Jorens P G, Michielsen P P, Pelckmans P A, Fevery J, Desmet V J, Geubel A P, Rahier J, Van Maercke Y M
Department of Gastroenterology, University Hospital of Antwerp (UIA), Belgium.
Liver. 1992 Dec;12(6):381-6. doi: 10.1111/j.1600-0676.1992.tb00592.x.
We report the case of a 35-year-old man who contracted vitamin A-induced liver cirrhosis. Five years before, he had been investigated for vitamin A-induced non-cirrhotic portal hypertension. In this case, the clinical and histopathologic evolution from non-cirrhotic portal hypertension to cirrhosis was documented. In spite of the cessation of pharmaceutical vitamin A intake, the disease progressed. Therapy with colchicine and phenobarbital apparently did not influence evolution to cirrhosis. This suggests that vitamin A can trigger largely unknown mechanisms of liver fibrosis which seem to be self-perpetuating.
我们报告了一名35岁男性患维生素A诱导的肝硬化病例。五年前，他因维生素A诱导的非肝硬化性门静脉高压接受过检查。在此病例中，记录了从非肝硬化性门静脉高压到肝硬化的临床和组织病理学演变过程。尽管停止了药用维生素A的摄入，但疾病仍在进展。秋水仙碱和苯巴比妥治疗显然并未影响向肝硬化的演变。这表明维生素A可触发很大程度上未知的肝纤维化机制，这些机制似乎会自我延续。
