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艾迪生病中的继发性垂体增生。

Secondary pituitary hyperplasia in Addison's disease.

作者信息

Clayton R, Burden A C, Schrieber V, Rosenthal F D

出版信息

Lancet. 1977 Nov 5;2(8045):954-6. doi: 10.1016/s0140-6736(77)90891-1.

Abstract

In patients with Addison's disease, whether treated or untreated for the previous 24 hours, hydrocortisone produced only a partial suppression of their elevated adrenocorticotrophic-hormone (A.C.T.H.) levels. This is comparable to untreated myxoedema, in which administration of triiodothyronine fails to inhibit secretion of thyrotrophin (T.S.H.). In myxoedema, however, continued treatment produces normal T.S.H. levels. Inadequate A.C.T.H. suppressibility in patients with Addison's disease while on treatment may be due to the maintenance of a secondary pituitary hyperplasia by inadequate replacement therapy. This may be clinically important, especially in the genesis of Nelson's syndrome.

摘要

在患有艾迪生病的患者中,无论之前24小时是否接受过治疗,氢化可的松仅能部分抑制其升高的促肾上腺皮质激素(ACTH)水平。这与未经治疗的黏液性水肿情况类似,在黏液性水肿患者中,给予三碘甲状腺原氨酸无法抑制促甲状腺激素(TSH)的分泌。然而,在黏液性水肿患者中,持续治疗可使TSH水平恢复正常。接受治疗的艾迪生病患者ACTH抑制能力不足,可能是由于替代治疗不足导致继发性垂体增生持续存在。这在临床上可能很重要,尤其是在尼尔森综合征的发生过程中。

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