Abstract
Porphyria cutanea tarda, which is the most common and readily treated form of porphyria in humans, results from a deficiency of uroporphyrinogen decarboxylase in the liver.1 2 3 It is characterized by cutaneous photosensitivity. The disease is usually classified as sporadic if uroporphyrinogen decarboxylase is deficient only in the liver, and as familial (autosomal dominant) if the enzyme is also deficient in nonhepatic tissues such as erythrocytes.3 4 5 There is also a familial form in which only the hepatic enzyme is deficient.6 Increased iron content in the liver is a major contributing factor in both sporadic and familial porphyria cutanea tarda,7 as are.
Original language | English (US) |
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Pages (from-to) | 315-317 |
Number of pages | 3 |
Journal | New England Journal of Medicine |
Volume | 322 |
Issue number | 5 |
DOIs | |
State | Published - Feb 1 1990 |
ASJC Scopus subject areas
- General Medicine