SKIN PIGMENTATION IN RELATION TO ADRENAL CORTICAL FUNCTION*

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Abstract
PIGMENTATION of the skin and mucous membranes constituted one of the cardinal features originally described by Thomas Addison in adrenal cortical disease (1). The pigment responsible has been shown histolcgically and chemically to be melanin (2), and many theories have been offered to explain the mechanism of the melanosis. An inability to utilize epinephrine precursors due to the loss of adrenal medullary function, with resulting conversion of these materials to excess melanin, was an early theory (3). The adrenal was also suggested as a necessary link in the sympathetic control of neural crest melanoblasts, disease of the adrenal thus resulting in skin melanosis (4). Absence of adrenal steroidal hormones has been thought to cause pigmentation by interfering with storage of vitamin C, or to result in loss of reduced ascorbic acid secondary to the lowered sodium level (5). These theories have been discussed by Jeghers (2, 6), Sodeman (7) and Lerner and Fitzpatrick (8). Recently Calkins (9), Johnsson and Hogberg (10), Sulman (11) and Reifenstein (12) have offered the hypothesis that the pigmentation of adrenocortical insufficiency may be caused by excess intermedin or melanophore-expanding hormone, which may be produced in excess in association with adrenocorticotropic hormone (ACTH), or which may be identical with it. The occurrence of pigmentation as a complication of long continued ACTH therapy gives the problem an added clinical interest and lends force to the latter theory, although it is recognized that the chromatophores of human skin are not expansile.

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