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Endogenous ochronosis with a predominant acrokeratoelastoidosis‐like presentation

years, and may present for the first time with advanced liver disease. It has been associated with leukocytoclastic vasculitis, cryoglobulinemia, lichen planus, porphyria cutanea tarda, erythema nodosum, erythema multiforme, urticaria, pruritus, malakoplakia, polyarteritis nodosa, and recently with NAE. NAE differs from other necrolytic erythemas in its acral distribution and universal association with HCV infection, remaining a cutaneous marker for HCV infection, being a clinical clue for the diagnosis of HCV infection. However, the physiological reason why NAE presents in patients with HCV infection remains unknown. Three cases associated with zinc deficiency have been reported until now and, even when empiric, responses of NAE to zinc therapy suggest association between zinc deficiency and NAE. A low zinc level and the response to oral zinc may suggest an association between zinc deficiency and NAE, and also a physiological basis for classifying NAE among necrolytic erythemas. Previous cases of NAE that responded to empiric zinc therapy despite normal plasma zinc levels may have resulted from physiological zinc deficiency. It has been proposed that overtly decreased serum zinc levels are a late sign of zinc deficiency, and that skin manifestations of zinc deficiency may occur despite normal plasma zinc levels. Even with its limitations, determination of serum zinc levels must be warranted for these patients. Moreover, even when plasma zinc level is normal, treatment with oral zinc should be considered as a therapeutic option for patients with NAE.