Disclosures. None. Seth Compton, MD Fellow of Rheumatology University of Mississippi Medical Center. Thank you for coming

Transcription

1 Disclosures None Seth Compton, MD Fellow of Rheumatology University of Mississippi Medical Center Steroids Steroids Thank you for coming 1

2 Outline Osteoarthritis Rheumatoid Arthritis Monoarthritis Systemic Lupus Erythematosus Fibromyalgia Arthritis in Mississippi Approximately 650,000 affected 30% of the state population 35% of women affected 27% of men affected Arthritis: Joint inflammation/swelling/warmth/erythema Joint deformity (visual or by imaging) Loss of range of motion Characterized symptomatically by prolonged (> 1hr) AM stiffness Rheumatoid Arthritis Arthralgia: Joint pain (with no observable inflammation) 2

3 Rheumatoid Arthritis What are we looking for in RA? Synovitis Erosions Extra articular Manifestations Kelley s Textbook of Rheumatology, 8 th Edition, Key Words for Inflammatory Arthritis AM stiffness > 1 hour Symmetric joint involvement Joint swelling Erosions on imaging Rheumatoid nodules Rheumatoid Factor RA RF in Rheumatic Disease Disease Incidence RA 75% JIA 20% AS <15% Reactive negative Psoriatic negative SLE 40% Sjogrens 90% Cryoglobulinemia >90% RF in Non Rheumatic Disease Infection Endocarditis Hepatitis Acute Viral Parasitic TB Lung Disease Interstitial Fibrosis Chronic Bronchitis Silicosis Other Cirrhosis Sarcoidosis Chronic Hepatitis Malignancy Post Vaccination MI Aging Anti-CCP antibodies: Specific (90-95%), low sensitivity (50-60%) Kelley s Textbook of Rheumatology, 3 rd Edition. 3

4 Early RA vs OA Rheumatoid Arthritis Osteoarthritis Age at Onset Childhood & adults; peak 50 s Increases with age Predisposing Factor Smoking, susceptibility epitopes (HLA DR4) Trauma Congenital abnormalities Early Symptoms Morning stiffness Increases through the day and with use Joints Involved MCPs, wrists, PIPs most often DIPs and weight bearing Physical Findings Soft tissue swelling, warmth Bony osteophytes, minimal soft tissue swelling early Radiologic Findings Laboratory Findings Periarticular osteopenia, marginal erosions Increased CRP, RF, anti CCP, anemia Subchondral sclerosis, osteophytes Normal ACR Classification Criteria (2010) Joint Involvement Score Acute Phase Reactants 1 med large 0 Normal ESR & CRP 2 10 med large 1 Abnormal ESR or CRP 1 3 small small 3 Duration >10 (>1 small) 5 <6 weeks 0 Serology >6 weeks 1 RF & CCP neg 0 Low (+) RF or 2 CCP High (+) RF or 3 CCP Score 0 1 ACR Classification Criteria (2010) Score >6 consistent with RA Med large joints: elbows, shoulders, hips, knees, ankles Low (+) serology <3x ULN Treatment of RA NSAIDS Hydroxychloroquine (Plaquenil) Methotrexate (Gold Standard) Leflunomide (Arava) Sulfasalazine (Azulfidine) TNF Blockers Enbrel, Humira, Remicaid Other Biologics Others Azathioprine, cyclosporine STEROIDS Avoid >10 15 mg of prednisone 4

5 Gold Immunosuppressants Antimalarials Cortisone Penicillamine Sulfasalazine Tocilizumab Certolizumab and Golimumab Rituximab Abatacept Adalimumab Anakinra Methotrexate Infliximab Etanercept Leflunomide History of DMARD Use Changes in the Treatment of RA Old New Emphasis on treating symptoms of the disease Less aggressive treatment in early stages NSAIDs considered least toxic. MTX and Steroids considered most toxic Emphasis on limiting destruction of joints Earlier diagnosis and use of aggressive treatments Higher doses of MTX Combination DMARD therapies Biologics (BRMs) shown to be highly effective (alone and esp. in combination with DMARDs) Pearls If checking a Rheumatoid Factor, would check hepatitis panel concomitantly Most DMARDs count as High Risk Medication Typically we only give 3 4 month supply of drugs like MTX, SSZ, etc due to lab monitoring If pt asks for temporary refill of DMARD, would: Defer to rheumatologist OR If filling, get a CBC/CMP Pearls Plaquenil: Annual eye screening TNF therapy: Malignancy risk unclear Continue age appropriate cancer screening Increased risk of infections DO get flu shot DON T get Varicella vaccine 5

6 Pearls Most Rheumatic drugs take time to work Plaquenil: 4 6 weeks Methotrexate: 3 6 weeks TNF s: 1 3 weeks Prednisone: Yesterday Osteoarthritis Incidence of OA Osteoarthritis Arthritis (million) Osteoarthritis Rheumatoid Arthritis Gout 27 6

7 Hand Radiograph OA General Features Clinical Lab Radiograph Age >50 ESR <40 mm/hr Osteophytes AM Stiffness <30 minutes RF Titer <1:40 Joint space narrowing Crepitus Noninflammatory synovial fluid Subchondral cysts and sclerosis No inflammation Malalignment Bony enlargement or tenderness Osteoarthritis Treatment Algorithm Diagnosis Physical Measures Patient Education Medications Analgesics Anti inflammatory Intra articular Acetaminophen Tramadol Capsaicin Opioids NSAIDs (COX 2) Corticosteroids Hyaluronate Adapted from ACR Subcommittee on Osteoarthritis. Arthritis Rheum. 2000;43: Surgery 7

8 Pearls If DIP hand involvement, think: Osteoarthritis Psoriatic Arthritis Gout Pseudogout Sjogren s, SLE, etc Less commonly RA Systemic Lupus Erythematosus What Is SLE Origin of Lupus Autoimmune disease body s defenses against infection mistakenly attack the body s own tissues causing inflammation. Chronic disease Can involve a number of organs and organ systems. 8

9 Organ Effects Systemic lupus erythematosus: alopecia Types of Lupus Discoid Sub acute cutaneous Systemic (SLE) Undifferentiated connective tissue disease (UCTD) Mixed connective tissue disease (MCTD) Raynaud s phenomenon SLE Classification Criteria Cutaneous 1. Malar Rash 2. Discoid Rash 3. Photosensitivity 4. Oral/nasal ulcers Musculoskeletal 5. Nonerosive arthritis Cardiopulmonary 6. Serositis Renal 7. Proteinuria Neurologic 8. Seizures or psychosis Hematologic 9. Hemolytic anemia Or low WBC/PLT Serologies 10. ANA 11. Anti ds DNA, anti Sm, or antiphospholipid >4 of 11 meets criteria 9

10 Discoid lupus erythematosus Systemic lupus erythematosus: Jaccoud s arthropathy Copyright Science Press Internet Services Lab Monitoring in SLE Standard labs: CMP verify renal and hepatic function (often on hepatotoxic medications) CBC ensure stability of blood counts RUA and spot urine protein/creatinine screen for lupus nephritis C3 and C4 complements low levels could suggest current or impending disease activity ESR and CRP because we re rheumatologists Treatment Lifestyle modifications Sun protection! Avoid infection (basic principles of hygiene) Infection often precipitates SLE flare Healthy lifestyle (exercise, weight loss, healthy eating) Increased risk of coronary artery disease Regular cancer screening Vaccinations: pnemonia, flu, meningococcal 10

11 Pharmacologic Treatment Corticosteroids Antimalarials (Hydroxychloroquine) Immunosuppressive therapies: Azathioprine (Imuran) Methotrexate Cyclophosphamide (Cytoxan) Mycophenolate mofetil (Cellcept) IVIG Benylsta Red Flags Increasing proteinuria New proteinuria >500mg is significant Low complement levels Changes in mental status Cerebritis/vasculitis? Lupus psychosis (treat like regular psychosis) Significant SOB/DOE Pneumonitis or DAH? Pearls If known SLE, starting plaquenil usually safe Steroids effective for flares but minimize use as much as possible Easy to get from 40mg to 10mg, tough to get from 10mg to off Best time to get pregnant: stable disease Potential markers for flare: C3, C4, ESR, CRP, AntidsDNA Monoarthritis 11

12 Differential for Monoarthritis Crystal induced Gout CPPD Infection Hemarthrosis Trauma Clotting disorder Systemic Rheumatic Disease Osteoarthritis Intraarticular derangement (tears, fractures) Gout Uric acid is the end product of purine metabolism present in serum and tissues in the form of monosodium urate. With uric acid levels > 6.7 mg/dl monosodium urate supersaturates the serum and precipitates into tissues. Prolonged tissue deposition gout and tophi. Most patients with elevated uric acid do not experience clinical disease. Two Reasons for Gout Impaired renal excretion of uric acid Most common Overproduction of uric acid Typically inherited Fibromyalgia 12

13 Fibromyalgia I ll let you know if I find something that works 13