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History of PMR 1888 First described as senile rheumatic gout (Bruce) 1936Secondary fibrositis 1945Periarthrosis humeroscapular 1946Peri-extra-articular.

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Presentation on theme: "History of PMR 1888 First described as senile rheumatic gout (Bruce) 1936Secondary fibrositis 1945Periarthrosis humeroscapular 1946Peri-extra-articular."— Presentation transcript:

1 History of PMR 1888 First described as senile rheumatic gout (Bruce) 1936Secondary fibrositis 1945Periarthrosis humeroscapular 1946Peri-extra-articular rheumatism 1951Special arthritis of old age 1952Myalgic syndrome of aged with systemic reaction 1953Pseudo-polyarthrite rhizomelique 1954Anarthritic rheumatoid disease 1950sHenk discovered anti-inflamm effects of prednisolone 1957Polymyalgia rheumatica (Barber - Manchester)

2 Diagnostic Criteria BSR working group (Dasgupta 2008) 1.Age >50 years 2.Shoulder and/or pelvic girdle pain 3.Morning stiffness >45mins 4.Duration of 2 weeks at least 5.ESR>30 mm/hr or CRP >6 mg/l Jones & Hazleman 1981 Absence of inflammatory arthritis, RA or malignancy Absence of muscle weakness / disease Prompt & dramatic response to steroids

3 Differential Diagnosis Rheumatoid arthritis Inflammatory myopathy Drug-induced myalgia (statins) Endocrine disease (thyroid, parathyroid, Addison’s) Malignancy, metastases, myeloma Occult sepsis Shoulder capsulitis, rotator cuff disorders Osteoarthritis, spondylosis Depressive illness Parkinsonism Fibromyalgia or pain syndromes Multiple pathology GP or hospital condition?

4 Management Start with plain prednisolone 15mg – expect 70% response within one week Immediate bone protection (alendronate) Monitor Clinical : pain stiffness, disability, steroid effects, other rheumatic problems may intervene Lab : FBC, esr/CRP, U&E, glucose

5 When to refer? Atypical features Younger patient Chronic onset Lack of shoulder involvement Lack of inflammatory stiffness “Red flag features” : weight loss, night pain, neuro signs, systemic features ++ Peripheral arthritis or signs of CTD/muscle disease Normal or v high acute phase response [esr or CRP ] Treatment Dilemmas Incomplete or non-response to steroid or ill-sustained response or unable to reduce dose or C/I to steroids

6 What’s new? Strong relationship between starting dose and maintenance dose of steroid Initial esr correlates with duration of treatment ESR > CRP for prediction of relapse (also calprotectin from WBC) Intramuscular methyl-prednisolone (Depomedrone) Deflazacort - no better than prednisolone Methotrexate – only small steroid-sparing effect Etanercept modest effect : Infliximab doesn’t work Tocilizumab may ameliorate via interleukin-6 PMR with normal esr in 7% : PMR with normal CRP in 1% Diagnosis & follow-up : GP or hospital

7 What’s the cause? Subclinical vasculitis Extra-capsular oedema on MRI Subacromial or subdeltoid bursitis on U/S Glenohumeral inflaamation onU/S No clinical or lab features to differentiate PMR from RA, although HLS class II associations are different

8 Temporal arteritis, aka. cranial arteritis, giant cell arteritis GCA Age >50yrs Headache- subacute onset, usually bilateral, may be unilateral Jaw claudication Systemic upset; fever, wt loss Temporal arteritis = medical emergency because of risk of sudden irreversible blindness

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10 Treatment Steroids – Prednisolone high dose 1mg/kg or intravenous methylpred - start before biopsy Steroid sparing agents sometimes used in chronic phase (MTx azathioprine) Aspirin

11 Duration of steroid therapy Most patients one to two years No consistently reliable predictors of the duration of therapy have been found. NEJM 2002;347:261-271 Steroid doses to be tapered according to inflammatory markers and clinical picture. IL6 is a better predictor of disease flare and ?can be used to monitor disease activity and gauge rate of steroid reduction Weyand CM, HunderGM Arthritis Rheum 2000;43:1041-1048

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