Reactions to Light on the Normal and Pellagrous Bantu Skin

Abstract

SUMMARY. In dark skinned subjects, delayed or “secondary” pigmentation from ultra‐violet light may be the only clinical sign of sunburn. It results from necrobiosis limited to the outer Malpighian layer and hardly extends deeper than this even when the dose exceeds the maximum possible from a day's natural sunshine. Preceding erythema is not merely masked by the pigment, but is often virtually absent. On the background of this natural skin resistance, the hyperkeratotic pellagrous lesion is interpreted as a marked reaction to mild or repeated ultraviolet injury followed by retention and ultimate cracking of the abnormal layers so produced. These layers are formed below the normal stratum granulosum when the initial damage is severe, but lie above the new stratum granulosum which forms underneath as the cells keratinize.

Pellagra: a still existing disease

“…It has been reported that 50% of the Bantu who were examined in the various clinics for a number of diseases presented with skin manifestations of pellagra (Pretorious, 1968). The increase of the disease among the Bantu has also been shown by Findlay et al (1969) and Hankes et al (1971). Adrian et al (1972) also observed that the disease is endemic in a few areas of Western Africa, notably Angola.…”

Is the Cracking in Pellagrous Hyperkeratoses due to Disturbed Water Binding?

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Correspondence

Is the Cracking in Pellagrous Hyperkeratoses due to Disturbed Water Binding?SIR,-^We were puzzled that the natural keratotic pellagrous lesion showed coarse cracking and the experimentally induced lesion did not (Findlay et al, 1969). Two possible reasons were-(a) the experimental lesions were shielded from the dry outdoor climate, (b) the cracking was due to a solid pile-up of hastily keratinized and adherent cells whieh dissected off with difficulty and cracked into large plates before being shed.

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