Gharib H, Carpenter P C, Scheithauer B W, Service F J
Mayo Clin Proc. 1982 Sep;57(9):556-63.
Two patients with overproduction of thyroid-stimulating hormone (TSH) are described. The first patient, a 25-year-old man with recurrent hyperthyroidism, had a pituitary adenoma and highly elevated levels of TSH. While the patient was receiving 0.3 mg of thyroid daily, and basal TSH level was 161 microM/ml. Despite an increase in the thyroid hormone therapy, serum TSH levels remained elevated. The administration of thyrotropin-releasing hormone (TRH) or dexamethasone resulted in no changes in TSH level. The second patient was an 18-year-old man who had inappropriately elevated levels of TSH 3 months after radioiodine therapy for hyperthyroidism. A gradual increase in thyroid hormone replacement therapy decreased the serum TSH levels from 250 to 14.8 microM/ml. The administration of TRH led to huge increases of TSH. Dexamethasone inhibited basal TSH but not TRH-stimulated TSH levels. The overproduction of TSH was attributed to autonomous, neoplastic secretion in the first case and to partial, selective pituitary thyrotroph resistance to thyroid hormone in the second.
本文描述了两名促甲状腺激素（TSH）分泌过多的患者。首例患者为一名25岁男性，患有复发性甲状腺功能亢进症，存在垂体腺瘤且TSH水平显著升高。该患者每日接受0.3 mg甲状腺素治疗时，基础TSH水平为161 μmol/ml。尽管增加了甲状腺激素治疗剂量，血清TSH水平仍居高不下。给予促甲状腺激素释放激素（TRH）或地塞米松后，TSH水平未发生变化。第二例患者是一名18岁男性，在接受放射性碘治疗甲状腺功能亢进症3个月后，TSH水平出现异常升高。逐渐增加甲状腺激素替代治疗剂量后，血清TSH水平从250 μmol/ml降至14.8 μmol/ml。给予TRH后，TSH大幅升高。地塞米松可抑制基础TSH水平，但对TRH刺激后的TSH水平无抑制作用。首例患者TSH分泌过多归因于自主性肿瘤分泌，第二例则归因于部分选择性垂体促甲状腺细胞对甲状腺激素抵抗。
