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Light produces endothelial necrosis in the upper dermis causing typical pain and oedema Porphyria cutanea tarda PCT is the commonest of the porphyrias Due to an acquired or inherited deficiency in the activity of the hepatic enzyme uroporphrinogen decarboxylase which usually converts uroporphyringoen III into Coproporphyrinogen III Decrease in activity of this liver enzyme can be multifactorial It is due to an inhibitor UROD called uroporphomethene This is produced particularly in the presence of an oxidising environement and increased iron in the liver Certain conditions predispose to an environment in which this inhibitor is produced leading to PCT: Haemochromatosis (20%) Hepatitis C (15%) Alcohol (50%) Oestrogen: eg HRT (50% females) Smoking So in summary, inhibition of UROD leads to a build up of uroporphyrinogen III Genetic factors may be present: A UROD mutation which is seen in 25% of patients makes the enzyme not as effective Therefore it requires less inhibitor activation to produce the disease so often get the disease at an earlier stage Reduced activity of UROD leads to accumulation of porphyrins (eg uroporphyrin) which can be transported to the skin