Pathogenesis, diagnosis and treatment of non-alcoholic fatty liver disease.

Non-alcoholic fatty liver disease (NAFLD) includes a broad spectrum of alterations that go from simple steatosis to steatohepatitis and cirrhosis. Type 2 diabetes mellitus (DM-2) and obesity are the principle factors associated to NAFLD. A 20-30 % prevalence in general population has been described. The survival of this type of patient is lower than the general population's, showing a higher incidence of hepatic and cardiovascular complications. The aetiopathogenesis is still unclear, but we know the intervention of different factors that produce fatty-acid accumulation in hepatic parenchyma, causing oxidative stress, oxygen-free radicals and the synthesis of an inflammatory cascade, that determine the progression of this disease from steatosis up to advanced fibrosis.The diagnostic gold-standard is still the liver biopsy, even though the development of newer non-invasive techniques, like serological and imaging (radiology), have opened a new field for research that allows bloodless testing of these patients and better study of the natural history of this disease. Nowadays, there is still no specific treatment for NAFLD. The development of healthy life habits and moderate exercise continue to be the pillars of treatment. Different pharmacological approaches have been studied and applied, such as the control of insulin resistance, lowering cholesterol levels, antioxidants, and other alternatives in experimental trials.

Etiopatogenia, diagnóstico y tratamiento de la enfermedad del hígado graso no alcohólica / No disponible

La enfermedad por hígado graso no alcohólica (EHGNA) comprende un amplio abanico de alteraciones que va desde la esteatosis simple hasta la esteatohepatitis y la cirrosis. La diabetes mellitus tipo 2 y la obesidad son los principales factores asociados a la EHGNA. Se ha descrito una prevalencia en la población general de entre el 20-30 %. La supervivencia de estos enfermos es menor que la población general, presentando una mayor incidencia de complicaciones hepáticas y cardiovasculares. La etiopatogenia es desconocida en parte pero se conoce la intervención de diferentes factores que provocan la acumulación de ácidos grasos en el parénquima hepático, produciendo una situación de estrés oxidativo, la formación de radicales libres de oxígeno y la síntesis de una cascada inflamatoria de citocinas que determinan la progresión de la enfermedad desde esteatosis hasta fibrosis avanzada. La prueba diagnóstica de elección continúa siendo la biopsia hepática, si bien el desarrollo de diferentes técnicas no invasivas, tanto serológicas como de imagen, ha abierto un nuevo campo de investigación que permite una evaluación incruenta de estos pacientes y un mejor estudio de la historia natural de la enfermedad. En la actualidad no existe un tratamiento específico. El desarrollo de hábitos de vida saludables y el ejercicio físico moderado continúan siendo los pilares básicos. Se han investigado y aplicado diferentes aproximaciones farmacológicas incluyendo el control de la resistencia a la insulina, hipolipemiantes, antioxidantes y otras alternativas en vía experimental (AU)

Non-alcoholic fatty liver disease (NAFLD) includes a broad spectrum of alterations that go from simple steatosis to steatohepatitis and cirrhosis. Type 2 diabetes mellitus (DM-2) and obesity are the principle factors associated to NAFLD. A 20-30 % prevalence in general population has been described. The survival of this type of patient is lower than the general population’s, showing a higher incidence of hepatic and cardiovascular complications. The aetiopathogenesis is still unclear, but we know the intervention of different factors that produce fatty-acid accumulation in hepatic parenchyma, causing oxidative stress, oxygen-free radicals and the synthesis of an inflammatory cascade, that determine the progression of this disease from steatosis up to advanced fibrosis. The diagnostic gold-standard is still the liver biopsy, even though the development of newer non-invasive techniques, like serological and imaging (radiology), have opened a new field for research that allows bloodless testing of these patients and better study of the natural history of this disease. Nowadays, there is still no specific treatment for NAFLD. The development of healthy life habits and moderate exercise continue to be the pillars of treatment. Different pharmacological approaches have been studied and applied, such as the control of insulin resistance, lowering cholesterol levels, antioxidants, and other alternatives in experimental trials (AU)

Hepatitis crónica por virus de la hepatitis C genotipo 4 / Chronic C hepatitis genotype 4

El virus de la hepatitis C (VHC) es uno de los agentes causales más importantes de enfermedad hepática. El genotipo 4 es responsable del 20% de las hepatitis crónica y en varios países de la cuenca mediterránea se ha comunicado que la prevalencia está aumentando. La infección por el VHC evoluciona a la cronicidad en más del 90%, un 20% puede presentar cirrosis y entre un 5–10% desarrollar un hepatocarcinoma. Se ha especulado sobre una posible asociación del genotipo 4 con el desarrollo de hepatocarcinoma, pero parece relacionado con otras causas concomitantes de hepatopatía. El tratamiento se basa en el uso de interferón pegilado α-2a (a dosis de 180μg/sem) o interferón pegilado α-2b (1,5μg/kg/sem) más ribavirina (1.000–1.200mg/día) durante un año. Con este régimen terapéutico se han observado tasas de respuesta virológica sostenida (RVS) en torno al 65%. Se han apreciado diferencias en las tasas de RVS según el grado de fibrosis, las infecciones concomitantes asociadas y la presencia de determinados marcadores serológicos. Se ha utilizado la nitazoxanida en combinación con el tratamiento combinado clásico, alcanzándose una mejoría en los resultados (AU)

The hepatitis C virus (HCV) is one of the most important causal agents of liver disease. Genotype 4 is responsible for 20% of chronic hepatitis and in several countries of the Mediterranean area it has been reported that the prevalence is increasing. The HCV infection develops to chronicity in more than 90%, 20% may have cirrhosis and 5–10% develop hepatocellular carcinoma. There has been speculation about a possible association of genotype 4 with the development of hepatocellular carcinoma, but it seems related to other concomitant causes of liver disease. Treatment is based on the use of pegylated interferon α-2a (180mg/week) or pegylated-interferon α-2b (1.5mg/kg/wk) plus ribavirin (1000–1200mg/day) for one year. With this regimen, there have been reported sustained virological response (SVR) rates around 65%. There are differences in the SVR rates according to the degree of fibrosis, associated concurrent infections and the presence of specific serologic markers. Nitazoxanide has been used in combination with the classic combination therapy, achieving an improvement in the results (AU)

[Chronic C hepatitis genotype 4]. / Hepatitis crónica por virus de la hepatitis C genotipo 4.

The hepatitis C virus (HCV) is one of the most important causal agents of liver disease. Genotype 4 is responsible for 20% of chronic hepatitis and in several countries of the Mediterranean area it has been reported that the prevalence is increasing. The HCV infection develops to chronicity in more than 90%, 20% may have cirrhosis and 5-10% develop hepatocellular carcinoma. There has been speculation about a possible association of genotype 4 with the development of hepatocellular carcinoma, but it seems related to other concomitant causes of liver disease. Treatment is based on the use of pegylated interferon α-2a (180 mg/week) or pegylated-interferon α-2b (1.5mg/kg/wk) plus ribavirin (1000-1200 mg/day) for one year. With this regimen, there have been reported sustained virological response (SVR) rates around 65%. There are differences in the SVR rates according to the degree of fibrosis, associated concurrent infections and the presence of specific serologic markers. Nitazoxanide has been used in combination with the classic combination therapy, achieving an improvement in the results.

Spectrum of anemia associated with chronic liver disease.

Anemia of diverse etiology is a common complication of chronic liver diseases. The causes of anemia include acute or chronic gastrointestinal hemorrhage, and hypersplenism secondary to portal hypertension. Severe hepatocellular disease predisposes to hemorrhage because of impaired blood coagulation caused by deficiency of blood coagulation factors synthesized by hepatocytes, and/or thrombocytopenia. Aplastic anemia, which is characterized by pancytopenia and hypocellular bone marrow, may follow the development of hepatitis. Its presentation includes progressive anemia and hemorrhagic manifestations. Hematological complications of combination therapy for chronic viral hepatitis include clinically significant anemia, secondary to treatment with ribavirin and/or interferon. Ribavirin-induced hemolysis can be reversed by reducing the dose of the drug or discontinuing it altogether. Interferons may contribute to anemia by inducing bone marrow suppression. Alcohol ingestion is implicated in the pathogenesis of chronic liver disease and may contribute to associated anemia. In patients with chronic liver disease, anemia may be exacerbated by deficiency of folic acid and/or vitamin B12 that can occur secondary to inadequate dietary intake or malabsorption.

Enfermedad hepática en la telangiectasia hereditaria hemorrágica (enfermedad de Rendu-Osler-Weber) / Hepatic disease in hereditary hemorrhagic telangiectasia (Rendu-Osler-Weber disease)

No disponible