Zamkoff K, Rosen N
Neurology. 1979 Mar;29(3):340-5. doi: 10.1212/wnl.29.3.340.
Two adult brothers became ill within 48 hours of each other, and both had severe myoglobinuria. One brother died of oliguric renal failure. The other did not have renal failure and survived. Acute influenza A infection was documented serologically and from throat washings in the surviving brother, and by isolation of the influenza A virus from throat cultures and lung tissue of the brother who died. It is not certain whether a genetic myopathy made these brothers susceptible to viral-induced myoglobinuria, but a normal response of venous lactate to ischemic work excluded lack of phosphorylase or phosphofructokinase as a cause of the myoglobinuria in the surviving brother. Neither brother had a history of recurrent episodes of myoglobinuria precipitated by exercise, cold, or fasting, thus making carnitine palmityl transferase deficiency unlikely.
两名成年兄弟在彼此发病后的48小时内均患病，且都出现了严重的肌红蛋白尿。其中一名兄弟死于少尿性肾衰竭。另一名兄弟未发生肾衰竭并存活下来。通过血清学检测以及对存活兄弟的咽拭子样本分析，证实其感染了甲型流感病毒；同时，从死亡兄弟的咽拭子培养物和肺组织中分离出了甲型流感病毒。目前尚不确定是否存在遗传性肌病使这些兄弟易患病毒诱导的肌红蛋白尿，但存活兄弟静脉血乳酸对缺血运动的正常反应排除了磷酸化酶或磷酸果糖激酶缺乏是导致其肌红蛋白尿的原因。两名兄弟均无因运动、寒冷或禁食诱发的复发性肌红蛋白尿病史，因此肉碱棕榈酰转移酶缺乏症的可能性不大。
