Chapter 32: Osteoarthritis & Gout – Anti-Inflammatory Therapy

Chapter 32 details the pathophysiology, diagnostic criteria, and comprehensive pharmacologic management of Osteoarthritis (OA) and Gout, two prevalent forms of arthritis. OA, a progressive disease often linked to aging, obesity, and joint injury, involves the deterioration of articular cartilage and a reduction in protective proteoglycans, leading to subchondral bone remodeling and osteophyte formation. Treatment for OA emphasizes a multimodal, patient-centered approach that prioritizes nonpharmacologic therapies like weight loss and exercise. Pharmacologic interventions typically begin with topical agents, such as diclofenac, for localized joint pain, followed by oral Nonsteroidal Anti-inflammatory Drugs (NSAIDs) for greater efficacy, though careful monitoring is required due to significant cardiovascular and gastrointestinal risks associated with systemic NSAID use. Acetaminophen, once first-line, is now conditionally recommended due to questionable efficacy and hepatotoxicity concerns. Other options include central analgesics like tramadol, the SNRI duloxetine, and intra-articular corticosteroids. The chapter also explores Gout, an inflammatory condition caused by hyperuricemia (uric acid greater than 6.8 mg/dL) resulting from the overproduction or underexcretion of uric acid, which leads to monosodium urate crystal precipitation in joints. Chronic gout is managed using Urate-Lowering Therapy (ULT), primarily Allopurinol (a Xanthine Oxidase Inhibitor or XOI) to maintain serum urate levels below 6 mg/dL, often adding Probenecid if goals are unmet. Febuxostat is generally reserved for patients intolerant to or inadequately controlled by Allopurinol. Acute gout attacks are treated with NSAIDs (naproxen, indomethacin, sulindac), systemic corticosteroids, or colchicine, often combined for severe attacks. Clinicians must be vigilant about complex drug interactions, particularly with colchicine and CYP3A4/P-gp inhibitors, and must perform genetic screening for the HLA-B*5801 allele in high-risk patients before initiating allopurinol.