Infección por virus C oculto en hepatopatías criptogenéticas Sr. Director: Desde que Brechot y colaboradores publicaron la primera serie de pacientes con Hepatitis B crónica sin hallazgo del antige-no de superficie en el suero (1) se ha venido hablando de virus B "oculto". Nosotros hemos colaborado en un trabajo de reciente publica-ción (2) en el que se ha estudiado una serie de 100 pacientes con alteración persistente de aminotransferasas y/o gamma-glutamil-transpeptidasa que no podía ser achacada a ninguna de las etiolo-gías habituales, incluyendo la negatividad de los marcadores virales (RNA-HVC, DNA-HVB) y en los que en cambio se encontró, en el 57%, por hibridación in situ, la presencia del RNA-HVC del genotipo lb en el tejido hepático y con una activi-dad necroinflamatoria y fibrótica superior a la histología de los pacientes sin RNA-HVC intrahepático. La reflexión, como clínico, que estos hallazgos implican me han hecho sumarizar las posibles consecuencias del mismo. Primero, en cuanto al diagnóstico, este hallazgo hecha por tie-rra la aseveración de que la ausencia en el plasma de marcadores del virus C (preferentemente el RNAHVC) elimina el diagnósti-co de Hepatopatía Crónica por virus C y, áun recogiendo los datos de mayor potencial necróticroinflamatorio y de fibrosis, desconocemos su evolución futura que precisará de seguimiento de estos pacientes. En cuanto a posibilidad de contagio, no tenemos aún el con-vencimiento de que el material genómico detectado sea infeccio-so, aunque con copias suficientes para identificar el genotipo 1b. Por otro lado el hecho de que, al menos en nuestra serie, los pacientes presenten elevaciones enzimáticas significativas, elimi-na el peligro de que puedan ser donantes en bancos de sangre, etc., pudiendo igualmente prevenirse posibles contagios parente-rales individuales. El hecho de no conocer aún la evolución específica de estos enfermos con virus C oculto, así como su pertenencia al genotipo Ib y que, únicamente por hibridación in situ de una nueva biopsia tras el tratamiento, pueda juzgarse de la eficacia del mismo, implican que, de momento, sólo deban emprenderse seguimien-tos y tratamientos muy controlados. A. Pérez Mota Servicio de Aparato Digestivo. Hospital Virgen de la Torre. Madrid 1. Bréchot C, Thiers V, Kremsdorf D, Nalpas B, Pol S, Paterlini-Bréchot P. Persistent hepatitis B virus infection in subjects without hepatitis B surface antigen: clinically significant or purely "occult"?. Hepatology 2001; 34: 194-203. 2. El hepatocarcinoma es el tumor primario maligno hepático más frecuente. Una de sus manifestaciones clínicas es la produc-ción de síndromes paraneoplásicos. Entre los más frecuentes se encuentran la poliglobulia, la hipercalcemia, la hipoglucemia y la hiperlipidemia. De forma más rara, se han descrito reacciones leucemoides secundarias a hepatocarcinoma (1-3). El primer caso fue descrito por Ranke y cols. (1) en 1965. Tras realizar una bús-queda bibliográfica en Medline desde 1966-2002 existen escasos artículos publicados referentes a dicho tema y...
SUMMARY BackgroundOccult hepatitis C virus infection is defined by the presence of hepatitis C virus-RNA in liver but with undetectable anti-hepatitis C virus and serum viral RNA.
Hepatitis B virus (HBV) DNA may persist in the liver in the absence of serum HBV-DNA after a self-limited acute hepatitis B. This may also occur in patients with chronic hepatitis C virus (HCV) infection but its prevalence and its impact on liver histology is unknown. HBV-DNA was tested by polymerase chain reaction (PCR) and by in situ hybridisation in liver biopsies from 98 patients with chronic hepatitis C who were hepatitis B surface antigen negative and serum HBV-DNA negative by PCR. HBV-DNA resulted positive in the liver of 37/98 (37.7%) patients without serum HBV-DNA. To test whether these patients had serum HBV-DNA levels under the detection limit of the PCR assay used in this study (50 copies/ml), PCR products in which HBV-DNA was undetectable after visualization of agarose gels were analysed by dot-blot hybridisation. With this method, HBV-DNA was positive in serum of 12/37 patients with liver HBV-DNA. Thus, 25/98 (25.5%) patients have HBV-DNA detectable only in liver. This was confirmed by in situ hybridisation, the percentage of infected hepatocytes ranging from 0.1% to 12%. In patients in whom the HCV infection was shorter than 20 years, HBV infected patients had higher (P = 0.01) fibrosis score (1.64 +/- 1.21) than HBV negative cases (0.53 +/- 0.66). In conclusion, a significant proportion of patients with chronic HCV infection have HBV-DNA in the liver in the absence of viral DNA in serum. The impact of this finding on liver histology deserves further research.
The intramuscular administration of interferon-beta (IFN-beta) at a dosage of 6 million units three times per week for 6 months has been evaluated in 90 patients included in a multicenter, randomized, controlled trial for the treatment of chronic hepatitis C. Transaminase levels were significantly reduced in IFN-beta-treated patients (p = 0.015) and were significantly lower with respect to those of the untreated controls (p = 0.040 at 6 months). Four treated (8%) and one untreated (2.5%) patients had normal transaminase values after 6 months. At study end (12 months), three quarters of the IFN-beta-treated patients had sustained transaminase normalization, whereas the untreated case had relapsed. Hepatitis C viremia was cleared in 6 (12%) treated patients but in none of the untreated controls (p = 0.058). Side effects of IFN-beta were infrequent (a mild flu-like syndrome in < 10%, asthenia in 16%, anorexia in 8%, headaches and weight loss in 8%, and hair loss in 4%). Leukocyte and platelet counts decreased during IFN-beta treatment, but no dose modifications were necessary. Such decreases were not statistically significant when compared with the levels in the untreated controls. Intramuscular IFN-beta at the dosage used has little efficacy in the treatment of chronic hepatitis C. Because of IFN-beta tolerance, higher doses and alternate routes of injection might prove beneficial for the treatment of this disease.
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