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Brain and Nerve No to Shinkei Volume 33, Issue 11 （November 1981）

Brain and Nerve 脳と神経 33巻11号（1981年11月発行）

Japanese English

原著

高プロラクチン血症を呈する下垂体腺腫の内分泌学的考察 ENDOCRINOLOGICAL ANALYSIS OF PITUITARY ADENOMAS ASSOCIATED WITH HYPERPROLACTINEMIA 佐藤修 ¹ , 堀田晴比古 ¹ , 中川俊男 ¹ , 相馬文勝 ¹ , 蓮沼正博 ¹ , 土田博美 ¹ , 田辺純嘉 ¹ , 小林計理 ² , 井上慶俊 ² Osamu Sato ¹ , Haruhiko Hotta ¹ , Toshio Nakagawa ¹ , Fumikatsu Sohma ¹ , Masahiro Hasunuma ¹ , Hiromi Tsuchita ¹ , Sumiyoshi Tanabe ¹ , Keiri Kobayashi ² , Yoshitoshi Inoue ² ¹札幌医科大学脳神経外科 ²王子総合病院脳神経外科 ¹Department of Neurosurgery, Sapporo Medical College ²Department of Neurosurgery, Ohji General Hospital pp.1115-1123

発行日 1981年11月1日 Published Date 1981/11/1

DOI https://doi.org/10.11477/mf.1406204846

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Abstract 文献概要
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I．はじめに

　高プロラクチン（PRL）血症をきたす視床下部下垂体の病態には^13），1）原発性視床下部障害によるPIFの減少ないしはPRFの増加による正常細胞からのPRL分泌，2） PRLを産生しない種々の腫瘍が，視床下部あるいはその連絡路を圧迫し，二次的PIF減少による正常細胞からのPRL分泌，3） PRL産生下垂体腺腫からの自動的な分泌が考えられる。このうち，下垂体腺腫による高PRL血症には，2），3）の機序が考えられる。PRL産生下垂体腺腫は，特に治療成績の上から，その直径が10mm以下のmicroadenomaと，11mm以上のmacroadenomaとに区別して論じられるのが通常である。Microadenomaとmacroadenomaは，内分泌学的障害の程度に差異が考えられ，また，microadenomaは，特発性高PRL血症との内分泌学的鑑別診断が問題となる。一方，PRLを産生しない下垂体腺腫が，視床下部を圧迫して高PRL血症を呈する場合（以下，視床下部腺腫と記載）に，PRL産生下垂体腺腫との間で内分泌学的に差異がみられるか否かも興味ある点である。われわれは，高PRL血症を呈した下垂体腺腫について，これらの点について着目し，内分泌学的比較対照を行い，また，特発性高PRL血症例とも比較したので，その結果を報告する。

The authors analysed the preoperative endocri-nological examinations in 40 hyperprolactinemic patients with pituitary adenomas and also compared the results with those of six idiopathic hyperpro-lactinemic patients.

Pituitary adenomas were classified as PRL-secret-ing macroadenomas, PRL-secreting microadenomas and hypothalamic adenomas which were non-secret ing but caused hyperprolactinemia by hypothalamic invasion. In 35 female patients, galactorrhea and amenorrhea were less often found in hypothalamic adenomas compared to PRL-secreting adenomas.

The all of the patients with PRL levels more than 300ng/ml had PRL-secreting adenomas with high possibility of macroadenomas, whereas the patient with PRL levels below 300ng/ml had hy-perprolactinemia of several causes such as PRL-secreting adenomas, hypothalamic adenomas, idiopathic hyperprolactinemia or pharmacological hyperprolactinemia. The basal PRL levels were more elevated in macroadenomas than in micro-adenomas. The basal PRL levels and the size of adenomas were well correlated in macroadenomas but such correlation was not found in microadeno-mas.

The endocrinological comparison could not dif-ferentiate hypothalamic adenomas from PRL-secret-ing macroadenomas except for the moderate re-sponse of PRL to TRH stimulation in hypothalamic adenomas.

The endocrinological comparison between micro-adenomas and other macroadenomas or hypothala-mic adenomas showed that the HGH reserve was rarely involved in microadenomas but was mostly involved in other adenomas. The TSH reserve was rarely involved in any adenomas but, if in-volved, the impairment was hypothalamic dysfunc-tion in microadenomas compaired to pituitary dysfunction in other adenomas. The LH or FSH reserve was very rarely involved in microadenomas but was often involved in other adenomas and, if involved, the impairment was hypothalamic dysfuc-tion in microadenomas compaired to pituitary dysfunction in other adenomas.

The endocrinological differentiation was impos-sible between PRL-secreting microadenomas and idiopathic hyperprolactinemia.

The loss of positive feedback to the decreased LH or FSH levels by premarin was observed not only in idiopathic hyperprolactinemia but also in hyperprolactinemia adenomas.

The elevated activity of dopamine in the hypo-thalamus was not confirmed in hyperprolactinemic adenomas and idiopathic hyperprolactinemia by primperan test.