Watanabe K, Kameya T, Yamauchi A, Yamamoto N, Kuwayama A, Takei I, Maruyama H, Saruta T
Department of Internal Medicine, Keio University School of Medicine, Tokyo, Japan.
J Clin Endocrinol Metab. 1993 Apr;76(4):1025-30. doi: 10.1210/jcem.76.4.8473377.
A 21-yr-old female with hyperthyroidism is described. Though her serum-free T3 was 17.8 pmol/L and free T4 was 60.2 pmol/L, TSH was as high as 10.7 mU/L. TRH stimulated an increase in TSH from 10.7-91.7 mU/L. T3 administration in gradually increasing doses of 100, 200, and 400 mg/day resulted in gradual reduction in serum TSH. Cranial computed tomography and magnetic resonance imaging revealed a microadenoma of the pituitary gland. Histology of the surgical specimen showed a TSH-producing adenoma with TSH cell cluster islets and decreased numbers of TSH cells in the nonneoplastic pituitary. Cultured cells from the adenoma secreted TSH spontaneously and in response to TRH. This TRH-stimulated TSH secretion was suppressed by T3 in a dose-dependent manner. One year postoperatively, neither residual tumor nor recurrence were seen by computed tomography and magnetic resonance imaging. However TSH, as well as free T3 or T4, was still high and overresponsive to TRH.
本文描述了一名21岁的甲状腺功能亢进女性患者。尽管其血清游离T3为17.8 pmol/L，游离T4为60.2 pmol/L，但促甲状腺激素（TSH）高达10.7 mU/L。促甲状腺激素释放激素（TRH）刺激后，TSH从10.7 mU/L升高至91.7 mU/L。每日逐渐增加剂量至100、200和400 mg的T3给药导致血清TSH逐渐降低。头颅计算机断层扫描（CT）和磁共振成像（MRI）显示垂体微腺瘤。手术标本的组织学检查显示为分泌TSH的腺瘤，伴有TSH细胞簇状小岛，且非肿瘤性垂体中的TSH细胞数量减少。腺瘤培养细胞可自发分泌TSH，并对TRH产生反应。这种TRH刺激的TSH分泌被T3以剂量依赖的方式抑制。术后一年，CT和MRI检查未见残留肿瘤或复发。然而，TSH以及游离T3或T4仍处于高水平，且对TRH反应过度。
