内分泌
词汇介绍
拓展阅读
解析
Carbimazole
释 义 n. 甲亢平;卡比马唑
例 句 Carbimazole is used to treat an overactive thyroid gland. 卡比马唑用于治疗甲状腺过度活跃。
概述
概述
卡比马唑,用于治疗甲状腺功能亢进症。卡比马唑是一种前药,因为它在吸收后会转化为活性形式甲他唑。甲基咪唑可防止甲状腺过氧化物酶与甲状腺球蛋白上的酪氨酸残基偶合和碘化,从而减少甲状腺激素T3和T4(甲状腺素)的产生。
不良反应
虽然皮疹和瘙痒很常见,但通常可以用抗组胺药治疗而不会停止使用卡比马唑。对于无法控制敏感性反应的患者,可以使用丙硫氧嘧啶作为替代品。这些药物之间的交叉敏感性很罕见。它最严重的罕见副作用是骨髓抑制,引起中性粒细胞减少和粒细胞缺乏症。这种情况可能在治疗期间的任何阶段发生,并且没有警告,监测白细胞计数没有用。建议患者立即报告感染症状,例如喉咙痛或发烧,以便安排全血细胞计数检查。如果这证实了中性粒细胞计数低,则停药可导致恢复。但是,如果未报告提示性症状或在考虑免疫抑制及其检测的可能性时出现延误,可能会导致死亡。
禁忌症
卡比马唑适合大多数成年人和儿童,但任何有以下情况的人都不应服用:血细胞有严重问题;严重的肝脏问题;以前服用卡比马唑时曾出现胰腺发炎(急性胰腺炎)。
注意事项
有些人对吡咯烷酮过敏,一些唑类药物有不良副作用。一些唑类药物可能会干扰妊娠期雌激素的产生,影响妊娠结局。怀孕期间应谨慎使用卡比马唑,因为它会穿过胎盘屏障。它(很少)与先天性缺陷有关,包括新生儿的皮肤发育不良,但没有禁忌证。但是,它更可能导致胎儿甲状腺功能减退,因此(最小剂量)可用于控制孕妇甲状腺功能亢进。据报道,胎儿出现甲状腺肿和胆道闭锁。此外,母乳喂养是可行的,但前提是必须使用最低有效剂量并密切监测新生儿的发育。由于上述原因,最好在怀孕期间使用PTU,尤其是在孕早期,因为在孕中期和孕中期可能会改用卡比马唑。
Graves病的胰岛素敏感性和 β 细胞功能及其与卡比唑诱导的甲状腺功能正常的关系
发表时间:2019-04-01
影响指数:3.0
作者: Nandhini Lakshmana Perumal Jayakumar
期刊:Eur Thyroid J
Graves’ disease (GD) is one of the most commonly encountered disorders in clinical practice with an annual incidence of 20–50 cases per 100,000 persons. Thyroid hormones (THs) play a key role in intermediate metabolism, and abnormal glucose tolerance and diabetes mellitus have been reported to occur in a significant proportion of patients with hyperthyroidism. Several factors like changes in insulin resistance, beta-cell function, abnormal gastric emptying, and intestinal absorption of glucose have been proposed as potential mechanisms that result in abnormal glucose homeostasis. THs contribute to a state of insulin resistance in the liver and peripheral tissues through several mechanisms. They induce the expression of enzymes such as phosphoenolpyruvate carboxykinase (PCK1) and glucose-6-phosphatase catalytic subunit (G6PC), the key mediators of gluconeogenesis and glycogenolysis, and glucose transporter 2 (GLUT2) in the liver, which contributes to increased hepatic glucose output. In adipose tissue, TH increases lipid oxidation and augments the sensitivity of adipocyte lipolysis to catecholamines and indirectly increases fatty acid efflux. In skeletal muscles, the rate of glycogen synthesis is reduced, and glucose, through conversion into lactate, is shunted to the Cori cycle in the liver. This results in increased glucose output. The rate of glycogenolysis has shown to be increased in animal models. However, changes in insulin sensitivity/resistance in patients with GD have not been consistently demonstrated in the literature. The other potential mechanism that can contribute to abnormal glucose tolerance is suboptimal beta-cell function. Studies measuring insulin secretion rates in response to stimulation by secretagogues like L-arginine and β2-receptor agonists and oral glucose load have also yielded conflicting results.
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