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Dockets ManagementBranch(HFA-305)Food and Drug Administration5630 FishersLanem. 1061RockvilleMD 20852USA 21St un

Dear Sirs

I am writing in response o the notice publishedMonday 2 1”’May 2001 regardingDevelopmentProgram or D rugs, Biological Productsand Devices for the treatmAnkylosing Spondylitis (AS) and related disorders Dodket No: OlN-0197).

Specifically, I write in terms of my role of Medical Director of the National AnkySpondylitis Society n Britain, ConsultantRheumatologistat the national referral Royal National Hospital for RheumaticDiseases, nd memberof the internationaspondylitis assessment roup .

In conjunction with the National Ankylosing Spondylitis Society of GreatBritain,the Royal National Hospital for RheumaticDiseases ome5,800 patients with ankspondylitis. Over the last 15 years, since left StanfordUniversity, California, I up a research eam focusing on this condition as per the enclosedcurriculum vitaethe last ten years one of de main focuseshas been hat of ankylosing spondylitis oresearch,and response o treatment.

We have published a seriesof studies,defining the important outcomedomains.Specifically, in eachcasewe have validated outcome nstruments,many of whichtranslated nto numerous anguages. Virtually every study now carried out in anspondylitis, world-wide, uses these utcomemeasurements, oth in terms of therastudies e.g non-steroidalanti-inflammatory drugs, use of biologics) and genetic srelating to the definition of susceptibility and severity gene oci. The self-adminiinstrumentshave been ranslated nto many anguages nd re-validated n their ow



In eachcase hese ndices have beenexplored and re-exploredand as n timated nof numerousoutcomesstudies.

In conjunction with the ankylosing spondylitis assessment roup, we have used hinstruments o assesshe relative contribution of the index as a whole, or sub-com

the index, and have further used hese nstruments n defining both clinicalIy impchanges nd he definition of partial remission and other relevant ssues.

In terms of the key factors raised n your notice, I would tentatively comment as

SCOPE

In large part, ankylosing spondylitis can be studiedas a whole, allowing for indwith ankylosing spondylitis having uvenile onset,psoriatic disease;nflammat

diseaseand other components. I believe we have somethingof a consensushatterm “ankylosing spondylitis” is appropriate. On our own database f 5,800pa40% have ritis while 14% have psoriatic spondylitis and 7 or 8% have n flammadisease i.e. enteropathicspondylitis associatedwith Crohn’s Diseaseor ulcerativIn large part our studieshave ncluded all sub -groups nd we believe hat this is tadvantage, ather han subsetting-at he outset.

CLAIMS

BASRI - the Bath Ankylosing Spondylitis Radiology Index - very simply definradiological statuswith four radiographs .e. pelvis anteroposterior iew to includsacroiliac oints, lumbar spine ateral and anteroposterior ilm, and a single laterafilm. As per the enclosedC.V and papersyou will see hat the BASRI index prowith a two-year follow up revealing sensitivity to change. Of course,over a showe would anticipate mprovement n terms of me trology, function, disease ctivitstatus,but not radiology.

MEASURES OF DISEASE ACTIVITY

I believe we have a global consensushat BASDAI is a simple, straightforwardavalidated nstrument hat, developed n conjunction with patients,physiotherapischnicians, addresses ll aspectsof disease ctivity (pleaseseepublication enclos

TRIAL DESIGN



outcome nstruments,although&e appreciate hat in terms of radiological changover two or more years, different weighting would be required n terms of struct

Naturally, our patients (the 5,800 ndividuals on our database) re anxious o takfurther evolution of this important approach o defining outcome.

I look forward to have further discussionswith you, and would be anxious o pla

Consultant Rheuma tologist.

Encs

PS: The BAS indices have beenpublishedextensively as outcomevariables or ankylosing spondylitis with:

1) Non-steroidal anti-inflammatory drugs

2) Cox-specific anti-inflammatory d rugs

3) Pam&one, Thalidomide etc

4) c1TNFlother biologics



1’ I ?.

Dear MS W alling_,.

., Re: FDA - Docket No: OlN-0197 - Clinical Development Program for Drug

Products and Devices for the treatment of A&dosing Spondylitis (AS) andDisorders

I should be most grateful for any additional nformation regarding his issue. I

written comments or the Dockets ManagementBranch, but would appreciateainformation that you believe should be incorporated o support his submission

.s,.,.:,...,“.: Yours sincerely,

z ,.:,., ,:. . Andrei Calin, MD, FRCP

. . Consultant Rheumatologist...

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CURRICULUM VITAE

ANDREI CALIN MD FRCP

lst May 2001



.‘NAME

DATE OF BlkTH ._

PLACE OF BIRTH

MARITAL STATUS

IMMEDIATE.PAST.

PRESENT POST

January 7 1944

Andover, England

Married (August 1,973,Jane Weller MB BCh)Three daughters, Tara (born 9.7.79), Sasha ‘an5.1.83).

Associate Professor of Medicine, Division Stanford University S chool of Medicine, Stanford,

Chief, Rheumatology Section, Medical ServiceVeterans Administration Hospital, Palo Alto, C1983.

Consultant RheumatologistRoyal National Hospital for Rheumatic Diseases,

EDUCATION

1957-61

1962-65

1965 Qualified BA (Cantab) Class 2:2

1965-68 Guy’s Hospital Medical School, London Unstudies)

1968

1970

1976

1978

1978

1986

Honorary Senior Lecturer

School of Postgratuate Medicine, University of Ba

Epsom College Medical Foundation

Clare College, Cambridge University (pre-clinkal

Qualified MA, MB, BChir (Cantab), LRCP, MRCS

,MRCP (UK)

Diplomate: American Board of Internal Medicine

MD (Cantab)

Subspeciality Boards: Rheumatofogy

FRCP (UK)



. . . A . , ,

PRIZES, SCHOLARSHIPS AND AWARDS

Epsom College Leaving Award

/ ,-’

’ 1965

1966

1967 Guy’s Hospital Medical School Travelling Scholarship

I995

Clare College Scholarsh[p

Scott Polar Travel Award (Atlas Mountains, Morocco)

Medical Research Council Travel Award; Wenner-Gren Research Award

Grant from the Royal Society of London

(The above three for medico-anthropological investigation and rAinu Tribe, North Japan.)

Cambridge University Travel Scholarship

Clare College Travel Scholarship (Tropical Medicine, Chagas’ D

Guy’s Hospital Medical School Scholarship

First Prize Cardiology Clinical Examination

Lawrence Atwell Travelling Award to Massachusetts General HMassachusetts, USA to ‘study Neu rology (Professors RaymoPierre Dreyfus) and Immunological Aspects of Lymphoma

Aisenberg)

Fulbright-Hays Travel Scholarship; Guy’s Hospital Travel Grant

Arthritis and Rheumatism Council for Research (Boots) Award

Back Pain Association Ltd Award: (For year at Stanford Universi

Margaret Holroyd Prize, British Society of Rheum atology

SOCIETIES: HONORARY AND SCHOLASTIC

1. American Rheumatism Association



6. Diplomate, Rheumatology Board, 19777. Fellow of the Royal College of Physicians (United Kingdom)

8. Chairman, National Ankylosing Spondylitis Society (United Kingdom)

9: International Society for Rheumatic Therapy

COMiWEES AND EDITORIAL BOARDS

1. American Rheumatism Association:, Programme Subcommittee

American Rheumatism Associafion: Reiter’s Syndrome CriteriaSubcommittee

5.

6.

7.

8.

9.

10.

11.

12.

’ 13.

14.

15.

Editor, Comprehensive Therapy, Rheumatology Section

Co-Editor, Annals of Rheumatic Disease, 38 (Supp l)

Editorial Board, Clinical Rheumatology, Belgium

Editorial Board, Advances in Rheumatology, New York

Editorial Board, European Journal of Internal Medicine

Treasurer, International Society for Rheum atic Therapy

Medical and Scientific Committee (Heberden), British Society forRheumatology

Consultant,,Steering Committee, RAD-A-R (Risk Assessment ofDrugs -Analysis and Response)

Chairman, Division of Rheumatology, Royal National Hospital forRheumatic Diseases, Bath

Past Chairman, Therapeutic & Ethical Committee, StanfordUniversity Medical School

Past member. Ethics Committee, Royal United Hospital

Editorial Board, Rheumatology in Practice

Editorial Board, Stand J Rheumatol

198

197

-19

198

198

198

198

198

198

198

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199



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19686 months

Guy’s Hospital, LondonHouse Physician to Dr Charles Baker (cardiologist) an(Dean of the Medical School)House Surgeon to Mr Sam Wass (gastro-intestinal chief)(Only one resident is invited to stay on to complete a full at Guy’s)

1969-706 months

/

Guy’s Hospital, LondonSenior ‘House Physician to Professor W J Butterfield and(general internal medicine)

19703 months

19706 months

’ Ship’s SurgeonCaribbean Line

Royal Post-Graduate Teaching ,Hospital (Hammersmith),Senior House Physician to Department of Medicine (Pro

and Dr C Pallis; Neurology)

19713 months

19716 months

Middlesex Teaching Hospital, LondonRegistrar in general internal medicine

Brompton Hospital for Diseases of the Chest, LondonHouse Physician to Professor J Scadding (ProfessoLondon University)

1971-721 year

Guy’s Hospital, LondonRegistrar (clinical, research and teaching post) to (general internal medicine), Dr R Grahame (physician inConnective Tissue Disorders, Rheumatology and AlliedDr M Abrams (general medicine). First year in clinica

immunology

1972-742 years

Guy’s Hospital, LondonFirst two years of a four year rotating Senior Regist

Grahame and D r H Burty in the Division of Connective TRheumatology and Allied Diseases (clinical, teaching anThird year of rheumatology/immunology at Royal SSenior Registrar to Dr C Quinn and B Latham

1974-75 USA

F--Y ‘.

\ I<,. Y

TRAINING AND EXPERIENCE

1968

3 months

St Bartholomew’s Hospital, London

Resident in thoracic surgery



1975-76

1 Ott 1976-Dee 1983

Dee 1983

Fifth year.‘.in clinical -‘rheumatology/immunology (as foinvolvement in Fellowship training programme, patient cresearch)esearch)

Assistant Professorof Medicine (immunology/rheumatolossistant Professorof Medicine (immunology/rheumatoloStanford University Medical Center and Chief, Rheumtanford University Medical Center and Chief, RheumMedic&Service, Veterans Administration Hospital, Palo Aedic&Service, Veterans Administration Hospital, Palo A

Associate Professor of Medicine (immunology/rheumatUniversity Medical Center and Chief, Rheumatology ; SService, Veterans Administration Hospital, Palo Alto, Calif



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Calin A. lberic influence on Moorish civitization. Scott Polar In

Cambridge University, 1050-60, 1963.

Calin A. The Ainu Tribe - medical and anthropological studies. Guy’s H12:5-l 0, 1965.

Calin A. Chagas’ Disease (Studied in Brazil). Guy’s Hospital Gazett1965.

Calin A. Immunological factors in Hodgkin’s Disease. (Following e

Professor Aisenberg, Massachusetts General Hospital). Guy’s Ho14:651-655, 1967.

Calin A. Bronchorrhoea.’ BMJ 4:274-275, 1972.

PowellJackson, Calin A, et al. Excess deoxycorticosterone sadrenocortical carcinoma. BMJ 2:32-33,1974.

Calin A, Grahame R . Double blind cross-over trial of flurbiprofen and phe

ankylosing spondylitis. BMJ 4:496-499, 1974.

Grahame R, Calin A, et al. Ankylosing rheumatoid arthritis. Brit J Rheu14:24-30, 1975.

Calin A. Renal glomerular function in ankylosing spondylitis. Stand4:241-242, 1975.

Calin A. Raised serum creatinine phosphokinase activity in ankylosing spRheum Dis 34:244-248,1975.

Calin A, Fries JF. Striking prevalence of ankylosing spondylitis in W27 and Fem ales: A Controlled Study. New Engl J Med 293:835-839, 1975.

Calin A, Fries JF. An ‘experimental’ epidemic of Reiter’s Syndrome revMed 84:564-566, 1976.

Calin A, Porta J, Fries JF, et al. The clinical history as a screening tesspondylitis. JAMA 237:2613-2614, 1977.

Calin A, Bennett PH, Jupiter J, et al. HLA B27 and sacroiliitis in Passociation in males only. J Rheumatol4:44-48, 1977.

Calin A, Bennett RM, Sukhupunyaraksa S, et al. Double-blind multi-cenof ketoprofen and ibuprofen in the treatment of rheumatoid arthritis.



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Hirshman HP, Schurman DJ, Calin A. Neutropenia and rheumatoid Med 129:235-236, 1978.Calin A. ‘. MD Thesis: The relative contribution of the environment an

pathogenesis of HLA B27 related rtieumatological disorders. Camb1978.

Rosenthal AR, Egbert PR, Calin A, et al. Association of HLA spondylitis and uveitis. International Congress Series N. 450 Ophthalmologicum, Kyoto, 1978, Ed K Shimizu - Co-Ed JA OosteMedica, Amsterdam - Oxford, Elsevier North-Holland, 940843.

Calin A, McShane D, Powers R. Objective measurements in evaluatin

ankylosing spondylitis. Current Therapeutic Research 24:838- 842, t97

Calin A. Ankylosing spondylitis sine sacroiliitis. Arthritis Rheum 22:303

Fox R, Calin A, Gerber J, Gibson D. The chronicity of symptoms Reiter’s Syndrome: an analysis of 131 consecutive patients. Ann Int M1979.

Calin A. Keratodermia blennorrhagica and mucocutaneous manifesta

Syndrome. Ann Rheum Dis 38 S:68-72,1979.

Calin A, Fox R, Gerber RC, Gibson DJ. The prognosis and natural hSyndrome. Ann Rheum Dis 38 S:29-31,1979.

Calin A. The management of Reiter’s Syndrome. Ann Rheum Dis 38 S

Wilkens RF, Arnett FC, Bitter T, Calin A, et al. Reiter’s Syndromproposed criteria. Ann Rheum Dis 38 S:8-11, 1979.

Kaslow RA, Ryder RW, Calin A. Search for Reiter’s Syndrome followinShigella sonnei dysentery. J Rheumatol6:562-566, 1979.

Gottlieb M, Hoppe RT, Cafin A, et al. Arthritis in a patient with myccomplete remission after radio-therapy. Arthritis Rheum 22:424-425, 19

Calin A, Britton MD. Sulindac in ankylosing spondylitis: double-b lind 6-parallel evaluation of sulindac and indomethacin in the managemen

spondylitis. JAMA 242:1885-l 886, 1979.

Gottlieb M, Calin A. Discordance for psoriatic arthropa thy in monArthritis Rheum 22:805-806, 1979.

Calin A. The relationship between genetics and environment in the



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Calin A, Kaye B, Sternberg M, et ai. The prevalence andnature of industrial complex: a questionnaire, radiographic and HLA analysis. S1980.

Calin A. HLA B27: To type or not to type? Ann lnt Med 92:208-211, 198

Calin A. Reiter’s Syndrome: epidemiology and immunogenetics. Stan32:178-l 83, 1980.

-Calin A. Reiter’s Syndrom e and reactive arthropathy: sex distribuRheumatol32:42-44, 1980.

Goodwin DA, Heckman JR, Fajardo LF, Calin A, et al. Kinetics and miglabelled human lymphocytes. Proceedings of International Symposium oImaging ih Medical Radionuclide Imaging 1:487-497, 1986.

Rosenbaum JT, Theofilopoulos A, McDevitt HO, Perreira A, CarsonPresence of circulating immune complexes in Reiter’s Syndrome aspondylitis. Clin lmmun and lmmun Path 18:291-297, 1981.

Strober S, Kotzin BL, Hoppe RT, Slavin S, Gottlieb M, Calin A, et al. T

intractable rheumato id arthritis with lymphoid irradiation. Int J Radiat O7: --7, 1981.

Kaslow R, Simon D, Calin ,A, et al. Reiter’s Disease following epidemicRheumatol8:969-973, 1981.

Calin A, Marks S. The case against seronegative rheumatoid arthrit70:992-994 1981.

Willkens RF, Arnett FC, Bitter T, Calin A, et al. Reiter’s Syndromepreliminary criteria for definite disease. Arthritis Rheum 24:844-849, 198

Kotzin 8, Strober S, Engleman E, Calin A, et al. Treatment of intractaarthritis with total lymphoid irradiation. New ‘Engl J Med 305:969-976, 19

Tucker CR, Fowles RE, Calin A, et al. Aortitis in ankylosing spondy litis:of aortic root abnorma lities with two-dimensional echocardiography. 9:680-686, -I982.

Lisse JR, Bennett PH, Knowler WO, Gofton JP, Calin A, Mann DLsacroiljitis in HLA B27 positive Pima Indian men. Arthritis Rheum 25:236

Calin A, Calin HJ. Oligoarthropa thy with chronic iridocyclitis - a dchildhood? J Rheumatol 9:i 05-l 06, 1982.

^ .-



49. Marks SH, Calin A. ‘A”“case-control study of juvenile- and adult-ospondylitis. J Rheumatol 9:739-741, 1982.

:50. Willkens RF, Arnett FC,’ Bitter T, Calin A, et al. ,Reifer’s Syndrom‘proposed criteria. Bul! Rheum Dis 32:31-42, 1982.

-“.,i :*_

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Hollingswotth PN, Cheah PS, Dawkins RL, Owen. ET, Calin A, Wood Pvariation in grading sacroiliac radiographs in HLA-B27 positive individual10:247-254, 1983. .,

Marks SH, Barnett M, Calin A. Ankylosing spondylitis in women andcontrol study. J Rheumatol 10:624-628, 1983.

53: Burns T, Calin A. The hand radiograph as a diagnostic discrimseropositive and seronegative ‘rheumatoid arthritis’: a controlled study. 42:605-612, 1983.

54. Calin A. In common clinical usage, nonsteroidal anti-inflammatoryidrgproduce adverse effects on the kidney. Am J K idney Dis 2:485-488, 198

55. Engleman EG, Calin A, Grumet FC. Analysis of HLA B27 antigen w

antibodies. J Rheumatol special issue 10:59-61, 1983.

56. Calin A. Spondylathropathy in Caucasians and non-Caucasians. J Rhissue 10:-l6-l 9, 1983.

57. Bobrove AM, Calin A. Efficacy and tolerance of a novel precision-dosindomethacin: double-blind trials in rheumatoid arthrkis and osteoarMedical Research and Opinion 8:55-61, 1983.

58. Calin A, Marder A, Becks E, Burns TM. ‘Genetic differences betweepatients with ankylosing spondylitis and B27 positive healthy controls. 26:1460-i 464, -I983.

59. Field EH, Strober S, Hoppe R, Calin A, et al Sustained improvemenrheumatoid arthritis after total lymphoid irradiation. Arthritis Rheum 26:93

60. Calin A. Clinical use of tolmetin sodium in ankylos ing spondylitis: aPharmacol23:301-308,1983.

61.

62.

Calin A. Reiter’s Syndrome. In Hospital Medicine November 1983, p. 73

Calin A, Marder A, Marks S, Burns T. Familial aggregation of Reiter’sankylosing spondylitis: a comparative study. J Rheumatol 11:672-677, 1



69.

72.

G&met FC, Calin A, Engleman EG, Fish L, Foung SKH. Studies.of monoclonal antibodies: ethnic and disease associated.variants. Advanc

9:41-53. In: ,The Spondylathropathies, ed. M Ziff and SB Cohen. RaYork, 1985.

Strober S, Tanay A, Field E, Hoppe RT, Calin A, Engleman EG, KotziKaplan HS. Efficacy of total lymphoid’irradiation in intractable rheumatoIntern Med i 02:441-449, 1985.

Lowthian PJ, Calin A. Geode development and m ultiple fractures in rheuAnn Rheum Dis 44: 130-33, 1985.

Calin A. Patterns of the Spondyloarthropathies. Advances.in lnflam ReThe Spondyloarthropathies. ed. M Ziff and SB Cohen. Raven Press, Ne

Calin A. When - and Why - to order x-ray films for RA patients. J Mu2(7):14-20, 1985.

Calin A. Osteoarthritis - more questions than answers. Geriatric M1985.

Calin A. A placebo-controlled cross-over study of azathioprine in ReAnn Rheum Dis 45: 653-655, 1986.

Calin A. Treatment of ankylosing spondylitis with oxaprozin: A cindomethacin. Seminars Arthritis Rheum (suppl). 15:95-l 00, 1986.

Calin A. Drug Trials by Fleet Street. (Editorial). Brit J Hosp Med. 35(6):

Calin A. NSAIDs, Misinformation and the Media. (Editorial). MIMSept;T6, 1986.

Calin A. Bowe l flora in ankylosing spondy litis. (Editorial). Lancet. ii, 125

Calin A. Focus on physician - patient communication. Am J Med. 80(6A

Calin A. The epidemiology of rheumatoid disease: past and present. D4:-i-6, 1986.

Calin A. Do NSAlDs need built-in protection? MIMS Magazine. Dee 11

De Souza Meirelles E, Calin A. Sindrome de Reiter nos Sexos MascuUrn Estudo de Caso Controle. Rev Hosp Clin Fat Med S Paulo 43; 3: 1



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Calin A. Assessing disease activity in ankylosing spondylitis. ‘(Ed!:1072,1987.

Elswood J, Calin A, Berg C, Rogers F. Ankylosing spondylitis: comparSwedish (n = 780) and British (n = 1500) experience - the natispondylitis societies. Stand J Rheum 16:437-440, t 987.

Calin A. Diagnostic criteria (new and old) for the spondy larthropath ies. exp Rheum. 5(2):101-?02,1987.

Calin A. Pathogenesis of ankylosing spondylitis: the state of the art. B(supp II): 106-709,1988.

Reilly PA, ,Elswood J, Calin A. Therapeutic intervention in rheumatoidcontrolled comparison of seronegative and seropositive disease.27:-i 02-l 05, 1988.

Calin A, Cawley MID; Pal B, Rosenberg JN, Silas AM, Williams PI. Mublind comparison of sustained action formulations of tiaprofenic acid anin osteoarthrits. Drugs 35(S1):57-63, 1988.

Calin A, Elswood J. The relationship between pelvic, spinal and hipankylosing spondylitis - one disease process or several? Brit J Rhe1988.

Calin A. Seronegative (reactive) arthropathy. The precipitating factors. (ii, 200-201, 1988.

Calin A. The natural history and prognosis of ankylosing spondylitis. (EdRheumatol, 15: 1054-l 056, 1988.

Doube A, Calin A. Bacterial endocarditis presenting as acute monRheum Dis 47:598-599, 1988.

Calin A. Leadership role of the rheumatologist: toward reaching Gerontology 34(%):42&I, 1988.

Calin A. From Rome to Bath and back again. (Editorial) Ann ltal Med 1

Calin A. Royal National Hospital for Rheumatic Diseases, Bath - a 250t(Editorial)., J Rheumatol 151733-734,1988.

Calin A, Elswood J, Rigg S, Skevington SM. Ankylosing Spondylitisreview of 1,500 patients: the changing pattern of disease. J Rheumato1988.



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Carette S, Calin A, McCafferty JP, Wallin BA. The Auranofin Cooperarette S, Calin A, McCafferty JP, Wallin BA. The Auranofin Cooperdouble-blind placebo-controlled study of auranofin in patients with psouble-blind placebo-controlled study of auranofin in patients with ps

Arthritis Rheum 32:158-j 65, 1989.rthritis Rheum 32:158-j 65. 1989.Calin A, Elswood J. The ,outcome of 138 total hip replacements andalin A, Elswood J. The ,outcome of 138 total hip replacements andankylosing spondylitis: high success rate after a mean follow-up ofnkylosing spondy litis: high success rate after a mean follow-up ofRheumatol 16:955-958, 1989.heumatol 16:955-958, 1989.

Calin A, Elswood J. Relative role of genetic and environmental facexpression: s ib-pair analysis in ankylosing spondylitis. Arthritis’ Rheum 3

Calin A, Elswood J, Klouda P. Destructive arthritis, rheumatoid fa

susceptibility versus severity:- a case-contro l study. Arthritis Rheum1989.

Calin A, Elswood J. Retrospective case-control analysis of 376 irradiatankylosing spondylitis. J Rheumatol 16:1443-l 445, 1989.

Fries JF, Singh G, Bloch DA, Calin A. The natural history of ankylosingthe disease really changing? J Rheumatol 16:860-863, 1989.

Calin A. Is there an association between ankylosing spondylitis and mulAnn Rheum Dis 12:971-972, 1989. ’

Calin A. Topical NSAIDs: a gimmick or a godsend? (Editorial). La1989.

Calin A. Clinical aspects of the effect of NSAlDs on cartilage. 16:S18,43-44, 1989.

Will R, Palmer R, Bhalla, AK, Ring F, Calin A. Marked osteoporosis is ankylosing spondylitis and may be a primary pathological event. Lance1989.

Herrero-Beaumont G, Zarco P, Armas J, Calin A. El deficit de IgA es upronostico en la, evolution del sindrome de Reiter. Rev Esp Reuma1989. \

Magaro L, Miall E, Elswood J, Calin A. Retrospective analysis of metho

experience in 81 patients from a British rheumatology unit. Submitted, 19

Calin A, Elswood J. A prospective nationwide cross-sectional study oover two years in 1331 patients with ankylosing spondylitis. 17:801-803,199O.

O’Brien BJ, Elswood J, Calin A. Percep tion of prescription drug risk



116.

Herrero -Beaum ont G,.Armas: J, Elswood J, Will R, Calin A& Selective IgAspondylarthropathy: a distinct disease? Ann’ Rheum Dis 49:636-637,19Hererro-Beaumont G, Elswood J, Will R, Armas JB, Calin A. Postsalm

phenomena in 2 patients with ankylosing spondy litis: no modifioation odisease. J Rheumatol,,l7:250-257,199O.

Calin A. Juvenile and adult systemic-onse t Still’s disease. (Edi2:92,1990.

Will Rj Elswood J, Edmunds L, Calin A. Serum keratan sulphate: a maturnover in rheumatic ‘conditions?. Current Research in Osteoporosis anMeasurement. 6:41-42,1990.

Will R, Elswood J, Edmunds L, Calin A. Serum keratan sulphaterheumatoid arthritis patients but fall in ankylosing spondylitis patients normal individuals. Biochem Sot Trans 18:964-965, 1990.

Will R, Palmer R, Bhalla AK, Ring F! Calin A. Marked osteoporosis is ankylosing spondylitis and progresses in late disease. CurrenOsteoporosis and Bone, Mineral Measurement. 9:74-751990. _ I

Will R, Elswood J, Calin A, Edmunds L. Is there sexual inequalityspondylitis? A study of 498 women and 1202 men. J Rheumatol 17, t 64

O’Brien B, Elswood J, Calin A. Willingness to accept risk in the treatmedisease. J Epid’ Comm Health 44:249-52, 1990.

Prowse M, Madd ison P’J, Calin A. Ankylosing spondy litis followed by reactive arthritis: an unusual or unique phenomenon? Brit J Rheum (In p

Calin A. Why do patients with, a chronic rheumatic disease sometim(Editorial). In “Scritti in onore di Ugo Carcass? (written in honour ofUniversita Degli Studi di Cogliari Page 58-60, 1991.

Calin A, Elswood J, Edmunds L. Late onset ankylosing spondylitis - disBrit‘J Rheum 30:69-70, 1991.

Edmunds L, Elswood J, Kennedy LG, Calin A. Primary ankylosing sponand enteropathic spondylarthropathy: a controlled analysis. J Rheum 18

Edmunds L, Calin A. New light on uveitis in ankylosing spondylitis.18:50-2, 1991.

Calin A. Gold therapy in rheumatoid arthritis. Lancet (Editorial). 338:19-



141.

Herrero-Beaum ont G, Gon&% $&abrero J, &ii& J, Gonzalez J, Zarc

~Egido J, Calin A. Disturbances of IgA immune response in patientsspondylitis. In Press 1991.

Tooke A, Stevenson FK, Calin A. Release of cell surface MHC Classynovial fluid: Correlation with disease type and-severity. Submitted 19

Will R, Calin A, Kirwan J. Increasing age at presentation with a&y/losAnn Rheum Dis 52:340-42;1992.

Calin A. Diagnostic precoce des spondylarthritides. La letter du 179:3-5; 1992.

Bernstein RM, Calin A, Calin HJ, Oilier S. A comparison of the efficacyof lornoxicam and indomethacin in ankylosing spondylitis. EuropRheumatology and Inflammation. Vol12 (3):6;1992.

Kennedy LG, Edmunds L,Calin A. Does ankylosing spondylitis prospective 2-year study. J’ Rheum atol20:688-92,1993.

Calin A, Kennedy LG, Edmunds L, Will R. Familial versus spor

spondylitis: two different diseases ?. Arthritis Rheum. 36:676-681 I 993.

O’Neill T, Simpson J, Smith SJ, Lovell C, Calin A. Case Report: Potarda associated with methotrexate therapy. Brit J Rheum 32:411-412,-l

Calin A, Edmunds L, Kennedy LG. Fatigue in ankylosing spondylitis - wJ Rheumatol. 20:99I-9951993.

Kennedy LG, Will R, Calin A. Sex ratio in spondylarthropathies and it

phenotypic expression, mode of inheritance and age at onset. 20: 1900-l 904; 1993.

Jones S, Calin A. The monitoring of patients on disease-modifyingdrugs. Brit J Rheum 32:87;1993.

Calin A. H’lA-B27, the atthritogenic peptide and the effector T cell. (E342:629, I 993.

Burney RO, Pile KD, Gibson K, Calin A, Kennedy LG, Sinnott Wordsworth BP. Analysis of the MHC Class II encoded components of antigen processing pathway in ankylosing spondylitis. Ann Rheum Dis 5

Calin A. Can we define the outcome of ankylosing spondylitis anphysiotherapy management? (Editorial) J Rheumato121 I 86-188:1994.



144. :, Caljn A, ,Garrett SL, W hrteloc%HC;Kennedy ‘LG;‘d’Rea’ J, .Ma!!orie PA,, . ‘:y,“;,: <, ‘S >.: \FQ, ;<:

A new approach to defining fun@ional abilityjn ankydsing ‘spondylitis: th

$of #he Bath ~Ank$sing Spondylitis. Fui%tionai”lndex~ BASFI):‘i::LI,Rheu

5;1994:’ :,

145. Garrett ,.SL;~~Jenl$~sonR, Whitelock,‘~~,;;~~~~y.:LG,,.~~~~sford’ P, CW” ..fapproach ‘to+ defiriing disease status’.in / ankylosing spondyliti$,‘!i;.The -Spondylitis Disease Activity Index (BASDAf)$g Rheumatol21~~2286~91

146. Kabasakal Y, Garrett SL, Calin A. The epidemiology of spondylodiscitspondylitis - a control!ed study. Bdt J Rheum. 35;660-663, 1996.

147. Dougados M, van der Linden S, Amor B, Calin A et al. Sulphasalazine of spondylarthropathy: a randomized, multicentre, double-blind, plastudy. Arthritis Rheum. 1995; 38: 618-627;

I

148. Kennedy LG, Jenkinson TR, fviallorie PA, Whitelock HC, Garrett Ankylosing spondylitis (AS): the correlation between a new metrolradiology. Brit,J Rheum 1995;34:767-770.

149. Koh WH, G arrett SL, Calin A. Cervical spine surgery in ankylosing sp

outcome good? Clinical Rheumatology, 16;5:466-470. 1997.

150. Jones SD, Koh WH, Steiner A, Garrett’SL, Calin A. Fatigue in ankylosinprevalence and relationship to disease activity, sleep and other factors23: 3; 487490.1996

151. Calin A, Garrett SL, Whitelock HC, Kennedy LG , O’Hea J, Mallorie PA,A new approach to-defining functional ability in arrkrylosingspondylitis:, >of the Bath ~AnkylosingSpondylitis Functional ‘Index (BASFI). ‘,.J Rheu

5;i 994.

152. Calin A. The Dunlop-Dottridge Lecture. Ankylosing spondylitis: Definingand the relationship between radiology, metrology, disease activityoutcome. J Rheumatol. 1995; 22: 740-744.

153. Calin A. The Margaret Holroyd Essay (BSR). The individual with ankylosspondylitis: de fining disease status and the impact of the illness. Brit. J. R34:7;663-672.1995.

154. Brown MA, Pile KD, Kennedy LG, Calin A, Darke C, Bell J, WordswortF. HLA Class I associations of Ankylosing Spondy litis in the white pUnited Kingdom. Ann Rheum Dis 55: 268-270. 1996.

155. Gomez KS, Raza K, Jones SD,. Kennedy LG, Calin A. Juvenile onset a



158.

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spondylitis: Relationship between o&x&ion and disease activity. J Rh24;5:908-911 ,I 997 .

Will R, Magaro L, Kennedy G, Elswood J, Calin A. Peripheral joint involvankylosing spondylitis - Pattern and correlation with spinal disease and areactant levels. Submitted to J Rheumatol 1997.

Brown M . . . .Ca lin A. Susceptibility to ankylosing spondylitis in twingenes, HLA and the environment. Arthritis and Rheumatism 40; October 1997.

Calin A. Editorial - HLA-B27, rheumatoid factor and spondyloarthritis. C

Exp Rheum 15:3;229-231, 1997.

van der Heijde D , Bellamy N, Calin A, Dougados M, Khan A, van der LindPreliminary core sets for endpoints in ankylosing spondylitis. J.Rheumato2225-2229,1997.

Brown MA, Kennedy LG.....,..CalinA, Wordsworth BP. The effect of HLAon susceptibility to and severity of ankylosing spondylitis. Arth & Rheu465,1998.

Brown MA, Piie KD........Calin A, Wordsworth P. A genome-wide screen susceptibility loci in ankylosing spondylitis. Arth & Rheum 41; 4: pp 588-

Brown MA , Calin A, Wordsworth BP. The role ofgermline po lymorphisms in the T-cell receptor in susceptibility to ankylosispondylitis. Brit J Rheum 37; pp 454-458,1998 .

Band D, Jones SD . . . . . Calin A. Which Patients with Ankylosing Spo

Most Benefit from an Inpatient Managem ent Program? J Rheumat2384: 1997.

Mackay K, Mack CS, Brophy S, Calin A. The Bath,Ankylosing SpondylitiIndex (BASRI): A New Validated Approach to Disease Assessment. Art12: 2263-2270 , December 1998.

Dougados M, G ueguen A . . . .Calin A. Ankylosing Spondylitis: What Duration of a Clinical Study? A one-year versus a six-week NSAID trial.

38:235-244, 1999.

Calin A. Editorial - Survival, alcohol and deaths in ankylbsing spoRheum. 37;6:pp600-601, 1998.

Calin A, Nakache J-P, Gueguen Al Zeidler H, Mielants H, ,Dougados



”L--ii :G8,;.

/,.

,171 Taylor AL, Balakrishnan C and Calin A. Reference Gentile charts fdisease activity, functional impairment, and metrology in ankylosing spoRheum 41; 6: 1119-1125,1998.

172. Taylor AL, Balakrishnan C and Cafin A. Defining disease severity

spondylitis. Submitted 1998.

173. van der Heijde D, Calin A, Dougados M et al. ‘Selection o f specific instrudomain in core set for DC-ART, SMARD, physical therapy and clinical rin ankylosing spondylitis. Progress report of the ASAS working group26;951-4, 1999.

174. Brown M . . . . . Calin A . . . .Wordsworth P. Polymorph isms of the CYP2D6susceptibility to ankylosing spondylitis. Human Molecular Genetics V1563-l 566,200O.

175 Santos H, Brophy S, Calin A. Exercise in Ankylosing Spondylitis: How MOptimum? J Rheumatol25: 11; 2156-2160; 1998.

176.

177.

178.

179.

180

181

182

183.

Catin A . . . . . . .Dougados M. Outcome variables in Ankylosing Spondylitistheir relevance and discriminant capacity. J Rheumatol26: 975-9; 1999.

Calin A . . ,, .~. ..Brophy S. A new dimension to outcome: Application of theAnkylosing Spondylitis Radiology Index. J Rheumatol26: 988-92; 1999.

Mackay K, Brophy S, Mack C, Cal@ A. The development and validation radiograph ic grading system for the’ hip in ankylosing spondylitjs: the Ba thSpondylitis,Hip Index (B&RI-h) - J Rheumatol 27 (i2)$2866-72. “Dece

Caiin A, Brophy S, Blake DR. Impact of sex on inheritance.of ankylosing

cohort study. Lancet Vol354, pp 1687-1690, November 1999.

Brown M . . . . .Calin A. Recurrence risk modelling of genetic susceptibilitankylosing spondylitis. Ann Rheum Dis 59 (11): 883-6,200O.

Mackay K, Gillen D, Taylor G, Brophy S, Calin A. Is Chest expansion a vmeasure in ankylosing spondylitis? Submitted 2000.

Will R, Kennedy G, Elswood J, Edmunds L, Wachjudi R, Evison G & Cali

Ankylosing spondylitis and the shoulder: Commonly involved but infrequeJ Rheumatol2000 27: 177-I 82.

Berthelot J-M, Saraux A, Calin A. The problematic nosology of atypical replies of 20 international experts to a survey of paper cases from 10 realclinic patients. 2000. In preparation .



186. Hamersma J.. . . . . .Calin A and Brown MA. Is Disease Severity in AnkySpondylitis genetically determined? Arthritis & Rheumatism In Press Au

187. Hoyle E, Lava1SH, Calin A$Wordsworth BP, Brown MA. The X-chromosusceptibility to ankylosing spondylitis. Arth & Rheum Vol43, No 6, pp

June 2000.

188. Lava1SH.. . . . Calin A, Wordsworth BP, Brown MA.- Whole genome screankylosing spondylitis -evidence of non-MHC genetic susceptibility loci.Genet 68 (4): 918-26, 2001.

189 Berthelot J-M.. . .Caiin A. . . .Saraux A. Lessons from an international sur

cases from ten real early arthritis clinic patients. Submitted J Rheumatol.

190. Calin, A. Defining outcome in ankylosing spondylitis: where have we beewe and where do we go from here? Submitted to Joint Bone Spine, RevRhumatisme; International Edition. Elsevier. December 2000.

191. Dougados M, .Behan J-M, Jolchine I, Cal@ A,van er Heijde D, Olivieri I, ZHerman H. Efficacy of Celecoxib, a Cyclooxygenase 2Specific Inhibitor

treatment of ankylosing spondylitis.Arth & Rheum 44,1; pp 180-185, J

REVIEW ARTICLES

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7.

Calin A, Fries JF. The single hot joint. Comp Therapy, 2:4-l 0, 1976:

Calin A, Fries JF. Polyarthralgia and polyarthritis. Comp Therapy 2:l l-1

Fries JF, Calin A. Ankylosing’spondylitis: genetics versus environment. 2: 17-22, 1976.

/

Calin A. Immunologic aspects of aging. Geriatrics 32:54-55 , 1977.

Calin A. The management of rheumatoid arthritis. American Family 89-94, 1978.

Calin A. Ankylosing spondylitis and the other seronegative spondylarthTherapy 5:41-47, 1979.

Calin A. Back pain: mechanical or inflammatory? American Fa20:97-l 00, 1979.



‘.

16.

Caiin A, Marks SH,. Management of ankylosing sbondylitis. Bull Rheu1981.

Calin A. Epidemiology of the rheumatic diseases, with a focus onTherapeutic Research 3O(S):i 5-23, 1981.

Calin A. The patient problem: the elusive triad. Hospital Practice 16:32

Calin A. Modern aspirin substitutes (non-steroidal;an ti-inflammatory dDrug Therapy 16:i -4,1982.

Calin A. Identifying nephrotic.syndrome. Hospital Medicine May:1 06-1.

Calin A. ‘Diagnosis, course and management of Reiter’s SyndromEducation June:40-48, 1982.

Calin A. Commonly encountered prob lems in the diagnosis of giant polymyalgia rheumatica. Geriatric Medicine Today 1(2):46-54, 1982.

Caiin A. Reiter’s Syndrome - 1982 . Clinical Rheumatology 1 I O-l 4, 198

Calin A. Classification of seronegative arthritis: recent developments. Ssuppl52;58, 1984.

Calin A. Clinical and pharmacological considerations in the use of ninflammatory d rugs in the elderly patient. Geriatric Medicine 3:77-84, 19Calin A. Gold: making better use of a valuable RA therapy. J M1:53-58, 1984.

Calin A. The relevance of the HLA system in the management of rheu

In: Novel technology for the management of rheumatoid, arthritis. ProInternational Symposium, Tokyo, 1983. Ed Y Shiokawa. Excerpta Medi

Calin A. When are corticosteroids worth the risk for PA patients? J M-I(13): 48-53, 1984.

Calin A. X-radiation in the management of rheumatoid disease. B33(5):261-265, 1985.

Calin A. When. are X-rays really needed for rheumatology disease? Med. Nov:l t-1 5, 1985.

Calin A. Because, many aspects of degenerative change remain a research needs to be done on the pathogenesis of the disease. Ger15(6):8, 1985.



36.

calin A . ~~~~~~~ ~ 6s~~~an ~“ritiSi inii! Fii~de oi di’ugs and advice. Ge

~29-31, 1985.

Calin A. How to characterize and manage ankylosing spondylitis.. J M3(3):14-24, 1986.

Calin A. How to characterize and manage Reiter’s syndrome and reaMusculoskel Med 3(4):21-27, 1986.

Calin A. Degenerative Joint Disease. American Family Physician. 33,i

Calin A. Is it polymya lgia rheumatica or giant cell arteritis? J Mu

8:28-31, 1986.

Calin A. Nephrotic syndrome. Hospital Medicine Oct:53-57, 1986.

Calin A. Reactive Arthropathy. In: Reactive Arthritis extra-articulaire veDequeker J. Pubfication Uitgeverij, Leeven. ~9-21, 1986.

Calin A. The spondylarthropathies - clinical aspects. Clin Exp Rheu1987.

Calin A. From wiliow bark to nonsteroidals. MIMS Magazine 1st Se1987.

Calin A. NSAlDs in practice - variations in action. MIMS Magazine 1st29, 1987.

Calin A. The GP’s top 50 - Voltarol. MIMS Magazine 15th September: 6

Calin A. The GP’s top 50 - Naprosyn. MIMS ‘Magazine 1st January: 43-

Calin A. Piroxicam. Brit J Clin Practice 42: 161-l 64, 1988.

Calin A. Indocid. MIMS Magazine. 15th March: 117:118, 1988.

Calin A. Low back pain. Medicine Digest.’ April; 28-32, 1988.

Calin A. Low back pain. Spectrum International 29 (2): 17-20, 1988.

Calin A. The history of the seronegative spondylarth ropathies. Brit J R1988.

Calin A. Osteoporosis. Brit J Rheum. 28: 165-166, 1989.45.

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60.

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63.

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65.

66,

Calin A. HLA 827 and peripheral arthritis. Rheumatology Now. 4: 35, 1

Calin A. Seronegative arthritis. Medicine International. In press 1990.

‘Calin A. Overview of NSAID safety. ,Proceedings Supplement (JA

Satellite. November 1989.

Calin A. Controversies+ NSAID usage. M IMS Magazine. In press 198.

Calin A. Differentiating rheumatoid arthritis from other arthropathieOpinion in Rheumatology 2: 446-449, 1990.

Calin A. Seronegative spondylarthritides. Medicine International 3073-3

Calin A. Auranofine et Rhumatisme Psoriasique. La lettredu rhumatol

1990.

Calin A. What criteria should be used to select drugs for second-line Magazine;; 1st October: 29-30, 1990.

Calin A. Non-steroidal anti-inflammatory drugs - some idiosyncratiIbuprofen - where next. Royal Society of Medicine Services Round Tab

30, 1990.

Calin A. Tackling disease of ,the oints. Doctor p39-45,5th April 1990.

Calin A. The drugs available for second-line therapy. Prescriber 12: 25-Calin A. Rheumatoid arthritis. GP 37-38, 12th October.! 990.

Calin A. Auranofin and psoriatic arthropathy. Rev Rheum. Paris. In pre

Calin A. The diagnosis and management of osteoarthritis. Doctor In pre

Calin A. Methotrexate finds its place in rheumatology - second look. 1B(8): 45-46, 15th April 1991.

Calin A. Safety and side-effects profiie of etodolac in European studMusculoskeletal Medicine 8 (4): S34-39, April 1991.

Calin A. Gold therapy in rheumatoid arthritis. Lancet 338:19-20, 1991.

Calin A. Current concepts of spondyloarthritis. In: Bone. Ed IT Boyle eIn press 1991.

, , _ . , . . ~ . , . - - . . I . _ “ . , . _ I __ ._, ,. _. ._: .,v _.._ *L . . h&,.” ,,._ ..j.. ., _ . .._. ,. .,._ _ .- .- ..

PI

\



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.d’

Calin A. Whom do patientS’ blame wnen a drug causes a side eViewpoint. (Journal of the Primary Care Rheumatology Society) p4, July

Calin A. When should a second line drug be added to a- non-management of rheumatic disease? MIMS Magazine.. In press 1991.

Calin A. Focus on methy lprednisolone (Depo-Medrone) in hospital Pharmaceutical Practice (Supplement). pi 6-I 8, January 1992.

Calin A. How G.P.s can treat polymyalgia (Editorial). MIMS Magaz ineFebruary 1992.

Calin A. What is the treatment of choice in OA and RA? MIMS MagazinFebruary 1992.

Calin A. Should you inject more joints? MIMS Magazine 19(1):7, 1st Ja

Calin A. Efficacy of topical NSAIDS. MfMS Magazine 19(l): 44, 15th Ja

Calin A. How x-ray films enhance the cfinicaf picture in RA. Journal of Medicine. g(5): 99-107, May 1992.

Calin A. What Clinical problems can G.P.‘s expect to see following infections? MIMS Magazine 19(28): 4850,29th September 1992.

Calin A. The spondylarthropathies. Proceed ings of the E.ULAR CongreElsevier Science Pub lishers, North Holland. In press 1992.Calin A. When to (and not to) use x-ray films in rheumatological diseaMusculoskeletal Medicine 9(10): 88-95, October 1992.

Calin A. Who and when to refer to a rheumatologist. Practice UpJanuary 1993.

Calin A. Safety profile of a sustained-release formation of etodolac rheumatoid arthritis and osteoarthritis. Advances in Therapy (The Internof Drug, Device and Diagnostic Research). 1O(1): I-8, Jan/Feb 1993.

Calin A. Refractory Reiter’s Syndrome. Rheumatology Review 2(2): 77-

Calin A. Rheumatological referrals - who? when? to whom? Rheumatol1 I), Winter 1993. i

Calin A. The pharmacology of the long-term suppressive drugs rheumatoid arthritis. Precriber. In press 1993.



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Calin A. Ostoeporosis: increasing grounds for optimism. Rheumatol(4): 22-23, Autumn 1994.

Calin A. ‘Local steroid injections in general practice. Prescriber ~67-73,

Calin A. Ankylosing spondylitis and its management. Rheu,matologyWinter 1994.

Calin A. Performance stresses. Rheumatology in Practice. 2(l): 201995.

Calin A. Ankylosing spondylitis: Defining disease status and the relatradiology, metrology, disease activity, ‘function and outcome. (The DuLecture) J Rheumatol. 1995: 22; 740-744..

Calin A. Managing hyperuricemia and gout:’ Challenges, and pitfaMusculoskeletal Medicine 12(2): 42-46; Feb 1995.

Calin A. From rats to Renoir:- Review of EULAR 1995. Rheumatology2:4; 1O-l 1. Sept/Oct 1995.

Caiin A.. Evolution, course and prognosis in spondylarthritis. Rev Esp R230-240, 1995.

Calin A. Calin’s Corner: Heart Surgery and the Rheumatologist. In RhePractice, Vol 3, No 2. Summer 1996.

Calin A. Calin’s Corner: “Please speak clearly” - communication in medRheumatology in Practice, Vol3, No 3. Autumn 1996.

Calin A. Pain: a geriatric/rheumatological perspective. Therapy ExpreAdvances in Therapy. No 106. December 1996.

Calin A. Keeping control of NSAID side-effects. Musculoskeletal MedicVol4, No 1. ~~13-15. January 1997.

Calin A. Non-steroidal anti-inflammatory drugs (NSAIDS) in OsteoarthriPrescriber April 1997

Calin A. Calin’s Corner. “Putting a face to the name” In Rheumatology Practice, Vol4, No t, p 23. Spring 1997.

Calin A. NSAlDs feedback. Prescriber Vol8, Issue 11,5th June 1997.



Calin A. Therapeutics: use of oral iijSAlDSs in Osteoarthritis. In RheumPractice Vol4, No 3, Autumn 1997.

Calin A. Cali,n’s Corner. “Profess ionally, it was the worse week of my lifeRheumatology inpractice, Winter 1997.

Calin A. ,Managemen t of early OA. Geriatric Medicine 27; IO: pp 4-5, O

Calin A. “Injections for Back Pain” in General Practitioner In Press 199

Ca1in.A. Interview-with an Expert. In General Practitioner In Press 1998

Calin A. Ankylosing Spondylitis. Medicine 26:6; 36-39. 1998.

Calin A. The ep idemiology of ankylosing spondylitis and reactive arthriReumatologia Supp Vol36, Warsaw ;1998.

Calin A. Is it time to stop the . . . . . Cinical Case Conference. Update 9”1998pp 314-316.

Calin A. Spondylatthritis in the year 2000. Pp55-56, Proceedings of the

of the Chinese Society of Immunology, Taiwan, and The Rheumatology ROC. 1999.

Calin A. Ankylosing Spondylitis. Update 7 September 2000, pp 236-239

Calin A. Spondylarthritis Update 2000. VII National Congress of RheumMamaia, Romania, 13-l 6 September 2000.

Calin A. What is the evidence that glucosamine helps with arthritis? Pu

number 48. December 2”” 2000.



5.

6.

7.

8.

9.

IO.

11.

12.

13.

Calin A. Reiter’s Syndrome. Medical.Cfinics of North America 61:3653

Calin A. Medicine. Scientific American Section 153, 7, 8, 11, 198

updates. -:-‘,” a^*-:

The SpondylarthropathiesAcute Rheumatic Fever

4d)

Infectious ArthritisThe Vasculitides

e> Fibrositis Syndrome

Calin A. Genetics and Environment in the HLA-related RheumaticTopical Reviews in Rheumatic Disorders. Ed AGS Hill. J Wright an

11O-132, 1980.

Calin A. Synovitis. In: Rheumatology. Ed JF Fries. Syntex Publication

Calin A. Enthesopathy/Spondylitis. In: Rheumatology. Ed JF Publications, 1980.

Calin A. Ankylosing Spondylitis. In: Prognosis: Contemporary OutcomEds JF Fries, GE Ehrlich. The Charles Press Publishers, Bowie, Ma1981.

Calin A. Ankylosing Spondylitis. In: Textbook of Rheumatology. EdHarris, S Ruddy, CG Sledge. WB Saunders, Philadelphia, 1017-1032, 1

Calin A. Reiter’s Syndrome. In: Textbook of Rheumatology. Eds WN S Ruddy, CG Sledge. WB Saunders, Philadelphia, 1033-l 046, 1981.

Calin A. Gerontologic Aspects of Rheumatology. In: Textbook of GeEbaugh. Addison-Wesley Publishing Company, Menlo Park, California,

Calin A. The Spondylarthritides. In: Introduction to Rheumatic D

Panush. John Wiley and Sons, New York, 197-216,198l.

Calin A. Ankylosing Spondylitis: Handbook,for Patients. Published throFoundation, American Rheumatism Association, Atlanta, Georgia, 1983

Calin A. Psoriatic Arthropathy: Handbook for Patients. Published throFoundation, American Rheumatism Association, Atlanta, Georgia, 1983

Calin A. Ankylosing Spondylitis. In: Primer of Rheumatic DisRodnan,SthEdition, Arthritis Foundation, Atlanta, 85-88, 1983.



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Calin A. Ankylosing Spondyl& In: &irent Therapy in Allergy and ImmM Lichtenstin, A S Fauci. Decker Inc, Ontario, 11 -1 16, 1983.

Calin A, The relevance of the HLA system in the management of rheuNovel Technology for the Management of Rheumatoid Arthritis (ProInternational Symposium, Tokyo). September 1983. Ed. Y ShiokMedica, Japan.

Calin A. Reiter’s Syndrome. In: Current Diagnosis. Ed RB Conn. Philadelphia, 1302-l 303, 1984.

Calin A. Reiter’s Syndrome. In: Spondylarthropathies. Ed A Calin. GruNew York, 119-l 50, 1984.

Burns T, Calin A. Undifferentiated Spondylarthropathy. In: SpondylarthCalin. Grune and Stratton, New York, 253-264, 1984.

Calin A. Spondylarthropathies: an overview. In: SpondylarthropathieGrune and Stratton, New York, l-8, 1984.

Calin A. Reiter’s Disease. In: Current Therapy in Internal Medicine (1

TM Bayless, MC Brain, RM Cherniack. BC Decker Inc, Philadelphia, 46-

Calin A. Ankylosing Spondylitis. In: Current Therapy in Internal MediciEds TM Bayless, M C Brain; RM Cherniack. BC Decker Inc, Philadelphia

Calin A. The Epidemiology of Ankylosing Spondylitis: ‘A Clinician’s PoEpidemiology of the Rheumatic Diseases. Ed RC Lawrence, LE ShulmaYork, 51-59, 1984.

Calin A. The Spondylarthropathies. In: Cecil Textbook of MedicWyngaarden, L S Smith, 1917 -I 922, Seventeenth edition, 1985.

Calin A. Ankylosing Spondylitis. In: Clinics in Rheumatic Diseases. EdSaunders, London. April 1985: 11 I), 41-60,1985.

Calin A. Ankylosing Spondylitis. In: Textbook of Rheumatology. SecoWN Kelly, ED Harris, S Ruddy, CG Sledge. WB Saunders, Philadel1985.

Calin A. Reiter’s Syndrome. In: Textbook of Rheumatology. Second EKelly, ED Harris, S Ruddy, CG Sledge. WB Saunders, Philadelphia, 100

Calin A. Ankylosing Spondylitis. In: Current Emergency Therapy. EdSpyker, BB Haury. Aspen Publication, Rockville, Maryland, 699-703, 19



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Calin A. The Spine in Ankylosing Sporidylitis and Related Conditions. Physical Medicine and Rehabilitation in Musculoskeletal Diseases. p 2Leek, M E Gershwin, W M Fowler. Grune.and Stratton, Orlando, Florida

Calin A. New Thoughts on Radiotherapy in the Management of ChroRecent Advances in Rheumatology, Vol 4:169-184. Eds J M H Moll anChurchill Livingstone, London. 1986.

Calin A. The Spondylarthropathies. In: Internal Medicine, Second EStein. Little Brown and Company, Boston, 1299-l 305, 1987.

Calin A. Splitting or lumping autoimmune diseases: a clinical pEurorheumatology. Ed’A Andrianakos et al, H Tagas, Athens. PI 34-l 3

Calin A. Gut inflalnmation and spine involvement in seronegative spondIn: Eurorheumatology. Ed A Adrianakos et al, H Tagas, Athens. P421-

Calin A. Enteric bacteriae causing Reiter’s syndrome - Spondylarthropathies: involvement of the gut. Eds H Mielants, EM VMedica, Amsterdam pp 87-92, 1987.

Calin A. Environmental factors causing tissue damage of the target or

AS with peripheral arthritis - possible mechanisms, In: Spondinvolvement of the gut. Eds H Mielants, EM Veys. Excerpta Medica,405-417, 1987.

Calin A. Ankylosing Spondylitis. In: Diagnosis and ManagemenDiseases. Ed WA Katz. JB Lippincott Philadelphia, pp 423432, 1988.

Calin A. Reactive Arthritis and Reiter’s Syndrome. In: Diagnosis and Rheumatic Diseases. Ed WA Katz. JB Lippincott, Philadelphia, pp 440-

Calin A. Ankylosing spondylitis. Chapter 108. In: Medicine for the Prac2nd Edition. Ed J W Hurst. Butterworths. ~183-186, 1988.

Calin A. The Spondylarthropathies. In: Cecil Textbook of MediWyngaarden, L S Smith, p 1917-I 922, Eighteenth edition ~2004 - 2009

Calin A. Ankylosing spondylitis and the spondylarthropathies. In: PrimDiseases. Ed R Schumacher. Professional Publications Arthritis Founpp 142-I 47, 1988.

Calin A. Reactive arthritis - treatment. In: Reactive Arthritis. Ed A aCRC Press Inc, Florida. pp 139-148, 1988.



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Calin A. Reiter’s Syndrome. In: Textbook of Rheumatology. Third EKelley, ED Harris, S Ruddy, CG Sledge. WB Saunders, Philadelphia, ~1

Calin A. Pathogenesis of ankylosing spondylitis. In: Spondylitis Ankbechterew. Ed. N Fellman and H. Spring. Verlag Hans Huber, Bern, p3

Calin A. Ankylosing spondylitis. In: Criteria for Diagnosis. Ed Butterworths, Boston. pp 57-59, 1989.

Calin A. Auranofin in the management of seronegative spondyloattAuranofin in’ Rheumatoid Arthritis. Eds MC Hochberg, Marcel DekkerPress 1989.

Sany J, Amor B, Calin A. Spondylarthropathies. Dossier des Euromedecine 90. pp 754-756, 7-I 1 November 1990.

Calin A. Ankylosing spondylitis and other inflammatory disorders ofPhysiotherapy: controlled trials and facts. Rheumatology. Ed P Schla

Basle. Vol 14:82-90; 1991.

Calin A. Ankylosing spondylitis . Chapter 6-3. In: Medicine for the prac

3rd Edition. Ed JW Hurst, Butterworths. Massachusetts 1991, pi 93-I 9

Calin A. The Spondylarthropathies. Chapter 6. Current Medicine Ill, RPhysicians. Ed. DH Lawson. Churchill Livingstone, Edinburgh. p79-95;

Calin A. Spondylarthritis, undifferentiated spondylarthritis and overlap. Oxford Textbook of Rheumatology. Eds P Maddison, DA Isenberg, P WOxford University Press. ~666-674, 1993.

Calin A. Ankylosing spondylitis. Chapter 5.53. Oxford Textbook ofEds P Maddison, DA lsenberg, P Woo, DN Glass. Oxford University P1993.

Calin A. The Spondylanhropathies, 1991. Elsevier Science PublishersCongress of Rheumatology. Budapest 1991. In Press 1991.

Calin A. The Spondylatthropathies. Chapter 259, In Cecil Textbook oJB Wyngaarden, LS Smith, JC Bennett. 19th Edition. W.B. Saunde

pi 515-I 520;1992.

Calin A. Recent progress and advances in rheumatism and arthritfs. Annual, the year book of General Practice 1992. Clinical Press Limited64-67.



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Calin. A. Spondylarthri%&i ‘!$ikj~&i Rheumatology. Eds A Ross, A

University Press. In Press 1993. , ,

Calin A. Ankylosing spondylitis., In: Handbook of current diagnosis andR Pounder and M Hamilton. Science Press Ltd., London, 1996.

Calin A. Evolution, course and prognosis in spondylarthritis. Rev. Esp

1995;22:230-240.

Calin A. Radiology and Spondylarthritis. Modern imaging Techniques.HA Bird and M Dougados. Bailliere Tindall, London. 1996. ~~455-476

Calin A. Terminology, introduction; diagnostic criteria, and oveSpondylarthritides, Eds. Calin A and Taurog J. Oxford University Press

Calin A. Reactive arthritis and Reiter’s syndrome - the clinical s

Spondylarthritides, Eds Calin A and Taurog J. Oxford University Press

Calin A. Ankylosing Spondylitis. A guide to the diagnosis, m

follow up of this painful and debilitation condition. Update 4 November 1

Calin A. Spondyloarthropathy, undifferentiated spondylarthritis, aChapter 55.1 Oxford Textbook of Rheumatology. Eds PJ Maddison,Woo, DN Glass. Oxford University Press 1998.

Calin A. Ankylosing Spondylitis. Chapter 5.5.3 Oxford

Rheumatology. Eds PJ Maddison, DA Isenberg, P Woo, DN Glass. OPress 1998.

ii., .’1’



BOOKS

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IO.

Calin A, Fries JF., Arikylosing Spondylitis: Discussions in Patient ManaExamination Publishing Company Inc, Garden City, New York, pp 1-I 1

Bitter T, Calin A, Hughes GRV, Editors. Symposium on Reiter’s

Rheum Dis 38:Suppl 1, 1979.

Calin A. Rheumatoid Arthritis. Addison-Wesley Publishing CompaCalifornia, pp l-266, 1983.

Calin A. Editor: Spondylarthropathies. Grune and Stratton, New York,

Calin A. Differential Diagnosis in Rheumatology: An Atlas for theLippincott Company, Philadelphia, pp f -220, 1984.

Calin A. Editor. Proceedings of a symposium. Factors affecting arth

Focus on physician-patient communication. Am J Med 80(6A)l-20,1986

Calin A. The National Ankylosing Spondylitis Society. A guide-book fBurleigh Press Ltd, Bristol.

Calin A, Cormack J. Arthritis and Rheumatism - your questions ansLivingstone, Edinburgh. 1996.

Calin A, Taurog J. Eds: The Spondylarthritides. Oxford Univ. Press. P



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Calin A. Extra-articular manifestations of rheumatoid arthritis. BMJ 359

Calin A, Grahame R, Tudor M, Kennedy L. Ankylosing rheum atoid artspondylitis and HL-A antigens. Lancet 1:874, 1974.

Grahame R, Calin A, Tudor M, et al. HLA as a diagnostic aid. Tel Avithe 12th Internal Congress of International Medicine 7974.

Grahame R, Calin A. Ankylosing rheumatoid, arthritis. Presented iAssociation of Rheumatology, June 1974.

Calin A. Nonsteroidal anti-inflammatory agents. New Engl J Med 292:1

Calin A. Drug treatment of rheumatoid arthritis. Lancet 2:38-39, 1975.

Calin A, Fries JF, Payne ‘R. HLA antigens and ankylosing spondylit1975.

Calin A, Fries JF. An extraord inarily high prevalence of ‘ankylosing spW27 positive males and females. A controlled study. Arthritis Rheum 1

Calin A, Fries JF Epidemic Reiter’s Syndrome. Genetics and enviroRheum 18:390-391, 1975.

Grahame R, Calin A. A controlled trial of Froben (flurbiprofen) in ankylocomparison with phenylbutazone. Stand J Rheumatol4:S8, 1975.

Calin A, Fries JF. Ankylosing spondylitis and Reiter’s Disease, thenvironment. Ann Rheum Dis 35:287, 1976.

Calin A, Bennett PLH, Jupiter J, et al. HLA B27 and sacroiliitis in Pima Rheum 19:791,1976.

Calin A, Bennett RM, Sukhupunyaraksa ‘S, et al. Double-blind multi-ceof ketoprofen and ibuprofen in the treatment of rheumatoid arthritis. 19:791, 1976.

Calin A, Fries JF, Schurman D et al. The close correlation between

disease expression in HLA B27 positive subjects. INSERM, HLA and D

Calin A, Fries JF, Stinson FB, et al. Normal frequency of HLAinsufficiency. INSERM, HLA and Disease 9:1976.



j .:.

, .:._ I 24.,- ‘T’/,’ :.:, \” 1 25.

26.

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28.

29. Calin A. Reiter’s Syndrome. Lancet 2:91 O-91 , 1979.

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Calin A , Porta, J, P.ayne R. HLA A28 in B27 positive controls a

ankylosing spondylitis. Arthritis Rheum 20:1428, 1977.

Britton M, Calin HJ, Calin A. Objective criteria in the assessmespondylitis, exemplified by a 6-month’ double-blind parallel trial indomethacin. Proceedings of XIV International Congress of Rheuma1977.

Bertken R, McShane D, Calin A. Objective criteria in assessmespondylitis, exemplified by a 3-month double-blind parallel trial oindomethacin. Proceedings of XIV International Congress of Rheum1977.

Bombardier C, Calin A, Rosen thal R, et al. Subsets of uveitis and assoin rheumatic diseases. Proceedings of XIV International Congress of R747,!977.

alin A. Ankylosing spondylitis and its early diagnosis. Lancet 2:1293,

Calin A. Allopurinol toxicity masquerading’as malignancy. JAMA 293:2

Calin A, Fox R, Gerber DJ, et al. The’natural history of Reiter’s SynRheum 21:548-549, 1978.

Calin A, Mitchell D. Kveim test status in ankylosing spondylitis. Abstrof Pan American Congress of Rheumatology 1978.

Calin A, Kaslow R, Simon D, et al, Reiter’s Syndrome and the seroShigella. Ann Rheum Dis 38:i 90, 1979.

Calin A, Fox R, Gerber R, et al. The chronicity of Reiter’s Syndrome.38:190-i 91, 1979.

Calin A. HLA DR4, rheumatoid factor and prognosis in rheumatoid 1:873-874, 1979.

Strober S, Hoppe J, Calin A, et.al. The treatment of rheumatoid arthlymphoid irradiation. Arthritis Rheum 22:632, 1979.

Simon D, Kaslow R, Calin A. Studies of Reiter’s Syndrome following epShigellosis. Arthritisem 22:659-660, 1979. I



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Calin A. Adverse reactions to D-penicillamine after gold toxicity. BMJ 2

Calin A, Barnett M. HLA 27 positive, negative or -,both? Ne

302: 1366-I 367, 1980.

Kaslow R, Calin A, Simon D, et al. Reiter’s Syndrome and reactive Salmonella Heidelberg gastroenteritis. Arthritis Rheum 23:702, 1980.

Calin A. Book Review: HLA and Disease: A Comprehensive ReviewBraun. Ann Int Med 92:885, 1980.

Marks S, Calin A. Inappropriate reliance on B27 and other tests in thpatients with spondylarthropathy: a comparative study. Arthritis Rheum

Calin A, Marks S. Reactive arthritis. BMJ 2:31 -312, 1980.

Rosenbaum JT, Theofilopoulos ‘A, McDevitt HO, Perreira A, CarsoPresence of circulating immune complexes in Reiter’s Syndrome spondy litis. Clin Res 28:41A, 1980.

Calin A. Ankylosing spondylitis and Reiter’s Syndrome: sequelaeQuestions and Answers JAMA 243:68,1980.

Calin A, Fries JF. On the reassessment of the prevalence of ankyloamong B27 positive individuals. J Rheumatol7:577, 1980.

Willkens R; Calin A, et al. Reiter’s Syndrome (RS) - suggested cridisease. Arthritis Rheum 24:844, 1981.

Marks S, Barnett M, Calin A. The natural history of juvenile ankylosincase-controlled study of juvenile- and adult-onset disease. Arthritis 1981.

Marks S, Barnett M, Calin A. Ankylosing spondylitis in women ancontrolled study. Arthritis Rheum 24:S119,1981.

Calin A, Marder A, Barnett M, Marks S. Evidence for a B27-susceptibility gene in spondylarthropathy. Arthritis Rheum 24:S109, 198

Calin A, Barnett M;Marder A, Marks S. The nature and prevalence oamong relatives of probands with ankylosing spondylitis and ReiteArthritis Rheum 24:S78,1981.

Lisse JR, Kuberski lT, Gofton JP, Calin A, Bennett PH, Mann DL





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75. Calin A. Gold therapy for asthma? ‘Clinical consultation’. J Resp Dis No

76.

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79. Calin A. On the prevalence of ankylosing spondylitis. J Rheumatol. 13 :2

80. Campion G, Jarner D, Calin A. The differential effect of rest and exercisearthritis (RA) and ankylosing spondylitis (AS). Brit J Rheum 25:123-124 ,

81.

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Burns TM, Rolleson TJ, Calin A. * Radiographic: subsets of juve‘rheumatoid’ seropositive (+) and seronegative (-) polyarthritis: a coanalysis. Arthritis Rheum 26:S25, 1983.

Lowthian P,*Woolf AD, Downes J, Gofton JP, Calin A. Seronegative rhe(RA): a distinct radiological entity. A controlled study versus seropositivRheum Dis 43: 117-I 18, 1984.

Calin A, Calin HJ, Field E, Tanay A, Strober S, Hoppe R, Kaplan Hcontrolled study of total lymphoid irradiation (TLI) in rheumatoid arthRheum Dis 43: 121-I 22, 1984.

Calin A. Intestinal perforation association with osmotic slow releasecapsules. ‘BMJ 288:240, 1984.

Calin A. Polymyalgia rheumatica. Q uestions and answers. JAMA 252(2

Calin A. A Review of ‘Progress in !Rheumatology Ed I Machtey, Wrigpages. In: Int Rehab Med 6(3):111, 1984.

Calin A. Prevalence of ankylosing spondylitis: Comment on Van derArthritis Rheum 27:1438, 1984.

Calin A. Diagnostic criteria for ankylosing spondylitis: Comment on Varticle. Arthritis Rheum 28:357-358, 1985.

Calin A. Lymphocyte proliferative responses to bacterial antigens in srthropathies (Letter to Editor). Brit J Rheum 2:227, 1985.

Campion G, Cumber P, Jamer D, Calin A. Creatinine phosphokinaankylosing spondy litis (AS): an indicator of ‘spondylitic myopathy’. 25(S2):97, 1986.

Cunningham T, Lowthian P, Calin A. Predilection for severe elbow “seronegative rheumatoid arthritis”? A distinct disease. Brit J Rheum 25(

Calin A. Reactive arthritis and overlap with septic arthritis. Brit J Rheu



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Calin A. The concept of seronegative rheumatoid arthritis. Brit J Rheu1986. ‘.

Nemeth R, Elswood J, Smith F, Calin A. Ankytosing spondylitis (AS) -the measurement of severity and outcome: the ankyiosing spondylquestionnaire (ASAQ). Brit J Rheum 26(S1):69, 1987.

Calin A, Elswood J. Ankylosing spondylitis (AS) - a nationwide analyticvariables determining surgical intervention and outcome,. Brit J Rheum 2

Calin A, Elswood J. Ankylosing spondylitis (AS): a review of 149 total hi(THR) in 86 patients. Brit J.Rheum 26(51):71, 1987.

Evison G,,Reilly PA, Gray J, Calin A.’ Comparison of erect and supinethe hip. Brit J Rheum. 26:393-94, 1987.

Calin A. Ulcerogenicity of piroxicam: an analysis of spontaneously repMed J. 294:i289-90, 1987.

Calin A. The prevalence of ankylosing spondylitis. J Rheumatol 14:175,

Carette S , Calin A. Evaluation of Auranofin in psoriatic arthritis: a doublcontrolled trial. Arthritis Rheum. 30:25, 1987.

Calin A, Elswood J. The natu ral history of juvenile onset ankylosingcontrolled study. Brit J Rheum. 26(52):114; 1987.

Calin A, Elswood J. The relationship between pelvic, spinal and hip ankylosing spondylitis - one disease process or several? Brit J Rheu1987.

Calin A, Elswood J. Genetic versus environmental factors influencing onof ankylosing spondylitis (AS) in 42 sib pairs concordan t for disease. 26(S2):105, 1987.

Calin A, Elswood J. HLA status of “seronegative rheumatoid arthritis” arheumatoid disease - matched for,disease severity. Brit J Rheum. 26(S2)

Calin A, Cawley MID, Pal 8, Rosenberg JN, Silas AM, Williams PI.

sustained release preparations of Tiaprofenic Acid and lndomethacin in Clin exp Rheum. 5(S2):215, 1987.Calin A. How Should I Treat This Patient’s Gout? MIMS Magazine Answers, 15th January:90, 1988.

Calin A, Elswood J. Sexual inequality in ankylosing spondylitis.



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Calin A. Ot/.:the Prevalence of Ankylosing Spondylitis. J Rheumatol 15:

Calin A, Elswood J. FamilW.versus sporadic ankylosing spondy litis - complementation: a controlled Study. l&it J Rheum 27(S2):9, 1988.

Calin A, Elswodd J. ,Parqnts tind children, concordant for ankylosingdiscordant for disease severity. ‘Brit J Rheum 27(S2):10, 1988.

Magaro L, Miall E, Elswood J, Calin A. Analysis of methotrexateouQom&: experience in 81. patients from a British rheumatology unit.28:25, 1989.

Will R, Elswood J, Calin A. The natural history of ankylosing spondylitis

study of pain and disability in men and women controlled for disease Rheum. 28(51):20, 1989.

Will- R, Palmer R, Ring F, Calin A. Ankylosing spondylitis (AS) is marked osteopenia of the lumbar spine and femoral neck in patients witand normal hips. Brit J Rheum. 28(51):19, 1989.

van der Linden S,,Amor B, Calin A et al. Preliminary criteria for the classpondylarthropathies. Arthritis Rheum 32:S47, 1989.

Will R, Elswood J, Calin A. Ankylosing spondylitis (AS) and the shouldejoint. Brit J Rheum 28(S2):100, 1989.

Will R, Magaro L, Elswood J, Calin A. Ankylosing spondylitis (AS) anreactants (APRs): a measure of peripheral joint inflammation - not axial Rheum 28(S2):11, 1989.

Calin A, Elswood J. Late onset ankylosing spondylitis (AS) - a distin

controlled study versus young& onset disease. Brit J Rheum 28(S2):12

Elswood J, Calin A. New light on uveitis in ankylosing spondylitis (AS28(52):12, 1989.

Dougados M, Amor B, Calin A et al. ,Preliminaty criteria for the classspondylarthropathies. Proceeditigs of XII International Congress of 1989.

Calin A. Reactive arthropathies with a focus on, environmental factors. XII International Congress of Rheumatology, 1989.

Calin A. Rheumatology. Eur J Int Med. 1:83-84,1989.

Calin A. The therapy of reactive arthropathy . Proceedings of IV



Calin A. True state of the art. &mm&it on van der Linden letter. Press, 1989.

Calin A, Elswood J, Will R. Rheumatoid arthritis: the prevalence and pa

(THR) and knee (TKR) replacements. Brit J Rheum 29(52):14,1990.

Will R, Elswood J, Herrero-Beaumont G, Calin A. Rheumatoid arpatients satisfied with their total hip (THR) and knee (TKR) replacements29(S2):88,1990.

Edmunds L, Calin A. Does ankylosing spondylitis (AS) burn outprospective controlled study. Brit J Rheum 29(S2):58,1990.

Will R, Evison G, Ring F, Calin A. Radiological and thermographic stdisease in ankylosing spondylitis. Brit J Rheum 2611990.

Armas J, Stevenson FK, Spellerberg MB, Calin A. Release of cell surfaantigen into synovial fluid: correlation ,with disease type and severity.29(Sl) p23,1990.

Will R, Evison G, Elvins D, Palmer R, Ring F, Calin A. Shou lder diseasspondylitis (AS): an assessment of disability, rad iology and thermography

29(S1):26,1990.

Will R, Elswood J, Edmunds L, Calin A. Serum keratan sulphate levelsrheumatoid arthritis (RA) but depressed in ankylosing spondylitis (AS) normal controls. Brit J Rheum 29(S1):29,1990.

Will R, Evison G, Edmunds, L, Elswood J, Calin A. Erosive seroncharacteristic radiological entity? B&J Rheum 29(S2):73,1990.

calin A. The Spondylarthropathies 1990. The clinical spectrum perspectives on therapy. Zeitschrift fur Rheumatologie 49(1):55,1990.

Will R, ‘Elswood J, Edmunds L, Calin A., Serum kera tan sulphaterheumatoid arthritis (RA) patients but fall in ankylosing spondylitiscompared with normal controls. Proc Bioch Sot Meeting, University of 1990.

Will R, Palmer R, Bhalla AK, Ring F, Calin A. Marked osteoporos is is

ankylosing spondylitis and progresses in late disease. ProceedConference on Osteoporosis and Bone Mineral Measurement. 25-27 Ju

Will R, Elswood J, Edmunds L, Calin A. Serum keratan sulphate: a maturnover in rheumatic conditions. Proceedings 2nd Bath Conference oand Bone Mineral Measurement. 25-27 June 1990.



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Calin A. Destructive aiithiitk.?; heumatoid factor, and HLA-DR4: suscseverity. Reply to comment by A Bartolucci. Arth and Rheum 33:1600,

Will R, Palmer R, Bhalla AK, R ing F, Calin A. Bone loss as well as bon

feature of progressive ankylosing spondylitis. .Brit J Rheum 29:498-499

Calin A. Rheumatology. Lancet 2:1056-l 057, 1990.

Will R, Elswood J, Calin A. A post world war II date of birth psubsequently developing ankylosing spondylitis is unexplained.17:1713-1714, 1990.

Calin A. NSAlDs in the 1990s. November 1990.

Kennedy LG, Will R, Calin A. Sex ratios in spondylarthropathies and itphenotypic expression, mode of inheritance and age at onset. Brit J Rh1991.

Palmer RG, Hayes G, Calin A, Daymond T, Pal B, Raman D, RosenbEfficacy of a new 600mg. od formulation of sustained-release tiaProceedings of Xllth European Congress of Rheumatology. Budapest,June - 6th July 1991.

Calin A. The Spondylatthropathies 1991. Proceedings of the VII EuropRheumatology. Budapest, Hungary. 30th June - 6th July 1991, p. 11.

Calin A. What do patients and rheumatologists regard as an ‘accepttreatment of rheumatic disease? (Letter) Brit J Rheum 30:318, 1991.

Calin A. Osteoporosis and ankylosing spondylitis. (Letter) Brit J Rhe1991.

Calin A. Book review “Pregnancy and the Rheumatic DRheumatologylBailiiere’s”. Lancet. In Press 1991.

Calin A. Spondylarthropathy and Children, 1991. Proceedings of SpRheumatology Symposium. Barcelona, 1991. In Press.

Will R, Calin, A. Delay between first symptoms and diagnosis in ankylo(Letter). J Rheum. 19:184-185, 1992,

Edmunds L, Elswood J, Kennedy LG, Calin A. Primary ankylosing sponand enteropathic spondylarthropathy: a controlled analysis.Rheumatology. Digest. 3:3;1992.

Calin A, Kennedy LG. The impact of social status on outcome and

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c ud



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Calin A. Controversy in the i&&N@-& (1992). In: Symposium - Tof arthritis; past, present and future. 7th APLAR Congress of RheIndonesia. 1992. Current Rheumatology. in Press.

Calin A, Will R, Kirwan J (Reply to letter) Age at presentation spondylitis. Ann .Rheum Dis 51 I 103, 1992.

Calin A, Hirst S, Garrett SL, Kennedy LG. A controlled prospective samong relatives’ of patients with HLA-related diseases: deviation fankylosing spondylitis. Brit J Rheum 32(S1):63;1993.

Bilgic A, Tutuncu ZN, Kennedy LG, Calin A. Interleukin-6, acute phaclinical status in ankylosing spondylitis. Brit J’ Rheum. 32(Sl):l65;1993.

Garrett SL, ,Kennedy LG, Calin A. Ankylosing spondylitisi disease onrelationship to childbearing status. Brit J Rheum 32(S1):66;1993.

Mallorie PA, Jenkinson TR, Whitelock HC, Kennedy LG, Calin A. mobility in ankylosing spondylitis (AS): a new metrology score. 32(S1):65;1993.

Jenkinson TR, Mallorie PA, Kennedy LG, Garrett SL, Calin A. Ankyl

(AS): The correlation between a new metrology score and radiolog32(S1):65;1993.

Kennedy LG, Jenkinson TR, Ma llorie PA, Garrett SL, Calin A. AnkyloThe relationship between self-assessment instruments, .metrology and Rheum. 32(S1):66;1993.

Calin A, Dougados M, Van der Linden S et al. (Australian SpondylaGroup). Double-b lind. multi-centre placebo (P) controlled study o

(SASP) in 351 patients with spondylarthropathy (SPA). Brit J Rheum 32

Garrett SL, Kennedy LG, Calin A. Patients’ perception of disease modinflammatory (rheumatoid atthritis/ankylosing spondylitis) andatthropathies. Brit J Rheum 32(S2):24;1993.

Garrett SL, Kennedy LG, Whitelock HC, Jenkinson TR, Gaisford PM,.OA new approach to defining disease status in ankylosing spondyAnkylosing Spondylitis Disease Activity Index (BASDAI). Brit J Rheum

Garrett SL, Kennedy LG, Calin A. Family history in ankylosing relationship between the sex of the index case and the numbers and relatives. Brit J Rheum 32(S2):23;1993.

Calin A, O’Hea J, Garrett SL, Gaisford PM, Whitelock HC, Jenkinson T



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Garrett SL, Kennedy LG, Calin A. The relationship between social/occand bad outcome (i.e. surgical intervention) in ankyiosing spondylitis33(S1):122,1994. :

Kabasakal Y, Garrett SL; Calin A. The epidemiology of spondylodiscispondylitis - a controlled study. Brit J Rheum 33(51):123, 1994.

Calin A, Edmunds L, Will R, Kennedy ,LG, Ford N. A prospectiveoutcome and disease kinetics in ankylosing spondylitis in terms ofmeasurement. Brit J Rheum 33(51):122, 1994.

Tutuncu ZN, Bilgic A. Kennedy LG, Calin A. Interleukin-6, acute phas

clinical status in ankylosing spondylitis. Ann Rheum Dis 53~425428, 19

Rudwaleit M, Pile KD, gurney R, Gibson K, Kennedy LG, Calin A, Worcell receptor germline polymorphism is not a major contributor to ankylo(AS) susceptibility. Brit J Rheum 33(S1):165, 1994.

Calin A. Why am I doing this? Rheumatology in Practice. Vol 1, No. 2, 1

Whitelock HC, Garrett SL, Mallorie PA, Calin A. Sexual relationships

spondylitis: the problem defined.~BritJ Rheum. 33(S2):28, 1994.\

Jones SD, Koh WH, Garrett SL, Calin A. Risks and determinants of uankylosing spondylitis (AS). Brit J Rheum 33(S2):28, 1994.

Calin A. Sex ratio in spondyloarthropathies. (Reply) J Rheum 21 :I 979,

Calin A. Nonstero idal antiinflammatory drugs and gastrointestinal toxicitthe article by Savage et al. Arthritis Rheum 37:1412, 1994.

Kennedy LG, Calin A. Sex ratios and age at onset in probands and secthe spondylarthropathies. J Rheumatol. 1995; 22: (4) 794-795.

Calin A. The presence of chronic wide spread pain in the generalRheumatol 1994;21: (3), 579-580.

Kennedy LG , Benlahrache S, Remita K, Calin A. Evidence for a posdifference between ethnic groups ? - a controlled study of British and Alg

Brit J Rheum 34(Sl): 143, 1995.

Jones SD, Steiner A, Garrett St, Calin A. The Bath Ankylosing SpondyGlobal Score (BAS-G). Brit J Rheum 34(Sl): 114,1995.



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Brown MA, Pile KD, Gibson K; Ken&& LG, Calin A et al. The HLA cgenetic contribution to ankylosing spondylitis. Bnt J Rheum 34(Sl): 76

Brown MA, Pile KD, Klinke J, Gibson K, Bunce M, Calin A et a

associations of ankylosing spondylitis. Brit J Rheum 34(Sl): 142, 1995i

Jones SD, Porter J, Garrett SL, Kennedy LG, Whitelock H, Calin A. scoring system for the Bath Ankylosing Spondyltis Metrology IndRheumatol. 22:8;1609.1995 -b

Koh WH, Dunphy J, Dixey J, Calin A, et al. Atypical antineutroantibodies (ANCA) in patients with ankylosing spondylitis. Brit J Rhe1995.

Calin A, Jones SD, Kennedy LG. Juvenile onset ankylosing spondyligirls than we thought? Brit J Rheum. 34:Abs supp 2;pp34,1995. ’

Jones SD, Garrett SL, Capper R, Canter RJ, Calin A. Ankylosing tonsillectomy, Brit J Rheum: 34:Abs supp2;pp35, 1995.

Koh WH, Garrett SL, Jones SD, Calin A. The relationship of fatiguspondylitis to disease activity, sleep and exercise. Brit J

supp2;pp36,1995.

Pande I, Mackay K, Chatfield K, Calin A. The Bath Ankylosing SpondyliRadiology Index (BASRI): a new validated approach to disease assessmBrit. J. Rheum.34:Abs supp2 ;pp37, 1995.

Calin A, Jones SD, Garrett SL, Kennedy LG.Index. (Letter) Brit J Rheum.34:793-794, 1995.

Bath Ankylosing Spondy

Jones SD, Calin A, Steiner A. An updat~e n the Bath AS Disease ActiviFunctional Indices (BASDAI & BASFI): Excellent Cronbach’s Alpha ScoreJ. Rheumatol. 23,407, 1996.

Koh WH, Pande I, Jones S, Samuels A, Calin A. A placebo-controlled sdose Amitriptyline in Ankylosing Spondylitis. B-J Rheum 35;abs supp 1

Haigh RC, Taylor AL, Calin A. An assessment of disease activity meaAnkylosing Spondylitis: their relationship with acute phase reactants.

abs supp I, p 153,1996.

Roussou E, Chowdhry KM, Kennedy LG, Calin A. Ankylos ing Spondy liDifferences. A comparative study between Pakistani and British patients35, abs supp I, p 149 1996. I

*

Cd’



193.

194.

195.

196.

19,7.

198.

199.

200.

201.

202.

203.

204.

205.

Calin A, Balakrishnan ^C,Tayior AL, Striking relationship between socstatus and outcome in Ankylosing Spondylitis (AS). Arthritis & RhS(supp); S256, Abs No:1373,1996.

Taylor AL, Balakrishnan C , Calin A. The development of reference cuand disability in ; Ankylosing Spondy litis (AS). Arthritis & R9(supp);S257, abs. no: 1374, 1996.

Kennedy LG, Gomez K, Taylor A, Calin A. Do childhood infections affedevelopment of Ankylosing Spondylitis ? Brit J Rheum 35, absno:39.1996.

Gomez K, Kennedy LG, Calin A. Does genetic anticipation occur

Spondylitis ? Brit J Rheum 35, abs supp 2, pp24, no:40, 1996.

Mack, CS, ‘Mackay K and Calin A. Radiology in Ankylosing Comparison of two Scoring Systems. Brit J Rheum 35, abs supp 2, ~23

Taylor AL, Balakrishnan CB and Calin A.Function in Ankylosing Spondylitis (AS).

Risk Factors for Worse DiseBrit J Rheum 35, abs supp

1996,and Arthritis & Rheumatism 39;9(supp);S257, abs. no:1375, 1996.

Mackay K, Mack CS, Pande l,.Roussou E, Calin A. The Bath AnkylosingRadiology Index (BASRI). Definition and correlation with functional, diseand metrology indices. Arth & Rheumatism Abs. supp. 39: 9;S206. Abs

Taylor AL, Balakrishnan CB and Calin A. Risk Factors for Worse D iseFunction k-r Arikylosing Spondylitis (AS). Atth & Rheumatism Abs. SAbs No: 1375. 1996.

Calin A, Balakrishnan CB and Taylor AL. Striking Relatio

Social/Occupational Status and Outcome in Ankylosing SpondylitisRheumatism Abs Supp. 39:9;S256, Abs No: 1373. 1996.

Kennedy LG, Calin A. “Does male:female sex ratio in AS change with reply: J Rheumatol 23:5;p948,1996.

Brown M, Bunce M, Calin A et al. HLA-B associations of HLA-B27 negatankylosing spondylitis: comment on the article by Yamaguchi et al. Ar1768-l 769, 1996.

Raza K, Kennedy LG, Calin A. Maternal age and risk of developing ankyspondylitis. Ann Rheum Dis 1997; 56 (3), p 209. ’

Versteeg J-P, Cleland L, Calin A et al. Polymorphism of human nramp in



207.

208.

209.

210.

211,

212.

213.

214.

215.

216.

217.

218.

Brown MA, Kennedy. LG, ‘Duncan EL et al. Twin study in ankylodemonstrating a significant non-HLA genetic susceptibility component. Abs Supp 1, pi 24.11997

Taylor AL, Balakrishnan C, Calin A. The development of a severity inspondylitis. Brit J Rheum 36 Abs Supp 1 pi 28.1997

Mackay K, Gillen D, Calin A. Chest expansion in ankylosing sponjRheum 36 Abs Supp 1 p130.1997

Bruges-Armas J, . Calin A. Ausencia de espondiloartropatias e dantigen0 HLA B27 em doentes corn pacemaker definitivo. RevistaCardiologia Vol 1G/suppl . April 1997.

Speden D, Taylor A, Calin A. The Prevalence of H.Pylori in AnkylosinJ Rheum Vol36, Abs Supp 2, p18,1997.

Roussou E, Petrou D, Calin A. Fatigue: An Overlooked Symptom in AnSpondylitis. Circadian variationof Fatigue compared to Pain and StiffneRheum Vol36, Abs Supp 2, p18,1997.

Brophy S, Mackay K, Mack C, Calin A. Ankylosing spondylitis: for a g

involvement who suffers more - men or women? Brit J Rheum Vol36Abs. Supp 2 pi 9,1997.

Band DA, Calin A. Complementary Therapies in Rheumatoid Arthritis, ASpondylitis and Fibromyalgia: Prevalence, Perceived Efficacy and CosVol36, Abs Supp 2, pi 9,1997.

Calin A, Zeidler H, Veys E et al.Piroxicam in ankylosing spondylitis.

Vol26; pp41, 1997.

Placebo-controlled comparison ofEULAR 1997.Rheumatology in Eu r

van der Heijde D, Bellamy N, Calin A et al. Preliminary core sets ankylosing spondylitis. Arthritis & Rheumatism Abs. Supp. Vol40; 9: S6

Calin A, Nakache JP, Gueguen A et al. Discriminant capacity of variabspondylitis (AS) between placebo and fast acting drugs. Arthritis &Rheumatism Abs Supp Vol40; 9: S63,1997.

Calin A, Nakache JP, Gueguen A et al. Defining disease activitspondylitis (AS): is a combination of variables (Bath AS Disease Activityan appropriate instrument? Arthritis & Rheumatism Abs Supp Vol40; 9:S63, 1997.

Bruges-Armas J, Cai$?~. .The ~prevalence of spondylarthritis .in



; .‘.

,:-j.; ,,,,,’ ,,:“. *, I 226.

227.

‘, . 228.

,:‘,. 232.

Caucasian community - ‘A population based study. Subm. to AC

November 1997.c

Masi AT . .Calin A. S/b-pair correlations of onset age (OA) and onset yof ankylosing spondylitis (AS): a reanalysis and reinterpretation of publisa..,*,,,Subm. to ACR Washington, November 1997.

Dougados M, Velicitat P, Veys E, .Zeidler H, Calin A. Meloxicam

spondylitis:, a 6 weeks doub le-blind comparison with placebo anProceedings-of ILAR 1997.

van der Heijde D, Bellamy N, Calin A, Dougados M, Khan A, van der Lin

Preliminary core sets for .endpoints in ankylosing spondylitis. AbstractWashington Nov 1997.

Dougados M Calin A. The preferential Cox-2 inhibitor Meloxicamspondylitis (AS): one year double -blind comparison with placebo and PiroProceedings of 3” APLAR Symposium, Manila, January 1998.

Roussou E,,Chowdhty KM, Calin A. “Ethnic Differences in Ankylosing Sp

Disease Expression in Pakistan Compared to Britain”, letter in reply: J Rh24:3;pp612-613, 1997.

Dougados M , Velicitat P.. ..,Calin A. Comparative assessment of Meloxiand Placebo in Ankylosing Spondylitis: Results of a l-year study. SuEULAR Symposium 1998.

Calin A. First symptoms of juvenile onset ankylosing spondylitis. Brit J Supp I, ~~37.1998.

Calin A, Brophy S. Ankylosing Spondylitis patients and the susceprelatives to the disease: Is sex the issue? Brit J Rheum 37 Abs Supp I, p

Brophy S, Calin A. Do Psoriatic, Enteropathic and lritis associated sfrom primary Ankylosing Spondylitis? Brit J Rheum 37 Abs Supp I, pp49

Band DA, Calin A. How .does a generic health status measure (SF-36disease-specific instruments ih relation to sensitivity to change inAnkylosing Spondylitis (AS)? Brit J Rheum 37 Abs Supp 1, pp 44. 1998

Calin A, Brophy S. The inheritance of ankylosing spondylitis (AS). Absto ACR, 1998

Calin A, Brophy S. Birth order in ankylosing spondylitis. Abstract sub . . _ . , . _ __ __ _. . _ ~.~~-.~~~~~~~~-~~~~~~-~~~~~~~.~~~~~-~~~

_ ., . _ . I ._ I . -_ “~. “ .. ._ . .^ . . .- I _.I ..- . j . .,” .._ -- .

1_,

235. Armas J, Laranjeira F, Riber% E . . . . &fin A. Clinical evaluation o



HLA B27 - ankylosing spondylitis (AS) patients f early onset of inflammin B27+ subjects. Abstract submitted to ACR, 1998.

236. Armas J, Laranjeira F, Ribeiro E.. . . . Calin A et al. HLA B*2703 and B2but not in patients with spondylarthritis from a Portuguese Caucasian pop

Abstact submitted to ACR 1998.

237. Calin A, Brophy S. Outcome of a cohort of patients with psoriatic spand interface with inflammatory bowel disease. J Rheumatol 25;

August 1998.

238. Calin A, Brophy S. The inheritance of ankylosing spondylitis - the.

Arthritis Rheum S287 presented ACR 1998.

239. Brown MA..... Calin A, Wordsworth BP. Polymorphisms of the CYP2D6

susceptibility to ankylosing spondylitis. Arthritis Rheum S355 presented

240. Calin A. “An anatomical explanati,on or good prognosis rheum atoid aresponse to D. McGonagle’s article. The Lancet - in press 1999

241. Calin A. ‘Yoga in treatment of carpal-tunnel syndrome” - letter in respo

W.Sequeira’s article. The Lancet, Vol353, ~~1185-6 April 3 1999

242. Brophy S, Doran M, Mackay K, Calin A. Ankylosing spondylitis (ASdisease. Is the rate of radiological progression equal? Abstract EULAR 1999

243. Sweeney S, Brophy S, Calin A. Outcome in Ankylosing spondylitis: An study. Abstract EULAR 1999. In press

244. Brophy S, Calin A. Birth order in Ankylosing’Spondylitis. Abstract EULA

In press.

245. Brophy S, Calin A. Ankylosing spondylitis (AS) and psoriasis: the resultor environment? Abstract EULAR 1999, in press.

246. Armas JB, Laranjeira F.. . . . & Calin A. The prevalence of spondylarthritisA Portuguese Caucasian community - a population based study. Abstract press.

247. Armas JB, Laranjeira F.. . . . & Calin A. Clinical evaluation of HLA B27+ aspondylarthritis patients: early onset of inflammatory back pain in B27+ subjectsEULAR 1999, n press.

248. Armas JB ., . . ..Calin A.. . .& Lopez-Larrea C. ‘Association of HL

250. Calin A . . . . . ..Gupta R. , The natural h&ry of total hip replacemen



spondylitis; 309 hips in 156 patients followed for a mean of 14 years. Arth &Suppl. Vol42, No. 9 Pp S402, ACR, Boston Nov 1999.

251. Sweeney S . . . . . .Calin A. Outcom e in ankylosing spondy litis (AS): routine care - an observational study. Arth & Rheum Abstract Suppl. Vol 42,ACR, Boston Nov 1999.

252 Brophy S, Calin A. The temporal relationship between onset ofinflammatory bowel disease (IBD), Iritis (I), and ankylosing spondylitis (AS)Abstract Suppl. Vol42, No. 9 Pp S371, ACR, Boston Nov 1999.

253. Brophy S . . . .-Cal@ A. Ankylosing spondylitis (AS): is rate of radiologlinear? Arth & Rheum Abstract Suppl. Vol42, No. 9 Pp S371, ACR, Boston Nov

254. Calin A, Brophy S. outcome in spondylarthntis: the impact of psoriasis (Pbowel disease (IBD) and iritis on ankylosing spondylitis (AS). ACR, Boston1999.

255.Speden D, Calin A, Bhalla A. Bone mineral density in ,women with anky

spondylitis. Arth & Rheum Abstract Suppl. Vol42, No. 9 PpS289, ACR, Boston

256.

257.

258.

259.

260.

261.

Hoyle E, Lava1 SH, Calin A . . et al. The X-chromosome and ankylosing spondylitis. Rheumatology 39, Abs Supp 1, No II 6, pp 6

2000.

Edwards S, Hoyle E, Campbell S, Lava1 SH, Calin A....et al.cytochrome P450 2D6 in ankylosing spondylitis - linkage, linkage disassociation studies. Rheumatology 39, Abs Supp 1, No 117 pp 65.2000.

Hamersma J, Cardon L, Brophy S, van der Horst-Bruinsma I, Calin A.. activity and functional impairment in ankylosing spondylitis are primdetermined. Rheumatology 39, Abs Supp 1, No 152, pp 84 BSR, Brigh

Brophy S, Calin A. Inheritance of phenotypic expression in AS: theRheumatology 39, Abs Supp 1 No 109, pp 61. BSR,,Brighton 2000.

Brophy S, Calin A. Flares in ankylosing spondylitis (AS). Rheumatolo1 No 106, pp 59. BSR, Brighton, 2000.

Sweeney S, Taylor G, Calin A. The effect of an exercise interventoutcome in ankylosing spondylitis - a randomised controlled trial. Rh

263. Doran M, Brophy S, Taylor G, &$ii A: Predictors of radiological



264.

265.

266.

267.

268.

269.

270

271.

272.

273.

274.

ankylosing spondylitis. Rheumatology 39 Abs Supp 1 No 112,Brighton 2000. _-

Dougados M,“Behrer J M, Jolchine I, Calin A, van der Heijde D, OliviHerman H. Efficacy of Celecoxib, a Cox-2 specific inhibitor in ankylosiplacebo and conventional NSAID (Ketoprofen) B-week controlled studRheumatism, in press September 2000.

Calin A, Brophy S, Blake D. Impact of Sex on Inheritance of ankylosiAuthors reply to letter: Lancet Vol355, pp 1098, March 25,200O.

Lava1 SH, Bradbury L, Darke C, Brophy S, Calin A, Brown M. The Rgenes in ankylosing spondylitis complicating inflammatory bow

Rheumatology Abs Supp 1, no 115, pp 64. BSR, Brighton, 2000.

Brown M, Lava1S, Brophy S, Calin A. Recurrence risk studies in ankylosupport oligogenic epistatic model of disease susceptibility. Rheumatol1, no 119, pp 66. BSR, Brighton 2000.

Lava1 S, Timms A, Bradbury L7 Edwards S, Rubin L, Siminovitch K, CWhole genome screening in ankylosing spondylitis confirms presenceMHC susceptibility loci on chromosomes ‘7, 10, 16 & 19. Rheumatolog

no 151, pp 83 BSR, Brighton 2000.

Hamersma J, Cardon L, Bradbury L, Brophy S, van der Horst-BruinsBrown M. Disease activity and functional impairment in ankylosing primarily genetically determined. Submitted ACR, Philadelphia, USA, 2

Calin A, Brophy S, Taylor G. Factors affecting phenotypic expression in aspondylitis. Arth & Rheum Abs Supp. 2000 Ann Scientific Mtg ACR, Vol4(Supp), Abs No 229, pp S105. Sept 2000.

Brophy S, Al-Saidi A, Calin A. Ankylosing Spondylitis - when does the Submitted to ACR, Philadelphia USA, 2000.

Brophy S, Calin A. Inheritance of phenotypic expression in ankylosing impact. of sex. Arth & Rheum Abs Supp 2000. Ann Scientific Mtg ACR(Supp), Abs No 1190, pp 5265. Sept 2000.

Sweeney S, Taylor G, Calin A. The effect of an exercise intervention

ankylosing spondylitis: a randomised controlled trial. Arth & Rheum AAnnua l Scientific Mtg, ACR, Vo l43;,No 9 (Supp), Abs No 222, pp Si 03.

Sweeney S, Taylor G, Calin A. Exploring outcome of primary (276) antotal hip replacements (THRS) .in ankylosing spondylitis (AS) over a mean



276.

277.

278

279

280.

281.

282.

283.

284.

28.5.

286.

287.

Doran M, Brophy S, -Taylor G, Calin A. Predictors of rad iologicaankylosing sponclylitis. Arth & Rheum Abs Supp 2000 Ann Scientific No 9 (Supp) ‘Abs no 1202, pp S267. Sept 2000.

Sweeney S, Taylor ,,G, Calin A. Disease specific versus generiankylosing spondylitis (AS). Submitted to ACR Philadelphia USA 200

Calin A. Outcome variables in ankylosing spondylitis. XX III Congress oBrazil. September 16-20 2000.

Calin A. Genetic susceptibility in ankylosing spondylitis.

Rheumatology, Brazil. September 16-20 2000.

XX

Calin A. Radiology in spondylarthritis. XXIIJ Congress of Rheum16-20 September 2000.

Edwards S.. . . . .Calin A. Cytochrome P450 2D6 and Ankylosing International Congress on Spondyloarthropathies, Gent, Belgium OttRheum Vol27, Supp 59, pp 26 August 2000.

Calin A. A long-term follow-up study on radiographic changes in ankylusing BASRI. 2”d nternational Congress on Spondyloarthropathies, G4-7,200O. J Rheum Vol27, Supp 59, pp 17. August 2000.

Timms AE . . . . ..Calin’ A, Brown MA. HLA Genes in ankylosing spondyby inflammatory bowel disease. 2”d International Congress on SpondGent, Belgium Ott 4-7, 2000. J Rheum Vol27, Supp 59, pp 27 Aug

Brophy S, Al-Saidi A, Calin A. Ankylosing Spondylitis (AS): When dstart? 2”’ International Congress on Spondyloarthropathies, Gent, Be2000. J Rheum Vol27, Supp 59, pp 48. August 2000.

Sweeney S, Gupta R, Taylor G, Calin,A. Outcome of 340 total hip replain ankylosing spondylitis (AS). 2”6 International Congress on SpondGent, Belgium Ott 4-7 2000. J Rheum Vo127, Supp 59, pp 43. Aug

Dougados M, Behier JM, Jolchine I, Calin A et al. Celecoxib, a Cox-2in ankylosing spondylitis (AS): a 6-week efficacy study. Arth & RheumAnnual Scientific Mtg ACR. Vol43; No 9 (Supp): Abs No 221, pp S103

Brown MA, Lava1 SH, Timms A, B radbury L, Edwards S, Rubin LA, Calin A, Wordsworth P. ‘Confirmation of non-MHC genetic loci bylinkage studies in ankylosing spondylitis. Arth & Rheum’Abs Supp 200Mtg ACR. Vol43; No 9 (Supp), Abs no 1971, pp S395. Sept 2000.



301. Hickey S, Trophy S, Pavy S and Gilin A$a 5 year prospective study.

Predicting outcome in ankyAbstract submitted to ACR, 2001



302.

302.

Pavy S, Marks-S and Calin A. Approaching the cdncept of minimum cdifference with the Bath Ankylosing Spondylitis Indices. Abstrabt submto ACR, 2001.

Pavy S, Brophy S, Hickey S and Caiin A.Ankylosing spondylitis?

Iritis: is it a predictor of longAbstract submitted to ACR, 2001.

_ -_ -. _ _ ..-. _-< . . _ --. .--- -L-.4----. -..” . -____ . .

;4 New Ap.proach to Defining Functional Ability in



Ankylosing Spondylitis: The Deve[opment of the

Bath Ankylosing Spondylitis Functional Index ... ANDREl CALIN, SARAH GARRETT. HELEN WHITELOCK, L. GAIL KENNEDY, JULIETTE

PATRICIA MALLORIE, and TIM JENKINSON

ABS7?ACT. Objecfivtz Afccr pain and stiffness, one of the rnos~ imponanr complaints of paticnrs wirh ankyl

ing spondytitis (AS) is disability. The main aims of tre;ltment are IOcontrol pain bur also to impfuncrion. Various merhods of assessing function cxisl but are either not specific for rhe disease

have not been adcquarcly validared. As a rcsul~ of rhis deficiency we dcvelopcd the Barb AnkyTosi

Spondyliris Func[ic,nal lndcx (BASFI) as a new approach10defininp and monitoring functional ab

in patients u-irh AS.

Methods. This self-asscssmcnf insrrurnenl was dcsigncd.by a team af mcdtc;d prol?ssionals in

junction with patients, and consists of 8 spccilic questions regarding funcGc)n in AS and 2 queslio

rctlec:ing rhc paricnl’s ahilily IO cope with cvcryday life. Each qucsiion is answered on a IO

horizontal visual an&g scatc. the mean of which gives $c BASFI score (0- 10). The yucsrionnair

was comptcrrd 257 Limes in tocat: once by I 16 oucpaticnrs and by 47 inpatients on 3 occasions o

a 3-week intensive physiochcrapy cour.sc. In addition. Ihc insrrumcnr was con1p3rcd with the Dou~do

funclionat ‘index.

Resukv. Parisnr scores covcrcd 95% of the BASFI range. giving a normal d islrihuiion of resu

In conrras[ only 6Zi%of the Dougados functional index scatc was used. Furrhcrmorc. over rh

week period of tnpaticnr rrcarn~cn~, the &SF1 rcvcalcd a si@icanr improvcmcnt in function (20p = 0.004) <.hitc thcrc was a less imprcssivc change in the Dougados functional index (6%.

0.03). Thisdcnmnsrratcs [hc superior sensitivity ofrhc BASFI. Coinsislcncy was good for both indi

(p <O.OOt). BS U’BS the rctarianship bctwccn pa~~cnr pcrceprion of funcrion and function as asscs

hy an external obscrvcr (p <O.OOt).

Conclrrsion. Thi: BASFI &sfics ihc criteria rcquircd ol>a functional in&x: ir is quick and e

to comple~c. is r<liahlc and is sznsitivc to chan_rc ;ISTWS rhc u*holc spcctrurn oi’dix~tsc. (J Rheurwr

Key Induirq Tccnrrst

ANKYLOSIIU’G SPONDYLITIS

FUNCTIONAL INDEX,

‘he control of pain and rhc preservation of function remain

;hc goaIs or trcatmcnf in ankylosing spondylitis (AS)‘. Non-

sreroidal anriinflammatory drugs (NSAID) and physiothcr-

apy. in the form of specific exercises, are the main methods

of therapy’. however the relationship between disease

activity, disease progression and its functional consequences

is tenuous3. Clinical and laboratory indicators of disease

activity are poor predictors of radiological damaged. The

maintenance of optimal function is of paramount importance

i‘ ram the Royal National Hospiral /or Rheumak Diseases. Both. UK.

Supported by lhe Anhriris and Rheumatism Council. Ihe National

A~t!qlosing Spondyliris Socicry. rhe Pikingron Trw and rhc CoaresTi2l.U.

A. Calin. MD, FRCP. Consulrnnr Rheumoroiogist: S.L. Garret. BA.

FUNCTIONAL ABILITY

VALIDITY

to the patient. thus any method of as

bc clinically relevant and reflect th

view’.

The. ideal self-administered instru

validity criteria: content [the choice an

of each component is appropriate fo

index]; face [the methods of weighting

ponevts into an index are sensible];

produces consistent results that reflect

of the patient]; discriminanr [the inde

clinically significant differences betwee

construct [the index agrees with expec

the hypothesis of the investigatorle.

reliable, reproducible and reflect the‘e

,

(SD.&O?.; inpatients: 23.8, outpa

di&se duration of 24.7 years (inp



AS Functional Index (BASFI) as a new approach to defin-

ing and monitoring functional ability in patients with AS.-

MATERIALS AND METHODSThe BASFf was designad, through cxtcnsivc discussion. by a team of heu-

matologists. physic&crapisrr and rexarch associate&i& a major inpul front

paticms with AS. fnirially. over 20 questions wcrc considered. crrcompass-

ing a wide range of activities. Questions which were tither rc@i&c in

terms of rquiriq the same movcmcnt. or which were ambiguou.+‘nor cn-

tidy clear COpricnts were cxcfudcd. The final v&on consists of 8 qua-

rims ‘on activiticc r&ring to the lunctional anatomy of patients. and 2

additional qocstions rh;tt awzss the patient’s ability to cope with wayday

fife. The questions rcffcct actix ?tics o f daily living and inch&: .‘putling

an socks or ti_chts without hcfp or aids”: “bending forward from the W&SC

lo pick up a pa from the flcwr without an Ilid”: “rcsching up w ;I high

rhcfr’: “getting out of an arrltl<sj din+:-room chair withcw using your

hands”: “getting up oti’thc tlc~u without help frctro lying c,n your fuck”:

“sranding unwpponcd 12~ IQ o~inuws withow di.xwr~~fwt~‘; “climhin; I?- I.5

steps without using ;I handmil <>r walking aid”: ‘Ofooking OVCT y<xur *h<tui-

dcr wirhoor turning your body”: ‘.doing pHysically dcrlwodin~ ;Ictwiticn

(c.g.. physiotherapy cxcrciscs . spom nod gxrd&ing )“: and “doing a full

day’s activities whcthcr at hnmc or at work” (Figure I ). The qucs&ws xrc

sinqdc to ondcrstand. spdic in r&lion to i p;rnicuix aclicrrt and rcfcwnt

lo ~%scssrncnI of fumxicm in AS.

fXxh question is answcrlrd on a IO cm visual analog scxlc (V ASi. 2% [his

irnpnwcs both the wmitivity t~l ihc in&x to change and its capacity to cfiw

a range of rcsponscs across the cntirc scale. The VAS have no distinpursh -ing%arks. in nccordancc with previous wori?. the only guidclincs b&g

rhc words “Easy-’ and “lnlp>\sihfc” at either end of the iinc to indicate

the direction of severity (Figur c I I. The mwn of the 10 scc;~is~ :i\‘c* rhc

EASFI WCC (o-10).

A ~c~ai of I63 paricnts look psfi 10 the study (47 consccutivc inpxlmxs.

t>n an intcnxivc 3.wcck physicuhcmpv course x xi I I6 rand~u~ rl\ ~ciscr~d

ourp~~~nts). The pt~cn~\ iwlod~cl in Ihe study rcllcct rhc v&k rsogc <,I’

dkcasc l’rtm cariy AS 1‘1 chtahlirhzd i;ltcdi~c:asc. The HASFI ~3s 3nsi!~d

in icrms of ail validity critwa and wx cwwpxcd with a pohiishcd fLrl~--

tionai index (DwgxJorf’. The O-IO wxing ~ybtcw c*i the la~rcr w;lb cow

vcncd to a O-10 scale frwcasc of w~px~iw~ All 163 p&cm< wcw $vcn

both mdiccs and a direct c wnp;lrixm was made. using the i4Y pclticnrs who

fully coolplctcd rhc qucsticmn ;liws. Uclth the BASFI and Dougados fuunc-

lion;1 index wcrc cmmpfacd by 30 inpatients at the s&a. 2nd day and end

of the 3-week pcricti of physinthcmpy . To assess rcprtdu cibiiity of’ the 7

indicts. inpatient scows clkcn 21 hours apan (Day 0 and Day I of treat-

mcnc). at ~boul rhc same time ofday. wcrc compared. An cx~crnal \xlida-

lion or both indicts was pcrfomxd on 20 of the inpaicnts. On compicticln

of 8 specific lasks by each of the paucnt?;. 2 physiorhc rapirts indcp-ndcn liy

scored rhc rclcvanr questions or rhc BASFI and rhc Dougados fimcrional

index. The patients compfetcd the qucstionnairc s scpardccly . Finally. s een-

silivity to change over rhc 3 weeks of inrcnsive physiorhcrdp y was analyzed

for both indices by comparing rhe inpaticnl scores o n Day 0 and Day 18of CrcatmcnL.

The analyses were carried out using the UNISTAT statistical software

on an IBM compatible PC. Correlations were performed using the Pearson

correlation cocfficienr and analyses of difference using the Kruska l-Wallis

one-way ANOVA and the Wifcoxon ranked sign ten.

24.6)..

The BASFI and Dougados funct

lent amount of time to complete

preference was expressed for patients. However, the distribution

superior to that of the Dougados

O-9.5 (mean 4.03, SD 2.16) comp

SD 1.68). respectively (Figures

In a comparison between the

inpatients a nd those of the outpatien

of the former was significantIy hig

IhoSpital patients: mean score = 5.06

mean score = 3.55 (SD 2.0); p <

f<>or the Dougados functional indethe inpatients rhan the outpatients

1.56) vs mean score = 2.29 (SD

The reproducibility of both instru

of consistency of inpatient scores ta

time orthe day (BASFI: mean at tim

vs mean at +2’4 h = 5.26 (SD 1.9

Dougados FI: mean t&c at zero =

at i-24 h = 3.46.(SD 1.55): r =

An cxtcmal validation oflhc BAS

and obscrvcr scores to bc reliably

score = 2 .76 vs mean Observer A

Obscrvcr B score = 2.65: r = 0.8

same intcrobscrvcr consistency wa

FI (rncan Paricnt sawc = 1.93 vs

= 2.29; r = 0-Y. p <O.(K)I).

Over an intcnsivc 3 week trcat

scores improved significantly f’rotn

on Day 0 to 3.75 (SD 2.1 1) on Da

score change = - I .07 [ 19.6% -5. IS IO +3.23). The Dougados

significant change over the .samc per

= 3 .09 (SD 1.43) vs Day 18: me

= 0.19. mciln scorcchangc = -0.3

range = -4.0 10 +3.0).

DISCUSSION

The aims of treatment in AS are to

tain or improve function. and thus

and function arc improved by ph

exercise programmes”.‘“. Function

measure in AS. Most of the previou

have been directed towards patients

ease. primarity assessing the functio

PLEASE DRAW A MARK ON EACH LINE BELOW TO INDICATE YOUR LEVEL OF ABILIP( WITH EACH



FOLLOWNG ACTIVITIES. DURING THE LAST WEEK.

N-8 An aid ir a piece of equipment which helps you to perform an action or movement

EXAMPLE:

EASY I LMPOS

I) Puning on your socks or fights \+out help or aids (c.g sock aid)

EASY LMPOSS

/

2) Bending fonvard From the waisr 10 pick up a pen from Ihe floor withour an aid

EASY

.3) Keaclun~ up IO a hi@ shelf withour help or aids (c .g hclpin~~ hand)

EASY Ihll’OSSI, -.-

4) Gcning up OUIof an armless dinins room c hair without using your hands or any other help

EASY IhiPOSSI

, r.

5) Gctring up off rhe floor wi[hout help from tyins in your back

EASY IMPOSSI

G) StandinS unsupporred for IO minurcs wirhoui discomfon

EASY Ihlf’0hSll3_i_-._ -__--.-_-. _-_ _- _.... -. - _... _

7) Climbing i 2 . Ii steps wirhout using a handrail or walking aid 011e foor 011each srct~

EASY IhlPOSSff__..__.~~

S) Lookln~ over your shoulder wirhour turnins your body

EASY Ihlf’OSSlB___-_-___

9) DoinS physically demanding activiries (e g physiorherapy exercises. gardening or spans)

EASY

IO) Doing a full days activities whether il be at home or ar work

Ihlf’OSSIB

EASY

Fig. 1. A copy of ihe BASFI.

IMPOSSIB

,. I,.

) '". . ..



ry arkI cons;is~s (11 70 qui’~~ri~r~~ i~t~rr~s~~~~r~l~r~~ 10 ;ictivitre>

trftl;Ill! Ilvirlp. A \<llW t1l 0 I\ ?:I\‘crr il’ tl1c usk car, hc ;ii.

cr~rnplrshcrl W~I~IOUI d~l‘li~~r!;~ I II in is pcl\hrhlc hut difficult

anIl 2 II’ II is rlllpo\lll/~ l-b?< ;Ill\LvCrh Arc‘ llddctl 1<1 g,w ;1

Lruili \iorc of tly\lu 11~111111 i-h ihi~iy;!tl~l\ f'l Iv;!?; <lcsl~rlccl

hy phyiicianr with ;I ~p~t2Ir\t rrrtcrcst rn AS. Apparcntl>

thcrc \VX no input frorrl ph\ \rclrhcrapr\t\. who arc closclv.

invul\cd with the nwnrtorrno of patient function. or from

the p~i~nts thcnlscl\w 2%~ ~~,ipor~ncc of the patrent’s pornt

of \Gu. has rcccntly been ~,trcsscd”. Orhcr problems cn-

countered with this particu!ar functional index include the

fact Ihat patients often find tiw qucstrrms drflicult to answr

without qualification. ,Mlan\ ol’ the questions arc not spccrfic

cnoush in terms of the exact movcmcnt or task required and.

It WaS as a EsU~t Of thes~apparen~ inadequacies in the CUT-

^._[n cdndli;sio:n,thk~A-~~~~atisfies the

necessary in the design of a functional



rent methods of assessing function in AS that a team of phys-

iocherapists, physicians, research associates and patients

designed a new functional index: the BASFI. This instru-

menI consisrs of 10 questions, sp&ific in their insrruction.

considered to be clinically relevant and to encompass the ap-

propriate anatomy and reflect the overall level of function

of the parienr. The questions were answered on a 10 cm VAS

in order fo improve both :he sensitivity of the index an d its

capbciry-to.make use of rhe entire scale of the index. The

questions relating IO specific movemcnls arc concise an d do

not require further explanation: They ,spccifically cxcludc

the U SC of he lp or aids.

The BASFI scores prtduccd J normat distribution which

covcrcd 95 % ofrhc rotzl scale whcr~25 rhc Dou~~Ios Cum-

~ional index iscd only 65% ,af rhc (o~tl range. This skew

was hi~hlighlcd by Ihc low mean <)I’ rhc paricnr scores on

ihc Dcqxlos FI: (2.58). conlparcd to that of rhc BASFI.

C4.03). As the inpaticnrs assessed covcrcd a broad spcc~run~

I( diwasc scvcriry, ;1 full rancc of 5corcs for- bolh in&cc>_ .

1’. would bc cxpccrcd, with a mean score near the middle of

‘, _ 1hc sc;~Ic. The superior score disrribucion of ~hc BASFI wxs

Icnlonsrrarcd in almost SO consccutfvc inpatients a5 well 2s

: aver IO0 randoritty sclectcd outpatients and gives it a dis-

lnct advantage over the cxisrinf functional index.

Paricnrs did nut cxpresr a prcfcrsnce for cithcr rhc BASFI

lr Douzados FI, in terms of time taksn IO complctc- thcn~ or

Ivcrall user fricndlincs<. but 3s c\plaiocd above. SO I~IC of

ilc qucnims in the Dtru~ados f-I n&cd qualificaiiorl in ordl‘i

~1bc answcrcd accurately. The rcproducibili[y ofthc BASFI

;yr. ,y”“Q+>:::3: 1.x _L / ,. \; fli@ly significant and. in addition. the patients‘ pcrccp

~ . .I \ _(__ ‘,I. Y:,.% :;

1‘: ::’ iion of their lcvcl of function accurately rnirrorcd that ol’

.,,,-“-I,, ‘.““,: ;. ,, ‘Z,

~xtcrnal obscrvcrs.

-, _ -+ :.;ic F.-;” (i Any index which is MI bc used in the analysis of function

,,;,:., lccds no{ only to bc ;Iccuratc but ;IIW scnsitivc to change.

.,_ .’),. ,, i’hc BASFI was shown II> bc sufficicnrly scnsirivc 10 dcmon-

-,.trarc an improvement in the functional ability of paricnts

‘. 1.~,. ; , :r” ,.),i /; -1

lvcr a 3 week period of inpatienr rhcrapy. This was not

,I”’ ,;;+dz” *,“.!:...~“:.o cflected by rhe Dougados FI. There is an inevitable tradc-

i’ 2.3, . ,;< -i,t:,-,-, :_,,_

)ff bctwccn sensitivity IO change and reproducibility: by in-

‘“.. -‘: -, 1../, J,::::.,I,.’ .,, ‘4

reasins one. the other is usually decreased. This is reflect-

. .“, -i ii -d in rhe BASFI where its superior sensitivity is balanced-ch “& ,‘_i -Ii

:‘.,-’ ;.:

:gainsr a lower de gree of reproducibility compared IO the

:’ -.i)ougados index. However, the high degree of reproduci-

,.,,;a,.:., i ,, lilicy shown by the Dougados is prima&y a function of irs,_? ,..a .:: .-) ,‘.‘_,_ . J.:. ,::

oti sensitivity, whereas the greatly increased sensitivity of

I ,.. ., he BASFI does not resull in a comparable decrease in iLs,-. .>

:, 1’_: ?, ,: ,: _ ’

eproducibility.

i’ .; .;, ~ :

to change across the whole spectrum of

not only does the BASFI satisfy the need

tioners and their physiotherapy colleaguerelevance is also heightened by the inclusi

by patients with AS during its design

assessmen(.

REFERENCES

I. Calin A: Ankylosing Spndyliris. In: Maddis



THE BATH ANKYLbsIN$ivSPONilYLITIS RADIOLOGY INDa-.

A Ney7 Validated Approach to Disease Assessment

KIRSTEN MACKAY, CHRISTOPHER MACK;SINEAD BROPHY, and ANDRE1

Obiecfire. To develop a reproducible and-simpleradiologic scoring system for the spine in patients withanhylosing spondylitis (AS): the Bath Anhyiosing Spon-dylitis Radiology Index for the spine @ASR.I-s).

hefhds. Radiographs of’470 patients with AS

were scored using the New York criteria for the sacro-iliac joints and, similarly,, grading the lumbar .and’

cervical s@ineon a scale of O-4 (for normal, suspicious,mild, moderate, and severe). These 3 scores were addedtogether to produce the BASRI-s score (scored 2-12).

Radiographs of 185 patients were used to test reproduc-ibility. Blinded radiqgraphs of 89 non-&S patients wereincluded, randomly, to assess disease specificity. Sensi-tivity to change was assessed using 177 radiographsfrom 5s $5 patients.

Results. Intra- and interobserver variation

showed 7556% and 73-79s complete agreement at allsites, respectively. Specificities of 0.53-0.59 suggestedthat the lumbar and cervical spine BX5RI scores weredisease specific. Sensitivity to change became apparent

at 2 years (P < 0.001). Using a laterai view and ananteroposterior view of the lumbar spine was moresensitive than using a lateral view alone. Grading a setof radiographs (sacroiliac joints, lumbar spine, and

cervical spine) took 30 seconds.Corrchsiorz. B?&RI isa reliable method, for grad-

ing radiographic changes in patients with AS. It isdisease specific? sensitive to change, valid, simpIe, andrapid to perform.

Supporrsd by a grant from the Coates Cbarit:lble Trust. theCol. W. WV.Pilkington Trust. the Harris Charirable Trust. and theNational Anbiosiq Spondylitis Society.

Kirstrn R. MacKq, MRCP, Christopher Mack. FRACP.Sinead Brophy. BSc. Andrei Caiin MD. FRCP: Royal NationalHospital for Rheum&tic Diseases..Bnth, UK.

Address reprint rsqursts to Andrei Calin. MD. FRCP. Royal

Ankylosing spondylitis (AS)

sive condition with fluctuating dis

ber of measures are used simult

outcome (l-lo), and these are funthe natural history of AS and ti>,e

nunagtxnent strategies in terms

( 11). Characterist ic radiologic chan

diagnosis of AS and is_considerod

for disease status. hut little work hdisease progression in radiologic

have the advantage over other mctive and uncomplicated by diurnal

No classification definingchange in AS esists. The New 1’0~

include the only \vidcly acc?ptcspecific fo r [he disease. but th& sacroitiac (SI) join ts ( 13-15). The presence of radioiogic sacroiliitis igore the rest of the’ spine ( 10). E

tl!mbar spine disease may 1x2 re

terms of a .-bamlwo spine. . hut Ics5

not been adequa~cl~ dcscriberl. A scoring some part of the spine ilished (12.17-10). but these are nothem score the whole spine. Some

ibility. are insensitive to diseaw slow to use (71). All ignore the pthe spine. classif’ying those \vhoelement fusion as normal or as

graphic chaqges when in fact thpletely fused (see Figures IA and

The Bath Anlqlosing Spo

dex for the spine (BASRI-s). a system. was designed to addressreport describes the BASRI-s, its

1

.

.

2264



Table 1. Bath Ankyiosing SpondylitisRadiology ndex (BASRI),forthe spine* i

Systemapplies o both the lumbar andthe cervical spine *

Score Grade (grade each as O-4) . -

0 Normal No change-1 Suspicious No definite change2 Mild Any number of erosions,squaring, or

sclerosis,with or withoutsyndesmophytes,n 52 vertebrae

3 Moderate Syndesmophytesn ~5 vertebrae,withor without fusion involving 2vertebrae

4 Severe Fusion involving ~3 vertebrae

* For the lumbar spine. examineboth the anteroposteriorand lateralradiographs ogether.The score or the lumbar spine s a composite ofthe 2 views. f. as n Figures IA and 8, one view shows yndesmophytesand fusion but the other view shows esserchanges. he overall scorewill relate o the view showina he more significantchanse.This systemappliesequally o the ce&aTspine, but only tb the ateral radiograph.See Figures 1 and 2.

patients whose disease occurs at a younger age (22-26)..& index documenting radialogic hip change is being

developed.

PATIENTS AND METHODS

A consensus approach (27) was used to determine asuitable scoring system for radiographs of patients with AS.Radiographs ‘07470 patients who had been diagnosed accord-ing to the NY criteda were scored open!y and assigned to 1 of5 severity grades based on the NY gradrng of SI joint disease(0 = no disease, 1 = suspicious for disease. 2 = minimaldisease, 3 = moderate disease. and 4 = severe disehse).‘Theradiographs used were an anteroposterior (AP) pelvis film, APand lateral lumbar spine films, and a lateral cervical spine film.The SI joints. lumbar spine, and cervical spine were eachassessedseparately. The lumbar spine was defined as extend-ing from the lower border of Tl2 to the upper border of SI,and the,cervical spine as extending from the iower border ofCl to the upper border of C7.

The discriminating features of each radiologic severitygroup were defined and used as the basis to describe a methodof assessing he severityof radiologic change n AS. The systemwas then repeatedly tested in a blinded manner by 3 experi-

enced readgrs (KM, CM, and AC)’ and modified openly onseveral occasions before the final format was determined.Rules for scoring the lumbar and cervical spine are shown inTable 1. The NY criteria were used to score the SI joints (15).

To assesswhether an AP or lateral radiographic viewwas more appropriate for scoring the lumbar spine, 58 sets oflumbar spine radiographs with both AP and lateral views were

FolIowing definition of theof 188 consecutive patients with Ascored randomly and blindly by th

BASRI. The mean (ZSD) age44.5 -t 10.9 years, and the sex raTwo hun dred sixty-three SI joint,‘cervical spine radiographs from tassessing ntra- and interobsemer vwere nonparametrically distributedisease duration, to cluster towadisease), a kappa statistic was uscance of the intra- and interobserv

Sensitivity to change ovescoring serial radiographs of5S p

intervals of 1, 2, 3, and 4 years. Ra2 occasions 12. 24, 3fi1 and 48 montin 20, 31, 28, and 23 cases, respecdiagnosis of these 58 patients was All radiographs were blinded as tradiograph; and a Wilcoxon signeddata was used to determine the etivity to change became apparent.

The specificity and positiother rheumatic conditions was asfrom the AS cohort and 7s radio

parients. Radiographs of non-X? with the AS patients’ films, such tthe diagnosis. A cutoff of grade 2and all radiographs were then cithose with and those without AS not viewed at this point.

The non-AS cohort \ve strive outpatients who xvere attendipital for Rheumatic Diseases. a who had had cenical or lumbar spevaluation o f symptoms. Their m16.S years. and the sex ratio tsas

cohort included 41 patients a-ith mechanical back pain. LO \virh fporosis, and 7with psoriatic arthr

RES

Lumbar and cervical spused? Using 58 sets of AF’ radiographs. 3 scores were deThis third, or combination, sc

or lateral scores if syndesmopat differeent levels on each proof the 58 patients. The “comfrom the AP score alone in 9

and from the lateral score al

BATH ANKYLOSING lSPONDYLITIS RADIOLOGY INDEX



In the cervical spine, this situation was not evi-dent (see Figure 2). Only 20 cases were available in the

population studied, since AP views of the cervical spinewere rarely taken. The AP view intluenced the overallscore 0nIy once.

Validation of the BASRI. I~~rrmbserrer ~m~ariorz.

complete agreement). respectiveThe ma in errors were reading trather than grade 3 in I? of 700

lumbar spine as grade 4 rather cases (7%). and in distinguishinfrom m ild (grade 2) disease in

!a, 1

Id



Figure 2. Cervical spine adiograph, showing fusion of the posteriorelemeats but no anterior fusion. Any scorin g system that ignored theposterior elements would classify the findings on this film as normal.

scored by each assessor on separate occasions. Therewas 78% complete agreement between observers, with akappa score of 0.55. The 160 sets of lumbar spine

radiographs used reached.73% complete agreement (K

= OH), and the 145 cervical spine radiographs reached79% complete agreement (K = 0.69) (see Tables 2 and3). Both the lumbar and cervical spine scores outper-formed the established NY criteria for SI joint assess-ment. Considerable difficulty in separating grades 3 and4 existed in SI joint assessment (8 occasions), while

Table 2. Summ ary of intra- and interobserver variations at thevarious skeletal sites scored as part of the Bath A&losing Spondyl itis

Radiology IndexIntraobserver Interobserver

variation variation

Complete , Complete

agreement Kappa apreement Kappa

Skeletal site statistic (%) statistic

Table 3. Kappa statistics and strength

Kappa

statisticCO.20.2-0.40.4-0.6

i&OSo.s-1.0

distinguishing mild from suspicio

problem for the Iumbar and c

occasions). Discrepancies of >1scoring the SI joints in 3 of 263in j of 160 films, and the cerv

radiographs.Diwnse ~peciJc$~. Spe

spine was 0.89, and that for theThe positive predictive value fo0.97, and that for the cervical s

Sensiticir~ ro clzni~g~‘.U

rank test for nonparametric da

strated a significant change in0.001) at 24 months for the SI and the cervical spine. Where tradiographs was 11 months. changes of at least I grade wit\vas not statistically significant

SconQtgspecd. he meanof films (SI joints, lumbar spine

less than 30 seconds.

DISCUSSI

Any measure that docum

be reproducible and sensitive disease specific and have both tive validity (11). To be clinicaeasy and quick to use, with feThe use of standard measur

comparison of results between is illustrated well in the rheuma

the frequent use of rad iologic the Larsen and Sharp scores fo(American College of Rheumaor EULAR (European LeaguCore Data Set (29-32). Using

BATH ANKYLOSING SPONDYLITIS RADIOLOGY INDEX



insights into causal factors and provide patients withprognostic information and expectations (33). Distin-

guishing between markers of disease activity and thosethat attempt to measure damage and function is imp@;tant (11). The BASRI was designed to fill ‘a perceived. -_

gap in the range of outcome measures for AS.Given that the NY criteria for the SI joints are

well established, they were incorporated into the BASRI’without change. To gain credibiIity, any newly developedscore needs to perform as well as these criteria, and wehave used the performance data for the NY criteria asthe “gold standard.” The BASRI was reproducible, with

intra- and interobserver variations equivalent to or bet-ter than those of the NY criteria. The main problem forgrading the lumbar and cervical spine was distinguishingsuspicious disease from mild disease on 5 occasions

because of difficulty in determining whether squaringwas present. Difficulty in distinguishing between grades1 and 2 was not seen with the SI joints because bilateralgrade 2 or unilateral grade 3 sacroiliitis was part of the

entry criteria for the study., A potential method .ofovercoming this problem for the spine would be ‘tomeasure each vertebra individually to determine thepresence or absence of squaring compared with thepopulation mean, as done in the method described byRalston and colleagues (18). However, t,his would con-siderably increase the time taken for scoring, therebyreducing the clinical usefulness of the BASRI.

The lumbar and cervical spine were shown to be

disease specific, but the SI joints were excluded from thispart of the study because the presence of sacroiliitis (as

part of the NY criteria) was one of the entry criteria forthe AS cohort. Since only 7 of the 89 non-AS cohort hadpsoriatic arthritis, further work is under way to deter-mine whether the BASRI would be able to differentiateAS patients from those with Reiter’s disease or psoriaticarthritis.

Little information has been available regardingradiographic sensitivity to disease progression and the

frequency with which repeat radiographs should beperformed. The BASRI was found to be sensitive to

change over a 2-year period, which suggests that radio-graphs at intervals of <2 years, for either routine orstudy purposes, are not warranted. The radiographs inthe study were blinded for the date, confirming that theBASRI could determine “forward progression” (i.e.,

syndesmophyte formation and fus

can be missed. The score generaalone differed from the combined

AP and lateral views) 15% of the t

than with the lateral view alone, the time. The best screening v

lumbar spine appears not to be

projection. but rather, the AP change is seen on this view, no fu

required, but if lesser disease iseAP and lateral views are essent

severity of change. This did notspine. The combination of viewdetermine the BASRI for the

cemical spine. an AP and lateralAP pelvis.

The use of the AP lumbar increase the radiation dose sligh

spine radiograph incurs a dose

(mSv). the addition of an AP lum

increases the dose by 7.0 mSv (34)the radiation esposure incurred flighr. The total radiation exposur

and lateral lumbar spine radiogra

No data are available for the cnearest comp3rable~esamination w

radiograph. incurring a dose of 0of death from a fatal cancer fol

radiopraph is -1:10.000 ’(35). The

traffic accident in 1 year is l:S.O

The thoracic spine has no

BASRI-s because of technical d iradiation exposure. The scapulae

the \ertebrae. making a good vie

difficult to produce a well-penetr

disease will also add to any difficu

overlie the thordcic spine in thtempts to improve the penetra

radiation exposure by an amount

the individual (e.g., muscle thiction). Standard radiographs (as u

conditions) (29) have not been uavaiiable “gold standard” rad

BASRI was compared with th

I .

I)

2268

that his index should be used with caution in these

M

than 12, may inappropriately d



conditions (29).

The BASRE was easy to use and to explain. Themean rime taken to score a set of radiographs fqr. 1subject was <30 seconds, and the required training wasminimal. Cross-sectional data generated using the orig-inaf cohort of 470 patients suggest that the diseaseascends with time ‘(36), which is consistent w ith manyearIier studies and supports the instrument’s face valid-

ity. Additionally, these data suggest that radiology mayhelp in defining subgroups of patients, especialiy if usedin conjunction with a variety of other indices. Studies

using longitudinal data to confirm the validity of theBASRI as a prognostic marker are in progress. A pilotstudy investigating the relationship between metrologyand an earlier version of the BASRI revealed a goodcorrelation b’etween the 2 scores (37). FoIlowing from

this, the relationships between radiologyX metrology,function, and disease activity (3-5) are currently beinginvestigated.

The BASRI, as described above, is a modified

version of studies previously published in abstract form

(38) involving the entire axial skeleton: including thehips. Further work has since been undertaken delineat-ing the spinal score, or BASRI-s, allowing for a moreprecise interpretation of the grading system, and thissystem has been compared with other available radio-logic scoring systems (20,21). The present study uses aseparate cohort of patients from those used in theprevious studies and was undertaken to validate theBASRI-s in a new AS population.

Hip changes have not been included in the

BASRI-s because patients who develop h ip diseaseappear to represent a distinct subgroup. H ip arthritis isassociated with the age at disease onset, occurring at ayounger age. Ascending spinal disease seems to be aproduct of time-the longer the disease, the greater thespinal change (22). The majority of patients, with hipdisease have developed some radiographic change by theage of 23 (23). In a prospective study begun in 1947, 150war veterans with AS were followed up for 33 years.

Peripheral joint disease occurred early, and those whosehips were normal after 10 years of AS did not subse-

quently develop hip arthritis (24). Other evidence hasshown that hip d isease is associated with a more severeoutcome. Amor and colleagues (25) include hip, arthritisas 1 of 7 entry variables correlating with disease severity

majority of AS patients. Those wspinal disease without hip arthritisa l&point global scale despite h

poor metrology, and poor functiograde these populations separatefor one and the BASRI-g for the

To maintain simplicity, th

up m inor radiologic change. Thewith each additional erosion. Ev

sclerosis will always remain grauntil fusion between 2 vertebrae

syndesmophytes is identified. Trestriction in patients without brmay be related to soft tissue inttiaily reversible factors, and there

as mild disease (12’;2?). As well damage that occurs in AS (eros

mophytes), the BASRI also incothe involvement (i.e;. number osyndesmophytes or fusion). Howeentiate between those with a com

and those who have ~3 fused vgrade 4. or SL’IWCdisease. Thidisease has been used because involves at least 60% of the lumspinal movement significantly. correlating radiology xvith metrolbut it does mean that the B?ISReffect. However. the same platgrading system are seen in the I

been widely accepted for scoring

the blueprint for the BASRI.The limited scale of t-

broad categories of radiologic gr

lvhy sensitivity to change for thyears. However, it might be that rslow and can only be seen at 2 yeof t.he index. Thus, the 72 -poi

Ankylosinp Spondylitis Spine Scomore sensitive to change (21). Untis, where erosions tend to occ

years: progression in AS appears Only 35% of a 470-patient cohotion 21 years, range 2-50 yeachanges in the Iumbar spine (3majority are diagnosed with grad

Various other radiologic scores for AS have been to use, and easy to explain. It is a



published in the past 10 years (l&17-19). These havenot attempted to define.progression in the entire axial

skeleton. The SASSS, as mentioned above, grades thelumbar spine alone, using a scale of O-72. It scores the..edges of each vertebral body from the lower border of -TI2 to the uppe; border of SI, using a O-3 scale (1 forerosions, squaring, or sclerosis; 2 for syndesmophytes;and 3 for a total bony bridge). The maximum possiblescore is therefore 72, which represents a completelyankylosed spine. The SASSS does not take into accountthe posterior elements. This means that a subject with

only posterior fusion would have a low score, and thelow SASSS would be inconsistent with the clinical pic-ture (see Figures 1A and B and Figure 2). Using theSASSS is slow, taking more than twice the time of theBASRI to grade just the lumbar spine (21). It does notuse the AP .lumbar spine film, which we have shown to

be necessary (see Figures 1A and B). It is less reliablethan the BASRI and isnot sensitive to progression (21).

The Glasgow Radiological Index (GRI) (1%19)is a composite score. The SI joints are scored using the

NY criteria, but a maximum score of S can be attained(unlike the hY criteria. the mean of the SI joints is nottaken). The lumbar spine score includes the VertebralConcavity Index. which measures the concavity of an

individual vertebra. comparing it with a normal refer-ence range. If the vertebra is squared. it is scored 1. The

maximum concavitv score is 5. In addition. each syndes-mophyte identified- is scored 1. allowing for a masimumpossible score of f?. All 3 scores are added for apotential total of 73. The GRI applies only to the lumbar

spine and SI joints. It is slow to perform, taking 23minutes (18). It scores syndesmophytes but not fusion. Itignores erosions. the posterior elements, and uses only a

lateral radiograph. The followup study (19) evaluated 41patients at, j-year intervals. The abstract states thatprogressive change was detected. There’was do correla-

tion behveen the GRI and other clinical and Iaboratoryparameters, namely. chest expansion, spondylometry,the erythrocyte sedimentation rate: and IgG levels.

In conclusion, radiology is fundamental to thediagn,osis and tracking the subsequent progression ofAS. Apart from the New York criteria for the SI joints,no widely accepted radiologic criteria exist. The BASRI,as a radiologic classification system, aims to satisfy theOMEKACT (Outcome Measures in Rheumatoid Ar-

the SI joints and the lumbar and c

ACKNO?VLEDGME

The authors hank MS P. Porcfor her help with labe ling of radiogCharifableTrustswho have provided fthe CoatesCharitableTrust, the Cof. the Harris Charitable Trust, and thSpondylitis Society.

REFERENCES

1. Dougados M. Gueguen A. Nakachr JP.8. ,Evaluation of a functional index ankyiosingpondylitis. J Rheumatoi 19

‘2. Dougados hl. Gueguen A: Nak achr Evaluation of a functional indrs forspondylitis [letter]. .I Rheumatol lY90:

3. Calin A. Garrerr S. Whitelock H. lisnnrP. et al. A nw approach to defining fuing spondvlitis: the development of thelitis Fu&ionsl Index J’Rheumatol 19

4. Garrett S. Jenkinson T: Kenned! LG. Calin A. .21 ew approach to defining d

spondylitis: the Bath Ankylosin$ SpIndex. J Rhsumntol 19Y-l:~l:I~SO-~l.

5. Jenkinson TR. hlalloric PX. LVhitelockSL. Calin .X. Drfinins spinal mohiiity(AS): rhr Barb .%SMetrofo~ Indc~. J R

6. Jones SD. Steiner A. Garrett SL. CaliSpond!,litis Patient Giobal Score [a19955-i Suppl I:1 14.

7. Creemers &lC\V. van ‘t Hof XI.4. FranLB.& Gribnau FWJ. !zn Riel PLC11. ing spundylitis: selection of a c‘ox set in the development of’ a diseaw acti\11196:35:867-5.

8. Daltrov L. Larson M. Roberts \yX. Lthe Health .~sszssmenrQuestionnaire thies. .I Rheumatol 1990:17:9X-50.

9. blander M. Simpson JM. kfclcllan ACarson Dick W . Studies with an enrhclinical assessme nt in ankxlosing spo19S7:46: 97-102.

10. Laurent MR. Buchanan WW. Bellamyused in anlxlosing spondyiitis clinical mat01 1991:20:3X-9.

11. Rigby AS. Silman .AJ. Outcome assan!-ccbsing spondylitis. Br J Rheumato

12. Averns L. Oxtoby 3. TaylorHG. JonPT. Radioiopical outcome in an@losStoke Ankvlosine Spondvlitis Spine Sctol 1996;35:373-16. . .

13. Bennett PH . Burch TA. Populariondiseases.Amsterdam: Excerpia hledic

14. Van der Linden S. Valkenhurg H

2270

2s. F&on DT. Choosing a core set



rheumatism. Vol. I. Oxford: BLackweft Scientific publications;1963.

17. T&or HG, War&e T. Beswick El, Dawes PT. The relationship of

cli&al and laboratory measures to radiological change in Linky-losing spondylitis. Br J Rheumatol IYY ;30:330-5.

IS. Ralston SH. Urquhart GDK, Brzeski M. Sturrock RD.‘& rtcwm&hod for the radiological assess ment of vertebrai squaring.inanhylosing spondylitis. Ann Rheum Dis 1992;51:330--3.

19. Chaudhuri K. Armstrong S, Murphy E. Zoma A, York J, SturrockRD. Evaluation of a rddioiogical index of spinal disease inanhylosins spondylitis-1O’year follow-up study @bstraCt]. 6r JRheumatol 1997;36 Suppl 1:1X

20. MacKav K. Mach C.5: Pande i: Roussou E. Calin A The BathAnhylo;ing Spondylitis Radiology’ Index: definition and correla-tion with functional. disease activity and metrolo_gy indices [ab-stract]. Arthritis Rheum 199639 Suppl 9:S206.

2 I. Ma& CS, Macriay KR. Calin A. Radiology in ankyiosing spondy-liris: a comparison of two scoring systems. Br J Rheumatol 1996;35Suppl 123.

22. Khan MA. Ankyiosing spondylitis: clinical features. In: Kiipprl J.Diepps P. editors. Rhrumatoiog. MoSby-Year Book EuropeLimited: 1994. p. 3:15.1-X10

13. Calin A, Elswood 1. The rckltionship between pelvic. spinal andhip involvement in ank--losine spondylitis-one disease process orst\,eral? Br J Rheumatol 1988:17:393-5.

74. Carette S. Graham D. Little H. Rub enstein J: Rosen P. Thenatural disease course of nnkviosiw spondvlitis. Arthritis Rhwm-. .1363:36: %-90.

7-5. Xmur B. Santos RS. Nahal R. Listrat V. Dougdos M. Predictive

facrors for the ions term outcome of spundvloarthropathirs..I Rheumarol 1991:21:1W-7.

76. Rilsy hLI. hnsell B&I. Bbwzters EGL. Radiological manifestationsof anh:losing spondylitis accordin,~7 o age at onset. Ann RheumDis 1971.3135~1%_ c

17. Bellam\- %. Buchanan WW. Outcome measurement in v>teoarthri-tis .clin&l trials: the ~3% for srandardisatiun. Clin Rhcwncltol19S4:3:IY~-3U~.

rheumatoid arthritis clinical ;rials.29. Larsen A, Dale K, Eek M. Radioa

arthritis and related conditions byRadio1 1977;18:481-91. .

30. Sharp J,T. Lidsky MD,‘Collins-LC. the prosTession of radioioeic ccorrelation of rndiologic. clinicalArthritis Rheum 1971;14:706-20.

31. Tugwell P, Beers M. OMERACT sures in Rheumatoid Arthritis Cli

mat01 199320590.57. Scott DL. A simple index to asse

arthritis. .I Rheumatol 19Y3:X58233. Little H. The natural historv olan

.tol 19SS:lS:I 179~SO.34. Hart D. Hillier h,lC, Wall BF. Sh

patients from medical s-ray esaminformation held in the National PRadiolog ical Protection B oard. RMajesty’s Stationers Office: IYY5

35. Annals of the ICRP series. RecomCommission fk Radiological proPrrwnon: 1991. pp. I-3.

Erratum

In the article entitled “Ou tcome of Renal Transplantation in Ninety-Sev en Cyclosp orine-E

Systemic Lupus Erythematosus and Matched Controls” published in the August 1998

Rheumatism (Stone et al, pp 143%1445), the name of the third author of reference 4 wasThe correct reference is Reveille JD, Bartoiucci A, Alar&n GS. Prognosis in systemic lup

negative impact of increasing age at onset, black race, and thrombocytopenia, as well a

Arthritis Rheum 1990;33:37-48. We regret the error.

British Journal of Rheumatology 1996;35:66-71



THE BATH ANKYLOSING SPONDYLITIS PATIENT GLO.L+-.: < SCORE (BAS-G)

S. D. JONES, A. STEINER,* S. L. GARRETT and A. CALIN

Royal National Hospitalfor Rheianatic Diseases, Upper Borough Walls, Bath BAI IRL and *InPolicy Studies, School of Social Sciences, University of Southampton , Southampton S

SUMMARY

in the absence f an ideal objectivemeasure or assessingnkylosingspondylitis (AS), self-adminisactivity (the Bath Ankylosing Spondylitis Disease Activity Index, BASDAI) and function ( the BathFunctional Index, BASFI) have been developed, in addition to an objective measure of spinal mobili

Spondylitis Metrology Index, BASMI). However, a more globai assessment s also desirable. We rvalidation of a global measure (the Bath Ankylosing Spondylitis Patient Global Score, BAS-G) whichon the patient’s well-being . A pilot study was performed to select the most appropriate wording for BAwith AS, BAS-G’s construct and predictive validity and test-retest reliability were assessed.CorrelatioBASDAI/RASFI were calculated, and multiple regression was used to examine the significant correlateresponses ove red the whole scale. As predicted, BAS-G correlated best with BASDAI (F = 0.73), followThe best fitting regression quation ncluded hesescales s well as patients’ genderand current agescores were significantly different (P < 0.001). Construct validity was good: BAS-G correlated mcomponent of BASDAI and BASFI,than with BASMI or with gender. Predictive validity was saimprovement (mean = 29%) in in -patient BAS-G scores over a 2 week treatment period (p < 0.001). Texcellent (1 week r = 0.84,6 months I = 0.93). BAS-G correlates well with both BASDAI,and BASFIactivity and functional ability play a major role in patients’ well-being, whereas metrology does not.

change, eliable, and meets ace, predictiveand construct validity criteria.KEY WORDS:Ankylosing spondylitis, Global score, Validation, Well-being, Outcome.

THERE is no ideal objective measure for assessingankylosing spondylitis “(AS). The radiograph is thecurrent ‘gold standard’, but X-rays are insensitive tochange, expensive, time consuming to perform andpotentially dangerous [l]. Thus, subjective measuresmay be better [Z, 31.

For example, Hidding et al. [4] found only a negli-gible discordance between self-report questionnairesand observed functional disability in patients with AS,in contrast to patients with fibromyalgia. Further, ‘ithas previously been demonstrated that a single-itemself-assessment ndicator is a better predictor of out-come than assessment y a physician [5]. In recognitionof this; two self-administered indices to measure diseaseactivity (the Bath Ankylosing Spondylitis DiseaseActivity Index, BASDAI) and function (the BathAnkylosing Spondylitis Functional Index, BASFI)have been created and validated [6,7]. An objectivemeasure of spinal mobility, the Bath AnkylosingSpondylitis Metrology Index (BASMI), has alsorecently been developed [S]. However, if clinicians are

In this paper, we report on thment of a single-item global Ankylosing Spondylitis Patient which reflects the effect of AS ‘over a particular period of timbetween BAS-G and’patients’ reand function is hypothesizedassociation between BAS-G an

PATIENTS AND M

In a pilot study, the most for the global measure was question (in two versions) askthe effect of AS on their weweek/6 months, using a 1Oanalogue scale, where none = (Fig. 1). We chose the periodcomparison with BASDAI and because his is often the time betations.

JONES ET AL.: AS GLOBAL SCORE



I

The Bath Ankylosing Spondylitis Patient Global Score.

@AS-G) I

1. Pleaseplace a vertical mark on the scale below to indicate he effectyour

diseasehas had on your well-being over the ast week.

NONEONE WRY SEVERRY SEVER

,

2.. Place a vertical,mark on the scalebelow to &Ii&e the effect your diseaselace a vertical,mark on the scalebelow to &Ii&e the effect your diseasehas had on your w ell-being oyer’the, ast six mo&hs.as had on your w ell-being oyer’the, ast six mo&hs.

‘((

NONEONE VERYSEVJZERYSEVJZ

J

TFKANK YOU

FIG. f.-The Bath Ankylosing Spondylitis Patient Global Score (BAS-G).

Respondents reflect the whole range from early AS to 2 week programme. We hypestablished late disease [7].

Correlations between BAS-G and BASDAIIBASFI,change n the 1 week’question an

and between 1 week and 6 month scores, were assessedin the 6 month question. One-daywas examined‘in 44 in-patients.

for the full sample. Since overall disease status is

assumed to be multidimensional [9], ordinary leastsquares (OLS) regression was used to examine thesignificant correlates of BAS-G. Initial predictorsincluded BASDAI, BASFI, gender, current age andage at disease onset. For ease of interpretation,continuous vanables in the regression analysis were

RESULTS

Responses to BAS-G coverscale, for both time frames (Figshowed that the difference betwemonth scores was statistically



70

60

50

$jg 40F

2 30

s20

1c

C

7 WEEK BAS-G SCORES .. ” = 392MEAN = 5.17

i_

6 MONTH BAS-G SCORES .n = 39.2MEAN = 5.70

FIG. 2.-Use of the whole O-10 s@e by the 1 week and 6 month scores.

JONES, ET AL.: AS GLOBAL SCORE

,,



7 WEEK BAS-G v BASDAI (n = 392)

0

0 2 4 6 8

BAS-G

FIG. 3.-Correlation between the 1 week BAS-G score and BASDAI (r = 0.73).

BASDAI (Table II) and BASFI (r = 0.30&0.59) thanwith BASMI (r = - 0.16) or gender (T = 0.09). Of thefive BASDAI items, spinal pain correlated best withBAS-G (r = 0.69), followed by fatigue (r = 0.66). One-way ANOVA demonstrated that the associationbetween BAS-G and occupational status was notstatistically significant, although it may become sowith a larger sample (P = 0.12). Comparison of separ-ate regressions of BAS-G on BASDAI, BASFIand occupationa categories showed that the R* stat-istics for BASDAI and BASFI (0.51 and 0.30, respect-

ively) were much higher than th(0.06).

There was satisfactory sensitivimprovement over a 2 week intenprogramme was expected, and oglobal scores for the week priorcourse m inus post-course, meS.E. = 0.31, P < 0.001). Overall,improvement in 1 week scoreimproved; Fig. 4) and a 6% impscores. The 24 h test-retest reli(1 week Y = 0.84, 6 months Y =



JONES ET AL.: AS GLOBAL SCORE

.’



physician can just as easily obtain an adequateverbal answer? The value of BAS-G, and thus thesecond way of considering these results, is thatwith patien ts answering the question on a visual ana-logue scale, numerical scores can be entered intothe medical notes ..to compare with scores at theprevious o r next consultation. From a practical per-spective, this may be helpful where patients do notnecessarily consult the same rheumatologis t on ,eachoccasion. The uatients should not have access toprevious scores when answering the question at a later

date.

&FkRENCES

Theoretically, it will now be possible to plot thescores over time to track changes in the perceived effectof the disease on patient well-being. The most subtlechanges-certainly changes more subtle than thoseshowing up in radiographs or in laboratory tests-should be detected. We propose the BAS-G as avaluable quantitative measure, developed to aidthe clinician in assessing how patients perceive theeffects of AS on their well-being. BAS-G may also bea useful instrument in clinical studies of AS. Further

research could lead to an understanding of howthe patient’s perception compares to the physician’sassessment. Finally, BAS-G is not disease specific incontent (as are BASDAI, BASFI and BASMI), andmay thus be applicable to other ch ronic or rheumaticdiseases.

1. Calm A. Can we define the spondylitis and the effect of phyJ Rheuniatol 1994;21:184-5.

2. B&ker C, Boers M, van der Lindankylosing spondylitis: taxonommendations. J Rheumatol 1993

3. Read JL, Quinn RJ, Hoefer health: an evaluation of threeJ Chronic Disability 1987;4O(s

4. Hiddlng A, van Santen M, vComparison between self- repo

observations of functional dspondylitis, rheumatoid arthrJ Rheumatol 1994;21:818-23.

In conclusion, we have formalized and validated asimple question universally asked of patients by clini-cians. The BAS-G generates a measurable answer inthe form of a numerical score which lends itself tosubtle comparisons over time. The score records

change where change is expected, is reliable, and meetsface, predictive and construct validity criteria. BAS-Gcorrelates well with both BASDAI and BASFI,suggesting that disease activity’ and functional abilityplay a major role in the patient’s perception of well-being. The contribution of pain and fatigue to thisperception is particularly significant, and merits furtherstudy.

ACKNOWLEDGEMENTS

We would like to thank the Arthritis and Rheuni-

atism Council for Great Britain, the National Ankylos-ing Spondyhtis Society, the Pilkington Trust and theCoates Trust for their financial support.

5. Mangen DJ, .PetersonWA. Resegerontology, Vol, 3, Health, proggraphy. Minnepolis: University1984.

6. Garrett SL, Jenkinson TR, WhitGaisford PM, Calm A. A newdisease,status in AS: the. BathDisease Activity Index (BASDA21:2286-91.

7. Calin A, Garrett SL, Jenkinapproach to defining functionspondylitis the development oSpondylitiss Functional Index 199+21:2281-5.

8. Jenkinson TR, Mallorle PA, WLG, Garrett SL , Calin A. Defankylosing spondylitis (AS): TIndex (BASMI). J Rhewnatol 1

9. Meenan RF, Gertman PM, Masstatus in arthritis. The ArthritisScales. Arthritii Rheum 1980;23

10. Goldthorpe JH, Pope K. The pation and a new approach tostudies of social mobility. Oxford

11. Bombardier C, Tugwell P. A mto develop and select ndices forand judgmental approaches. J R

1.2. Calin A, Edmunds I.,, Kennedyosing spondylitis-Why is it- 1993:20:991-5.

13. Calin A, Elswood J, Rigg S, Skespondylitis-An analytical revthe changing pattern of disea15:1234-8.

14. Kennedy LG, Eclmunds L, Calinof ankylosing spondylitis. Does i1993;20:688-92.



SARAH GARRETT, TIM JENKINSON. L. GAIL KENNEDY. HELEN WHITELOCK, PENNY

ANDRE1 CALIN

Kc!- ldc.rirtg Tmrr.~: -

AiKYLOSING SI’ONDYLITiS

SELF-AD1IINfSTERED INSTRUMENT

Discasc status. in terms of disease activity, discasc progrcs - _

sion and prognos is is di[ficulI IO tJcf?nc in ankyfosing spon-

dylitis (AS)‘. Fundamcnlal to investigating the natural his-

tory of the disease is the as~~ssmcnt of OuCcornc~. or which

radiology. metrology. and measures of functional (dis)ahil-

ity ,arc tool+J. Such measurerncnts of damage and its func-

tional consequences should. however. be distinguished from

measures of disease activity’. The assessmenf of disease -

activity in a predominantiY axial d isease such as AS is notori-

ously difficult and. as yer. no gold s tandard existsr,4. In

contrast to the situation in rheumatoid arthritis (RA). tabora-

tory indicators of disease activity refitit neither clinical

I>ISllnSE

activity nor radiological progrc

conrrovcrsial In RA. a core se

has been inrrcKluccd~-‘. prc@Iin

tcchniqu& I”. In AS. such

Newcastle Enlhcsis Index ” and

Index (DAI)rz have been dcscr

Iruc mcasurcmcnts ofdiscdsc a

quatcly validated. In addition.

sive, For example. recent rcs

Hospital for the Rheumatic Dis

skated that fatigue is a major

patient+ and this should now

measurement of disease activity

index is therefore ncccssary. To

ing Spondylitis Disease Activity

administered instrument, has b

.,,_.-.,.. . ,_ .

>

: Eprsdii6;b,*~*+$iip.&-lJ*g

severity. It needs, in addition, to be qui

plete. Finally it has the advan tage of p



choice and relative importance of each component is appro-sive method of obtaining clinical inf&

p&e for the purpose of the index); face (the methods of safely and frequently repeated.

weighting and aggregating components into an index are sen- MATERIALS AND METHODSsible); criterion (the index produces consistent results chat The index BASDA I was developed. on chc basis

reflect the true clinical state of the patient); discriminant (the a team of physiolhcr;lpists. rcscarch asscciatcs

index detects the smallest clinically significant difference ;I major input hm paticn!s w ith AS. The rcsulri

betwmn and within patients); and construct (the index agrees 6 questions rclarin~ >o 5 nxtjor syrtxprorrts rclev;

with expected results based oh the hypothesis of the investi-pain. joint pztinlswelling. xcc3s of localircd lcnd

IICSS (Figure I). The Ixr is rwasurcd in tcrws

gator). A self-assessment instrument should be reliable. stiffness) and qmntily (lcngtb oftimc for which w

,’ ,, f 4

‘( .,; _ ,‘? ‘.. . ;.I.._’ ::,cy&.,. 1 L .,_. IlASD.‘\Id

*, : :;c;, :.,,:”The l3ath Anl~ylosing Spcmdylitir Okcase Acci\icy lndcx. xi:- .i

Ten ccnriwtrc visual analog scales (VAS) wcrc used Co mea.wrc k

______h’a$art (D$ b of treatment: m

Day I: mean score = 5.438, S

The capacity of the BASDAI



patient’s rcsponx. to each question as chcy allow maximum reliability. and

sensitivity to change and improve rhc capacity of a” index 10 elicit a range

of rcsponscs across the entire scale. In accordance with previous Work”

the VAS wcrc’unmarkcd. CXCC+X by rhc words “none” ac tic start and “VCrY

scvczc” ac chc end of each line. The cxccption was a O-2 h time scale (mark&

at cvcry quancr ofan hour) used IO mcdsurc quantity of morning sriffncss.

TIC time scale given for this mca~urcmtn~ was dcrivcd from an ahal+

of rctrospcctivcdxta regarding durarion of morning stiffness. in aboul 2m

pticnc qucstionnaircs (unpublished dam). From rhc rang< of porriblc ~IISWC~S

(“ovc’r 4 h”Grs” to “do no< have horning niffncsr”) the rnca” rcspo”K

tV=s found ~0 bc 30 min to I h. Thus I h wvas taken as rhc “xidpoi”: of the

rinlc rcalc. wirh 2 “r more h bci”,n _eivcn the maximum score.

Each visual acwlog scale was scored from 0 10 10. The “XX” “f the 2worcs rclxing w “wming Gffncis uzc tzkcn. providing a” aggrcga~c SC”TC.

Thus each syn~pcon~ is given cqusl wcighcing. The rcsulring O-50 wore for

[he o~er~il iodsl ,,x ~~~“~cncd LO I 0- IO w;lk (0 give [hc fiwl BASDAI

A pilot qucni”““zirc wxs given ICI .I group of paticnls o” a 3-week intcn-

sive physiothcrlpy CORN. Modificxutms ICI’I~C index. such PS IIIC wording

of qucstionr and the intlusion of quxlity of “toming stiffness WC~C nude

as a rcsulr “I p;lricnr feedback.

The fin;ll vcrziw “f the BASDAI u-as c<icimplcrcd hy 4 .scts vf inpacienls

(n = 46) “n 4 yp~rzc crcxsions during their physiotherapy course: Days

0. I. 8 and IX. One hundred and cishr othcrsplndylitics. including RNHRD

uu+tricnrs and “~cmbcrs “f vari”u< h:AsS (National Ankyiasing Sp”ndy-

liris S”cirty) self-help group?; ~11s” compictcd the iosrrumcnc. This rc~uhcd

in ;L mcztl of 292 qucstionnxircz complc(cd by I54 pacicnts.

As x “wxns rrfcomparison, ~hc carlicr Bath DAI’? WIS given w paticnl?.

cxh rir~rc [hey c”mpicGi rhc BASDAI. I” addition. chc Ncwcaztlc Enthc-

sis Index” wils carried wt by z phystorhcmpiar on Days 8 arid IX “ftrcat-

mcnt with 25 inpaticms. Brah th< DAI and the Ncwcastls Enthesix lndcr

scn~cs wcrc convcncd m a O-IO scale IO cnablc direct coolp~risci” with thz

OASDAI.

User friclidlincsl. ICS‘C-rctcst rclmbil”y. score distriburkm ;rnd .scnsr[ivit)

w change wcrc all tinalyzcd for [hc BASDAI and wcrc compared tu resuh~

frum the DAI and rhc Ncwcns(le Enlhcsis Index. Rcliabili[y was as.u~~.xdby testing thccorrzlation bctwcc” B~SDAI,SC~~CS taken a( (hc ~lmc tirrxe

ofday rm Days 0 and I “f the inpalicnc cwcsc: approprialc USC uf the scale

wils a.sccnaincd from the range and mc~+n of sccorcs given by the total paricnr

population (using the Day 0 scars f”r the inparicnc cohort): while scnsi-

livily of (hc BASDAI w change was analyzed by a comparison “I inp;rticn(

scores. on Day 0 and Day IX of ~rcarnsnr.

Pmsihtc redundancy within the mnde~ wax rcncd for by analyzing drz degree

elf xsnriarion bctwccn scows given for fach nf the 6 questions.

Analysis of rcwltr wxs carriuf our using the UNLSTAT s[a[is(ical soft-

k+rc on a” IBM compariblc PC. The Pearson correlation cocfftcienr was

usul to perform corrclaGons: the Wilcoxon signed rank CIX and the Kntrkai-

Wallis one way ANOVA ior analyses of difference.

RESULTS

The mean age of the 154 patients (I IS men: 39 women -

a 2.9:1 ratio) who completed the BASDAI was 47.7 (SD

across the scale was good, witthe whole patient sample (n

4.31, SD 2.12 (Figure 2). Th

inpatients (5.06) was significan

patients (4.0; p = 0.005).

Ah o f the individual sympto

bution, with scores spread ac

Correlations between each set

tween r = 0.34 (-‘fatigue”

0.66 (“spinal pain” versus

correlation bctwccn quality aness was closer: r = 0.79.

The comparison of inpatien

on Day I8 of physiotherapy s

sitivc to change. The mean s

5.31 (SD 1.74) and 4.46 (SD

a significant improvcmcnt o

(p = 0.009: rncan score chang

mcnt]: rang e = -4.0 to +2

I.

Table 1 Comparisor? oj- DAi

validify crireria arwlwed

DAI

Time 75

(mea” seconds)

Rcproducibilicy r = 0.96

(Day 0 vs Day I,

,

. ..- ..

__ ._, - _ _-. eL---..s

The BASDAI correlated weII with the DA1 in ali aspects

of validity criteria (TabIe I). However, a significantly higher

- _ _-.

DiSCUSSION

The development of the BASDAI



.number of patients (x2 = 7.21, b = 0.009) felt that the

BASDAI contained the most suitable questions for obtain-

ing information on the symptoms of those with AS. Inpatients

took a mean of 75 s (SD: 34.59) to complete the DA1 which,

like the BASDAI. was highly reliable (mean score on Day

0 of treatment = 5.38, SD 2.29: mean score on Day .I .-=

5.66. SD 2.46: r = 0.96. p <O.OOI). Score distribution

across the scale was equal IO hat of the BASDAI (mean score

= 4.12. SD 2. IO; range 7 O-9.5; Figure 3). and there was

a good correlation between the 2 sets of scores (r = 0.75;

p <O.OOl). The mean inpatient DAI score(s.13) was againsignificantly higher rhan that of the outpatien ts (3.79:

p = 0.001). The DAI reilccted the sensitivity IO change

shown bv rhc BASDAI. with mean inpatient scores improv-

ing fron; 5.34 on Day 0 of the 3 week course to 4.12 by

Day IS (p = 0.002; mean score change = - I .22 [22X%

improvcmcnt]:~iangc 3 -6.3 to +2. I). There was no sig-

nificant partiality am ong the patients for tither the DAI or

the BASDAI in terms of which questionnaire was the easi-

cst to understand and complete. or overall qucstionnairc

prcfcrcnce.Among the cohon of 25 inpatients on whom the Ncwcastlc

Enthcsis Index was also carried out. the BASDAI showed

superior distribution of scores across the scale and greater

sensitivity to change over IO days of physiotherapy. The

mean Enthesis Index score on Day 8 of treatment was 1.96.

with a range 010-5.33. compared to a mean BASDAI score

of 5.06. with a range of 0.83-8.79. While the mean BAS’-

DAI score improved significantly from 5.06 to 4. I5 by Day

18 of rrcatmcnr (p = 0.009: mean score change = -0.9 I ;

range = - 3.7 to + I .66). there was no comparable changein the Enthesis Index scores over thfs period (mean score

on Day 8 = 1.96 vs mean on Day I& = I .79,. p = 0.35;

mean score change = -0.18: range = -1.73 to i-1.22).

Reliability of the Newcastle Enthesis Index has already been

shown to be poor”.

satisfaction with existing measure

For example, the Newcastie Ent

Specificaliy, it is very limited in

on the entheses, and thus does n

of symptoms in AS. It exhibits ne

score range. nor sensitivity to cha

advantage of the measurement is

clinician or physiorherapisf to ‘pe

is thus expensive in terms of tim

the earlier Bath DAI is not fully

ally. it omits rcfcrence to fatigue.

ncss and localized tcnderncss.

Naturally. rhc components inclu

strumcnt arc not exhaustive. but r

yxGhlc questions. If rhcrc is a ver

rhc rcsponscs tu 2 diffcrcnt qucsri

obraincd from one question mirro

other (intcmal redundancy). It is th

indices which adcquatcly rcprcsen

(cg.. discasc activity) without spe

possible question’? This is an impis an invcrsc correlation bctwccn

included in an instrument and th

obtained’“.

The five components of thc,BASD

in ascertaining a comprchcnGvc

cxc activity. Fatigue. previously u

ciudcd in the light of rcccnt icsc

an important and common sympto

rc.scarch was a dirccr resu lt of palicnizcd that thcrc arc 2 main xourccs

and pain in pcriphcral joints. T

symptoms and need to bc meas

tcndcrncss was included in order t

sitis. Morning stiffness was rccag

nificant aspects: no1 only is the

- morning stiffness persists imporran

ness should also be raken into accou

with on ly I5 min of stiffness each

severe debility during this period affected as a patient with stiffness

who suffers very little reduction o

inclusion of both the quality and q

ness does no : however give this sy

“.

_.--_- 7_ _ ‘. . _ “- . _ - , - . . . -

noncorrela tion to justify the inclusion of both aspects of the

symptom (Figure 4).

Although, after validation, the DA1 showed greater change

- .--rr . ,- ._-.

3 weeks of physiotherapy is l

nificance. Further study is requ

tivity of the index in relation to



over 3 weeks of treatment than did the BASDAI (22.8 vs16.4% score improvement: NS), ,this may be, a result o f its

bias towards pain and its inclusion of a-scale measuring the

patient’s well-being. The score change is, arguably, more

likely to be a reflection of the effects of the intensive phys-

iotherapy program on these aspects than a greater sensitivity

ofthe DA1 to change in disease activity as a whole. The

BASDAI does not differ from the DA1 in any of the other

areas analyzed (reliability, use of the scale and user friend-

liness), bu1 s superior, from the pcrspecrive of both patients

and clinicians, in 1crms of face and content validity, com-

prehensiveness of symptoms and their, weighting. The BAS-

DAI has. in addition. proved to bc susrior in all aspects

to the Ncwcasdc &thesis Index as a measure of discaso

activity.

The diffcrcncc apparent bctwecn the mean scores of the

inpatients and outpatients for both the BASDAI and rhc DA1

wet-c predictable , since patients on an intensive hospital

course would naturally tend to bc those with worst discasc.

The ability of the BASDAI ‘to distinguish clinically sig-

nificant diffcrenccs in both inter and intrapaticnt rcsponscs

(discriminant validity)” was shown by the tota range of-

scores among patients. rcflccting’thccntire disease spectrum,

and further by rhc scnririviry of 1hc index to change within

patients on the 3-week physiotherapy course. The 16%

(men) improvcrncnt in the symptoms of those paticms a fter

a more dramatic effect on resultgram of physiotherapy. Although

ing drug for AS (in contrast to th

nonsteroidal antiinflammatory d

on symptoms and therefore on

could thus be incorporated in

studies.

In summary. BASDAI is a co

the measurement ofdisease activ

highly reliable. reflccfs the enti

cxhibils the ability to be sensitivstriking is its recognition of the f

cnccd by patients with AS. som

addrcsscd in previous ntcasurcn

more prccisc &inition of disca

cnhanccd understanding of outc

I‘ _

KEFEKENCES

IO. Mallya RK. Mace BEW: The nsscs

rheumatoid anhritis wing a multivari

Rchotd 198/rZOrl4-7.

Il. Mandcr M. Simpson JM. McLcflan

JA. Carson Dick W: Srudics with

of clinical asscssme‘nt in ankylosing

1.

18. F&x IF. S piu PW , Young DY: Touccomcs: he He&h AssessmentQ

pain xafcs. 1 lueuma~0l1982,-9:78



L .

19. LcVy P. Lcmcihow S: Samphg for

Belmont: Wadswoti Publishing. 120. Calin A: Editorial. Can we dcfrnc

spondyliris and chc effect of physiof Rlwamarol 1994:2 1: 184-5.

I

‘Defining Spinal Mobility in Ankytosincj Spondy

The Bath AS Metrology IndexTIM R. JENKINSON, PATRICIA A, MALLORIE, HELEN C. WHITELOCK, L. GAIL KSARAH L. GARRETT, and ANDRE1 CALIN



ABSTRACT. Objective. To determine the most appropr iate clinical measurements or the assessming spondylitis (AS).and to develop the new metrology index.Methods. One hundred and ninety-three individuals with AS were studied. The pat

the entire spectrum of casesof AS. Metrology was performed on 327 occasions. Firs

.-s gy (20 measurements) f 43 patients was analyzed. From this, 5 simple clinical measdefined which most accurately reflect axial status: cervical rotation, trap to wall diflexion, modified Schober’s, and intermaIIeolar distance. These measurementswerreliabitity, speed and both inter and intraobserver variability in another 40 patient

Results. Analysis of the first group of 43 patients and a subsequentgroup of 54 patie5 measurements hat constitute this new Bath AS Metrology index (BASM I), demonst

accuratelyand reliably mirror the 20 clinical measurements ssessed reviously (r = 0.9In a new group of 40 patients the measurementswere demonstrated o be accurateandfor both intraobserver variability (r = 0 .99, p <O .OOl) and interobserver variabilitp ~0.001). In a further 56 patients, admitted for inpatient therapy, an improvement from 3.34 (SD 2.71) to 2.16 (SD 2.42) was noted over a period of 3 weeks (regardlseverity) wh ich indicates a sensitivity to change (x2 = 6.55, p <O&1). The ma- over baselinewasabout 30%.Conclusion. Five clinical measurements provide a composite index (BASMI) and d

status n AS. The BASMI is quick (7 min), reproduc ible and sensitive to changeacrospectrum. (J Rhematoi 1994;21:1694-8)

Key Indexing Terms:METROLOGY INDEX SPINAL MOBILITY AXLRELIABILITY SENSITIVITY DISEASE PR

Disease tatus n ankylosing spondylitis (AS) can be definedby metrology, radiology, Laboratory ariabIes and functionalcapacity’. The relationship between these and diseaseactivity, disease progression, and response to treatmentremains uncle&. Limitation of spinaI movement is an early

feature of AS and its importance as a clinical sign is empha-sized by its ificlusion in the New York diagnostic criteria].

Methodsof determining diseaseprogression include sequen-tial assessment f spinal mobility. Numerous physical meas-urementshave consequently become widely used since theoriginal assessmentsdefmed by Go11 aid Wright4. Fre-quCntIy hesemeasurements re not standardizedor assessedfor reliability, validity, or sensitivity to changes.

Historic&y up to 20 separate measurementshave beenused n the assessment f patientswith AS attending he Royal

From the Royal Notional Hospital for Rhewndc Diseaxr, Eka~h Al

1R.L.

Suppo+d by the Arthritis and Rheumadsm Cow zcil of Great Britain;

the Narionql~akyiosing Spondylitis Society, the Gxztes Tmtr. and thePilkington Trust.

T. R. Jenkinson. MRCP; P.A. M allorie. RSc, MCSP; H. C. Wkite~ock,~

MCSP;L-G) Kennedy, BSc Horn: S.L . Garrett, BA Horn; A. Gziin.MD, FRCP.

National Hospital for Rheupatient population encompasease in AS. Inpatient treatme

patients with severedisease ua11 atients in&ding those wspecific exercise therapy is con

with AS in order to maintain

as a consequence their overailof life. Our aim was to determ

clinically appropriate measuraxial status i.e., cervical, dorpelvic soft tissue) and from th(the Bath Arikylosing Spondylit

to define clinically significant

MATERIALS AND METHOD

In total.193 onaeeuti~enpatients etrum of diseasen AS, and metroloccasions. First the metrology of 4criteria3 or definiteAS wasanalyzedmatologists, hysiethetapistsndcesein AS. Intuitively, and following an simple clinical measurementshichreflectaxial statuswerede!&& cervic

. ,

table from which a total score oft&lO/patieni could be derived (Table 1).

Subsequent xam ination of the metrology on a further 54 patients was per’

formed comparing the total me trology score of the 20 measurements er-sus he compositescore (also with a range of O-10) of the 5 me asurements

that comprise the BASMI (Table 2).

Thesemeasurementswere assessedor interobserver, intraobserver yar-iation and reliability. The observerswere 3 physiotherapists,all of whom

Table 2. BASMI (bath ankyloindex)

I. Tramps o wall,

0

c 15c-0

2. Lumbar flexion 7 4c



hadexperience n assessing S. Twenty patientscompleted he interobserverassessments . ach patient was measured, sing the 5 clinical measurem entsmat form the BASM I, by eachof the 3 observers eparatelywith the remoValof any skin markings following each assessment. he resulti were alsodocumented eparately o hat the observerswere blinded o their COk?WS

results. The intraob server assessments ere determined by each of the 3observersmeasuring a further 20 patients on consecutivedays at about thesame ime. Meastiements were recorded from mid-morning to allow for,resolution of morning stiffne ss and were documentedseparatelyso that the’

observersWereblinded to their previous esultsand thoseof their c01leagueS.Cervical otation was measuredwith a grav ity action goniometer. he mean

of right and left results being calculated. The patient lies supine n the neu-

tral position and the goniometer is placed centrally on the forehead. The:patient s then asked o turn the headas far as possible o the right and then.to the lef@. For measurements f the tmgus to wall distance the patient!standswith heelsand buttocks ouching the wall, kneesstraight, shoulders

back and piaces the head as far back as possible, keeping the chin in’.’Lateral spinal flexion is measured y Fingertip o flwr distance n full Iateralflexion without flexing forward or bending the knees, using a ruIe mount-ed on a floor &nd5. The patient bends aterally to push the middle finger

of the right or left hand down the rule and the difference between start andend points s recorded and the meancalculated. Lumbar flexion is assessedby the Macrae and Wright modification of the Schober nde xs. A ma rk isplacedat the lumbosacral unction, which is represented y the spinal nter-

section of a line joining the dimples of Venus. Further marks are piaced5 cm below and 10cm above he htmbosacral unction. The patient s asked

to bend orwards as far a s possible, keeping the kneesstraight, and the dis-traction between hese2 marks s recorded. Intenalleolar distance s meas-ured with the patient supine, he kneesstraight and the feet pointing straight

Table 1_ Original metrology assessment (20 measurements).

score0 1 2

1. Tragus to watl <I5 cm 15-30 cm 7 30 em

2. Lumbar flexion >4cm 2-4 cm <2cm3. Intermalleolar distance >lOOc m 70-100 cm < 70 cm

4. Cervical rotation (L) > 70” 20-70” < 20”

5. Cervical rotation (R} > 70” 20-70” < 20”

6. Lumbar side flexion (L) > 1Ocm S-10 cm < 5 cm

7. Lumbar side llexion (R) > 10 cm 5-10 cm <SCUl

8. Cervical side flexion (L) > 40” 1040” < 10”

9. Cervical side flexion (R) > 40” 10-40” < IO”

IO. Fingers to floor < 20 cm 20-40 em > 40 cm

11. Lumbar extension > 1.5 cm 1.5-0.5 cm < 0.5 cm

12. Cervical extension > 40” 15-40” < 15”

13. Cervical flexion > 45” 20-45” < 20”

14. Vi& capaci&y .> 3.51 2.0-3.51 < 2.0115. Chest expansion >6cm 3-6 cm < 3 cm

16. Height loss 0 cm O-I cm 7 I cm

17. Shod~er flexion (L) > 140” 110-140” < 110”

18. Shoulder llexion (R) > 140” 110-140” < 110”

19. Shoulder abdnction (L) > 140” 100-140” < 1oQ”

3. Cervical rotation> 70

4. Lumbar side flexion > IOb

5. Intermalleolar distance 7 1Oi

BASM I 0 indicates mild disease nvolv2 = severedisease nvolvement. Resu

side lexion are the meansof the eft and

O-10. :

up. The patient is as ked o separate he

tance between the medial malleoli is.m

A further 56 patientswere assessedt admission for an intensive exercise eg

for sensitivity to changeover a short trwas performed through the UNIS TATS

PC, using Pearson’s orrelationcoeflicie

bility and sensitivity respectively.

RESULTS

The total metrology scores deon each of 43 patients (39 mento the new BASMI. The meanyears (SD 11.4 years), the mea22.6 years [SD 7.8 years) and hyears. BASMI correlated with disease-duration@ <0.004) a&(Age p <O.OW, diseaseduratison between BASMI and the ora good correlation value (r = 0To verify the reliability of the2nd cohort of 54 patients (40 mrent age 43.4 years (SD 9.3), 23.5 years (SD 7.51) and mean

(SD 9.4) was analyzed. The BAthe total metrology score (r =The BASMI was assessedn

terobserver variation. The patiedently by 3 physiotherapists. Cp <O.OOl), tragus to wall (r =side flexion (r = 0.94, p <O.O0.96, p <O.OOl), and interma<O.OOI) demons trated ittle in

A further 20 patients were as

Lion. Cervical. rotation (r ,= +i.lI (r = -&&,~p <OkI); h&

p <O.OOl), modified Schoberintermalleo iar distance (r = 0to be accurate and reproducib

I

8 0



3 -- a.&..

0 . ..I.. 0--0 q r30 DO

Cl D cl 0 0D 00 cl Cm 0 01 -- ..“..~.,y&

DO m q D 0

0

0-m ; I , ,I t

0 10 20 30 40 50 60 70. 80

SUBJECT NUMBER

Fig. 1. A graph to show the relationship between BASMI and the original measuremen ts n 97

p <O.OOI). m BASMI score, 0 = original assessm ent core (both on scale of O-10).

over baseline. Themean currentage of the cohort (46 men:10 women) was 41.3 years (SD lO.l), mean age at symptomonset21.5 years (SD 6.5) with a mean diseaseduration 19.9years (SD 11.6) Seventy-one percent of the patientsimproved, 29% remained the same and no patients deterio-rated over the 3 week treatment period (Figure 2). Of the16 patients who failed to improve 8 had an initial BASMIscore of 0, with a further 4 having an initial score of 3 orless out of IO.

ZERO TIME + 3 WEEKS

n-4 6 6 n-2

n-3 5 5 n-7

n-7 4 4 n-5

n-7 3 3 n-5

n-5 2 2 n=2

“i-12 1 1 n-11

n-8 0 0 n=21

MEAN 3.34 MEAN2.16

(SD 2.421

Table 3. Inter and .intraobser

Interobserver ReliabilityMeasurement

Tragus to wallLumbar flexionIntermalleoIar distance

Cervical rotationLumbar side flexion

Intraobsewer ReliabilityTragus to waN

Lumbar flexionIntermaIieolar distance

Cervical rotationLumbar side flexion

DISCUSSION

The present study was prompavailable for measuring spinalnot validated or reliable and so

tation or radiography. There isof measurements hat are simand clinically relevant. Standspinal movement not only proof diseaseprogression n AS, b

“ I ,_ _ - .

a.,! ,_

The hip is the most commonlinsidious loss of movement andmore incapacity than a rigid spment of the hip is often neglectFurthermore st&dard,assessmeurementsare unreliable. We havlar straddle as a simple and accu

:. ! ment as there is no universal agreement on the methods of’ measuringdisease activity or iunction’in AS”. In, addilibti,

it is possible that diseaseactivity indices should be ikparat-

ed from those purporting to measurediseaseprogression andits functional Consequences12.

With this in mind, a team of rheumatologists, ‘physio-i therapists and research associateswith a specialist interest



hip ahd pelvic soft tissues.’HistoricalIy, up to 20 separatbeen performed as part of the ASonly is this expensive n terms ofbut many of the measurementsreliability. We have .demonstrtotalling almost 100 patients, th(BASMI) ,mirrors the informati‘numberof &asurements and is astatus p <O.OOl). In addition, o

and intraobserver reliability of wall distance, lumbar flexion a

Furthermore, the BASMI dchange across the whole diseaspatients with severe diseaseof lotant as it is often considered thaits disability during the first decresponse o treatment in late disprovements may be clinically ireversal of a deteriorating tren

Almost half of the patients (14%began the treatment with a BASprovement noted n 7 1% of patieperiod of intensive exercise and

In conclusion, (1) 5 simple clina composite score (BASMI) andand (2) this metroIogy score is qble, reproducible and is sensitivease spectrum. Further studies arelationships betweenmetrology,and function.

j in AS undertook an extensvie eview of the literature to deter-’ mine those measurements ound to be most reliable and clin-I

ically useful. The measurements onsidered most accurately1 to reflect axial status nclude cervical rotation, tragus to wail

distance, IateraI spinal flexion, modified Schober’s, and in-termalleolar distance.

Cervical rotation occurs at the atlantoaxial joint, is a, reproducible measurementand is an important reflection of

neck functionl3. Cervical rotation was measured with ai

/

gravity action goniometer and this method has been demon-

strated to be simple, cheap, accurate and reliable13. Rota-/ tion can also be measured by means of a neck protractor;

the neutral position being O”, with the 90” mark over theacromioclavicular oints and a perpendicular ine through thenosebeing the interceptm.This method has also been shownto be highly reproducibles. Although lateral cervical spineffexion is often reduced n AS, significant interobserver var-iations have been demonstrated n its measurementIs.

Tragus o wall d istance s a measureof lower cervical spineflexion and upper thoracic kyphosis. It provides an accurateassessmentof proximal axial disease progression and ishighly reproducible7.

7Lateral spinal flexion occurs at the lower thoracic and the

lumbar spine Bnd is often the earliest movement restricted-

in AS14.The fingertip to floor distance on lateral flexionusing a rule is considered to be the most reliable method ofassessment’s. umbar side flexion was initiafly found to bethe most variable measurement.Attention has to be paid tothe starting position and downward movement of the ruleshould be a consequence of lateral flexion only. Using trick

movementspatients can attempt o depress he rule by down-ward movementof the arm without lateral flexion. The differ-encebetween he start and end positions is recorded and the

mean calculated. This ensures that the assessment s notaffected by the initial position of the rule which can be in-

fluencedby the degreeof kyphosis of the patient. Once thesepractical changes were adhered o, lumbar side flexion wasfound to be as reliable as the other measurementsused inthe index.

., .L-;.I

:,:.::

; ,:. 1, ;, _:: are

!.’ ... len-__:: ‘. ij I set,.:z.,./ ,. .’!,.,, .“’ i lble;’ ’ : 1

; It ofi ._, :-4 ‘. I lent: :!

ved 1

.~ \:: I :

‘. :ria- ’.‘( .: :,

Fingertip to floor distance was originally described as ameasurementof erector spinae and hamstring extensibility,and includes not only spinal movement but also hip mobility,Posterior leg muscle and ligament tightnesszl. Although ithas been shown to be a reproducible measurement, t is in-

ACKNOWLEDGMENTWe thank our researchsecretariesJeanW

secretarial assistance.

REFERENCES

I. Rigby AS. Silman AJ: E ditorial ou

trials of AS. Br J Rheumatol 19??

2. Taylor HG, Wardle T, Beswick El

clinical and laboratory measureme

AS. Er J Rheumatoi 1991;30:330-5.

3. Bennett PH, Wood PHN, eds. Pop

Rheumatic Diseases. Amsterdam: E1968:456-7.

4. Mall JMH, Wright V: Normal rang

i WI. L-

’ 6. Joint Motion. Method of &feoswing and Recording. Chicago:

American Academy of Orthopacdic Surgeons. 1965:#-64.7. TomJinson MJ, Bare foot J. Dixon .A St I: Inte ri& iii+tiknt

physiotherapy courses mprove movement and posture of AS.Physiockerapy 19%6;72:238-40.

8. Macrae IF, Wright V: Measurementof back movement. Anf~

Rkeum Dir 1%9;28:584-9.

9. Calin Ai Ankylos‘ing spondylitis. In: Kelly WN , Harris ED,

Ruddy S, Sledge CB, eds. Tatbook of Rheumatology, 2nd ed.

k &tad’IS. Reynolds PMG: Measurem

of ttirv methods. Rheumor

16. Dudley Hart F, StricMand Dmobility. Ann Rhewn Dis 19

17. Schober Vpn P: The lumba

Much Med WSCW 1937,.8

18. Carette A, Graham D, Littlecourse of AS. Arthritis Rkeu

19. Roberts WN, Barefoot I. C



PhiladeIphia: WB %unders, 1985:993-1005.10. Sturrock RD, Wojtulewski SA, Hart DF: Spondylometry in a

normal $opuIation and in AS. Rheum&l Rehobil

1973;12:135-42:

1 . Editorial. Assessingdiseaseactivity in AS. Lancet 1987;1:1072.

12. Beflamy N. Buchanan WW: Clinical evaluation in rheumatoid

diseases. n: McCarty DJ, ed. Arthritis and Allied conditions.

PhiiadeIph ii: L ea and Febiger, 1989:158-86.

13. Moffet JAK. Hughes I, Griffiths P: Measurement of cervical

spine movements using a simple inclinometer. Phys leer

1989;75:309-12.

14. Mall JMH, Liyanage SP,’ Wright V: An objective clinicalmethod to measure !a&1 spinal flexion. Rhe um Pkys Med

1972;11:225-39.

i

anthropome tric techniques fRheumaoi 1989;28:40-5.

20. O’DriscoII SL, Jayson MIV,in A S and their response o

1978;37:64-6..2 I. Kraus E, J+cmnenger-Web

structuural nd functional me

1945:25:267-71.22. Klippers V, Parker AW: To

validity. Pkys ilzer 198X67:‘1

c

A New Dimension to Outcome: Application

Bath Ankylosing Spondylitis Radiology IndANDRE1 CALIN, KIRSTEN~MACKAY, HELENA SANTOS, and SINEAD BROPHY



Ankylosing spondytitis (AS) is a chronic inflammatory pro-gressive disorder mainiy affecting the axial skeleton and theperipheral joints. The disease is a result of interactionbetween genetic and environmental triggers. A number ofmeasurescan be used simultaneously to monitor outcomeand these are fundamental in assessing he natural history ofAS’“. Characteristic radiological appearancesat the sacroil- .iac (SI) joints are essential o r diagnosis of AS’, but no,dlas-sitication completely defining axial and hip radiologicalchange exists in AS. The Bath Ankylosing SpondylitisRadiology Index-total (BASRI-t) is a new system for scor-ing radioiogical change or the spine and hip in AS8. Resultscan be divided into Bath Ankylosing Spondylitis RadiologyIndex-spine (BASR-I-s), which combines the scoresof the SIjoints, lumbar spine, and the cerGca1spine, and the BASFU-hip (BASRI-h). We describe BASRI-t, BASRI-s, and

From the Epidemiology Depamnen~, Royal Nationnl Hospital for

Rhewzaric Diseases, Both. UK.

Supponed by the Nationo[ An/$osing Spondylitis Society. John Comes

Charitable Trust, and Cof. W.W. Piikington Chnrirobie Trrtst.

A. C&r, MD. FRCP. Corrs&mu Rheumatologist; K. Mackay, MRCP.

BASRI-h and demonstrate thstudy.

MATERIALS AND METHOValidorion of BASRI. Existing. Rnd

using the yew York criteria for AS. w

were-scored openly dnd placed in on

scale for SI joint disease. The radiopelvis, an AP and lateral lumbar sp

lumbar spine was defined as extendin

upper border of S 1, and the cervical

the upper border of C7. The discrim

defined and used as the basis CO esc

radioio$cal change in AS . The s yblinded fashion by 3 experienced re

occasions before a final format was

bar, cervical nd hip radiographs areTo assesswhether AP or lateral

sets of Lumbar and ce rvical spine

views Were scored using f 1) AP aloviews’ contribution (as a compositeeach view was determined and comp

After definition of the scoring s

patients with AS and 89 without AS

the 3 readers CO alidate B ASRI. The

ABSTRACT. Our aim was to develop a reproducible and simple radidlogical scoring system f

spondylitis (AS) to use in cross sectional and prospective studies. Regarding valBASR I (Bath Ankylosing Spondylitis Radiology Index), rad iographs of 470 patients

scored using the New York criteria for the sacroiliac joints. The lum b& and cervical s

were similarly graded O-4. These scores were added together to give BASRI -t (total)

are excluded to give B ASRI -s (spine). Ra diographs of 188 paiients were used to test

ty. Blindeh radiographs of 89 non-AS patients were incIuded randomly to assess disea

Sensitivify to change was assessed using 177 radiographs from 40 patients. Regarding

tional study, 2200 radiographs of 550 (104 F:446 M) patients were randomly selecte

using BASRI. The frequency disiribution of BASK I-t rind BASR I-s were plotted using

Inter and intraobservation showed between 73 and 82% and 73 and 88% complete agspecificity of 0.78-0.89, suggesting scores are disease-specific. Sensitivity to change b

ent at 2 years (p < 0.05). S coring required 30 secbnds to complete. BASRI-t was fou

mally distributed using a probit plot. The mean BASR I scores (total, spinal, hip) incre

ease duration. The correlation, however, was poor (I. = 0.293,0.347,0.263, respectively

hip invokement had more severe spinal disease (p 2: 0.0001). Men had more severe

than women (p < 0.0001). We conclude BASRI is a reliable and rapid m ethod to grad

ic chat&s in AS. Using this scoringsystem t can be seen hat AS is a slowly progwith m uch individual variation. Hip patients have more severe spinal disease than thos

involvement ndmen havemoresevere pinaidiseasehanwomen. (J Rheumatol 199

Key O&xing Terms:ANKYLOSING SPONDYLITIS RADIOLOGY BASRI ~

Table IA. BASRI-spine..I . ::. . .

score Grade ,:,.;b_ System Applies to Both Lumbar and Cervical Spine

0 Normai No change

1 Suspicious No definite change

2 Mild Any number of erosions, squxin~, cierosis syndeson 2 2 vertebrae



3 Moherate Syndesmophytes on >- 3 vertebrae r fusion involving 2

4 Severe A,; Fusion involving 5.3 vertebrae

Table IB. BASRI-hip.

score Grade Description

0 NormaI No change

I Suspicious FocaI joint space narrowing

2 Mild Circumferential joint space narrowing z 2 mm

3 Moderate. Circumferential joint space narrowing c 2 mm or bone-

apposition of ~1 cm

4 Severe Bone deformity or bone-on-bone apposition >I cm

NB: Increase the grade by 1 if 2 of 3 of the following bony changes are present: erosions, osre

sion.

pelvic radiographs taken. Their mean age was 57.9 + 16.8 years, sex ratio

1:3 (M:F). T he cohort included 41 rheumatoid arthritis, 21 mechanical back

pain, 10 fibromyalgia, 10 osteoporosis. 7 psohatic arthritis.

Cross secrionai study. We randomly selected and scored 2200 sets of films

of 550 (4:1, M:F) patients with AS, using BASRI-t. The frequency distrib-

utions of BASRI-t and BASRI-s were piotted using a probit plot to estab-

lish parametric distribution. The probit plot is a scatter diagram that is lin-car if data are normally distributed and curved if they are not. Of the 550

patients, there were 423 with known disease duration.

Srarisrica[ n ~er/mdx. For validarion of BASRI: The data were nonparamer-

rically distributed: therefore an unweiphted kappa statistic was used to

determine the significance of inter and intraobserver variability. The

Wilcoxon signed rank test was used to assess significance of change over

time. For the implementation of BASRI: correlations were established

using Pearsdn’s correlation coefficient for normally distnbuted variables or

Spearman’s rank order for non-normally distributed variables. Independent

t tests or Wilcoxon nnk sum test and chi-squared were used to evaluatemean scores. ‘llxe SPSS software program was used for all analyses.

RESULTSLumbar spine: ~yhich ilm should be used. Using 58 sets ofAP and laterai lumbar spine radiographs, 3 scores werederived as described above. The combination score differedfrom both the AP and lateral scores if syndesmophytes orfusion was seen at different levels’ on each projection and

occurred in 3/58 cases.The cthe AP alone in 9/58 (16%)21/58 (36%) cases. Over changed the score 46% of th

Irztruobserverva~iation. The

scores were (Table 2): 86% SI joints, 75% agreement (ka81% agreement (kappa 0.73and 87 and 88% agreemenright and left hip.

Inter-observer variariorz. Rerevealed 78% agreement (kaagreement (kappa 0.64) for ment (kappa 0.69) for the cagreement (kappa 0.64 and

Disease speczficity. To vahdradiographs of 89 non-AS ohip component 51 non-AS owas taken as the cutoff. A swas used (disease durationSpecificity for the lumbar sspine it was 0.83, and for the

Tub/e 2. Summary of inter and intraobserver variation in BASRI-total.

Skeletal Site Intraobsewer Variation

Complete Kappa

Interobserver Varia

Complete

Agreement, ‘% Agreement, lo

SI joints 86 0.69 78

Sensitivity to change. Serial radiographs of 40 patients Were

scored over ‘177 time intervals (4.4 intervals/patient). Allradiographs were blinded for the name and date of radio-graph. Scoring was performed by a single observer. The

patients were assessed ver a time period of one year [yearsbetween radiographs: 1 yr.(n = 24), 2 yrs (n =.3 l), 3 yrs (n

tion between the 2 groups (20

0.2).The m ean BASRI-t was high

women (n = 72) (8.9 vs 7.2,

Disease duration was compar(Figure 3). More men than wom



= 30), 4 yrs (n = 26)]. A significant change in radiologicalscore (p < 0.05) at 2 years was observed for the SI joints,lumbar and cervical spine, and the hips. The magnitude ofchange for the BASRI-spine was from 7.0 to 7.9 in a 2 yearperiod. Forty-two percent of patients had a change inBASRI-s score in a 2 year period. The smallest detectabIedifference betweenscores over a 2 year period is a change nBASRI-s of 0.5, i.e., 0.5 change in SI joints score,,and achange n score of 1 for the lumbar spine and cervical spine .

Frequency distribution of BASRI-t axd BASRI-s. BASRI-twas normally distributed using a probit plot. BASRI-s wasnot norm&y distribured.

Cross sectional study. The mean BASRI-t and BASRI-sscores over 5 year intervaIs were plotted against diseaseduration (Figure 1). Correlation was poor: r = 0 ,293, p <0.01 and r = 0.347, p < 0.01, respectively.

BASRI-s for those patients with hip disease n = 101) andthose without (n = 322) was plotted against diseaseduration(Figure 2). The BASRI-s was higher for those with hip dis-

ease (p < 0.0001). There was no difference in disease dura-

12

6

SI joints (odds ratio, OR = 1.CI, 1.1-2.7; p < 0.016). More lumbar spine disease OR = 2.6More men than women had s(OR = 2.3,95% CI 1.3-3.9; p <and women with severe hip dstages of disease.

DISCUSSIONThe BASRI is reproducible,

variation equivalent to or bettBASRI was found to be sensperiod, which suggests adiog2 years are not .warranted.Themean time taken to score a se30 seconds.To maintain simpliminor radiological change. Theach additional erosion or sclegrade 2 or mild disease until ttebrae or 2 3 s)ndesmophytes

The changes in BASRI-t a



Figure 2. BASRX-spine - patients w ith hip disease (n = 101) versus DO hip disease (n = 321). 81 B

d BASRI-s (NH). p < 0.001.

indicate that AS is a slow progressive disease,or of course,that BASRI is too insensitive to pick up clinically relevantchange. However, lack of correlation between BASRIscoresand diseaseduration shows that outcome is extremely

variable for different individuaIs. The change n BASRI-s inpatients with and without hip involvement shows thatpatients with hip disease have more severe axial disease.

This supports ather studies that suggest hip involvement is

*k-Ji

impoflant outcome mea

(BASMI)‘, functional in

index (BASDAI)‘, and glment of our patients.

REFERENCES1. Jenkinson T. Mollorie P. W

A. Defining spinal mobilit

Metrology Index. J Rheum



predictive of more severe diseaseg.Comparison of male ver-sus femaIe hasshown that men have more severe disease, nthe SI joints, lumbar spine, and the cervical spine, but not inthe hips. Clearly, clinical significance does not equate withstatistical significance. Further studies will be required todefine the value of these findings.

The correlation of severity with disease duration is poorif taken ndividually. In the scoring of the lumbar spine, onlyhalf the patients develop severe disease after 45 years. Forthe cervical spine, 25% never develop any ce rvical involve-ment.

In conclusion, radiology is fundamental to diagnosis andprogressionof AS. Apart from the New York criteria for theSI joints, no widely accepted radiological criteria exist.BASRI as a radiological classification system is a valuabletool that is reproducible, specific, sensitive to change at 2years, simple, and fast to use. Using the B.&SRI in cross set-tional study of AS shows that this is a slowly progressive

diseasewith much individual variation. Some of this varia-tion can be accounted for: patients with hip involvementhave more severe spina diseaseand men have more spinalinvolvement than women. In conclusion, BASRI is an

2. Dougados M. Gueguen A

Evaluation of a functional

ankylosing spondylitis. J

3. Calin A, Garrert S, Whitel

functional ability in ankyl

, Bath Ankylosing Spondyii

1994;21:2281-5.

4. Mander M, Simpson JM..

Carson Dick W. Studies w

clinical assessment in ank

1987;46:191-202.5. Garrett S, Jenkin~on T. Ke

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7. Rigby S, Silmnn A. Outco

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