Langlois M F, Lamarche J B, Bellabarba D
Department of Medicine, Faculté de Médecine, Centre Universitaire de Santé de I'Estrie, Sherbrooke, Québec, Canada.
Thyroid. 1996 Aug;6(4):329-35. doi: 10.1089/thy.1996.6.329.
A 63-year-old female patient was referred to our hospital in February 1994 for a pituitary tumor. On a previous examination, in 1973, she had a goiter, nonspecific symptoms and only an elevated serum T3. In 1984 she had become hypothyroid, her goiter had increased, serum T4 was 69 nmol/L, TSH 34.4 mU/L, and TPO antibodies were positive. Hypothyroidism due to autoimmune thyroiditis was diagnosed and she received L-T4 100 micrograms/day. In 1985 and 1986, serum TSH had decreased but remained slightly elevated, while T4 was at the upper limits of normal. From 1987 to 1989 her serum TSH rose from 9 to 20 mU/L and remained at that level for the ensuing 4 years in spite of increasing L-T4 up to 150 micrograms/day. In October 1993, after discontinuing L-T4 for 6 weeks, TSH was 23.7 mU/L, T4 170 nmol/L, 131I thyroid uptake 52%, and the CT scan showed a large pituitary tumor with suprasellar extension. On preoperative investigation TSH was 40-51 mU/L with no response to TRH or GnRH. The alpha-subunit was increased at 6.33 micrograms/L with the alpha-TSH/TSH molar ratio of 1.23. Prolactin was elevated, but plasma cortisol, FSH, and LH were low. At surgery, we found a large chromophobe adenoma with few PAS-positive granules and with immunostaining positive for TSH and prolactin. From the clinical and biological data, we can conclude that the patient had probably a TSH-secreting adenoma since the goiter was first detected. The development, however, of autoimmune thyroiditis with hypothyroidism considerably modified the presentation of the disease and may have accelerated the growth of the tumor.
一名63岁女性患者于1994年2月因垂体瘤被转诊至我院。在之前的检查中,1973年她患有甲状腺肿,有非特异性症状,仅血清T3升高。1984年她出现甲状腺功能减退,甲状腺肿增大,血清T4为69 nmol/L,促甲状腺激素(TSH)为34.4 mU/L,甲状腺过氧化物酶(TPO)抗体呈阳性。诊断为自身免疫性甲状腺炎所致甲状腺功能减退,她开始接受每日100微克左甲状腺素(L-T4)治疗。1985年和1986年血清TSH有所下降但仍略高于正常,而T4处于正常上限。1987年至1989年,她的血清TSH从9 mU/L升至20 mU/L,并在随后4年维持在该水平,尽管L-T4增加至每日150微克。1993年10月,停用L-T4 6周后,TSH为23.7 mU/L,T4为170 nmol/L,131I甲状腺摄取率为52%,CT扫描显示一个巨大的垂体瘤并向鞍上延伸。术前检查时TSH为40 - 51 mU/L,对促甲状腺激素释放激素(TRH)或促性腺激素释放激素(GnRH)无反应。α亚基升高至6.33微克/升,α-TSH/TSH摩尔比为1.23。催乳素升高,但血浆皮质醇、卵泡刺激素(FSH)和黄体生成素(LH)降低。手术时,我们发现一个巨大的嫌色细胞瘤,PAS阳性颗粒很少,TSH和催乳素免疫染色呈阳性。从临床和生物学数据来看,我们可以得出结论,自首次发现甲状腺肿以来,该患者可能患有分泌TSH的腺瘤。然而,自身免疫性甲状腺炎伴甲状腺功能减退的发生极大地改变了疾病的表现,可能加速了肿瘤的生长。