...
首页> 外文期刊>The Endocrinologist >Treatment With Lithium Prevents Serum Thyroid Hormone Increase After Thionamide Withdrawal and Radioiodine Therapy in Patients With Graves disease
【24h】

Treatment With Lithium Prevents Serum Thyroid Hormone Increase After Thionamide Withdrawal and Radioiodine Therapy in Patients With Graves disease

机译:锂治疗可防止Graves病患者亚硫酰胺停用和放射碘治疗后血清甲状腺激素增加

获取原文
获取原文并翻译 | 示例
   

获取外文期刊封面封底 >>

       

摘要

Background: Antithyroid drugs (ATD) are frequently given for a few months before ~131I therapy, primarily to reduce the degree of thyroid hormone rise after the administration of ~131I. Propyl-thiouracil pretreatment is associated with a higher failure rate of ~131I therapy, whereas methimazole (MMI) does not affect the cure rate (Thyroid 2002; 12: 131). There is controversy about the origin of the transient rise in serum thyroid hormone that occurs after ATD withdrawal and ~131I treatment of thy-rotoxic Graves disease. Whether it is caused by withdrawal of ATD or is caused by ~131I-induced disruption of the follicular cells has been a matter of debate.Materials and Results: This prospective, randomized, blinded study addresses these questions and explores the use of lithium as an adjunct to ~131I treatment of thyrotoxicosis. The study confirms that MMI withdrawal causes a prompt rise in serum free T4 and free T3 concentrations within 2 days, approaching a plateau within 5 days that can be prevented by lithium. Furthermore, ~131I therapy produced a further increment in serum free T4 levels on day 1 after ~131I that peaked on day 5, whereas patients treated with lithium had a slight rise in serum thyroid hormone levels on day 1, with a rapid decline in the next 3 to 5 days. The abrupt rise in serum thyroid hormone levels in all study groups on the first day after ~131I therapy suggests that it is caused by discharge of preformed thyroid hormone from ~131I-induced lysis of thyroid follicular cells. Although the therapeutic dose of ~131I did not differ in the three treatment groups, the two lithium-treated groups retained ~131I longer than the group not so treated, as would be expected, and thus received a significantly higher absorbed dose of ~131I. Cure of hyperthy-roidism occurred in 67% of the group not treated with lithium and in 92% in each of the lithium-treated groups.Comment: The authors advise giving a short course of lithium as an adjunct to ~131I therapy, which provides prompter control of thyrotoxicosis and avoids the transient exacerbation of symptoms accompanying MMI withdrawal and ~131I administration. The fact that serum thyroid hormone concentrations after ~131I did not differ in the two lithium-treated groups suggests that lithium could be withdrawn 1 week after ~131I administration. No adverse effects were noticed from lithium except for a slightly higher (but not statistically significant) incidence of nausea and neck tenderness in the group receiving lithium for 19 days. Lithium has been used for longer than a week in hypothyroid patients with thyroid cancer being treated with ~131I, without producing adverse effects. The observations offer a new and effective paradigm in the ~131I treatment of thyrotoxicosis. (EM)
机译:背景:〜131I治疗前几个月通常要服用抗甲状腺药物(ATD),主要是为了减少服用〜131I后甲状腺激素升高的程度。丙基硫氧嘧啶预处理与〜131I治疗的更高失败率相关,而甲巯咪唑(MMI)则不影响治愈率(Thyroid 2002; 12:131)。关于在ATD停用和〜131I治疗甲毒性Graves病后发生的血清甲状腺激素短暂升高的起源存在争议。是否由ATD引起或由〜131I诱导的卵泡细胞破坏引起的争论一直在争论。 〜131I辅助治疗甲状腺毒症。该研究证实,MMI戒断会导致2天之内血清T4和T3游离浓度迅速升高,并在5天之内达到平台水平,这可以通过锂来预防。此外,〜131I治疗在〜131I后的第1天在第5天达到峰值,使血清游离T4水平进一步升高,而接受锂治疗的患者在第1天的血清甲状腺激素水平略有上升,而在第1天血清甲状腺激素水平迅速下降。接下来的3至5天。在〜131I治疗后的第一天,所有研究组的血清甲状腺激素水平突然升高,表明这是由〜131I诱导的甲状腺滤泡细胞裂解释放出预先形成的甲状腺激素引起的。尽管在三个治疗组中〜131I的治疗剂量没有差异,但是两个锂处理组的〜131I保留时间比未进行此类处理的组长,这是可以预期的,因此吸收的〜131I剂量明显更高。未接受锂治疗的组中有67%的人甲状腺功能亢进症治愈,而经锂治疗的每个组中有92%的人甲状腺功能亢进。评论:作者建议给予短期锂疗作为〜131I治疗的辅助手段,可以更快地控制甲状腺毒症,避免因MMI停药和〜131I给药而引起的症状的暂时加重。在两个锂处理组中,〜131I后血清甲状腺激素浓度无差异这一事实表明,可以在〜131I给药后1周撤出锂。除了接受锂治疗19天的组中恶心和颈部压痛的发生率略高(但在统计学上不显着)外,锂没有发现任何不利影响。在使用〜131I治疗的甲状腺癌甲状腺功能减退患者中,锂使用时间已超过一周,但未产生副作用。这些发现为〜131I治疗甲状腺毒症提供了一种新的有效范例。 (EM)

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号