Gout and Pseudogout dr. MUH. ARDI MUNIR, M.Kes., Sp.OT., M.H., FICS

Background Gout and pseudogout are the two most common crystal-induced arthropathies. Gout is caused by monosodium urate monohydrate crystals; pseudogout is caused by calcium pyrophosphate (CPP) crystals and is more accurately termed calcium pyrophosphate disease (CPPD).

Pathophysiology Gout can be considered a disorder of metabolism that allows uric acid or urate to accumulate in blood and tissues. When tissues become supersaturated, the urate salts precipitate, forming crystals. In addition, the crystals also are less soluble under acid conditions and at low temperatures, such as occur in cool, peripheral joints (eg, the metatarsophalangeal joint of the big toe).

Signs and symptoms Podagra (initial joint manifestation in 50% of gout cases and eventually involved in 90%; also observed in patients with pseudogout and other conditions) Arthritis in other sites – In gout, the instep, ankle, wrist, finger joints, and knee; in pseudogout, large joints (eg, the knee, wrist, elbow, or ankle) Monoarticular involvement most commonly, though polyarticular acute flares are not rare, and many different joints may be involved simultaneously or in rapid succession

Signs and symptoms In gout, attacks that begin abruptly and typically reach maximum intensity within 8-12 hours; in pseudogout, attacks resembling those of acute gout or a more insidious onset that occurs over several days Without treatment, symptom patterns that change over time; attacks can become more polyarticular, involve more proximal and upper-extremity joints, occur more often, and last longer In some cases, eventual development of chronic polyarticular arthritis that can resemble rheumatoid arthritis

Physical findings may include Involvement of a single (most common) or multiple joints Signs of inflammation – Swelling, warmth, erythema (sometimes resembling cellulitis), and tenderness Fever (also consider infectious arthritis) Migratory polyarthritis (rare) Posterior interosseous nerve syndrome (rare) Tophi in soft tissues (helix of the ear, fingers, toes, prepatellar bursa, olecranon) Eye involvement – Tophi, crystal-containing conjunctival nodules, band keratopathy, blurred vision, anterior uveitis (rare), scleritis

Complications of gout include Severe degenerative arthritis Secondary infections Urate or uric acid nephropathy Increased susceptibility to infection Urate nephropathy Renal stones Nerve or spinal cord impingement Fractures in joints with tophaceous gout

Diagnosis Joint aspiration and synovial fluid analysis Serum uric acid measurement (though hyperuricemia is not diagnostic of gout) 24-hour urinary uric acid evaluation Blood studies (including white blood cells [WBCs, triglyceride, high-density lipoprotein, glucose, and renal and liver function tests)

Plain radiographs may show findings Erosions with overhanging edges are generally considered pathognomonic for gout (though also found in other diseases). Characteristics of erosions typical of gout include the following: - Maintenance of the joint space - Absence of periarticular osteopenia - Location outside the joint capsule - Sclerotic (cookie-cutter, punched-out) borders - Asymmetric distribution among the joints, with a strong predilection for distal joints, especially in the lower extremities

Other imaging modalities Computed tomography (CT) – Complementary to plain radiography for recognizing erosions in gout Magnetic resonance imaging (MRI) – MRI with gadolinium is recommended when tendon sheath involvement must be evaluated and when osteomyelitis is in the differential diagnosis Ultrasonography

Management Gout is managed in the following 3 stages: - Treating the acute attack - Providing prophylaxis to prevent acute flares - Lowering excess stores of urate to prevent flares of gouty arthritis and to prevent tissue deposition of urate crystals

Acute treatment Nonsteroidal anti-inflammatory drugs (NSAIDs), such as indomethacin Corticosteroids Colchicine (now less commonly used for acute gout than it once was) Adrenocorticotropic hormone (ACTH) Combinations of drugs (colchicine plus NSAIDs, oral corticosteroids plus colchicine, intra-articular steroids plus colchicine or NSAIDs)

Long-term management Therapy to control the underlying hyperuricemia generally is contraindicated until the acute attack is controlled Long-term management of gout is focused on lowering uric acid levels. Agents used include the following: - Allopurinol - Febuxostat - Probenecid

Agent Prophylaxis Because these agents change serum and tissue uric acid levels, they may precipitate acute attacks of gout. This undesired effect may be reduced by prophylaxis with the following: - Colchicine or low-dose NSAIDs - Low-dose prednisone

Other Therapeutic Agents Uricase and pegloticase Vitamin C Anakinra Fenofibrate

Non Pharmacologic Measures Avoidance or restricted consumption of high-purine foods Avoidance of excess ingestion of alcoholic drinks, particularly beer Avoidance of sodas and other beverages or foods sweetened with high-fructose corn syrup Limited use of naturally sweet fruit juices, table sugar, and sweetened beverages and desserts, as well as table salt Maintenance of a high level of hydration with water (≥8 glasses of liquids daily) A low-cholesterol, low-fat diet, if such a diet is otherwise appropriate for the patient Weight reduction in patients who are obese

Operative Treatment

Conclusion

Telima Casihh