Recent developments in the diagnosis of canine hypothyroidism

Hair thinning in a hypothyroid dog.Dermatological abnormalities occurin around 80 per cent of cases

Recent developments in the diagnosisof canine hypothyroidism RICHARD DIXON

HYPOTHYROIDISM is a relatively common endocrine disorder of dogs, with a reported prevalence ofbetween 0.2 and 064 per cent compared with estimates of 0*0005 to 1.5 per cent for canine diabetesmellitus. However, accurate confirmation of the diagnosis of this disease is difficult as the clinical signsvary in terms of severity, type and number and often mimic other common conditions. In addition,numerous diagnostic tests are available with a wide range of recommendations for their use andinterpretation. This article summarises the current understanding of canine hypothyroidism and

Richard Dixongraduated fromGlasgow in 1993.After a spell in smallanimal practice inHull, he returned toGlasgow Universityas a small animalhouse physician.During this timehe was awarded theRCVS certificate inveterinary radiologyand developed hisinterests in smallanimal clinicalbiochemistry andendocrinology.He was recentlyawarded a PhDfor investigationsinto the diagnosisof caninehypothyroidism. Heis currently workingas a veterinary clinicalpathologist in Devon,specialising inendocrinology.

outlines a practical clinical approach to its diagnosis.

AETIOLOGY

Hypothyroidism is a clinical syndrome that results frominadequate circulating thyroid hormone concentrations.The most commonly recognised underlying cause ofhypothyroidism is lymphocytic thyroiditis in which thethyroid gland becomes progressively infiltrated withlymphocytes, macrophages and plasma cells. Thyroidtissue is slowly destroyed, progressively reducing thecapacity for hormone production. Although the under-

The principal product of the thyroid gland is thyrox-ine (T4) although a small amount of tri-iodothyronineCT3) is also produced. The secretion of T4 and T3 isstimulated by the release of the pituitary glycopro-tein thyrotropin (thyroid stimulating hormone, cTSH).Thyrotropin secretion is stimulated by hypothalamicthyrotropin-releasing hormone (TRH) secretion. BothT4 and T3 exert a negative feedback effect on cTSHand TRH synthesis and secretion.

Thyroxine exists in the circulation as both protein-bound (99.9 per cent) and free hormone (0.1per cent). In peripheral tissues, T4 is converted tothe more metabolically active T3. Circulating totalT4 concentrations fluctuate throughout the day,and 'subnormal' total T4 concentrations are in facta common finding in perfectly healthy dogs. How-ever, there is no circadian rhythm to canine T4secretion.

lying cause of thyroiditis is not fully understood, a breedpredisposition has been demonstrated (Nachreiner andothers 2000) and, in one series of borzois studied, anautosomal recessive mode of inheritance was proposed(Conaway and others 1985).

Another common thyroidal pathology in caninehypothyroidism is idiopathic atrophy in which thethyroid becomes infiltrated with adipose and fibrousconnective tissue. Hypothyroid dogs with thyroiditis tendto be younger than those without thyroiditis and it has

Normal regulation of canine thyroid function

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been suggested that idiopathic atrophy may be the endstage of lymphocytic thyroiditis. Furthermore, euthyroiddogs with thyroiditis tend to be younger than both thesegroups. This is consistent with a theory of progressionfrom 'thyroiditis but euthyroid', through 'thyroiditis andhypothyroidism' to 'hypothyroidism without thyroiditis'(Nachreiner and others 2000). Clinical hypothyroidismonly develops after approximately 75 per cent of thetissue is destroyed. Thyroid pathology can thereforebe present for months or years before clinical signs ofhypothyroidism become apparent.

SIGNALMENT

Spontaneous hypothyroidism is most frequently recog-nised in medium to large breeds, particularly labradorretrievers, spaniels, dobermanns, Shetland sheepdogsand setters. It typically affects middle-aged dogs buttends to present at a younger age in the predisposedbreeds. It is rare in dogs less than two years of agealthough the underlying pathology obviously startsbefore clinical signs become apparent. Both entire andneutered males and females are affected.

CLINICAL SIGNS

Thyroid hormones perform myriad functions involvingmultiple tissues and organ systems. Deficiency ofthyroid hormones can therefore result in a variety ofpresenting signs (see table below). Contrary to popularbelief, polyuria and polydipsia are rarely (if ever) due tohypothyroidism, and their presence should generallydirect the investigation elsewhere. Metabolic abnormali-ties occur in over 80 per cent of cases. These includelethargy, weight gain or obesity and exercise intolerance.Dermatological abnormalities occur in around 80 percent of cases and include hair thinning, particularlyaffecting the flanks, tail and thighs, dry or poor coatquality, skin hyperpigmentation, seborrhoea and super-ficial pyoderma. Metabolic and dermatological signsoccur concurrently in approximately 70 per cent ofcases.

Less common signs include neuromuscular, repro-ductive, ocular, gastrointestinal and cardiovascularabnormalities. Laryngeal paralysis, megaoesophagus,peripheral vestibular disease, cranial nerve disorders,

wl c

Category Clinical sign

Metabolic LethargyWeight gainExercise intoleranceWeaknessCold intolerance

Dermatological

Other

Hair thinningPoor quality coatHyperpigmentationPyodermaSeborrhoeaOtitisSkin thickening

NeuropathiesPoor fertilityDiarrhoea

behavioural abnormalities and seizures have all previ-ously been attributed to hypothyroidism in the literature.However, the variation in assessment of thyroidal statusin many of these reports and the universally erraticresponse to thyroid hormone replacement therapy leavesthe role, if any, of thyroid dysfunction in these condi-tions to be clarified. It is probable that thyroid disease isassociated with a small percentage of such cases, buthypothyroidism is certainly an uncommon cause of each.Similarly, while a small number of cases of female infer-tility may be associated with hypothyroidism, it is anuncommon cause of this problem. Recently, diarrhoeasecondary to small intestinal bacterial overgrowth hasalso been reported as a feature of hypothyroidism.

DIAGNOSIS

The diagnosis of hypothyroidism is undeniably problem-atic. First, none of the individual clinical signs ofhypothyroidism are pathognomonic for the disease andare often associated with other diseases. Secondly, whilethere are a number of characteristic laboratory abnormal-ities, none are specific and many parameters are affectedby non-thyroidal illness (NTI) and a variety of medica-

Lymphocytic thyroiditis -the most common causeof canine hypothyroidism

Extensive hair loss causedby hypothyroidism

Frequency

Very commonVery commonVery commonCommonOccasional

Very commonCommonCommonCommonOccasionalOccasionalOccasional

OccasionalOccasionalOccasional

In Practice e J UNE 200 3 1 329




tions that have often been used prior to diagnostic test-ing. As a result of the diagnostic difficulties, and theease and apparent advantages of trial therapy, the 'pre-sumptive diagnosis' of hypothyroidism and the use ofthyroid hormone supplementation is widespread. How-ever, this approach causes a number of long-term diffi-culties (see later) and, while trial therapy has a role toplay in the confirmation of hypothyroidism in a few rarecases, its widespread use should be discouraged.

Despite the absence of a 'perfect' test, a number ofpractical steps can be taken to maximise the clinician'saccuracy and limit the use of the therapeutic trial, andthese are discussed below.

PRE-EVALUATIONThe first step in confirming hypothyroidism is not theinvestigation of thyroidal status but, rather, the evalua-tion of non-thyroidal factors, including recent drugtherapies and the investigation of NTIs that are mostcommonly associated with the presenting signs.

Various drugs widely used in veterinary practice inter-fere with thyroid function tests. Specifically, steroidsdecrease thyroid hormone concentrations and may alsodecrease cTSH secretion; sulphonamide-containing drugsdirectly inhibit thyroid hormone synthesis and may evencause a temporary reversible state of hypothyroidism; andbarbiturate anticonvulsants decrease both total and freeT4 concentrations. Thyroid hormone test results shouldtherefore be interpreted cautiously in dogs that havereceived these medications. If possible, assessment ofthyroid function should be postponed for around sixweeks after such medication has been stopped (or as longas is practical, bearing in mind the duration and dose ofthe therapies that have been used).

Many NTIs have been shown to cause a reduction incirculating thyroid hormone concentration, and therecovery phase of NTI has been associated with a tempo-rary increase in circulating cTSH values. Spontaneoushyperadrenocorticism is of particular concern as many ofthe clinical features of this disease are similar tohypothyroidism, and profound (but reversible) suppres-sion of thyroid function frequently occurs.

The exclusion of NTI and assessment of recent drugusage at the outset may completely eliminate the needfor subsequent evaluation of thyroid status. If pre-evalu-ation excludes the most likely alternative diagnoses, theninvestigation of hypothyroidism should be performed. Insuch cases where thyroid testing is required, adequatepre-evaluation allows a much more confident interpreta-tion of the results.

ROUTINE ABNORMALITIESThere are a number of well recognised routine clinico-pathological abnormalities associated with hypothyroid-ism. Hypercholesterolaemia and hypertriglyceridaemiaare reported in approximately 75 to 80 per cent of cases

and a mild non-regenerative anaemia is also common.Unfortunately, these abnormalities are equally, if notmore, common in dogs with NTI. Recently, studies com-

ENDOCRINE TESTSTotal thyroxineCirculating total T4 concentration is invariably decreasedin dogs with hypothyroidism. However, many non-thyroidal factors will also decrease total T4 and fluctua-tions below the reference range regularly occur inhealthy dogs. In addition, a decreased total T4 concentra-tion is common in NTI and is associated with certaindrug therapies. Consequently, a subnormal total T4 con-centration does not confirm hypothyroidism. However,total T4 measurement is a useful method for ruling outhypothyroidism as very few hypothyroid dogs havereference range values.

andsenitive Marker forhyotyoiim

* :Low vaues do notconfirm hypotyridismI Subnoml at the da* Decread by ste s bi non-sterdalanti-inflammatory*rus and sulphon*ades* D ereasd by N

Endogenous thyrotropin (cTSH)Decreased circulating thyroid hormone concentrationsresult in reduced negative feedback on the pituitarygland. Circulating cTSH concentration is thereforetheoretically increased in primary hypothyroidism. Thecombination of reduced T4 and increased cTSH values ishighly specific for hypothyroidism. However, approxi-mately 20 per cent of hypothyroid dogs have referencerange cTSH values. Dogs with this combination of testresults pose the greatest diagnostic dilemma as subnormaltotal T4 but reference range cTSH values are typical ofNTI. In this situation, if the index of suspicion forhypothyroidism remains high, the tests outlined beloware appropriate next steps. Abnormally high cTSH valuescan occur in euthyroid dogs receiving sulphonamide ther-apy or during recovery from NTI, although total T4 val-ues are usually normal. The use of the T4 to cTSH ratiohas also been employed but assessment of the individualvalues is of principal importance.

On balance, therefore, combined total T4 and cTSHmeasurement is an economic and fairly reliable approach,especially if pre-evaluation has been performed.

paring the routine biochemical and haematological resultsfrom hypothyroid dogs and those with clinically similarillnesses demonstrated that the most reliable abnormalitiesthat specifically helped identify hypothyroidism were

decreased red cell count, increased y-glutamyl transferase,hypercholesterolaemia and neutropenia (Dixon and others1999).

In Practice * JUNE 2001330




Free T4Free T4 is the metabolically active fraction of T4 and itsmeasurement is widely acknowledged to more closelyreflect tissue thyroidal status than total hormone determi-nation. Free hormone is less affected by NTI and variousdrug therapies than total T4, although barbiturate anti-convulsant therapy has recently been shown to decreasefree T4 concentrations in dogs (Muller and others 2000)and severe NTI can decrease free T4 concentrations inhumans. Free hormone is'potentially of particular valuein those dogs with subnormal total T4 and referencerange cTSH results because it helps distinguish genuinehypothyroidism from NTI.

However, measurement of free T4 has been compli-cated by the various assay methodologies available,some of which are unreliable when used in patients withNTI. The recommended 'dialysis' method for free T4measurement is now commercially available from sever-al UK diagnostic laboratories. The use of traditional'analogue' assays for free T4 estimation offers no addi-tional diagnostic information over total T4 measurementand is not recommended.

n Wbtrpthan total

art apcificfor hypo-

R~beby andi's more

abb inN I aorby

Thyroglobulin antibodiesThyroglobulin antibodies (TgAb) are produced duringthe development of lymphocytic thyroiditis. Until 1997,the commercially available methods for TgAb estimationwere based on human methods; they were unreliable andfalse positive results were common. However, a more

specific assay for canine TgAb is now commerciallyavailable and has recently been evaluated (Nachreinerand others 1998, Dixon and Mooney 1999). The mea-

=L~ D~;~

i Reliable methodavailable* A positive resultthyroid pathology

for determination is now

is extr tive of

Wd-."* Prod no t f thyroid functional

* A negative result does not rule out significant

surement of TgAb confirms the presence of thyroidpathology but does not provide an assessment of thy-roidal function. However, the principal limitation ofTgAb measurement is that not all dogs with hypothy-roidism have lymphocytic thyroiditis and, therefore,while a positive TgAb result provides strong evidence ofthyroid disease, a negative result cannot rule it out.Epidemiological analysis of the prevalence of TgAb hasshown a peak in dogs of up to four to six years of age,which subsequently declines, presumably as the thyroidtissue becomes ablated and the antigenic stimulusdecreases.

TSH stimulationThe bovine TSH response test is widely acknowledgedto be the single best test for the assessment of thyroidalstatus. The test provides an indication of thyroidal func-tion but, more importantly, functional reserve capacity.Approximately 10 per cent of cases give equivocalresults with this test and in these dogs it is usually appro-priate to wait and reassess after a period of severalmonths. However, bovine TSH is no longer widelyavailable in practice and its use is largely restricted toresearch institutions. The use of recombinant humanTSH has recently been evaluated (Sauve and Paradis2000) and may also prove to be useful, but at this timefurther studies are required.

TRH stimulationDue to the limited availability of bovine TSH, the TRHresponse test has been used as an alternative method ofassessing thyroidal reserve. Dogs with hypothyroidismfail to demonstrate a response to TRH administration, anda 'normal' response excludes hypothyroidism. However,with the recent availability of a reliable free T4 assay, bothof these conclusions can now usually be reached using thetests outlined above. In addition, failure to respond toTRH does not confirm hypothyroidism, and is a frequentfinding in both healthy dogs and, more commonly, thoseaffected by NTI. The TRH response test therefore offersfew, if any, advantages over the basal tests now available,and is no longer recommended by the author.

cTSH response to TRHIn humans with primary hypothyroidism, the TSHresponse to TRH administration is increased, presumablyas a consequence of thyrotroph up-regulation. In con-

trast, NTI typically blunts the TSH response to TRH.However, in dogs this test offers no advantages over theroutine basal tests outlined above.

THERAPEUTIC TRIALThe use of a therapeutic trial to confirm hypothyroidismis, initially at least, an appealing proposition. It avoidsthe diagnostic problems outlined above and adequatelytreated hypothyroid dogs invariably respond excellently.However, exogenous thyroid hormone suppresses cTSHand therefore endogenous thyroid function. Hence, once

thyroid hormone replacement therapy has been institut-ed, assessment of thyroidal status at a later date becomesprofoundly confusing. Furthermore, the administrationof thyroid hormone to dogs with 'normal' thyroidfunction is known to have physiological effects that are

easily interpreted as a clinical response. For example,increased hair growth has been proven to occur in euthy-roid dogs receiving thyroid hormone. Nevertheless, it is

In Practice o JUNE 2001

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332




",i

(right) 'Rat tail' appearancein a hypothyroid dog beforethyroxine treatment.(far right) The same tailafter treatment

cleari th'at adeqUately treated hypotiioild dlogs deimlonl-strate a marked clinical improx ement anid tailuIrC tocompletely respond caLin thelcfor-c bc consider-ed LsetulcV idence ol' a misdilatiosis.

On balance, the use of triall thel`apy shouldC bcreserxed foi cases in wxhich thiere aLre nio diagnlostic .alter-natixves. Oxneirs oft' thiese animals Should he made axwareco' the limitations that may ultilmaItel ike lonm-terpatient man iemieit more difficuilt, patticularlVn if theciinical rCslpon1se is, as is often tIle CaSC, equixocVal. Iftriial theriapy is used as a diagllostic tool, it is recolin-miienided thait, it there is a good clinical iesponse. thera-1pyshould be temlporari-Ix stopped. If thele is a- el meacal con-traindication to stopping treatment (eg. thc prcscnce ofconCuIrr1elIt panicreatitis). the othlt conIditionI shou0ld beIMt1eACted and thy roid lioriioeic replacemenit therapystopped xhen appropriate. If clinical signs ot Iwpothy-roidisIII teeiL. thenl treaCtm11enIt should he Ie instituted: itthe clinicatlaIbn-orm.alities do 1not Ietuilrn thell thele is

obh iouIslN nio nieed to e-n1stitteC thlCI aplry

TREATMENT AND THERAPEUTICMONITORING

H>pothy roidism is ulidoLihtedly otie of the imiost satisfy-ing eildocrinlie dliseaLses to tielat. Otice daily thierapy I-CsLiltsin a good clinical responise in x irtUally all eases. xw ithi

very fexw animials requinl-gll tw ice daily medication. Astartinm dose of 0)02 m,/ko tlhioxine (Soloxine: ima.nil-tflCturedl in the USA by Daniels andcldistributed in the UKbNy Aniiolds) should be Lsed. Approxinmately hallf of allIea.ses wx il reqire a suhsequLenit dose adCtjuLst ImIen t taehiexe optimal thetrapeltie coneentirations.

ThelLpuCtiC mon0itoulill shoctld bc peftor-niiet xwithintwx o xxeeks of statrtino thcrl-.lNr0ao afitcr ichanigLe ill dosagc

to elnsLIrIe adleqUate hloodl hoit none cotienitriations. B31hi(1Samples tIo tIioniitorinig peak totaLl T4 aud cTSH coiicc-tratiotiS mu1LSt he collecctcl SiX\IoLIIS p1oSt- pill andI thCI-C-toteC iii1OriiiIg tlet .laps iS LuSual>1 tIlh imost coixeniciIt. Flipeak circulating total I coticetit tioH ShoUld bc abox ethe tiormI1al ralIge. \ aIeIS Of apptp iImIate1 (i) to 70)nniillo/litle alre LILIallV assoliated xw ithi excellct clili cllcotiti-ol peak total T4 'oneeitrtitis (i less than11 *1tiiol/litre itidicate the iedlot alti iviilcase ill d(ose

Co1tiLu-r-ellt atialy sis ot' c [S H is 1tecotu1tctld1ed dotul1iiLtliCIa-IpeLItiC 1ii(littol tug1 aIS it itCidlcateS tilhe aIdeuCLIs!o\sglit ltiV lo0Iget -ternill thelCIapeuLtic colltrol.

Metabolic sitgs t'l-CIreLqCltit'I iipr-oxe xx ithill a niltterof dla s otf stat tilLt ti attimilt tIlathe CS1pou1Se is Li-all \

d-;ilamtic. DcrmiatoloLical abuotrmalItics take lottLcc toimiiproxve, bit Milost dooS .icCsSciitaillx> clilocallx' 1t0iltiiAxx ithilt 2 wc!ck,s ()f statiitigL, thieLt ap>. A less thiall Citt11pleCtC ICeSpOtisc s1i0oildl protlipt CotAisldrltatio of ci liici

iMaCleCteIL thict irap (i a Ivni scliagiiosis

PROGNOSIS

The pirogilosis tf i- xx elI ti catecl Ii>p(ot1vl-olch c(logs is

cxcelleiit. Thict-c is oV cx luce to suIggest that lifecX\pCCtalie>\ iS alteletcl. aticl tIlh ClLal it> Oi lite should be

cri CLoocl. Re1gu1lar rulot1itoltimtl. at vIi less thall Si\moutith>vi tittcrsals is ceomiitleclICICI. ITrcatcdl dioeLs maI.lxbe proie to titetl ittetit sceclacrxhactcrt ail ilifecoti'Saticl cpisodes of pv> o(cltv1ia ill pat ticuLlatl. A\lth1oLiLg fI>'lkctICe01iiiti01c. Ii> pot Old(itch clos ate a! so potetltially at riiskof d1cx clopilig othlct iiiiLHiC-mctliediatd ciuclocriniopatlhiics.k> ogn"I secpi°t1CilIglaticl; at sI ticSi(lil ies ii0st c0111111011aIV I-CCoLIIIiSCCI j)1VoLn1;Ll(tlCl A'l1 (V1ClO11C01tS iII tLOL's .1'C

1lN loth>tI oitchisili ill associatiou xx ithi diabctes iilillttlts oipi>ilac1 icl1octil ticisili.

334 lractice * Ju NE 200334




ReferencesCONAWAY, D. H., PADGETr, G. A. & NACHREINER, R. F.(1985) The familial occurrence of lymphocytic thyroiditis inborzoi dogs. American Journal of Medical Genetics22, 409-414DIXON, R. M. & MOONEY, C. T. (1999) Canine serumthyroglobulin autoantibodies in health, hypothyroidismand non-thyroidal illness. Research in Veterinary Science66, 243-246DIXON, R. M., REID, S. W. J. & MOONEY, C. T. (1999)Epidemiological, clinical, haematological and biochemicalcharacteristics of canine hypothyroidism. Veterinary Record145, 481-487MULLER, P. B., WOLFSHEIMER, K. J., TABOADA, J.,HOSGOOD, G., PARTINGTON, B. P. & GASCHEN, F. P. (2000)Effects of long-term phenobarbital treatment on thethyroid and adrenal axis and adrenal function testsin dogs. Journal of Veterinary Internal Medicine14, 157-164NACHREINER, R. F., BOWMAN, M. M., GRAHAM, P. A.,REFSAL, K. R. & PROVENCHER-BOLLIGER, A. (2000) Theprevalence of thyroglobulin antibody is strongly influencedby breed: a retrospective study of 45,131 canine thyroiddiagnostic test results. Journal of Veterinary InternalMedicine 14, 232NACHREINER, R. F., REFSAL, K. R., GRAHAM, P. A.,HAUPTMAN, J. & WATSON, G. L. (1998) Prevalence ofautoantibodies to thyroglobulin in dogs with nonthyroidalillness. American Journal of Veterinary Research59, 951-955SAUVE, F. & PARADIS, M. (2000) Use of recombinant humanthyroid-stimulating hormone for thyrotropin stimulationtest in euthyroid dogs. Canadian Veterinary Journal41, 215-219

Further readingDIXON, R. M. & MOONEY, C. T. (1999) Evaluation of serumfree thyroxine and thyrotropin concentrations in thediagnosis of canine hypothyroidism. Journal of Small AnimalPractice 40, 72-78FRANK, L. A. (1996) Comparison of thyrotropin-releasinghormone (TRH) to thyrotropin (TSH) stimulation forevaluating thyroid function in dogs. Journal of the AmericanAnimal Hospital Association 32, 481-487LOTHROP, C. D., TAMAS, P. M. & FADOK, V. A. (1984) Canineand feline thyroid function assessment with the thyrotropin-releasing hormone response test. American Journal ofVeterinary Research 45, 2310-2313PETERSON, M. E., MELIAN, C. & NICHOLS, R. (1997)Measurement of serum total thyroxine, triiodothyronine, freethyroxine, and thyrotropin concentrations for the diagnosisof hypothyroidism in dogs. Journal of the AmericanVeterinary Medical Association 211, 1396-1402SCOTT-MONCRIEFF, J. C. & NELSON, R. W. (1998) Changein serum thyroid-stimulating hormone concentration inresponse to administration of thyrotropin-releasing hormoneto healthy dogs, hypothyroid dogs and euthyroid dogs withconcurrent disease. Journal of the American VeterinaryMedical Association 213, 1435-1438SCOTT-MONCRIEFF, J. C., NELSON, R. W., BRUNER, J. M. &WILLIAMS, D. A. (1998) Comparison of serum concentrationsof thyroid-stimulating hormone in healthy dogs, hypothyroiddogs, and euthyroid dogs with concurrent disease. Journal ofthe American Veterinary Medical Association 212, 387-391SPARKES, A. H., GRUFFYDD-JONES, T. J., WOTTON, P. R.,GLEADHILL, A., EVANS, H. & WALKER, M. J. (1995)Assessment of dose and time responses to TRH andthyrotropin in healthy dogs. Journal of Small AnimalPractice 36, 245-251

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Recent developments in the diagnosis of canine hypothyroidism