Rosmorduc O, Richardet J P, Lageron A, Munz C, Callard P, Beaugrand M
Service d'Hépato-Gastroentérologie, Hôpital Jean-Verdier, Bondy.
Gastroenterol Clin Biol. 1992;16(10):801-4.
The authors report the cases of 4 patients with heavy chronic alcoholic intake who presented with hepatomegaly and jaundice without obvious hepatic failure and who died rapidly. In all 4 cases, histological examination of the liver showed massive microvesicular and macrovesicular steatosis involving approximately 100% of hepatocytes and, in 2 cases, minimal lesions of alcoholic hepatitis. Histochemical study, performed in 3 cases, showed that steatosis was constituted of triglycerides only, and that hepatic glycogen was completely depleted in 2 of 3 cases. No obvious cause of death was found in these 4 patients. Shortly, before their death, the 4 patients had increased their ethanol and decreased their food intake. The authors suggest that death as well as microvesicular steatosis could have be due to acute mitochondrial dysfunction.
作者报告了4例重度慢性酒精摄入患者的病例，这些患者出现肝肿大和黄疸，但无明显肝功能衰竭，且迅速死亡。在所有4例病例中，肝脏组织学检查显示大量微泡性和大泡性脂肪变性，累及约100%的肝细胞，2例有轻度酒精性肝炎病变。对3例进行的组织化学研究表明，脂肪变性仅由甘油三酯构成，3例中有2例肝糖原完全耗竭。这4例患者未发现明显死因。在死亡前不久，这4例患者增加了乙醇摄入量并减少了食物摄入量。作者认为，死亡以及微泡性脂肪变性可能是由于急性线粒体功能障碍所致。
