통풍의 합병증 치료
Management of Complicated Gout
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초록
통풍은 비교적 잘 조절될 수 있는 질병으로 인식되어 왔으나 선택할 수 있는 치료제가 제한되어 있고 장기적인 관리와 치료가 잘 이루어지지 않을 경우 만성통풍으로 발전하여 합병증을 가져올 수 있다는 문제점이 있다. 또한 환자의 동반 질환에 따라 치료약제의 부작용이 나타날 위험이 증가할 수 있으므로 이런 경우 신중한 약제 선택과 약제 부작용 감시가 필요하다. 통풍의 합병증과 특수한 상황에서의 통풍 관리는 환자의 동반질환, 병용약제 등을 고려해야 한다. 또한 통풍 환자가 만성결정성통풍으로 이행되지 않도록 꾸준한 관리와 치료가 이루어지도록 독려하는 것이 중요할 것으로 생각된다.
Abstract
Chronic tophaceous gout results from long-term uncontrolled hyperuricemia with accumulation of urate crystals in joints, soft tissues, tendon sheaths and bony prominence. Urate-lowering agents should be administered to reduce serum uric acid level to less than 5 mg/dL for tophi reabsorption. Surgical indications include restoration of joint and tendon dysfunction, nerve decompression, debridement of septic joints, pain relief and cosmesis. Gout patients are at greater risk of forming uric acid stones. The renal tubular abnormality related to gout and metabolic syndrome leads to excretion of acidic urine, which favors formation of the relatively insoluble uric acid than more soluble urate. The corner stone of treatment of uric acid stone is urine alkalinization. Lowering serum uric acid with allopurinol and increasing urine volume are also important. Allopurinol is poorly tolerated and ineffective or contraindicated in some patients. Benzbromarone, a uricosuric agent is a useful alternative but possible hepatotoxicity should be monitored. Desensitization of allopurinol can be attempted to patients with mild cutaneous hypersensitivity. For gout patients with chronic renal failure, allopurinol dose need to be adjusted and nonsteroidal anti-inflammatory drugs and colchicine may be contraindicated. (Korean J Med 2011;80:269-272)Chronic tophaceous gout results from long-term uncontrolled hyperuricemia with accumulation of urate crystals in joints, soft tissues, tendon sheaths and bony prominence. Urate-lowering agents should be administered to reduce serum uric acid level to less than 5 mg/dL for tophi reabsorption. Surgical indications include restoration of joint and tendon dysfunction, nerve decompression, debridement of septic joints, pain relief and cosmesis. Gout patients are at greater risk of forming uric acid stones. The renal tubular abnormality related to gout and metabolic syndrome leads to excretion of acidic urine, which favors formation of the relatively insoluble uric acid than more soluble urate. The corner stone of treatment of uric acid stone is urine alkalinization. Lowering serum uric acid with allopurinol and increasing urine volume are also important. Allopurinol is poorly tolerated and ineffective or contraindicated in some patients. Benzbromarone, a uricosuric agent is a useful alternative but possible hepatotoxicity should be monitored. Desensitization of allopurinol can be attempted to patients with mild cutaneous hypersensitivity. For gout patients with chronic renal failure, allopurinol dose need to be adjusted and nonsteroidal anti-inflammatory drugs and colchicine may be contraindicated. (Korean J Med 2011;80:269-272)
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