Woolliscroft J O, Colfer H, Fox I H
Am J Med. 1982 Jan;72(1):58-62. doi: 10.1016/0002-9343(82)90578-2.
To clarify the role of the serum urate level and its change as a potential marker for severe tissue hypoxia, we have measured serum urate levels and urine uric acid excretion in 16 patients with acute cardiovascular disease. The six patients who died had a baseline mean serum urate level of 11.1 mg/lg (range, 6.6 to 15.5 mg/dl) and reached a peak mean value of 20.7 mg/dl (range, 13.6 to 33.0 mg/dl). Five of these patients had findings to suggest increased production of uric acid, in addition to decreased excretion of uric acid from impaired renal function. The 10 survivors had a baseline mean serum urate level of 6.8 mg/dl (range, 1.3 to 14.0 mg/dl) and a maximal mean peak value of 7.1 mg/dl (range, 2.9 to 14.0 mg/dl). There was no consistent evidence for increased production or decreased excretion of uric acid. Patients who died had a lower systolic blood pressure, arterial pH and plasma bicarbonate level and a higher heart rate and serum creatinine level compared with the patients ho survived. The observations suggest that marked hyperuricemia at the height of an illness may predict a fatal outcome. Tissue hypoxia may contribute to this sequence of events by leading to the depletion of adenosine triphosphate (ATP) and activation of purine nucleotide degradation to uric acid.
为阐明血清尿酸水平及其变化作为严重组织缺氧潜在标志物的作用，我们测定了16例急性心血管疾病患者的血清尿酸水平和尿尿酸排泄量。死亡的6例患者基线平均血清尿酸水平为11.1mg/dl（范围6.6至15.5mg/dl），平均峰值达到20.7mg/dl（范围13.6至33.0mg/dl）。其中5例患者除肾功能受损导致尿酸排泄减少外，还有提示尿酸生成增加的表现。10例存活患者基线平均血清尿酸水平为6.8mg/dl（范围1.3至14.0mg/dl），最大平均峰值为7.1mg/dl（范围2.9至14.0mg/dl）。没有一致的证据表明尿酸生成增加或排泄减少。与存活患者相比，死亡患者的收缩压、动脉pH值和血浆碳酸氢盐水平较低，心率和血清肌酐水平较高。这些观察结果表明，疾病高峰期的明显高尿酸血症可能预示着致命结局。组织缺氧可能通过导致三磷酸腺苷（ATP）耗竭和嘌呤核苷酸降解为尿酸的激活而促成这一系列事件。
