Chiovato L, Marinò M, Perugi G, Fiore E, Montanelli L, Lapi P, Cavaliere R, Ciampi M, Patronelli A, Placidi G, Placidi G F, Cassano G B, Pinchera A
Department of Endocrinology, University of Pisa, Italy.
J Endocrinol Invest. 1998 Dec;21(11):758-64. doi: 10.1007/BF03348042.
A role of psychic stress in precipitating hyperthyroid Graves' disease has been suggested, but the evidence in support of this pathogenetic mechanism is conflicting. In this study we investigated the possible occurrence of Graves' disease in patients with panic disorder, a psychiatric condition characterized by recurrent endogenous stress. The study group included 87 consecutive patients suffering from panic disorder since 1 to 30 years: 17 males (mean age 31.3, range 26-43 years) and 70 females (mean age 37.6, range 15-73 years). Two hundred and sixty-two normal subjects with no present or past history of psychiatric disorder served as controls. Patients were submitted to a full evaluation of the thyroid that included physical examination, assays for free thyroid hormones, TSH, thyroglobulin (TgAb), thyroperoxidase (TPOAb) and TSH receptor (TRAb) antibodies, and thyroid echography. The prevalence of circulating TgAb and/or TPOAb in patients with panic disorder did not differ from that in the control group. Twelve patients with panic disorder (13.7%) had circulating TgAb and/or TPOAb, but none had TRAb. Three out of 12 patients with thyroid antibodies, indicating a genetic susceptibility to autoimmune thyroid disease, had a family history of clinical thyroid autoimmunity, and 4 of them had a hypoechogenic pattern of the thyroid at ultrasound suggesting autoimmune thyroiditis. None of the patients with panic disorder had a previous history of hyperthyroidism. On examination, clinical hyperthyroidism or endocrine ophthalmopathy were not found in any of them. A small goiter was appreciated by palpation in 16 patients (18.3%). Free thyroid hormones and TSH were within the normal range in all patients but one: a 55-year old lady with normal serum free thyroid hormones and undetectable TSH. During an 18-month follow-up she did not develop hyperthyroidism and her TSH spontaneously returned in the normal range. Considering the individual duration of panic disorder, evidence for previous or present Graves' hyperthyroidism was not found for a total of 478 patient-years of exposure to recurrent endogenous stress in the whole study group, and for a total of 39 patient-years in patients with a genetic susceptibility to autoimmune thyroid disease. In conclusion, we found that recurrent endogenous stress did not precipitate Graves' hyperthyroidism in a series of 87 patients with panic disorder, encompassing a total of 478 patient-years of exposure to stress. Failure to activate the hypothalamic-pituitary-adrenal axis by endogenous stress due to panic disorder as opposed to exogenous stress due to life-events might explain why panic disorder does not precipitate Graves' hyperthyroidism.
心理压力在引发甲状腺功能亢进的格雷夫斯病中所起的作用已被提及，但支持这一发病机制的证据存在矛盾。在本研究中，我们调查了恐慌症患者中格雷夫斯病的可能发生率，恐慌症是一种以反复出现内源性压力为特征的精神疾病。研究组包括87例连续患恐慌症1至30年的患者：17名男性（平均年龄31.3岁，范围26 - 43岁）和70名女性（平均年龄37.6岁，范围15 - 73岁）。262名无精神疾病现病史或既往史的正常受试者作为对照。患者接受了全面的甲状腺评估，包括体格检查、游离甲状腺激素、促甲状腺激素（TSH）、甲状腺球蛋白（TgAb）、甲状腺过氧化物酶（TPOAb）和促甲状腺激素受体（TRAb）抗体检测，以及甲状腺超声检查。恐慌症患者中循环TgAb和/或TPOAb的患病率与对照组无差异。12例恐慌症患者（13.7%）有循环TgAb和/或TPOAb，但均无TRAb。12例有甲状腺抗体的患者中有3例（提示对自身免疫性甲状腺疾病有遗传易感性）有临床甲状腺自身免疫的家族史，其中4例甲状腺超声显示低回声模式提示自身免疫性甲状腺炎。恐慌症患者均无甲亢病史。检查时，未发现任何患者有临床甲亢或内分泌性眼病。触诊发现16例患者（18.3%）有小甲状腺肿。除1例55岁女性血清游离甲状腺激素正常但TSH检测不到外，所有患者的游离甲状腺激素和TSH均在正常范围内。在18个月的随访中，她未发展为甲亢，TSH自发恢复到正常范围。考虑到恐慌症的个体病程，在整个研究组中，在总计478患者 - 年的反复内源性压力暴露中，以及在对自身免疫性甲状腺疾病有遗传易感性的患者中总计39患者 - 年的暴露中，均未发现既往或当前格雷夫斯甲亢的证据。总之，我们发现，在一系列87例恐慌症患者中，反复的内源性压力并未引发格雷夫斯甲亢，这些患者总计有478患者 - 年的压力暴露。恐慌症导致的内源性压力未能激活下丘脑 - 垂体 - 肾上腺轴，与生活事件导致的外源性压力相反，这可能解释了为什么恐慌症不会引发格雷夫斯甲亢。
