El virus C de la hepatitis y las enfermedades que produce / Hepatitis C virus and the diseases that it produces

In 1989, the main agent causing non A non B hepatitis was identified as a RNA virus of the flavivirus family, with several serotypes, and was denominated virus C. At the present moment, the knowledge about the infection features and diseases that it causes has expanded thanks to the availability of reliable laboratory techniques to detect the antibody and the virus. The prevalence of infection and the frequency of serotypes varies in different regions of the world. Chile is a country with a low prevalence. The detection of infected blood in blood banks has reduced the spreading of the disease. Other means of infection such as the use of intravenous drugs, hemodialysis and transplantation have acquired greater importance. Sexual, maternal and familial transmission is exceptional. Infected people develop an acute hepatitis, generally asymptomatic. Eighty percent remain with a chronic hepatic disease, that can be mild or progressive, evolving to cirrhosis or hepatic carcinoma. Chronic hepatitis, closely resembling an autoimmune disease, can be caused by the virus. Alcohol intake increases viral activity causing severe hepatic diseases, refractory to treatments. Several non hepatic diseases are associated to hepatitis C virus infection such as essential mixed cryoglobulinemia, mesangiocapillary glomerulonephritis, porphyria cutanea tarda, dysglobulinemias and probably type 2 diabetes mellitus. The only available treatment is interferon, that is successful in a minority of patients, frequently causing a transient improvement. The use of ribaravine associated to interferon improve the effectiveness of therapy. Liver transplantation is the only therapy for severe hepatic disease. The use of new antiviral drugs should improve the prognosis of the disease

Carácter adquirido de la porfiria cutánea tarda en pacientes infectados con virus C de la hepatitis / Acquired character of porphyria cutanea tarda in patients infected with hepatitis C virus

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

Excreción de porfirinas e infección crónica por virus C de la hepatitis / Porphyrin excretion and chronic infection by hepatitis C virus

Eighteen patients with cirrhosis Child-Pough A, eight infected with hepatitis C virus, were studied. Urinary excretion of Ù aminolevulinic acid, porphobilinogen, coproporphyrins, uroporphyrins and fecal excretion of coproporphyrins and protoporphyrins were measured. Red blood cell protoporphyrin was also measured. There were no differences in the measured parameters between patients with or without hepatitis C virus infection. No patient had uroporphyrin excretion values over the normal range. Some patients had slight elevations in some parameters, but always below the values observed in porphyrias. In these group of patients, hepatitis C virus infection of its associated liver diasease do not cause detectable alterations in porphyrin metabolism

Hepatopatía en dadores de sangre portadores asintomáticos del virus B de la hepatitis / Hepatopathy in blood donors who are asymptomatic carriers of hepatitis B virus

Los portadores crónicos de HBsAg tienen una alta probabilidad de infectar a quienes reciben su sangre y a sus contactos sexuales y evolucionar a daño hepático intenso. Se citaron a 56 dadores de sangre que resultaron (+) al ELISA para HBsAg para estudio de alteraciones hepáticas. El 57,1 por ciento concurrió a la citación. De ellos, 12,5 por ciento resultó negativo al repetírseles el ELISA. El 94 por ciento de los dadores repetidamente (+) al ELISA fueron confirmados por técnica de neutralización en el ISP. La prevalencia estimada de portadores asintomáticos de HBsAg en este grupo de personas es de 0,12 por cientom menor que lo señalado por otros autores, lo que puede atribuirse a un efectivo descenso por la práctica de medidas de control en los bancos de sangre. El 28 por ciento de los dadores HbsAg (+) refirió algún actor de riesgo de infección. Un alto porcentaje de dadores de sangre refirió un consumo exagerado de alcohol. Las alteraciones de las pruebas de laboratorio hepático fueron frecuentes, pero de muy baja intensidad. La excreción de bromosulfaleína fue la prueba de laboratorio mas frecuentemente alterada (36 por ciento). Sólo un paciente con indicación de biopsia aceptó relizársela, demostrándose hepatitis crónica persistente. Las pruebas de laboratorio pueden encontrarse levemente alteradas en dadores de sangre HBsAg (+), pero aún así es posible demostrar evidencias, a lo menos, de hapatitis crónica persistente