par Dumont, Jacques Emile 
;Roger, Pierre P. ;Lugdate, M.
Référence Endocrine Reviews, 8, page (448-452)
Publication Publié, 1987
;Roger, Pierre P. ;Lugdate, M.Référence Endocrine Reviews, 8, page (448-452)
Publication Publié, 1987
Article révisé par les pairs
| Résumé : | Graves’ disease is characterized by thyroid hyperfunction and hyperplasia which lead to thyrotoxicosis and goiter. Hyperthyroidism has been clearly related to the presence in plasma of immunoglobulins which stimulate the TSH receptor via its adenylate cyclase, the thyroid stimulatory immunoglobulins (TSI) (1–4). With regard to growth, several facts have suggested that additional mechanisms may be involved. There is no simple relationship between level of function in Graves’ disease and goiter size; indeed there are cases of hyperthyroidism with little increase in thyroid size and others with slight thyrotoxicosis and large goiters. Moreover, the presence of circulating growth-stimulating factors in euthyroid and hypothyroid patients with goiter has been reported (5–10). On the other hand, depending on the species, several biochemical pathways may be involved in the regulation of thyroid cell proliferation: 1) the TSH-activated adenylate cyclase-cAMP cascade (11–13); 2) the cAMP-independent epidermal growth factor mechanism, probably involving protein tyrosine phosphorylation (11,13); and 3) as in other types of cells, the phosphatidylinositol-Ca2+ cascade (14). It is, therefore, quite conceivable that some factors may activate growth of thyroid cells without influencing the rate of hormone synthesis and secretion. It should be pointed out, however, that in a careful study, Jin et al. (15) have been unable to dissociate the cAMP and the proliferative response to TSI in a rat thyroid cell line (FRTL5). © 1987 by The Endocrine Society. |
