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为了澄清伴发库兴氏病的高催乳素血症的发病机理,作者测定42例肾上腺皮质功能亢进(26例为库兴氏病;16例为肾上腺皮质腺瘤)和10例Nel-son征患者的PRL含量。结果在26例库兴氏病有6例血催乳素轻度升高(23%);16例Nelson征有5例升高(30%)。相反,所有继发于肾上腺皮质腺瘤的库兴氏病人,血浆PRL基础值是正常的。注射TRH可以肯定地引致PRL释放,但库兴氏病人和有高催乳素血症的Nelson病人反应都很迟钝。另一方面,短期摄取地塞米松并不能改变这类病人的PRL分泌;5例库兴氏病人,当切除双侧肾上腺,而且已出现Nelson征的典型临床表现时,再次测定
In order to clarify the pathogenesis of hyperprolactinemia associated with Cushing’s disease, the authors determined 42 cases of adrenocortical hyperfunction (26 cases of Cushing’s disease, 16 cases of adrenocortical adenoma) and 10 cases of Nel-son syndrome The patient’s PRL content. RESULTS: Six of 26 Cushing’s disease patients had mildly elevated prolactin (23%), and 5 of 16 (30%) Nelson signs were elevated. In contrast, all patients with Cushing who were secondary to adrenocortical adenoma had normal PRL basal values. Injection of TRH can certainly lead to the release of PRL, but Cushing’s patients and Nelson patients with hyperprolactinemia are slow to respond. On the other hand, short-term ingestion of dexamethasone did not alter PRL secretion in these patients; in 5 Cushing’s patients, the bilateral adrenal glands were resected and a typical clinical manifestation of Nelson’s syndrome occurred