Wajchenberg B L, Tsanaclis A M, Marino Júnior R
Acta Endocrinol (Copenh). 1984 May;106(1):61-6. doi: 10.1530/acta.0.1060061.
A 30 year old woman with primary hypothyroidism due to an ectopic (sublingual) thyroid, with a pituitary tumour invasive to the sphenoidal sinus presented with hyperprolactinaemia, amenorrhoea and galactorrhoea not corrected by long-term thyroid replacement. High basal TSH and TRH hyperresponsiveness were suppressed by thyroid therapy. After transsphenoidal removal of the tumour the Prl returned to normal. Light microscopy including differential staining and immunocytochemistry demonstrated that the tumour was composed of TSH cells. Ultrastructurally the adenoma cell contained small granules (90-150 nm) as described in TSH cells. This case provides evidence that a TSH cell adenoma probably arising from protracted overstimulation secondary to thyroid deficiency can induce hyperprolactinaemia. This did not appear to be produced directly by the adenoma nor was there any evidence of compression of the pituitary stalk.
一名30岁女性,因异位(舌下)甲状腺导致原发性甲状腺功能减退,同时患有侵袭蝶窦的垂体瘤,表现为高催乳素血症、闭经和溢乳,长期甲状腺替代治疗未能纠正。高基础促甲状腺激素(TSH)和促甲状腺激素释放激素(TRH)高反应性经甲状腺治疗后得到抑制。经蝶窦切除肿瘤后,催乳素(Prl)恢复正常。包括鉴别染色和免疫细胞化学的光镜检查显示肿瘤由促甲状腺激素细胞组成。超微结构上,腺瘤细胞含有如促甲状腺激素细胞中所述的小颗粒(90 - 150纳米)。该病例提供了证据,表明促甲状腺激素细胞腺瘤可能源于甲状腺功能减退继发的长期过度刺激,可诱发高催乳素血症。这似乎不是由腺瘤直接产生的,也没有任何垂体柄受压的证据。