首页 > 医学词汇大全 > Carbimazole
Carbimazole

内分泌

关键词内分泌 治疗药物 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

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

Insulin Sensitivity and Beta-Cell Function in Graves’ Disease and Their Changes with the Carbimazole-Induced Euthyroid State 复制标题

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

影响因子: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.

译文

格雷夫斯病(GD)是临床实践中最常见的疾病之一,每100,000人每年发生20–50例。甲状腺激素(THs)在中间代谢中起关键作用,据报道,甲状腺功能亢进症患者中相当一部分患者出现糖耐量异常和糖尿病。已经提出了诸如胰岛素抵抗,β-细胞功能改变,胃排空异常和肠内葡萄糖吸收等多种因素作为导致异常葡萄糖稳态的潜在机制。 THs通过几种机制促进肝脏和周围组织中胰岛素抵抗的状态。它们在肝脏中诱导酶的表达,例如磷酸烯醇丙酮酸羧激酶(PCK1)和葡萄糖-6-磷酸酶催化亚基(G6PC),糖异生和糖原分解的关键介体以及葡萄糖转运蛋白2(GLUT2),这有助于增加肝葡萄糖输出。在脂肪组织中,TH可增加脂质氧化作用,并增加脂肪细胞脂解对儿茶酚胺的敏感性,并间接增加脂肪酸外排量。在骨骼肌中,糖原合成速率降低,并且葡萄糖通过转化为乳酸被分流至肝脏的Cori循环。这导致葡萄糖输出增加。在动物模型中糖原分解的速率已显示出增加。但是,文献中并未始终证明GD患者胰岛素敏感性/抵抗力的变化。可能导致异常葡萄糖耐量的其他潜在机制是次佳的β细胞功能。测量响应促泌素(例如L-精氨酸和β2受体激动剂)刺激的胰岛素分泌率和口服葡萄糖负荷的研究也产生了矛盾的结果。