Experiences with methoxsalen in the Americam tropics.

The dermatologic potentialities of methoxsalen in populations living in the tropics are especially intriguing for several reasons. The nationals of tropical countries tend to be more or less darkly pigmented; in them such physically innocuous processes as vitiligo may have serious social and economic impact. White-skinned residents may be subject to greater actinic dermal injury than would be the case in their normal, temperate climates. Finally, the optimal source of ultraviolet energy (i.e., intense natural sunlight) is readily available. While the mode of action of the furocoumarins is not entirely clear, it has been shown that systemic administration of appropriate doses of methoxsalen followed by ultraviolet radiation will produce a series of morphologic changes in skin (1, 2). The stratum corneum thickens and a structure resembling stratum lucidum may appear within two weeks of daily exposures; there is a possibility this may be intimately related to the stratum corneum conjunctum of Szakall (3). Although more work remains to be done on the relation of altered structure to altered function, Imbrie et at. (4) have clearly demonstrated that a single ultraviolet exposure of methoxsalenconditioned skin nearly doubles the amount of energy required to induce a minimal erythema in the treated area five to six weeks later. Another change has to do with melanin pigmentation, which may become increased (as compared to skin areas exposed to ultraviolet without methoxsalen). Two explanations have been offered. The first, which seems to be the case in normal skin, is that the altered epidermis simply increases retention of melanin formed in ordinary amounts in response to sunlight. The second suggestion, that the melanocytes are somehow stimulated to increased production of melanin, seems to have application in one abnormal condition, vitiligo. This is a disease characterized by failure of pigmentation in areas of skin containing a normal complement of melanocytes, twice the normal amount of sulfhydryl, tyrosinase, and ample substrate, tyrosine (4). The reason for loss