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[甲状腺肿的发病机制问题]

[Pathogenetic problems of goiter].

作者信息

Aleshin B V

出版信息

Arkh Patol. 1981;43(4):88-93.

PMID:6112977
Abstract

The extrafollicular growth (hyperplasia) of the thyroid parenchyma resulting in the development of epithelial goiter begins with proliferation of thyrocytes of the follicular wall (sometimes called "clear cells" and erroneously identified with the parafollicular cells or C-cells). An important role in the pathogenesis of goiter disease belongs to the transition of the thyroid parenchyma hyperplasia from the initial adaptative (compensatory) reaction which arises under conditions of thyroid hormone production deficiency into the irreversible pathological process of indefinite duration after restoration of the euthyroid state of the patient. It may be assumed that this transition results from stabilization of gradually increasing shift of protein biosynthesis in the thyrocytes towards preferential thyroalbumin formation at the expense of thyroglobulin.

摘要

甲状腺实质的滤泡外生长(增生)导致上皮性甲状腺肿的发生,始于滤泡壁甲状腺细胞的增殖(有时称为“透明细胞”,并错误地与滤泡旁细胞或C细胞相混淆)。甲状腺肿疾病发病机制中的一个重要作用在于,甲状腺实质增生从最初在甲状腺激素产生不足情况下出现的适应性(代偿性)反应,转变为患者甲状腺功能正常状态恢复后持续时间不定的不可逆病理过程。可以推测,这种转变是由于甲状腺细胞中蛋白质生物合成逐渐增加的转移稳定下来,以牺牲甲状腺球蛋白为代价优先形成甲状腺白蛋白。

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