Introduction
Porphyria cutanea tarda (PCT) is the most frequent type of porphyria and resulted from a catalytic deficiency of uroporphyrinogen decarboxylase (UROD), the fifth enzyme in heme biosynthesis 1. Accumulation of photosensitive byproducts, namely uroporphyrinogen, leads to the fragility and blistering of sun-exposed skin in PCT patients. The common age of presentation is fifth to sixth decade and it occurs slightly more commonly in males. Three different types of PCT are currently distinguished: an acquired variant accounting for 80% of PCT cases, also referred to as sporadic or type I PCT, in which the enzymatic deficiency is limited to the liver; an autosomal dominantly inherited form, also known as familial or type II PCT, in which a decrease of enzymatic activity is found in all tissues; type III PCT is similar to type II concerning familial occurrence, but their erythrocyte UROD activity is normal 2. Patients with type I PCT is closely associated with liver diseases triggered by genetic and environmental factors, such as alcohol abuse, iron overload, hemochromatosis, and hepatitis C virus infection 3. We herein present 3 PCT cases with a history of alcohol abuse. Of considerable interest, the 3 patient showed complete remission after cessation or reduction of alcohol consumption during our follow-up that emphasize the importance of environmental factors in PCT development.