Larcan A, Lambert H, Laprevote-Heully M C, Delorme N
Diabete Metab. 1979 Jun;5(2):103-12.
Histopathological study of the liver has been undertaken on twenty-one diabetics with hyperlactatemia exceeding 5 mEq/1 of whom seven were treated with phenformin, six with metformin and eight not biguanide-treated. Hyperlactatemia occurred during the course or during resolution of severe ketoacidosis or of hyperosmolar coma. Hepatic lesions were invariably present. By light microscopy, massive steatosis, steatonecrosis or necrosis of variable extent were observed. Ultrastructural study showed constant mitochondrial abnormalities. These results support the hypothesis of a major role for mitochondrial changes in hepatic cells in provoking pathological hyperlactatemia. In diabetic patients, these mitochondrial lesions could be induced either by an anoxic process resulting from a variety of metabolic insults or by some as yet undefined toxic action of biguanides or by the combination of both of these factors.
对21名高乳酸血症超过5 mEq/1的糖尿病患者进行了肝脏组织病理学研究，其中7名接受苯乙双胍治疗，6名接受二甲双胍治疗，8名未接受双胍类药物治疗。高乳酸血症发生在严重酮症酸中毒或高渗性昏迷的病程中或缓解期。肝脏病变始终存在。通过光学显微镜观察到广泛的脂肪变性、脂肪坏死或不同程度的坏死。超微结构研究显示线粒体持续异常。这些结果支持了肝细胞线粒体变化在引发病理性高乳酸血症中起主要作用的假说。在糖尿病患者中，这些线粒体病变可能是由多种代谢损伤导致的缺氧过程引起的，也可能是由双胍类药物某些尚未明确的毒性作用引起的，或者是由这两种因素共同作用引起的。
