Revista medica de Chile · 1998
[Acquired characteristics of porphyria cutanea tarda in patients infected with hepatitis C virus].
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Wolff C, Stella A M, Armas R, Parraguez A, Silva H, Batlle A M
Аннотация
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 whether 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.
AIM: To study erythrocytic URO-D activity in order to find out whether 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.