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Les neurones à GHRH semblent être sensibles à une atteinte vasculaire, du fait de leur localisation centrale au niveau de l’hypothalamus. Les cellules somatotropes hypophysaires sont, elles, situées essentiellement dans les parties latérales et les cellules gonadotropes dans le pars tuberalis, ces 2 territoires sensibles vascularisés par le tronc porte hypophysaire long, alors que les cellules corticotropes et thyréotropes sont situées dans la partie centrale de l’hypophyse et sont sous la dépendance du tronc porte hypophysaire court. C’est d’ailleurs pour cela que d’une façon générale, après chirurgie et irradiation hypophysaire, ce sont les axes somatotropes et gonadotropes qui sont le
plus souvent concernés.
AITD are heterogeneous in their clinical presentation: the two main forms are autoimmune thyroiditis (AT) and Graves&apos; 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.
The weight of evidence from epidemiological and case-control studies supports an association between stress and GD. On the other hand, there is little information available on the effect of stress on HT, but there is evidence for an increase in postpartum thyroiditis, following the cellular immune suppressive effect of pregnancy. Whether stress has a causative effect on GD remains elusive. Circumstantial evidence supports the hypothesis that stress may influence the clinical expression of thyroid autoimmunity in susceptible individuals favoring the development of GD by shifting the Th1-Th2 balance away for Th1 and toward Th2. Conversely, recovery from stress or the immune suppressive effect of pregnancy may induce a Th2 to Th1 &quot;return shift&quot; leading to autoimmune (sporadic) or postpartum thyroiditis, respectively.
The most outstanding fact is that in genetically predisposed individuals, the disruption of these neuroendocrine-immune interactions by environmental factors results in thyroid autoimmune dysfunction. These interactions are able to incline the balance between Th1-Th2 immune response toward one side, resulting in a Th1-cell-mediated autoimmune reaction with thyrocyte destruction and hypothyroidism in Hashimoto&apos;s thyroiditis but to a hyperreactive Th2-mediated humoral response against TSH receptor with stimulatory antibodies leading to Graves&apos; disease hyperthyroidism