Department of General Medicine, Himalayan Institute of Medical Sciences, Swami Rama Himalayan University, Jolly Grant, Dehradun, Uttarakhand, 248016, India.
Department of Neurology, Himalayan Institute of Medical Sciences, Swami Rama Himalayan University, Jolly Grant, Dehradun, Uttarakhand, 248016, India.
J Med Case Rep. 2023 Mar 23;17(1):107. doi: 10.1186/s13256-023-03827-y.
High-dose vitamin E intake is known to inhibit vitamin K-derived coagulation factor synthesis, which can cause serious bleeding events such as gastrointestinal bleeding and intracranial hemorrhage. We report a case of coagulopathy induced by marginally increased levels of vitamin E.
A 31-year-old Indian man presented with oral bleeding, black tarry stools, and bruising over his back. He had been taking non-steroidal anti-inflammatory drugs for low backache and vitamin E for hair loss. He had mild anemia with normal platelet count, thrombin time, and prolonged bleeding time, activated partial thromboplastin time, and prothrombin time. Serum fibrinogen was slightly raised. Mixing studies with pooled normal plasma, aged plasma, and adsorbed plasma were suggestive of deficiency of multiple coagulation factors due to acquired vitamin K deficiency. Serum phylloquinone was normal, while prothrombin induced by vitamin K absence-II level was increased. Serum alpha-tocopherol was slightly raised. Upper gastrointestinal endoscopy showed multiple gastroduodenal erosions. A final diagnosis of vitamin E toxicity-related coagulopathy was made. The patient responded well to pantoprazole, vitamin K supplementation, multiple fresh frozen plasma transfusions, and other supportive treatments besides the discontinuation of vitamin E supplementation. The coagulation parameters normalized, and the patient was discharged with complete resolution of symptoms and remained asymptomatic during the follow-up for 6 months.
Vitamin E-related inhibition of vitamin K-dependent factors with coagulopathy may occur even at marginally increased levels of serum vitamin E. This risk becomes significant in patients receiving other drugs that may increase the risk of bleeding.
已知大剂量维生素 E 摄入会抑制维生素 K 衍生的凝血因子合成,这可能导致严重的出血事件,如胃肠道出血和颅内出血。我们报告一例因维生素 E 水平略有升高而引起的凝血功能障碍病例。
一名 31 岁的印度男性因口腔出血、黑便和背部瘀斑就诊。他因腰痛一直服用非甾体抗炎药,因脱发一直在服用维生素 E。他有轻度贫血,血小板计数、凝血酶时间、延长的出血时间、激活部分凝血活酶时间和凝血酶原时间正常。血清纤维蛋白原略有升高。混合研究用混合正常血浆、陈旧血浆和吸附血浆提示由于获得性维生素 K 缺乏导致多种凝血因子缺乏。血清叶绿醌正常,而维生素 K 缺乏诱导的凝血酶原水平升高。血清α-生育酚略有升高。上消化道内镜显示多发性胃十二指肠糜烂。最终诊断为维生素 E 毒性相关凝血功能障碍。除停止补充维生素 E 外,患者还接受了泮托拉唑、维生素 K 补充、多次新鲜冷冻血浆输注和其他支持治疗,反应良好。凝血参数恢复正常,患者出院,症状完全缓解,在 6 个月的随访期间无任何症状。
即使血清维生素 E 水平略有升高,维生素 E 相关的维生素 K 依赖性因子抑制也可能导致凝血功能障碍。在接受其他可能增加出血风险的药物的患者中,这种风险更为显著。