KEY CLINICAL UPDATES IN CRYSTAL DEPOSITION ARTHRITIS
In a 2020 randomized, controlled trial in patients with CKD and a high risk of its progression, urate-lowering treatment with allopurinol did not slow the decline in eGFR when compared to placebo.
In patients with concomitant coronary artery disease, long-term colchicine use can reduce major cardiovascular events.
Despite initial concern that febuxostat was associated with more cardiovascular events than allopurinol, a large, randomized, controlled trial in 2020 showed that the two drugs have similar cardiovascular safety.
ESSENTIALS OF DIAGNOSIS
Acute, monoarticular arthritis, often of the first MTP joint; recurrence is common.
Polyarticular involvement more common in patients with longstanding disease.
Identification of urate crystals in joint fluid or tophi is diagnostic.
Dramatic therapeutic response to NSAIDs.
With chronicity, urate deposits in subcutaneous tissue, bone, cartilage, joints, and other tissues.
Gout is a metabolic disease of a heterogeneous nature, often familial, associated with abnormal deposits of urate in tissues and characterized initially by a recurring acute arthritis, usually monoarticular, and later by chronic deforming arthritis. Urate deposition occurs when serum uric acid is supersaturated (ie, at levels greater than 6.8 mg/dL [404.5 mcmol/L]). Hyperuricemia is due to overproduction or underexcretion of uric acid—sometimes both. The disease is especially common in Pacific islanders, eg, Filipinos and Samoans. Primary gout has a heritable component, and genome-wide surveys have linked risk of gout to several genes whose products regulate urate handling by the kidney. Secondary gout, which may have a heritable component, is related to acquired causes of hyperuricemia, eg, medication use (especially diuretics, low-dose aspirin, cyclosporine, and niacin), myeloproliferative disorders, plasma cell myeloma, hemoglobinopathies, chronic kidney disease (CKD), hypothyroidism, psoriasis, sarcoidosis, and lead poisoning (Table 20–4). Alcohol ingestion promotes hyperuricemia by increasing urate production and decreasing the renal excretion of uric acid. Finally, hospitalized patients frequently suffer attacks of gout because of changes in diet, fluid intake, or medications that lead either to rapid reductions or increases in the serum urate level.
Table 20–4.Origin of hyperuricemia. ||Download (.pdf) Table 20–4. Origin of hyperuricemia.
Increased production of purine
Specific enzyme defects (eg, Lesch-Nyhan syndrome, glycogen storage diseases)
Decreased renal clearance of uric acid (idiopathic)
Increased catabolism and turnover of purine
Carcinoma and sarcoma (disseminated)
Chronic hemolytic anemias
Decreased renal clearance of uric acid
Chronic kidney disease
Drug-induced (eg, thiazides, low-dose aspirin, cyclosporine, niacin)
Ketoacidemia (eg, diabetic ketoacidosis, starvation)
Functional impairment of tubular transport
Diabetes insipidus (vasopressin-resistant)
About 90% of patients with primary gout are men, usually over 30 years of age. In women, the onset is typically postmenopausal. The ...