Effect of Graves' Disease on the “Thyrotroph” of the Adenohypophysis

Publisher Website
Google Scholar
Abstract
In sections stained by the aldehyde thionln modification of the periodic acid Schiff (PAS) technique one can identify 5 types of chromophils in the human adenohypophysis. These are designated alpha (acidophil), beta 1, beta 2, delta 1 and delta 2 (basophils). This study deals with the response of the beta 2 cell to thyroid disorders. In the normal gland, this cell appears in heavily granulated, lightly granulated and vesiculated forms. Cell counts were performed on pituitary glands from 21 cases of sudden death in adults (control group), 5 patients with hypothyroidism and 5 patients with hyperthyroidism, Including 3 due to diffuse hyperplasia of the thyroid and 2 due to toxic nodular goiter. Of special interest was an additional pituitary gland from a patient with Graves'' disease in whom radioactive iodine treatment resulted in hypothyroidism. In hypothyroidism there is a significant increase in the total number of the beta 2 cells. This increase occurs mainly in the lightly granulated and vesiculated forms, and suggests that these forms reflect hypersecretion of TSH [thyroid-stimulating hormone]. In hyperthyroidism there is a decrease in all the usual forms of the beta 2 cell; in their place small vesiculated cells are found. This form has Deen termed the "regressed vesiculate" variety of the beta 2 cell. Its small size suggests suppression of cellular activity and its content of vesicles links it with the beta 2 series. These changes in the beta 2 cells are found in glands from hyperthyroidism due to diffuse hyperplasia and to toxic nodular goiter. In a patient with Graves'' disease in whom treatment caused hypothyroidism the increase in number and vesiculation of the beta 2 cells resembled that in the other patients with hypothyroidism without Graves'' disease. The beta 2 cell changes in thyroid disorders strongly suggest that it is the human "thyrotroph." In both types of hyperthyroidism studied the cellular source of normal TSH appeared to be suppressed.

This publication has 10 references indexed in Scilit: