摘要
Assigning causality in drug-induced liver injury is challenging particularly when more than one drug could be responsible. We report a woman on long-term therapy with raloxifen who developed acute cholestasis shortly after starting fenofibrate. The picture evolved into chronic cholestasis. We hypothesized that an interaction at the metabolic level could have triggered the presentation of hepatotoxicity after a very short time of exposure to fenofibrate in this patient. The findings of an overexpression of vascular endothelial growth factor in the liver biopsy suggest that angiogenesis might play a role in the persistance of toxic cholestasis.
当超过一药能是负责的时,在导致药的肝损伤分配诱发性特别地是挑战性的。我们与 raloxifen 在长期的治疗上报导一个女人立即在开始 fenofibrate 以后开发了尖锐胆汁郁积。图画演变为长期的胆汁郁积。我们假设了那在新陈代谢的水平的一个相互作用能在这个病人在 fenofibrate 的暴露的一很短的时间以后触发了 hepatotoxicity 的演讲。调查结果一过去在肝活体检视的脉管的内皮生长因素的表示建议血管生成可能在有毒的胆汁郁积的坚持起一个作用。
基金
Supported by a research grant from the Agencia Espanola del Medicamento and Fondo de Investigaciones Sanitarias, No. FIS PI 04/1759 and PI 04/1688