Chronic recurrent stress due to panic disorder does not precipitate Graves' disease

Citation
L. Chiovato et al., Chronic recurrent stress due to panic disorder does not precipitate Graves' disease, J ENDOC INV, 21(11), 1998, pp. 758-764
Citations number
41
Categorie Soggetti
Endocrinology, Nutrition & Metabolism
Journal title
JOURNAL OF ENDOCRINOLOGICAL INVESTIGATION
ISSN journal
03914097 → ACNP
Volume
21
Issue
11
Year of publication
1998
Pages
758 - 764
Database
ISI
SICI code
0391-4097(199812)21:11<758:CRSDTP>2.0.ZU;2-F
Abstract
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 Gr aves' disease in patients with panic disorder, a psychiatric condition char acterized by recurrent endogenous stress. The study group included 87 conse cutive 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 pa st history of psychiatric disorder served as controls. Patients were submit ted to a full evaluation of the thyroid that included physical examination, assays for free thyroid hormones, TSH, thyroglobulin (TgAb), thyroperoxida se (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. Thre e out of 12 patients with thyroid antibodies, indicating a genetic suscepti bility to autoimmune thyroid disease, had a family history of clinical thyr oid 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, c linical hyperthyroidism or endocrine ophthalmopathy were not found in any o f 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 un detectable TSH. During an 18-month follow-up she did not develop hyperthyro idism and her TSH spontaneously returned in the normal range. Considering t he individual duration of panic disorder, evidence for previous or present Graves' hyperthyroidism was not found for a total of 478 patient-years of e xposure to recurrent endogenous stress in the whole study group, and for a total of 39 patient-years in patients with a genetic susceptibility to auto immune thyroid disease. In conclusion, we found that recurrent endogenous s tress did not precipitate Graves' hyperthyroidism in a series of 87 patient s with panic disorder, encompassing a total of 478 patient-years of exposur e 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 Grave s' hyperthyroidism. (C)1998, Editrice Kurtis.