RESUMEN
La toxicidad hepática por fármacos y su mecanismo han sido durante mucho tiempo desconocidos. Se ha observado que los pacientes con hepatitis aguda elevan los niveles séricos de ferritina. El objetivo de este estudio es determinar si existe una asociación de hepatotoxicidad por medicamentos y las mutaciones en el gen HFE asociadas con la hemocromatosis hereditaria. Material y métodos: Se analizaron10 pacientes ingresados en nuestro hospital con el diagnóstico de hepatitis aguda inducida por fármacos. A todos se les hicieron pruebas de laboratorio para el estudio de enfermedades hepáticas, la mutación del gen HFE y las características histopatológicas. Resultados: Un paciente con hepatitis secundaria a fármacos era heterocigoto para la mutación C282Y y uno heterocigoto para las mutaciones C282Y y H63D. Hubo un paciente homocigoto para la mutación H63D y seis fueron heterocigotos para la mutación H63D. La prevalencia general de las mutaciones del gen HFE en pacientes con enfermedad hepática inducida por fármacos fue del 90%. Conclusiones: La prevalencia de las mutaciones del gen HFE asociadas con hemocromatosis hereditaria está muy aumentada entre los pacientes que presentan hepatotoxicidad por medicamentos. Las mutaciones del gen HFE podrían estar involucradas en la hepatotoxicidad por fármacos...
Asunto(s)
Masculino , Femenino , Ferritinas , Hemocromatosis , Hígado , Mutación , Preparaciones Farmacéuticas , ToxicidadRESUMEN
Reversibility of liver fibrosis or cirrhosis involves complete restoration of normal liver architecture. This phenomenon has been well documented in chronic liver diseases such as autoimmune hepatitis, biliary obstruction, hemochromatosis, nonalcoholic steatohepatitis, and viral hepatitis. There are very few reports of reversal of cirrhosis after antiviral therapy in patients with chronic hepatitis B virus (HBV) infection. We report a case of disappearance of HBV-induced liver cirrhosis after years of treatment with distinct antiviral drugs, documented by successive biopsy results. This disappearance was accompanied by normalization of platelet count, gammaglobulin titers, and radiologic findings.
Asunto(s)
Antivirales/uso terapéutico , Hepatitis B/tratamiento farmacológico , Cirrosis Hepática/virología , Humanos , Masculino , Persona de Mediana Edad , Inducción de Remisión , Factores de TiempoRESUMEN
UNLABELLED: Iron deficiency anemia of unknown origin is a frequent cause of anemia in which etiological diagnosis is often not achieved, despite currently available diagnostic techniques. Recent studies suggest that, in the absence of digestive tract lesions, Helicobacter pylori infection could be the cause of iron deficiency anemia, due to the alterations produced in gastric iron absorption. OBJECTIVES: To evaluate whether H. pylori eradication resolves iron deficiency anemia and removes the need for oral iron administration. PATIENTS AND METHODS: We performed an observational descriptive study in patients with iron deficiency anemia refractory to treatment with oral iron administration and with out causes that could explain their anemia. Gastroscopy, ileocolonoscopy, intestinal transit study and/or endoscopic capsule were performed. Female patients also underwent gynecological study. All patients were H. pylori-positive and standard eradication therapy was administered until elimination was achieved. The patients were followed-up for a minimum of 3 months after H. pylori eradication and the need for oral iron intake after eradication was evaluated. RESULTS: Ten patients, aged 53+/-8.2 years, were included. Hemoglobin (Hbg) before treatment was 10.06+/-0.53 mg/dl, mean corpuscular volume (MCV) was 75.43+/-6.02 fl and ferritin was 6.1+/-3.28 ng/ml. Eradication therapy was administered until elimination of H. pylori. The mean time before disappearance of anemia was 4.5 months. Laboratory parameters after treatment were as follows: Hgb 12.86+/-0.75 mg/dl, MCV 85.02+/-4.8 fl and ferritin 28+/-22.19 ng/dl. CONCLUSIONS: In the absence of lesions that could explain iron deficiency anemia, this disease can be related to H. pylori infection. Eradication of this infection is closely followed by disappearance of anemia and ferropenia.