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.