Serrano Hernández N, García López F, Fedriani Gorria J
Unidad de Medicina Intensiva, Hospital General, Albacete.
An Med Interna. 1996 Nov;13(11):552-4.
We describe a 76-year-old male patient who developed a life-threatening acute hepatotoxicity possibly caused by flutamide, an antiandrogen drug given during the previous 10 months, in the scenario of a brief moderate hypotension secondary to atrial flutter. There was a sudden increase of liver enzyme levels AST = 4.521 IU/L, ALT = 1.716 IU/L (normal values 0-37 and 0-40 respectively), prothrombin activity decreased to 16%, and also felt the platelet count, with significant haemorrhages. We hypothesize this was triggered as a consequence of the transient diminished supply of oxygen to the subclinically flutamide-damaged hepatocytes by the well-known mechanism of the cytochrome P450 (3A and 1A)-mediated formation of electrophilic metabolites, and the inhibitory effect of flutamide on mitochondrial respiration and ATP formation.
我们描述了一名76岁男性患者，该患者在因心房扑动继发短暂性中度低血压的情况下，出现了可能由氟他胺引起的危及生命的急性肝毒性。氟他胺是一种抗雄激素药物，在之前10个月内一直服用。肝酶水平突然升高，AST = 4521 IU/L，ALT = 1716 IU/L（正常范围分别为0 - 37和0 - 40），凝血酶原活性降至16%，同时血小板计数下降，并伴有明显出血。我们推测，这是由于细胞色素P450（3A和1A）介导的亲电代谢产物形成的已知机制，导致向亚临床氟他胺损伤的肝细胞的氧供应短暂减少，以及氟他胺对线粒体呼吸和ATP形成的抑制作用共同引发的。
