Carácter adquirido de la porfiria cutánea tarda en pacientes infectados con virus C de la hepatitis

Background: Porphyria cutanea tarda (PCT) is due to a partial defect of hepatic uroporphyrinogen decarboxylase (URO-D). In the hereditary form, both hepatic and erythrocytic enzymes are altered, whereas in the acquired form, only the hepatic enzyme fails. There is a high prevalence of hepatitis C virus infection in patients with PCT, specially in those without family history of the disease. Aim: To study erythrocytic URO-D activity in order to find out wether hepatitis C virus infection is associated to the acquired form of PCT or unveils an inactive hereditary form. Patients and methods: URO-D activity was measured in red blood cells of normal controls, hepatitis C virus carriers without symptoms of PCT and patients with PCT, with and without family history of the disease, with and without anti hepatitis C virus antibodies. Results: URO-D activity was similar in normal controls, patients with chronic liver disease associated to hepatitis C virus, and in patients with PCT without family history of the disease with and without hepatitis C virus antibodies. URO-D activity was lower in patients with PCT and family history of the disease, with and without hepatitis C virus antibodies. Conclusions: PCT in patients with hepatitis C virus infection is due to an acquired alteration of hepatic URO-D. Hepatitis C virus does not modify erythrocytic URO-D