RESUMEN
Alcoholic hepatitis represents the most severe form of alcoholic liver disease Recent research points to an exaggerated inflammatory response, mediated by neutrophils,as the basic mechanism of liver damage. This entity has a distinctive clinical picture and a characteristic histopathology and a poor outcome.Recent investigation reveals a complex network of intracellular and intercellular communication signals involving hepatocytes, endothelial cells, monocytes, lymphocytes, neutrophils,Ito and Kupffer cells, leading to massive migration of neutrophils from blood to liver.When neutrophils reach the liver, multiple cytokines produced locally by endothelium, hepatocytes and Kupffer cells, up-regulate their function. Activation of neutrophils leads to increased production of oxygen radicals(mainly superoxide)and hydrogen peroxide production.To date there is general agreement that measurement of superoxide production by neutrophils is a reliable way of determining neutrophil function and its activation.Thirty one patients with acute alcoholic hepatitis, twenty with compensated alcoholic liver disease end seventeen controls were studied.Patients with alcoholic hepatitis and alcoholic liver disease were enrolled on admission to the hospital and if they had no features of infection, bleeding or renal failure.The neutrophil stimuli used were opsonized zymosan and fMLP.The production of superoxide was similar in the three groups when neutrophils were not stimulated.After stimulation with opsonized zymosan,there was an increase in the production of superoxide from patients with acute alcoholic hepatitis in comparison to those with alcoholic liver disease and controls. This increase was statistically significant when fMLP was the stimulant(p<0.05). This is a reliable technique that can be use in the evaluation of different therapeutic modalities in acute alcoholic hepatitis
RESUMEN
Actualmente, la relación entre consumo de alcohol y el desarrollo de daño hepático está claramente definida. Sin embargo, también debe considerarse la influencia de los factores genéticos, la existencia de enfermedades asociadas y el uso concomitante de otros agentes hepatotóxicos. Durante el etilismo crónico se producen grandes cantidades de radicales libres de oxígeno, se altera el equilibrio redox y se sobrepasa la capacidad defensiva de los antioxidantes naturales. Todos estos factores originan "stres oxidativo", que distorciona completamente la función hepatocelular. Asismismo, el incremento en la concentración intracelular de acetaldehido, modifica diversas proteinas celulares, lo que deteriora aún más la actividad hepática. Está aún por definirse la importancia de los "neoantígenos", entre componentes celulares y el acetaldehido, así como su rol en la formación de los cuerpos de Mallory. por otro lado, la complicada red de comunicaciones inter e intracelulares que comprende a las citoquinas, a las moléculas de adherencia y a los receptores de membrana son elementos indispensables a considerar en la génesis de la hepatopatía alcohólica. La endotoxina, el TNF-a, la IL-8, así como la producción de ROIs son al parecer los factores más importantes. En relación a hepatitis alcohólica, el desarrollo de una respuesta inflamatoria exagerada y mediada por neutrófilos sería el mecanismo básico de injuria hepatocelular. El diagnóstico definitivo de hepatitis alcohólica es histológico. Este permite además, graduar la severidad del daño y determinar la presencia de fibrosis y/o cirrosis en cuyo caso el pronóstico es más sombrío. Clínicamente el diagnóstico puede plantearse teniendo el antecedente de ingesta exagerada de alcohol. Existe gran variabilidad en el cuadro clínico, y no es infrecuente que algunos pacientes presenten las complicaciones de la hepatopatía crónica. Los que desarrollan insuficiencia hepática severa, presentarán leucocitosis, ictericia y fiebre. En estos casos la mortalidad puede llegar hasta 80 por ciento. La alteración de las pruebas de función hepática no guardan relación con al severidad del daño. La utilidad de los antioxidantes en cirrosis ha sido demostrada en modelos animales y en algunos estudios en voluntarios humanos. Su rol como terapia en el contexto de hepatitis alcohólica, esta por ser definida...
Asunto(s)
Hepatitis Alcohólica/diagnóstico , Hepatitis Alcohólica/terapiaRESUMEN
At present, the relation between alcoholic consumption and the development of hepatic injury is clearly defined. However, the influence of genetic factors, the existence of associated pathologies, and the concomitant use of other hepatotoxic agents should also be considered.During chronic drunkenness, great quantities of oxygen free radicals are produced, redox balance is disturbed, and the defensive capacity of natural antioxidants is exceeded. All these factors originate an "oxidative stress," that totally distorts the hepatocellular function. Llkewise, an increase in the acetaldehyde intracellular concentration modifies several cellular proteins, deteriorating even more the hepatic activity. The importance of the "neo-antigens" between cellular components and acetaldehyde is still undefined, as well as their role in the formation of the Mallory Bodies.On the other hand, the complex network of intercellular and intracellular communications that includes cytokines, adherence molecules and membrane receptors are essential elements to be considered in the alcoholic liver disease genesis. The endotoxin, the TNF-a, the IL-8, as well as the ROIs production seem to be the most important factors.With reference to Alcoholic Hepatitis, the development of an exaggerated inflammatory response with the existence of neutrophiles may be the main mechanism of hepatocellular injury (82, 167, 168.)The final diagnosis of Alcoholic Hepatitis is histological. This also enables to measure the injury severity and to determine the presence of fibrosis and/or cirrhosis, in which case prognosis is more uncertain.Should a history of exaggerated alcoholic ingestion exist, diagnosis could be clinically determined. There is a great variability of clinical symptoms, and some patients present chronic liver disease complications frequently. Those who develop severe liver insufficiency will present leukocytosis, icterus and fever. In these cases, mortality can be as high as 80 per cent. There is no relationship between the alteration of liver function tests and the injury severity.The usefulness of antioxidants in cirrhosis has been demonstrated in animal modeis and in some studies made in human voluntarles. However, their role as therapy within the context of Alcoholic Hepatitis has not been yet defined.In conclusion, several therapeutic approaches have been investigated and from all of them, only steroids have proven to be effective on patients properly selected. The discriminative function (DF) benefit has been confirmed in certain studies. Should a patient have a DIF of more than 93, he/she may receive corticosterold treatment. Contral ndicati ons are a bsol ute when the patientpresents infection, renal insufficiency or gastrointestinal bleeding.Once the patient has been compensated, ABSTINENCE is essential. Likewise, an appropriate nutritional support is an important part of the treatment.Where the possibility of Liver Transplant exists, this should be planned if there is a deterioration of the patient's general condition or if he/she compiles with the necessary criteria, since the survival rate in these cases is similar to those who received a transpiant due to other causes.
RESUMEN
La formación de una conexión extrapilórica no quirúrgica entre el antro gástrico y el bulbo duodenal está en investigación en los últimos veinte años. Expresiones tales como "píloro doble" "pseudopíloro", "úlcera en tunel", "diafragma pilórico" y "banda mucosa antral" probablemente describen la misma lesión. Reportamos 3 casos con evidencia radiológica y endoscópica.