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Rheumatic pain management In daily practice

Rheumatic pain indramayu 29june2013

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Page 1: Rheumatic pain indramayu 29june2013

Rheumatic pain management

In daily practice

Page 2: Rheumatic pain indramayu 29june2013

Pain GridI II III IV V VI

Acute (Incident Focused) Monophasic Pain

Acute (Diagnostically Focused) Recurrent

Pain

Chronic Malignancy Based Pain

Chronic Progressive Non-Malignancy Based

Pain

Chronic NonProgressive

NonMalignancy Based Pain

Chronic Benign Pain

Examples Examples Examples Examples Examples Examples

Post Operative, Major Trauma, Acute Phase of

Burns, Fractures, Pre- and Post-Procedural Scenarios, Acute Back Pain Syndromes

Sickle Cell Crisis, Acute Flare of Inflammatory Bowel Disease, Acute Flares of Inflammatory

Arthropathies, Hemophilic Arthropathy, Renal

Calculi, Forms of Back Pain, Dysmenorrhea,

Migraine

Self Explanatory based on local spread,

metastatic invasion, pressure or obstruction

A.I.D.S. Progression, Sickle Cell Patients, Hemophilia Patients,

Some Connective Tissue Diseases, Inflammatory

Bowel Disease with Short Gut and ExtraGut

Autoimmune Manifestations

Musculoskeletal Pain Syndromes

(Osteoporosis, spondylolisthesis), TMJ,

Neuropathic Pain Syndromes (Postherpetic

neuralgia, painful polyneuropathy, RSD),

Forms of Back Pain

Pain Associated with a Marked Discrepancy in

Pathologic Findings compared against Strong and Typical Axis I, Axis II

and Premorbid Psychosocial Features

           

Opioid Advisability Opioid Advisability Opioid Advisability Opioid Advisability Opioid Advisability Opioid Advisability

OK Ok (with cautions) Advised OKRelative

ContraindicationOpioid Avoidance

Courtesy of Craig Pratt, MD (with some changes)

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Rheumatic pain

3

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Symptoms

■ Joint pain

■ Joint swelling

■ Morning stiffness

■ Fatigue

■ Weight loss

■ Flu-like symptoms

4

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The goal of pain management

is

not necessarily pain relief – it is improving a

patient’s quality of life.

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Symptomatic Treatments

■ Education/support■ Rest/relaxation■ Joint protection■ Physiotherapy■ Analgesics■ Anti-inflammatory drugs■ Steroids■ Joint injections■ Pain Management Clinics

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Symptomatic Treatments

■ Education/support■ Rest/relaxation■ Joint protection■ Physiotherapy■ Analgesics■ Anti-inflammatory drugs■ Steroids■ Joint injections■ Pain Management Clinics

7

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What are the benefits and risks from NSAIDs?

How do I reduce the GI risks?How do I reduce the CV risks?

Are there specific safety concerns with NSAIDs?

*Note by NSAIDs we mean traditional NSAIDs (e.g. diclofenac, naproxen, ibuprofen); etodolac, meloxicam, or coxibs (e.g. celecoxib,

etoricoxib)

Key questions regarding NSAIDs*

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Common Rheumatic problems: Osteoarthritis and Rheumatoid Arthritis

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Prevalence of Arthritis in US Adults*

■ 49.9 million (22.2%) with self-reported, physician-diagnosed arthritis†1

■ 21.1 million (9.4%) with arthritis and arthritis-attributable activity limitation1

■ Affects more women than men in every age group2

0

20

40

60

80

100

18–24 25–34 35–44 45–54 55–64 65–74 75–84 85+

Women Men

Age Group, years

* Data sources: 2007-2009 data from the National Health Interview Survey (NHIS). † Includes multiple forms of arthritis.

HCP=health care professional.

1. CDC. MMWR Morb Mortal Wkly Rep. 2010;59(39):1261-1265.2. Graphic adapted from CDC. NHIS Arthritis Surveillance: Arthritis Prevalence in Women and Men.

www.cdc.gov/arthritis/data_statistics/national_nhis.htm. Accessed January 12, 2011.3. CDC. MMWR Morb Mortal Wkly Rep. 2009;58(16):421-426.4. Hootman JM, Helmick CG. Arthritis Rheum. 2006;54(1):226-229.

■ Arthritis and rheumatism leading causes of disability in US3

■ By 2030, a projected 67 million in US will have HCP-diagnosed arthritis4

US

Ad

ult

s (%

)W

ith

Art

hri

tis

US

Ad

ult

s (%

)W

ith

Art

hri

tis

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Factors Implicated in the Development of OA

Cartilage breakdown

ObesityObesity

Anatomic abnormalities

Anatomic abnormalities

Microfractures and bony

remodeling

Microfractures and bony

remodeling

Loss of joint stability

Loss of joint stability

TraumaTrauma

AgingAging

Genetic and metabolic diseases

Genetic and metabolic diseases

InflammationInflammation

Immune system activity

Immune system activity

Compromised cartilage

Biophysical changes• Collagen network fracture• Proteoglycan unraveling

Biochemical changes• Inhibitors reduced

• Proteolytic enzymes increased

Abnormal stresses Abnormal cartilage

Mandelbaum B et al. Orthopedics. 2005;28(2 suppl):s207-s214.Adapted with permission from 2002 Medtronic Sofamor Danek, Basic Bone Biology.

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EULAR Diagnostic Criteria for Knee OA (2010)

■ Based on review of studies from 1950-2008 and expert consensus

■ Focuses on clinical diagnosis: presence of three symptoms andthree signs correctly diagnoses 99% of cases

SymptomsSymptoms

1 Persistent knee pain √

2 Limited morning stiffness √

3 Reduced function √

SignsSigns

4 Joint crepitus √

5 Restricted movement √

6 Bony enlargement √

EULAR=European League Against Rheumatism.

Zhang W et al. Ann Rheum Dis. 2010;69(3):483-489.

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ACR Diagnostic Criteria for Knee OA (1986)

■ Clarified and standardized definition of osteoarthritis Joint symptoms and signs associated with defective integrity of

articular cartilage and changes in underlying joints at bone margin

■ Focuses on clinical examination of knee pain plus:

■ Sensitivity, 95%; specificity, 69%

Presence of 3 of the followingPresence of 3 of the following

1 Age >50 years √

2 Morning stiffness <30 minutes √

3 Joint crepitus on active motion √

4 Bony tenderness √

5 Bony enlargement √

6 No palpable warmth of synovium √

ACR=American College of Rheumatology.

Altman RD et al. Arthritis Rheum. 1986;29(8):1039-1049.

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Goals of OA Management:OARSI Recommendations

Reducejoint pain and

stiffness

Reduce physical disability

ImproveHRQoL

Educate patients

Limitprogression of joint damage

Knee and Hip OA: Goals of Treatment

HRQoL=health-related quality of life; OARSI=Osteoarthritis Research Society International.

Zhang W et al. Osteoarthritis Cartilage. 2008;16(2):137-162.

Maintain and improve joint

mobility

Page 16: Rheumatic pain indramayu 29june2013

Integrated Approach to Treating Patients With OA

NonpharmacologicNonpharmacologic PharmacologicPharmacologic

■ Patient education■ Phone contact (promote self-care)■ Referral to physical therapist■ Aerobic, strengthening, and/or water-based exercise■ Weight reduction■ Walking aids, knee braces■ Proper footwear, insoles■ Thermal modalities■ TENS■ Acupuncture

■ APAP■ Oral NSAIDs■ Topical NSAIDs and capsaicin■ Corticosteroid injections■ Hyaluronate injections■ Glucosamine, chondroitin sulphate, and/or diacerein■ Weak opioids and narcotic analgesics for refractory pain*

SurgicalSurgical

■ Total joint replacement■ Unicompartmental knee replacement■ Osteotomy and other joint preserving surgical procedures

■ Lavage/debridement in knee OA†

■ Joint fusion after failure of joint replacement

* Pain resistant to ordinary treatment. † Controversial.

TENS=transcutaneous electrical nerve stimulation.

Zhang W et al. Osteoarthritis Cartilage. 2008;16(2):137-162.

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US Prevalence and Burden ofRheumatoid Arthritis (RA)

■ May affect between 1.3 and 1.5 million adults1,2

Incidence lowest in individuals aged ≤34 yearsIncidence increases progressively with ageOccurs more commonly in women than in men

■ Societal costs3

* Costs in 2005 US dollars.1. Myasoedova E et al. Arthritis Rheum. 2010;62(6):1576-1582.2. Helmick CG et al. Arthritis Rheum. 2008;58(1):15-25.3. Birnbaum H et al. Curr Med Res Opin. 2010;26(1):77-90.

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Hand RA

Photos from Towheed TE, Anastassiades TP. Can Fam Phys. 1994;40:1303-1309. Used with permission.

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2010 ACR / EULAR Diagnostic Criteria for RA

CriterionCriterion ScoreScore

A Joint Involvement*

1 large joint 0

2-10 large joints 1

1-3 small joints (± large-joint involvement) 2

4-10 small joints (± large-joint involvement) 3

>10 joints (at least 1 small joint) 5

B Serology†

Negative RF and negative ACPA 0

Low-positive RF or low-positive ACPA 2

High-positive RF or high-positive ACPA 3

CAcute-Phase Reactants‡

Normal CRP and normal VHS 0

Abnormal ESR or CRP 1

DDuration of Symptoms§

Less than 6 weeks 0

6 or more weeks 1

Total score ≥6/10 Total score ≥6/10 needed to classify needed to classify

definite RAdefinite RA

Total score ≥6/10 Total score ≥6/10 needed to classify needed to classify

definite RAdefinite RA

* Any swollen or tender joint on examination. Excluded are distal interphalangeal joints, first carpometacarpal joints, and first metatarsophalangeal joints. Large joints = shoulders, elbows, hips, knees, and ankles. Small joints = metacarpophalangeal joints, proximal interphalangeal joints, 2nd through 5th metatarsophalangeal joints, thumb interphalangeal joints, and wrists. The >10 category can include large and small joints, and other joints not listed elsewhere (eg, temporomandibular, acromioclavicular, or sternoclavicular). † Negative: IU values ≤ULN for lab and assay. Low-positive: IU > ULN but ≤3x ULN. High-positive: IU >3x ULN. When only RF-positive or RF-negative is known, positive scored as low-positive. ‡ Normal/abnormal determined by local lab standards. § Patient self-report of duration of signs/symptoms of synovitis in joints clinically involved at time of assessment, regardless of treatment status.

ACPA=anti-citrullinated protein/peptide antibodies; CRP=C-reactive protein; VHS =erythrocyte sedimentation rate; RF=rheumatoid factor.

Aletaha D et al. Arthritis Rheum. 2010;62(9):2569-2581.

* Any swollen or tender joint on examination. Excluded are distal interphalangeal joints, first carpometacarpal joints, and first metatarsophalangeal joints. Large joints = shoulders, elbows, hips, knees, and ankles. Small joints = metacarpophalangeal joints, proximal interphalangeal joints, 2nd through 5th metatarsophalangeal joints, thumb interphalangeal joints, and wrists. The >10 category can include large and small joints, and other joints not listed elsewhere (eg, temporomandibular, acromioclavicular, or sternoclavicular). † Negative: IU values ≤ULN for lab and assay. Low-positive: IU > ULN but ≤3x ULN. High-positive: IU >3x ULN. When only RF-positive or RF-negative is known, positive scored as low-positive. ‡ Normal/abnormal determined by local lab standards. § Patient self-report of duration of signs/symptoms of synovitis in joints clinically involved at time of assessment, regardless of treatment status.

ACPA=anti-citrullinated protein/peptide antibodies; CRP=C-reactive protein; VHS =erythrocyte sedimentation rate; RF=rheumatoid factor.

Aletaha D et al. Arthritis Rheum. 2010;62(9):2569-2581.

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Goals of RA Management

Reduce painReduce painPrevent or

control joint damage

Prevent or control joint

damage

Prevent functional

decline

Prevent functional

decline

Maximizepatient

quality of life

Maximizepatient

quality of life

Early and SustainedSuppression of Disease Activity

ACR Subcommittee on Rheumatoid Arthritis Guidelines. Arthritis Rheum. 2002;46(2):328-346.

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Treatment Options for Patients With RA1-3

NSAIDsNSAIDs Symptomatic treatment to reduce joint swelling and pain

DMARDs DMARDs (biologic and (biologic and nonbiologic)nonbiologic)

Reduce/prevent joint damage, preserve joint integrity and function Methotrexate, leflunomide, hydroxychloroquine, minocycline,

sulfasalazine Etanercept, infliximab, adalimumab (TNF inhibitors) Rituximab (anti-CD20) Abatacept (cytotoxic T-lymphocyte antigen 4 immunoglobulin) Tocilizumab (anti-interleukin 6 receptor)

GlucocorticoidsGlucocorticoids Short-term use during flare-ups (oral or intramuscular) Local treatment for individual active joints (intra-articular)

SurgerySurgery Carpal tunnel release, synovectomy, resection of metatarsal heads,

total joint arthroplasty, joint fusion

Supportive Supportive StrategiesStrategies

Patient education, cognitive-behavioral interventions Rehabilitation interventions

DMARDs=disease-modifying antirheumatic drugs; TNF=tumor necrosis factor.

1. ACR Subcommittee on Rheumatoid Arthritis Guidelines. Arthritis Rheum. 2002;46(2):328-346.2. Saag KG et al. Arthritis Rheum. 2008;59(6):762-784.3. Smolen JS et al. Lancet. 2007;370(9602):1861-1874.

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Distinguishing OA From RA1

CharacteristicCharacteristic OAOA RARA

Prevalence in US adults 27 million2 1.3–1.5 million3,4

Pathophysiologic process Degenerative Autoimmune

Commonly affected jointsHips, knees, spine,

fingersHands, feet

Typically symmetrical involvement

No Yes

Morning stiffness Transient Persistent

Joint swelling Hard tissue Soft tissue

Hand involvement Distal joints Proximal joints

Extraarticular involvement No Yes

Elevated autoimmune markers No Yes

1. Goldman L, Ausiello D. Cecil Textbook of Medicine. 23rd ed. Philadelphia, PA: Saunders Elsevier; 2007. 2. Lawrence RC et al. Arthritis Rheum. 2008;58(1):26-35.3. Helmick CG et al. Arthritis Rheum. 2008;58(1):15-25.4. Myasoedova E et al. Arthritis Rheum. 2010;62(6):1576-1582.

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1991: A New Paradigm for COX Biology

GlucocorticoidsGlucocorticoids(block mRNA (block mRNA expression)expression)

Arachidonic AcidArachidonic Acid

COX-1COX-1(Constitutive)(Constitutive)

COX-2COX-2(Cytokine (Cytokine Inducible)Inducible)

StomachStomachIntestineIntestineKidneyKidneyPlateletPlatelet

Inflammatory Site:Inflammatory Site:• MacrophagesMacrophages• SynoviocytesSynoviocytes• Endothelial cells Endothelial cells

NSAIDsNSAIDsx x

Page 24: Rheumatic pain indramayu 29june2013

McKenna F et al. Scand J Rheumatol 2001;30:11–18.VAS=visual analogue scale.

Less P

ain

Patient’s Assessment of Pain (VAS): Mean change at week 6

Mea

n C

ha

ng

e (m

m)

*p=0.001 vs. placebo

placebo(n=200)

celecoxib100 mg BID(n=199)

diclofenac50 mg TID(n=199)

Coxib vs. diclofenac:6-week Knee OA TrialMcKenna et al. 2001: Patient’s Assessment of Pain

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McKenna F et al. Scand J Rheumatol. 2001;30:11-18.

American Pain Society (APS) Pain Measure:Worst Pain in the Past 24 Hours

Mean

Ch

an

ge in

Score p=0.05, active treatment vs.

placebo (days 1-7).

-4.0

-3.5

-3.0

-2.5

-2.0

-1.5

-1.0

-0.5

0.0Baseline Day 1 Day 2 Day 3 Day 4 Day 5 Day 6 Day 7

placebo (n=200)

celecoxib 100 mg BID (n=199)

diclofenac 50 mg TID (n=199)

Less P

ain

Coxibs vs. diclofenac:6-week Knee OA TrialMcKenna et al. 2001: American Pain Society – Pain Measure

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Gastrointestinal Safety

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Risk of upper GI ulcer bleedingLanas A, et al. Gut 2006;55:1731–38

0

1

2

3

4

5

6

7

8

9

10

11

12

13

14

15

Ad

justed

RR

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Guidelines for Prevention of NSAID-Related Ulcer Complications(ACG Practice Guidelines 2009)

Lanza FL et al. Am J Gastroenterol 2009;104:728-738

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Cardiovascular Safety

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Primary Endpoint: Cumulative Incidence of Thrombotic CV Events

30

Etoricoxib (320 events)

Diclofenac (323 events)

MonthsNo. of patients at risk*

EtoricoxibDiclofenac

16,81916,483

13,359 10,733 8277 6427 4024 80581538326213790110,14212,800

7.0

6.0

5.0

4.0

3.0

2.0

1.0

06 12 18 24 30 36 420

Cu

mu

lati

ve in

cid

ence

(%

) w

ith

95%

CI

Etoricoxib vs diclofenacHR = 0.95 95% CI = (0.81-1.11)

*Per protocol population.

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Boxed Warning for All Prescription NSAIDs

Cardiovascular Risk

NSAIDs may cause an increased risk of serious cardiovascular thrombotic events, myocardial infarction, and stroke, which can be fatal. This risk may increase with duration of use. Patients with cardiovascular disease or risk factors for cardiovascular disease may be at greater risk.

[Product] is contraindicated for the treatment of perioperative pain in the setting of coronary artery bypass graft (CABG) surgery.

Gastrointestinal Risk

NSAIDs, including Coxibs, cause an increased risk of serious gastrointestinal adverse events including bleeding, ulceration, and perforation of the stomach or intestines, which can be fatal. These events can occur at any time during use and without warning symptoms. Elderly patients are at greater risk for serious gastrointestinal (GI) events.

Cardiovascular Risk

NSAIDs may cause an increased risk of serious cardiovascular thrombotic events, myocardial infarction, and stroke, which can be fatal. This risk may increase with duration of use. Patients with cardiovascular disease or risk factors for cardiovascular disease may be at greater risk.

[Product] is contraindicated for the treatment of perioperative pain in the setting of coronary artery bypass graft (CABG) surgery.

Gastrointestinal Risk

NSAIDs, including Coxibs, cause an increased risk of serious gastrointestinal adverse events including bleeding, ulceration, and perforation of the stomach or intestines, which can be fatal. These events can occur at any time during use and without warning symptoms. Elderly patients are at greater risk for serious gastrointestinal (GI) events.

Page 32: Rheumatic pain indramayu 29june2013

So what does this mean for us?

■ BOTH NSAIDs and coxibs are associated to varying degrees with increased CV risk

■ We must consider co-morbidities and concurrent medications that may sway risk

■ Older patients are at increased risk of CV, GI and renal side effects – weigh up risk/benefit

■ Both NSAIDs and coxibs are viable and effective options to treat pain and have manageable side effect profiles

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33Arthritic patients with hypertension

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NSAIDs: Renal risksMHRA DSU. May 2009

Renal risk

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SUMMARY

■ Arthritis Pain is major health problem in our population

■ NSAIDs is scientifically proven to alleviate arthritis pain (OA, RA)

■ In patients with risk of GI tract afflection combine diclofenac with PPI

■ Diclofenac has a well-tolerated safety profille

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■ NICE advises against use of any NSAID in those taking low-dose aspirin

■ Avoid tNSAIDs and coxibs in those with history of heart failure

■ Avoid tNSAID or coxib in those with GFR <30, use with caution when GFR 30<60

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Practical Advice

■ Prescribe lowest effective dose for the shortest period of time

■ In chronic pain consider as required dosing and review regularly

■ Advise patient regarding potential side effects and do what you can to minimise risks

■ Monitor BP, renal function and liver function in those on long term

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Have an enjoyable learning

Thank you