Stress and Autoimmune Thyroid Diseases

Abstract

Autoimmune thyroid diseases (AITD) are the far most common autoimmune disorders, their prevalence in Western countries exceeding 5% of the general population. In the large majority of individual cases the clinical impact of AITD is not severe, however, their widespread diffusion renders them a significant health problem. AITD are heterogeneous in their clinical presentation: the two main forms are autoimmune thyroiditis (AT) and Graves’ disease (GD). Although they probably share, at least in part, a common genetic background and may occur in the same family as well as in the same individual, they are definitely two distinct diseases both in their clinical presentation and their pathophysiology. In fact, AT causes structural thyroid damage (mainly via cell-mediated immune destruction of thyroid follicular cells) which results, as a rule, in functional impairment (hypothyroidism); however, depending on clinical variants, evolution towards hypothyroidism may be very low, or thyroid function impairment occurs after an initial phase of mild thyrotoxicosis due to relatively rapid gland destruction. GD patients have hyperthyroidism, often severe, due to autoantibody-mediated thyrotropin receptor stimulation, with thyroid cell hyperplasia and hyperfunction. Such a functional heterogeneity is a key feature for the clinical management: as a matter of fact, therapy of AITD is mainly therapy of thyroid dysfunction. Moreover, since hyperthyroidism is quite early perceived by the patient as a cause of discomfort, the timing of the natural history of GD is relatively well defined; on the other hand, AT may be asymptomatic for a long time and defining its natural history in a single patient may be difficult. In some AITD patients (mainly, but not exclusively, with GD), clinical features not directly related to thyroid dysfunction, such as orbitopathy, are present. Graves’ orbitopathy is probably related, at least in part, to autoantibodies directed to thyrotropin receptor; it may be, in a minority of patients, severe and sight-threatening, and represents an independent clinical problem.

MECHANISMS IN ENDOCRINOLOGY: Role of emotional stress in the pathophysiology of Graves' disease

“…A review of the literature including seven case-control studies has highlighted the preexistence of a 'negative' stressful event in patients with Graves' disease (8,9,10,11,12,13,14,15). However, one can criticize the principle of case-control studies: it is difficult to assess the effect of a given stressful event in different individuals; the validity of filling out a questionnaire may be limited in an emotional context, the actual date of the onset of the disease is difficult to specify and nothing proves that it occurred after the stressful event (8). However, a prospective study conducted in Serbia shows that while the incidence of Graves' disease had been stable since 1971, it increased significantly between 1992 and 1995, i.e.…”

“…Conversely, thyroid hormones potentiate the effects of glucocorticoids and catecholamines. Therefore, there is a 'cross-talk' between the two axes, and a disruption resulting from an excessive secretion of thyroid hormones during thyrotoxicosis can lead to vicious circles between thyroid homeostasis and immune response (8).…”

Serum Proteomic Profiling Associated with Immune System Impaired by Stress Using ProteinChip Technology

“…It has been demonstrated that stress affects the immune system and can cause increased susceptibility to tumors [16][17][18] , infections [19][20][21] , and autoimmune diseases [22][23][24] . Therefore, determination of the protein and peptide composition during stress on the immune system may not only lead to an improved understanding of stress, especially in regard to psychosomatic illness, but may also offer new insights into the possibility of using selected peptides or proteins as markers of processes occurring during stress to explain the molecular mechanisms.…”

Stress and thyroid gland

“…В последние годы значительно выросло количество исследовательских работ, посвященных изучению эффектов стресса на функцию щитовидной железы (ЩЖ) и периферический метаболизм тиреоидных гормонов [1][2][3][4]. Это может быть обусловлено, по-видимому, несколькими составляющими.…”