, Volume 4, Issue 1, pp 91-92
Date: 04 Nov 2008

Can nonalcoholic steatohepatitis trigger porphyria cutanea tarda clinical manifestations?

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Porphyria cutanea tarda (PCT), the most common form of porphyria, is characterized by cutaneous lesions that appear after exposure to sunlight that are caused by uroporphyrin deposits. Reduced activity of hepatic urophorphyrinogen decarboxylase (URO-D) underlies the disease whose clinical manifestations are triggered by chronic HCV (hepatitis C virus) infection, alcoholic liver disease (ALD), drugs such as estrogens, and exposure to toxic compounds. Excess hepatic iron seems to be able to trigger PCT clinical manifestation in susceptible individuals, and it is still debated whether alcohol and HCV induce PCT by themselves or through their known effect on iron metabolism.

Mild iron overload is detected in the majority of patients with PCT, and iron depletion by phlebotomy induces disease remission and normalizes uroporphyrin levels in the majority of cases [1]. A high prevalence of mutations in the HFE gene of hereditary hemochromatosis has been reported in patients with PCT, with the C2