Pioro E P, Scheithauer B W, Laws E R, Randall R V, Kovacs K T, Horvath E
Department of Pathology, Mayo Clinic, Rochester, Minnesota 55905.
Surg Neurol. 1988 Mar;29(3):218-26. doi: 10.1016/0090-3019(88)90010-9.
Primary hypothyroidism accompanies more than 50% of clinically significant pituitary thyrotroph adenomas. Hypothyroidism may also produce pituitary enlargement secondary to thyrotroph hyperplasia and present with a sellar mass and hyperprolactinemia. Three hypothyroid patients who presented with presumed prolactin-producing adenomas are reported. Although laboratory and radiologic abnormalities of pituitary enlargement may resolve after corrective thyroid therapy, our patients showed no such response and underwent operation. Histologic examination revealed no adenomas, but thyrotroph and lactotroph hyperplasia were present. Thyrotroph hyperplasia probably results from lack of negative feedback of thyroid hormone upon the anterior pituitary. Whether this is due to hypothalamic release of thyrotropin-releasing hormone (TRH) or another mechanism is unclear. Lactotroph hyperplasia may result from excess TRH, which stimulates lactotrophs with resultant hyperprolactinemia, or from reduced hypothalamic dopamine, thereby facilitating prolactin secretion. This study suggest that (a) hyperprolactinemia in hypothyroidism is not necessarily due to the "stalk section effect" secondary to pituitary enlargement, and (b) patients with primary hypothyroidism and sellar mass should initially be managed medically so that potentially reversible pituitary hyperplasia is not mistaken for adenoma.
原发性甲状腺功能减退症在临床上具有显著意义的垂体促甲状腺激素腺瘤中占比超过50%。甲状腺功能减退症也可能继发于促甲状腺激素细胞增生而导致垂体增大，并表现为鞍区肿块和高催乳素血症。本文报告了3例表现为疑似催乳素分泌腺瘤的甲状腺功能减退症患者。尽管垂体增大的实验室和影像学异常在甲状腺纠正治疗后可能会消退，但我们的患者并未出现这种反应并接受了手术。组织学检查未发现腺瘤，但存在促甲状腺激素细胞和催乳激素细胞增生。促甲状腺激素细胞增生可能是由于甲状腺激素对垂体前叶缺乏负反馈所致。这是由于下丘脑释放促甲状腺激素释放激素（TRH）还是其他机制尚不清楚。催乳激素细胞增生可能是由于过量的TRH刺激催乳激素细胞导致高催乳素血症，或者是由于下丘脑多巴胺减少，从而促进催乳素分泌。本研究表明：（a）甲状腺功能减退症中的高催乳素血症不一定是由于垂体增大继发的“垂体柄切断效应”；（b）原发性甲状腺功能减退症和鞍区肿块患者最初应进行药物治疗，以免将潜在可逆的垂体增生误诊为腺瘤。
