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Gout and Osteoarthritis: What Works and What Doesn't?

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Gout and Osteoarthritis: What Works and What Doesn't? Gout and Osteoarthritis: What Works and What Doesn’t? Ahmad M Salah, DO Rheumatology, Franciscan Health Alliance, Midwestern University ACOI 2019 Annual Convention Disclosures None Osteoarthritis and Gout – Epidemiology Highlights, Clinical Relevance Brief Overview of Osteoarthritis and Gout Pathophysiology Review of Current Treatment Modalities and Evidence-Based Recommendations What is on the Horizon? Emphasis on Patient-centered Care and Education for Osteoarthritis and Gout Objectives Osteoarthritis OA affects ~30 million Americans (~35% of Americans ≥65yo)1 A leading cause of disability among older adults in the US, top 10 causes of disability worldwide1 5th most expensive condition treated in US hospitals @ $40 billion1 Annual direct per-patient cost $1500 - $20,0002 ~25% of OA patients have limitations in activities of daily living1 Increased CVD risk, depression, suicidal ideation2 Osteoarthritis Highlights Worse with activity Morning stiffness < 30 minutes “Gelling” Bony hypertrophy Limited mobility Crepitus Clinical Features Osteoarthritis Joint Distribution Heberden’s and Bouchard’s nodes signify primary nodal OA Google Image Search Pathophysiology Osteoarthritis Nat Rev Rheumatol. 2015 Apr;11(4):206-12. Trauma/Microfracture Chondrocyte transformation to inflammatory catabolic phenotype Articular Degradation of ECM Cartilage (metalloproteinases) Macrophage Activity/Cytokine Release Subchondral bone exposure Journal of Pharmacy Research 7 (2013) 132-138 Exposed to Suboptimal Rapid attempt Hypomineralized synovial fluid + shock to refortify bone growth factors absorption Subchondral Bone Ther Adv Musculoskel Dis (2013) 5(2) 77–94 Osteoarthritis not arthrosis Ther Adv Musculoskel Dis (2013) 5(2) 77–94 Kapoor, Mohit et al. “Role of proinflammatory cytokines in the pathophysiology of osteoarthritis.” Nature Reviews Rheumatology 7 (2011): 33-42 Nature Medicine Volume 19, pages 667–669 (2013) What Works for Osteoarthritis? Google Image Search • Nonpharmacologic • Patient Education, Low-impact Exercise, PT, Aqua PT, Weight loss Treatment for • Drugs (Tylenol, NSAIDs, Tramadol, Opioids) • Supplements (+/- glucosamine + chondroitin OA sulfate, curcumin) • Injections (CSI, HAI) • Clinical Trials (DMOADs) Education on disease, treatment and recommendations → improved pain and function long term Major obstacle is quality of education given by healthcare providers Multidisciplinary approach is generally beneficial for patient outcomes (physician, nurse, pharmacist, physical therapist) Patient Education American Academy of Family Physicians Am Fam Physician. 2012 Jan 1;85(1):49-56 American College of Rheumatology Arthritis Care & Research Vol. 64, No. 4, April 2012, pp 465–474 Journal of the American Geriatrics Society 49:808-823, 2001 American College of Rheumatology Glucosamine/Chondroitin Sulfate • Theory: Glucosamine is component of extracellular matrix • In vitro studies: glucosamine increases synthesis of proteoglycans by chondrocytes • Conflicting evidence • Relief should be noted in 2-3 months, otherwise discontinue Vogelgesang, Scott. “Osteoarthritis.” Rheumatology Secrets, Elsevier Health Sciences, 2014, pp. 389–390. Intra-Articular Tx Corticosteroids: • Q3-4 months • Short-term efficacy demonstrated Viscosupplementation • Q6-12 months • Shows some superior benefit for long-term efficacy ACR 2012 Guidelines for OA Treatment Action Plan It’s important to Patients oftentimes establish an action just want to know plan with your their options and patient how to use them Google Image Search Tanezumab: anti-NGF monoclonal Ab – SC/IV Tissue Gene-C: TGF-Beta 1 Transduced Chondrocytes – IA SM04690: WNT pathway inhibitor – IA DMOADs – Phase III Trials Tanezumab • Anti-Nerve Growth Factor monoclonal antibody – IV/SC Q8 weeks • Improved knee pain, stiffness, and limitations of physical function • SE: abnormal peripheral sensation, rapid progression of OA with NSAID use J Anaesthesiol Clin Pharmacol. 2018 Jan-Mar; 34(1): 111–116 J Pain Res. 2018; 11: 151–164. J Pain Res. 2018; 11: 151–164. J Pain Res. 2018; 11: 151–164. IL-1β elevates NGF TGF-β1 induces Mechanical expression in the NGF expression in loading stimulates synovium and the synovium and NGF expression by chondrocytes chondrocytes chondrocytes Role of Nerve Growth Factor (NGF) Tissue Gene-C (Invossa) Osteoarthritis Cartilage. 2015 Dec;23(12):2109-2118 https://www.tissuegene.com/en_US/technology/invossa • High quantities of TGF-β1 in articular cartilage TGF-β1 • Overexpression of TGF-β1 → chondrogenesis and growth of articular chondrocytes SM04690 • WNT pathway inhibitor – IA • Dual MOA: anti-inflammatory and reduces cartilage degradation • Clinically significant improvement in joint space width by x-ray Gout ~2% in men > 30yo, Prevalence increasing women > 50yo worldwide ~9% in men > 80yo Most prevalent inflammatory arthritis in men > 40yo Gout Positive Family History in 25% Highlights Risk Factors: diet, obesity, metabolic syndrome, HTN, diuretics, CKD, ARBs, β-blockers Protective: low-fat dairy, coffee, vitamin C, CCB, losartan Rheum Dis Clin North Am. 2014 May ; 40(2): 155–175. G. Ragab et al. / Journal of Advanced Research 8 (2017) 495–511 Clinical Features Gout Monoarticular Abrupt, Rapid Night or Early (85%) (hours) morning +/- Low-grade Articular and Acral fever Extra-articular distribution Google Image Search • Urate underexcretion (90%) • Impaired renal urate transport Gout • Hyperparathyroidism, hypothyroidism • Metabolic and respiratory acidosis Pathophysiology • Drugs (Cyclosporine – Alcohol – Nicotinic acid – Thiazides – Lasix – Ethambutol – Aspirin (<325mg) – Pyrazinamide Gout – Pathophysiology Basics Uric acid is the end product of purine degradation The human species lacks uricase – which oxidizes uric acid to more soluble allantoin Interestingly, we have the gene for uricase but it is inactive Hypothesized to be an evolutionary development as uric acid has potent antioxidant and free radical scavenger functionality Janson, Robert W. “Gout.” Rheumatology Secrets, by Sterling G. West, Elsevier, 2015, pp. 337–345. Underexcretion Pathway OAT1 OAT3 The genetics of hyperuricemia and gout - Scientific Figure on ResearchGate. Available from: https://www.researchgate.net/figure/The-uric-acid-transportasomeUrate-transporters-in- renal-proximal-tubules-are-involved-in_fig2_230791101 What Works for Gout? https://www.arthritis.org/about- arthritis/types/gout/articles/best-and-worst-gout-foods-12.php Adherence to gout Studies show 50-80% of management is very low patients stop taking ULT at compared to other chronic about 12 months diseases Gout education increases Knowledge about gout and its compliance dramatically treatment is lacking, both in (adherence at 1 year ↑ 40-70%, patients and HCPs 85% adherence at 5 years) Patient Education Systematic review of RCTs evaluated interventions that improve adherence Education on pathogenesis, co-morbidities and management of gout → increased adherence Patient Education cont… Hyperuricemia is primarily genetically driven – patient should not be ashamed or blame themselves Gout requires long-term treatment → goal is to reduce sUA → eliminate substrate for gout attacks Lowering sUA initially may lead to gout flares → goal is to eliminate crystal burden → no more attacks! NSAIDs, steroids, colchicine treat acute inflammation but do not treat gout/sUA Treatment is important → increased frequency of flares, affected joints → permanent/deforming joint damage Patient Education Talking Points Rheumatology 2018;57:i51-i58 Rheumatology 2018;57:i51-i58 Rheumatology 2018;57:i51-i58 Current Rheumatology Reports (2018) 20:12 Ther Clin Risk Manag. 2018; 14: 793–802. Ther Clin Risk Manag. 2018; 14: 793–802. Rheumatol Ther. 2019 Jun; 6(2): 179–193. Rheumatol Ther. 2019 Jun; 6(2): 179–193. Gout – Management Dietary Do not generally treat asymptomatic • Avoid purine-rich foods hyperuricemia • Meats (esp organ meats – liver, kidney, etc.) • only ~1/10 have gout • Seafood (esp shellfish, sardines/anchovies) • Uric acid >10mg/dL → 50% have gout • Avoid excess fructose (sodas, fruit juices) • Some suggest treating hyperuricemia to reduce • Vitamin C, reduced-fat dairy, tart cherries – reduce risk of nephrolithiasis but no consensus gout risk • Purine-rich vegetables (rich green leafy i.e. spinach) not associated with gout risk Rheum Dis Clin North Am. 2014 May ; 40(2): 155–175. G. Ragab et al. / Journal of Advanced Research 8 (2017) 495–511 Acute – 1.2mg → 1 hr → 0.6mg Prophylactic – 0.6mg daily Colchicine Probenecid • Inhibits proximal tubule urate reabsorption Uricosurics • Avoid in CKD, nephrolithiasis, elderly • Not commonly used as it is generally less effective and more limitations Lesinurad Arthritis Research & Therapy December 2016, 18:214, Patient Related Outcome Measures 2018:9 231–238 Arthritis Rheumatol. 2016 Aug; 68(8): 1793–1796 Inhibits function of (URAT1, OAT4) ≠ reabsorption of uric acid in the kidney Lesinurad Approved for combination therapy with an XOI, not monotherapy Patient Related Outcome Measures 2018:9 231–238 Arthritis Rheumatol. 2016 Aug; 68(8): 1793–1796 Allopurinol Febuxostat • Allopurinol Hypersensitivity Syndrome (0.1%- • 40mg – 80mg (can use higher doses) 0.4%) • More expensive than allopurinol • More common in patients who had • Safe in patients who had AHS maculopapular rash 2/2 allopurinol (5-10%) • Hepatic clearance • Caution in patients with CKD and/or on diuretics • Clinical: rash, fever, eosinophilia, hepatic necrosis, leukocytosis, worsening renal function • Tx: high dose steroids and dialysis • Start
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