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Clinical Pearls: Rheumatology

Clinical Pearls: Rheumatology. Sterling West, MD, MACP Professor of Medicine University of Colorado Denver SOM. Disclosures. None . Case #1: History. 60yo woman with RF+ RA x 15yrs MTX (10mg/wk), SSZ (500mgBID), folate, prednisone (5mg/d)

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Clinical Pearls: Rheumatology

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  1. Clinical Pearls: Rheumatology Sterling West, MD, MACP Professor of Medicine University of Colorado Denver SOM

  2. Disclosures • None

  3. Case #1: History • 60yo woman with RF+ RA x 15yrs • MTX (10mg/wk), SSZ (500mgBID), folate, prednisone (5mg/d) • PMH: HBP (lisinopril), obesity, osteopenia (alendronate). Nonsmoker • Chronic complaint: diffuse pain and fatigue • New problem: Rt knee pain

  4. Case #1: Physical Exam • VS: P=80, BP=132/80, BMI=31 • HEENT: Xerostomia, dental caries • CHEST/CVS/ABD: obese • EXT: RA deformities of hands/wrists/feet with continued active synovitis of isolated MCPs/PIPs, rt wrist, and left knee. She walks with a limp due to rt knee pain. She is tender inferior to medial joint line. • BACK: Multiple fibromyalgia tender points • NEURO: no ankle reflexes. Fall risk as evidenced by poor “get up and go” test. • SKIN: Rt elbow rheumatoid nodule

  5. Case#1: Laboratories • CBC: Hct 33% with MCV 82, WBC 7800 with normal diff, plts 438,000 • CMP: normal except fasting glucose 108, alk phos 135 (nl< 115), albumin 3.0, calcium 9.1 • U/A: WNL • ESR 45 mm/hr; CRP 2.6mg/dL (nl <1.0) • Iron studies: Iron 28, % sat 14%, TIBC 274, Ferritin 230 • TSH: 2.6 , Hgb A1C: 6.1% • Fasting lipid panel: Cholesterol 205, HDL 36, LDL 129, TG 156 • Stool for occult blood: negative x1

  6. Case#1: Radiographs • Bilateral weight bearing knee xrays: • Right: normal joint space, medial osteophytes • Left: medial joint space narrowing 50% • DEXA: Worst T score is -2.3 at rt FN. However, there has been a 5% loss of bone mineral density at spine and hips over past 2 years while on alendronate therapy.

  7. Case#1 Problem List • Fatigue • Fibromyalgia • Rt knee pain • Rheumatoid arthritis • Dysmetabolic syndrome: HBP, obesity, low HDL, glucose intolerance • Anemia • Osteopenia worsening on therapy

  8. Question#1: Fibromyalgia • Which one of the following is the next best step? • A. Send to physical therapy • B. Order 1,25 OH vitamin D level • C. Start amitriptyline 25mg qhs • D. Ask if she snores • E. Give her a shot of triamcinolone 40mg intramuscularly

  9. Question #1: Answer: D. Ask if she snores • Fibromyalgia associations (30%) • Sleep apnea • Sexual/physical abuse • PT and amitriptyline won’t work unless correct sleep apnea • Severely low vitamin D: measure 25OH vit D not 1,25OH vitD • IM triamcinolone helps RA transiently but not fibromyalgia pain

  10. Clinical Pearl #1 • Clinical Pearl: All patients with fibromyalgia should be asked about symptoms of sleep apnea. • Reference: • Parish J. Sleep-related problems in common medical conditions. Chest 135: 563-572, 2009.

  11. Question #2: Rt knee pain • Which one of the following should be done now? • A. Send to nutritionist for weight loss • B. Send to PT for quadriceps strengthening exercises • C. Consult orthopedist for hyaluronate injections into the knee • D. Order an MRI of knee • E. Inject triamcinolone/lidocaine into anserine bursa

  12. Question#2: Answer: E. Inject anserine bursa • Anserine bursitis common in obese patients and those that limp from any cause. • Weight loss and PT helps prevent recurrence but won’t help patient acutely. • Symptoms, exam of knee, and weight bearing xrays showing no JSN ruled out OA so hyaluronate injections won’t help and are expensive. • Symptoms and exam not compatible with an internal derangement of knee so MRI not indicated.

  13. Pes Anserine Bursa

  14. Clinical Pearl #2 • Clinical Pearl: All patients with medial knee pain should be examined for anserine bursitis. • Reference: • Hill CL et al. Periarticular lesions detected on MRI: prevalence in knees with and without symptoms. Arthritis Rheum 48: 2836-44, 2003. • Handy JR. Anserine bursitis: A brief review. Southern Medical J 90:376-7, 1997.

  15. Question#3: Rheumatoid arthritis • Which one of the following is the next best step to control this patient’s RA? • A. Add celexoxib 200mg BID • B. Increase prednisone to 5mg BID • C. Titrate methotrexate up to 20mg weekly • D. Start an anti-TNF agent • E. Start abatacept

  16. Question #3:Answer: C. Titrate MTX to 20mg/wk • At least 30% of RA pts respond to MTX but must dose must be optimized (MTX polyglutamate level > 60). • Variability of absorption. Watch MCV. Go to subq • Don’t use MTX if renally impaired • Use MTX early in disease: first 3-6 months • Celexoxib and prednisone are short term benefit, have side effects, and don’t prevent joint destruction. • Biologics are expensive and should be used after failure of MTX.

  17. Clinical Pearl #3 • Clinical Pearl: All patients with RA should be started on disease-modifying antirheumatic therapy as early as possible. In patients with normal renal function, MTX should be titrated to 20mg a week before it is considered ineffective. • References: • Visser K et al. Multinational evidence-based recommendations for the use of methotrexate in rheumatic disorders. Annals Rheum Dis 68: 1086-1093, 2009.

  18. Question#4: Rheumatoid arthritis • Which one of the following is this patient most likely to die from over the next 10 years? • A. Sepsis • B. Lymphoma • C. Myocardial infarction • D. Hip fracture • E. Ovarian cancer

  19. Question #4:Answer: C. Myocardial infarction • RA accelerates atherosclerosis by 10 years and increases RR 2x. • RA pts need aggressive risk factor reduction similar to a diabetic. • Sepsis, lymphoma, and osteoporosis are increased in RA pts but not as much as atherosclerosis. • Solid malignancies are not increased in RA.

  20. CV Risk in Newly Diagnosed RA Patients 10-yr absolute CVD risk in 60-yr-old female • Study of patients with RA and conventional cardiac risk factors • Given identical cardiac risk factors, patients with RA have a higher likelihood of having MI than non-RA patients • Important to control both inflammatory disease and conventional risk factors RA Non RA Without risk factor SMO SMO HTN SMO HTN DM SMO HTN DM DYS SMO HTN DM DYS OBE SMO HTN DM DYS Low BMI DM, diabetes mellitus; DYS, dyslipidaemia; HTN, hypertension; OBE, obesity; SMO, smoker 1 Kremers HM, et al.71st ACR, Boston 2007. #2185

  21. RA and cardiovascular risk • Retrospective database analysis (UK General Practice Research Database, GPRD)1,2 • Data from 1987–2002 (pre-biologic era in UK) • 34,364 RA pts; 103,089 well-matched controls • 73% used DMARDS or prednisone prior to MI • 966 MI in RA pts • Summary • Individuals with RA have an increased risk of MI that remains after adjusting for traditional risk factors • Lipid-lowering medications significantly reduce this risk whereas antihypertensives had little effect on the risk 1. Edwards CJ, et al. ACR 2008, San Francisco #687; 2. Edwards CJ, et al. ibid #688

  22. CVD Mortality Reduction • 19,580 pts; 1129 deaths; 63,811 pt-yrs f/u • CVD33%,cancer22%,lung dz19% • Therapy major impact on decreasing CVD deaths by 30-45% Abstract 296, ACR National Meeting,2005

  23. Clinical Pearl #4 • Clinical Pearl • RA, SLE, vasculitis patients die early of CVD (MI, strokes) • CVD occurs 10 years early • Traditional risk factors fail to explain premature atherosclerosis • RA, SLE, vasculitis patients should be treated like diabetic patients - aggressively • References: • Sodergren A et al. Increased incidence of and impaired prognosis after acute myocardial infarction among patients with serpositive RA. Ann Rheum Dis 66: 263-266, 2007. • Solomon DH et al. Cardiovascular morbidity and mortality in women diagnosed with rheumatoid arthritis. Circulation 107: 1303-1307, 2003.

  24. Question#5: Anemia • Which one of the following should be done now? • A. Start oral iron therapy • B. Start a proton pump inhibitor • C. Stop methotrexate • D. Control the rheumatoid arthritis • E. Order an EG&D and colonoscopy

  25. Question #5:Answer: D. Control the RA • Anemia is common in RA: iron deficiency vs ACD • Both have low iron and %sat. • TIBC > 400 ug/dl equals iron deficiency • Ferritin > 100 ng/ml equals ACD • Inflammation causes IL-6 release. IL-6 stimulates hepcidin that stops ferroportin from releasing iron stores. This causes iron sequestration.

  26. Anemia of Chronic Disease and RES IL-6 or sequestered in RES

  27. Clinical Pearl #5 • Clinical Pearl: RA patients with anemia and a ferritin greater than 100ng/ml do not have iron deficiency anemia. • Reference: • Gabay C, et al. Acute phase proteins and other systemic responses to inflammation. NEJM 340: 448, 1999 • Porter DR et al. The use of serum ferritin estimation in the investigation of anemia in patients with RA. Clin Exper Rheum 12: 179-182, 1994.

  28. Question#6: Osteopenia with worsening DEXA • Which one of the following is the next best step? • A. Order 25 OH vitamin D level • B. Order a PTH level • C. Switch to IV zolendronic acid • D. Switch to teriparatide • E. Send to PT for weight-bearing exercises

  29. Question #6:Answer: A. Order 25OH vitamin D • The two most common reasons for not responding to bisphosphonate therapy: • Vitamin D insufficiency • Failure to take bisphosphonate correctly • No reason to order PTH if calcium normal. • IV zolendronic acid or sub q teriparatide will not work if vitamin D deficient. • Exercise is great to prevent falls not to increase BMD

  30. Nonresponders to Osteoporosis Therapy • Vitamin D deficiency • Poor adherence to therapy • Taking the medication incorrectly • Co-morbid conditions • Malabsorption (celiac disease) • Wrong dose or dosing interval • Lack of efficacy (generics)

  31. Clinical Pearl #6 • Clinical Pearl: Rule out vitamin D insufficiency/deficiency in patients losing bone mineral density while receiving therapy for osteoporosis. • Reference: • Lewiecki EM. Nonresponders to osteoporosis therapy. J Clin Den 6: 307-314, 2003.

  32. Case#2: History • 25 yo woman with diffuse aching x 10yrs. Started as cheerleader in HS. • Pain worse in lower extremities. Joint swelling intermittently in knees after a hike. • PMH: Hypothyroidism age 21 (levothyroxine) • Other meds: prn aleve, OCPs x 5 yrs

  33. Case#2: PE/Labs • Physical examination is normal except for the following: • Mildly enlarged thyroid • CVS: midsystolic click, ? systolic murmur • Patellofemoral crepitus with small effusions • Hypermobility with pes planus. No synovitis. • Skin: normal • Laboratories: • CBC, CMP, CPK, U/A, TSH normal • ESR 2mm/hr, RF neg • ANA: 1:160 speckled

  34. Question#7: Arthralgias and a positive ANA • Which one of the following should be done now? • A. Order an anti-CCP • B. Order an ANA profile • C. Order radiographs of painful joints • D. Order an echocardiogram • E. Order a free T4 level

  35. Question #7:Answer: B. Order ANA profile • Strategy to determine if ANA is significant (next slides) • ANA can’t be ignored if patient has autoantibody against specific autoantigen • Physical exam not consistent with RA so antiCCP and xrays of little help • Echo may show MVP but not explain arthralgias • A free T4 not indicated with normal TSH

  36. Clinical Pearl #7: Evaluation of a positive ANA • Hx and P/E: rule out occult Sjogren’s • ANA titer (≥ 1:160) and pattern (rim, nucleolar) • ANA profile: • Anti-SS-A: SLE, Sjogren’s, UCTD • Anti-SS-B: Sjogren’s • Anti-U1 snRNP: MCTD, SLE, scleroderma • Anti-Sm (Smith): SLE • Anti-dsDNA: SLE • Anti-centromere: CREST • Anti-topoisomerase I/SCL-70: diffuse scleroderma • Anti-PM-SCL/PM-1: polymyositis/scleroderma overlap • Anti-histone: drug-induced lupus, SLE, others PEARL: A positive ANA against a specific antigen is never normal

  37. Clinical Pearl #7: Evaluation of a positive ANA • CBC (anemia:ACD vs hemolysis; leukopenia; thrombocytopenia), chemistries (kidney), LAEs (autoimmune hepatitis), CPK, urinalysis • ESR, RF, C3/C4 (hypocomplementemia) • Pearl: If any of these are abnormal then must respect the positive ANA • SPEP (polyclonal gammopathy), PTT (lupus anticoagulant), RPR (false positive) • Others (patient specific): antithyroid antibodies, antihistone antibodies (DILE), antiphospholipid antibodies (hx of clot), anti- ribosomal P antibodies (psychosis or severe depression)

  38. Question #7: References • Shmerling RH. Diagnostic tests for rheumatic disease: clinical utility revisited. So Med J 98:704, 2005. • Solomon DH, et al. Evidence-based guidelines for the use of immunologic tests: Antinuclear antibody testing. Arth Rheum 47: 434, 2002. • Wallace DJ et al. The “rule out lupus” consultation: Clinical outcomes and perspectives. J Clin Rheum 1: 158-164, 1995.

  39. Question#8: Knee pain and hypermobility • Which one of the following is the next best step? • A. Order gene testing • B. Stop oral contraceptives • C. Order shoe orthotics and muscle strenghtening exercises • D. Inject both knees with triamcinolone • E. Start tramadol

  40. Question#8:Answer: C. Order shoe orthotics and muscle strengthening exercises • Hypermobility causes arthralgias and patellar chondromalacia that can cause knee effusions. • Common in cheerleaders and dancers • Do not diagnose these patients as having Ehlers Danlos, type III • Must correct pes planus or other therapies unlikely to work. • Gene testing expensive and not helpful • Arthralgias predate OCPs so not the cause.

  41. Clinical Pearl #8: Hypermobility Syndrome

  42. Clinical Pearl #8 • Clinical Pearl: In any patient with patellofemoral disease, rule out hypermobility and pes planus. If present, shoe orthotics are a necessary part of therapy in addition to quadriceps strengthening exercises. • References: • Remvig L et al. Epidemiology of general joint hypermobility and basis for proposed criteria for benign joint hypermobility syndrome: a review of the literature. J Rheumatol 34: 664-665, 798-803, 2007. • Collins N et al. Foot orthoses and physiotherapy in the treatment of patellofemoral pain syndrome: randomised clinical trial. Br J Sports Med 43: 169-171, 2009.

  43. Thank you Questions ????

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