Suppr超能文献

[碘缺乏性甲状腺肿的病因发病机制与治疗]

[Etiopathogenesis and therapy of iodine deficiency goiter].

作者信息

Gärtner R

机构信息

Medizinische Klinik, Klinikum Innenstadt, Universität München.

出版信息

Z Arztl Fortbild (Jena). 1995 Feb;89(1):27-31.

PMID:7709641
Abstract

The main cause of endemic goiter is iodine deficiency. For the last four decades, it has been thought that the reason for goiter development is the increased action of thyreotropin (TSH) on thyroid cell proliferation. During the last years, however, it became evident that local growth factors may be more directly involved in goiter formation and, furthermore, iodinated derivatives of membrane lipids are modulators of this growth factor's actions. TSH modulates both, the growth factor and growth factor receptor expression as well as the iodine content of the thyroid gland. In addition, most of the effects of TSH on thyroid volume seems to be the induction of thyroid hypertrophy, but not hyperplasia which is related to the action of local growth factors. These new insights in the pathophysiology of goiter development are important for the regimen of endemic goiter therapy. The current concept of goiter treatment by a TSH suppressive therapy has been derived from the previous hypothesis that TSH alone is more effective in causal goiter treatment than the TSH suppressive therapy.

摘要

地方性甲状腺肿的主要病因是碘缺乏。在过去的四十年里,人们一直认为甲状腺肿发展的原因是促甲状腺激素(TSH)对甲状腺细胞增殖的作用增强。然而,在过去几年中,有一点变得很明显,即局部生长因子可能更直接地参与甲状腺肿的形成,此外,膜脂的碘化衍生物是这种生长因子作用的调节剂。TSH调节生长因子和生长因子受体的表达以及甲状腺的碘含量。此外,TSH对甲状腺体积的大多数影响似乎是诱导甲状腺肥大,而不是与局部生长因子作用相关的增生。这些关于甲状腺肿发展病理生理学的新见解对地方性甲状腺肿的治疗方案很重要。目前通过TSH抑制疗法治疗甲状腺肿的概念源于先前的假设,即单独使用TSH在病因性甲状腺肿治疗中比TSH抑制疗法更有效。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验