Dermatologic correlates of selected metabolic events.

Various metabolic events may lead to dermatologic pathology. Three illustrative examples are glucagonoma syndrome, uremic pruritus, and zinc deficiency. The glucagonoma syndrome, resulting from a glucagon secreting-tumor, is characterized by a distinctive dermatitis, necrolytic migratory erythema. This skin rash is a generalized, pruritic eruption which first appears as erythematous patches, then progresses to form superficial vesicles and bullae. Uremic pruritus is a clinical phenomenon seen in patients with chronic renal failure; it provokes vigorous scratching and may lead to numerous cutaneous lesions including extensive excoriations, lichen simplex chronicus, prurigo nodularis, keratotic papules, or secondary impetigo. Zinc deficiency may be evident as an inherited disease called acrodermatitis enteropathica, which presents clinically with a predominately acral and periorificial rash of sharply demarcated erythematous, exfoliative, and exudative patches. It may also result from an acquired defect with similar clinical findings. A brief review concerning the etiology, clinical manifestations, diagnosis, and treatment are given for glucagonoma syndrome, uremic pruritus, and zinc deficiency. Any pathophysiologic dysfunction that results in a loss of metabolic control of homeostasis in the body may demonstrate cutaneous manifestations. These skin findings may be of great clinical significance and may aid in the diagnosis or even be the first sign of a disease process. The glucagonoma syndrome, uremic pruritus, and zinc deficiency are three examples of dermatologic correlates of metabolic events.