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首页> 外文期刊>Endocrine journal >Liver dysfunction induced by Levothyroxine Sodium Tablets (Euthyrox?) in a hypothyroid patient with Hashimoto’s thyroiditis: case report and literature review
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Liver dysfunction induced by Levothyroxine Sodium Tablets (Euthyrox?) in a hypothyroid patient with Hashimoto’s thyroiditis: case report and literature review

机译:左旋甲基钠片(Euthyroxα)诱导肝功能障碍(Euthyroxα),患有Hashimoto甲状腺炎的甲状腺功能亢进患者:病例报告和文献综述

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A 49-year-old woman with hypothyroidism developed liver dysfunction after increasing dose of levothyroxine (L-T4) (Euthyrox?) from 25 μg to 50 μg. Viral hepatitis, autoimmune hepatitis and non-alcoholic steatohepatitis (NASH) were ruled out with examinations. She had no concurrent medication and had no history of infectious, chronic or any other autoimmune diseases. After cessation of Levothyroxine Sodium Tablets (Euthyrox?), liver enzymes gradually returned to normal. She was diagnosed levothyroxine-induced liver injury, based on criteria proposed in “Diagnosis and treatment guideline on drug-induced liver injury” issued by the Chinese Medical Association (2015). As an alternative 25 μg qod of Levothyroxine Sodium Tablets (Letrox?) was tried and increased gradually up to 75 μg daily. Since then liver enzymes have remained within normal range. The main difference of additive for both tablets is whether it contains lactose or not: Euthyrox? contains lactose which caused no liver injury, thus excluding the possibility that an additive of Euthyrox? contributed to liver injury. The relatively quicker and larger replacement with synthetic T4 for hypothyroidism inducing transient thyrotoxicosis was suspected, although thyroid function was normal. Immune-mediated drug-induced liver injury (DILI) was also not excluded. This is a rare case of drug-induced liver injury due to levothyroxine tablets. It reminded us that when replacement with synthetic T4 for hypothyroidism is done, smaller-dose initiation and slower-speed increase may be useful for treatment of cases similar to genetically susceptible individuals.
机译:一个49岁的女性,甲状腺功能减退症,在将左旋羟基嗪(L-T4)(Euthyroxα)增加到25μg至50μg后,发育了肝功能障碍。试论病毒性肝炎,自身免疫性肝炎和非酒精性脱脂性炎(NASH)被检测。她没有同时用药,没有传染病,慢性或任何其他自身免疫疾病的历史。停止左旋甲苯胺钠片(Euthyrox?)后,肝酶逐渐恢复正常。根据中国医学协会(2015年)发布的“诊断和治疗指南”中提出的标准,她被诊断为左旋噻嗪诱导的肝损伤。作为替代的25μg百分点钠钠片(Letrox?)的Qod,并每天逐渐增加至75μg。从那时起,肝酶保持在正常范围内。两种片剂添加剂的主要差异是它是否含有乳糖:Euthyrox?含有乳糖,导致没有肝损伤,从而排除了Euthyrox的添加剂的可能性?有助于肝损伤。虽然甲状腺功能是正常的,但怀疑诱导甲状腺功能亢进诱导瞬时溶毒性病变的合成T4相对更快和更大的替代。免疫介导的药物诱导的肝损伤(DILI)也没有排除在外。这是一种罕见的药物诱导肝损伤,由于左羟基甲胺片剂。它提醒我们,当用合成T4进行甲状腺功能亢进的替代时,较小剂量的启动和较慢的速度增加可能对于治疗类似于遗传易感个体的病例可能是有用的。

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