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Enfermedad Hepática Alcohol
- 3. Manos M, et al. Limitations of Conventionally Derived Chronic Liver Disease Mortality Rates: Results of a Comprehensive assessment. Hepatology , 2008 HCV 13% Mortalidad (excluyendo m. por HCC) según la etiologia Mortalidad en pacientes con Hepatopatia crónica El 61% de muertes en hepatopatas crónicos (73%, si se excluye mortalidad por HCC) se produjo en pacientes con hepatopatía alcohólica
- 4. Descompensación y mortalidad en CH por Alcohol Jepsen P. Clinical Course of Alcoholic Liver Cirrhosis: A Danish Population-Based Cohort Study, Hepatology, 2010 E.Hepática Ascitis y Hemorragia digestiva Se produce un incremento importante en la mortalidad al iniciarse las descompensaciones
- 5. Espectro de la lesión hepática por alcohol Gao B, et al. Alcoholic Liver Disease: Pathogenesis and New Therapeutic Targets. Gastroenterology, 2011 Progresión Severidad
- 6. Cantidad de alcohol ingerida e incidencia de cirrosis Mann RE et al. The epidemiology of alcohol liver disease. Alcohol Research & Health, 2003 * * * * CONSUMO DE RIESGO: Hombres: > 40 g/dia Mujeres: > 25 g/dia Factores de riesgo de progresión
- 7. Otros factores asociados a progresión Raynard B et al. Risk factors of fibrosis in Alcohol induced liver disease. Hepatology, 2002
- 8. Influencia del consumo de alcohol en la progresión de la fibrosis en pacientes con VHC A medida que se incrementa el consumo de alcohol, se incrementa la proporcion de pacientes con estadios mas avanzados de fibrosis. El consumo importante de alcohol (> 50 gr), estaria asociado a mayor fibrosis y cirrosis (p <0,01) % patients Monto A, et al. Risks of a Range of Alcohol Intake on Hepatitis C-Related Fibrosis. Hepatology ,2004. gr of alcohol / day
- 12. ESTEATOSIS HEPATICA ALCOHOLICA Esteatosis macrovesicular Megamitocondrias Esteatosis macro-microvesicular
- 13. Esteatosis: Patogenia Consumo de alcohol incrementa la expresión de SREBP-1c , con el consiguiente aumento de enzimas lipogénicas y síntesis de ácidos grasos. Por otro lado disminuye la expresión del PPAR-α, disminuyendo la β – oxidación de AG . SREBP : sterol regulatory element-binding protein (proteínas que se unen a elementos reguladores de esteroles) PPAR- α: peroxisome proliferator-activated receptor ( receptores activados de proliferación de los peroxisomas) Gao B, et al. Alcoholic Liver Disease: Pathogenesis and New Therapeutic Targets. Gastroenterology, 2011
- 15. Balonización Fibrosis perivenular HTP sin cirrosis HEPATITIS ALCOHOLICA Infiltrado por PMN Hialina de Mallory
- 16. Sistema inmune Innato: Activación de las células de Kupffer, células esteladas y hepatocitos. infiltración de neutrófilos y macrófagos) Sistema Inmune adaptativo: El alcohol induce la producción de especies reactivas de oxigeno y proteinas (adductos) que sirven de neoantigenos . infitración de linfocitos T y B. Hepatitis Alcohólica Patogenia: Gao B, et al. Alcoholic Liver Disease: Pathogenesis and New Therapeutic Targets. Gastroenterology, 2011 Serum level of cytokines: TNF-α, IL-1, IL-6 and IL-8 are elevated in acute alcoholic hepatitis. Studies have shown a linear relationship between TNF-α receptors and mortality from AAH [9].
- 19. Tratamiento Corticoides y pentoxifilina: solo en HA severa
- 20. Maddrey Discriminant Function: MDF = 4,6 * (TP paciente (seg) - TP control (seg) ) + bilirrubina (mg /dl) Mal pronóstico : MDF >=32 MELD MELD = 3,8*loge(bilirrubina, mg/dl) + 11,2*loge(INR) + 9,6*loge (creatinina, mg/dl) + 6,4 Mal pronóstico: MELD > 18 Alcoholic Liver Disease. O’Shea R et al. AASLD Practice Guidelines. Hepatology. 2010 H. Alcohólica: Scores predictores de mortalidad
- 21. Alcoholic Liver Disease. O’Shea R et al. AASLD Practice Guidelines. Hepatology. 2010
- 22. Corticoides en el tratamiento de HA (corticoides vs placebo) Rambaldi A, et al. Systematic review: glucocorticosteroids for alcoholic hepatitis – a Cochrane Hepato-Biliary Group systematic review with meta-analyses and trial sequential analyses of randomized clinical trials. Aliment Pharmacol Ther, 2008. Corticoides: Reducción de citoquinas pro-inflamatorias, factor de necrosis tumoral-α (TNF-α), IL-1, IL-8, moléculas de adhesión celular (ICAM-1), formacion de neoantigenos.
- 23. Corticoides en el tratamiento de HA (corticoides vs placebo) Rambaldi A, et al. Systematic review: glucocorticosteroids for alcoholic hepatitis – a Cochrane Hepato-Biliary Group systematic review with meta-analyses and trial sequential analyses of randomized clinical trials. Aliment Pharmacol Ther, 2008.
- 24. Pentoxifilina: Inhibidor de la fosfodiesterasa, con incrementado de AMPc lo que reduce la expresion: TNF-α, IL1, IL6; contraregulador de TGF-β, genes sintetizan pro-colageno Whitfield K et al. Pentoxifylline for alcoholic hepatitis (Review), The Cochrane Collaboration. 2009 M:P: (24% vs. 38%) 42/ 63/
- 25. Otros fármacos: . Anti TNF- α (infliximab, estudios comparatativos con esteroides demostraron mayor mortalidad en grupo de infliximab) . Silimarina, N- acetilcisteina, vitamina E, vitamina A (antioxidante) . Propiltiouracilo (modula el consumo de O2 a nivel del tejido hepático) . Colchicina (inhibidor de la síntesis del colágeno) . Fosfatidil colina (lecitina poliinsaturada que impide la activación de las células esteladas) En general los estudios tienen “n” bajas, en la mayoría de casos se compara la efectividad del fármaco con placebo, se valoran diferentes variables principales (ej. Mejoría en determinada escala, otros mortalidad), diferentes periodos de seguimiento; esto dificulta valorar la eficacia y seguridad real de cada fármaco.
- 27. Fibrosis cirrosis Patogenia Activación directa de las celulas esteladas por el acetaldehido. Los LPS activarian a las células esteladas via TGF-b directamente o previa activación de las celulas de Kupffer Las celulas NK activadas destruirian células esteladas activadas e inhibirian su proliferación via INF-gama y TRAIL, via inhibida por el alcohol Gao B, et al. Alcoholic Liver Disease: Pathogenesis and New Therapeutic Targets. Gastroenterology, 2011
- 32. 2.Pacientes descompensados: 2.1. Ascitis 2.2. Encefalopatia hepática 2.3. Sangrado variceal. 2.4. Peritonitis bacteriana espontanea 2.5. Sindrome hepatorenal. 2.6. Sindrome hepatopulmonar. 2.7. Carcinoma hepatocelular 2.8. Otros problemas: Hidrotorax hepatico, prurito severo o intratable, hepatitis alcoholica sobre cirrosis
- 33. Manejo de las complicaciones Lactulosa Neomicina Rifaximina Dieta Diureticos Paracentesis c/ albumina Antibióticos (PBE) TIPS Propranolol Terlipresina Endoligadura TIPS Etanolización (PEI) Radiofrecuencia Quimioembolización Resecciones quirúgicas Polaramine… Colestiramina Naltrexona MARS
- 34. Complicaciones y mortalidad en CH por Alcohol Clinical Course of Alcoholic Liver Cirrhosis: A Danish Population-Based Cohort Study Peter Jepsen, HEPATOLOGY, 2010 Encefalopatia Hepatica Ascitis y sangrado digestivo Mortalidad importante cuando desarrollan descompensacion
- 35. Pacientes con enfermedad hepatica terminal secundaria a alcohol deben considerarse para trasplante hepatico (TH) como cualquier otro paciente con enfermedad heaptica descompensada despues de una cuidadosa evaluación médica psicologica –psquiatrica que debe incluir un control formal de abstinencia. Los criterios mínimos de inclusión en lista son: Child ≥7, con una estimacion de sobrevida al año sin TH de menos del 50% , un episodio de PBE o presencia de EH grado (2) En caso de hepatocarcinoma, son suceptibles de TH los pacientes que cumplan con los criterios de Milan (1 nodulo < 5 cm, o no mas de 3 nodulos, menores de 3 cm, en ausencia de diseminacion extrahepatica) Robert S. O’Shea et al. Alcoholic Liver Disease. Hepatology, 2010. AASLD PRACTICE GUIDELINES Vibha Varma, et al. Liver transplantation for alcoholic liver disease World J Gastroenterol. 2010
- 37. Varma V, et al. Liver transplantation for alcoholic liver disease. World J Gastroenterol 2010. Indicaciones de TH según el ELTR (European Liver Transplant Register) 2008
- 38. Sobrevida despues de TH en pacientes con ALD, PBC y cirrosis viral Viral PCB Alcohol
- 40. GRACIAS
Notas del editor
- We investigated the CRONIC LIVER DISEASE MORTALITY (CLD) mortality rate and associated etiologies (derived from medical records) in a large managed care health plan. From the 16,970 deaths among health plan members in 2000, we confirmed 355 (2.1%) as CLD related, including 75 with HCC. STUDY based on medical records . The age-adjusted CLDmortality rate using the comprehensive codes was 11.9 per 100,000. Based on medical records, the underlying CLD was attributed to alcoholic liver disease (ALD) in 44% of deaths, HCV infection with ALD in 16%, HCV without ALD in 18%, and chronic HBV infection in 7%. Only 64% of HCV-associated, 48% of HBV-associated, and 64% of ALD-associated deaths ascertained by medical record had that specific etiology mentioned on the death certificate. Conclusion: CLD mortality burden was almost doubled by using a comprehensive list of mortality codes and considering HCC deaths as CLD related. Furthermore, the contributions of viral hepatitis and ALD to CLD mortality may be underestimated if based solely on death records. (HEPATOLOGY 2008;47…)
- JEPSEN, HEPATOLOGY 2010 The clinical course of alcoholic cirrhosis, a condition with a high mortality, has not been well described. We examined prevalence, risk, chronology, and mortality associated with three complications of cirrhosis: ascites, variceal bleeding, and hepatic encephalopathy We followed a population-based cohort of 466 Danish patients diagnosed with alcoholic cirrhosis in 1993-2005, At diagnosis of alcoholic cirrhosis, 24% of patients had no complications, 55% had ascites alone, 6% had variceal bleeding alone, 4% had ascites and variceal bleeding, and 11% had hepatic encephalopathy. One-year mortality was 17% among patients with no initial complications, 20% following variceal bleeding alone, 29% following ascites alone, 49% following ascites and variceal bleeding (from the onset of the later of the two complications), and 64% following hepatic encephalopathy. Five-year mortality ranged from 58% to 85%. The risk of complications was about 25% after 1 year and 50% after 5 years for all patients without hepatic encephalopathy. Although patients initially without complications usually developed ascites first (12% within 1 year), many developed either variceal bleeding first (6% within 1 year) or hepatic encephalopathy first (4% within 1 year). Subsequent complications occurred in an unpredictable order among patients with ascites or variceal bleeding. Conclusion: Patients with alcoholic cirrhosis had a high prevalence of complications at the time of cirrhosis diagnosis. The presence and type of complications at diagnosis were predictors of mortality, but not of the risk of subsequent complications.
- REVISION, GAO El espectro de la lesion hepatica por alcohol es amplio Asi de ha descrito que entre el 90 – 95% de las personas con ingesta significativa de Oh desarrolla esteatosis, de ellos SOLO entre un 20-40%, desarrollaran otras formas mas severas de ALD , como fibrosis, cirrosis y HCC En la progresión a formas más severas de ALD , ademas del consumo de alcohol persistente, intervendrian diferentes factores de riesgo (sexo, obesidad, tabaco,polimorfismos genéticos .. ) y enfermedades asociadas en particular las hepatitis virales (VHC)
- UNO DE LOS FACTORES ASOCIADOS A PROGRESION CON DESARROLLO DE CIRROSIS SERIA EL CONSUMO PERSISTENTE Y DE CANTIDADES IMPORTANTES DE ALCOHOL. Diferentes estudios realizados a finales de los años 80 demostraban que a mayor cantidad de alcohol ingerida mayor riesgo de desarrollo de cirrosis; COMO SE VE en la diapositiva y en “*” rojos, (mujeres) esto se producia cuando la ingesta estaba entre 25-35 gr /dia de OH Y en “*” azul , (varones) cuando la ingesta estaba entre el 45-50 g/ dia. ACTUALMENTE se acepta como que el consumo de riesgo seria >=40 g / dia en varones y 25 gr/dia en mujeres.
- FACTORES CLINICOS ASOCIADOS A PROGRESION A FIBROSIS …. Demostro que esto era mas frecuente en mujeres, mayores, con BMI alto, consumo (terminos de duracion) mas importante de alcohol, tendencia a hiperglicemias y deposito de hierro en la biopsia hepatica.
- El consumo de OH influiria aceleraria la fibrosis en pacientes con VHC; en este estudio se evaluo el grado de fibrosis en pacientes con HVC, clasificados segun el grado de consumo de OH. Entonces, en el eje x tenemos el consumo de OH en gr/ dia, en el eje “y” el % de pacientes , Los estadios de fibrosis estan representados por barras de diferentes colores, desde FO: ausencia de fibrosis, EN GEIGE, F!: fibrosis incipiente hasta fibrosis importante con nodulos en el F4. Observamos que los de pacientes con mayor consumo de alcohol, presentaban mayor grado de lesion histologica en la biopsia hepatica. Solo el Heavy alcohol use (more than 50 g daily) worsens fibrosis and increases risk of cirrhosis . Heavy alcohol intake (50 g daily) during therapy leads to lower response rates to antiviral therapy Cessation of heavy alcohol intake improves response to antiviral therapy abstinence from alcohol is recommended during therapy Alcohol intake was associated with a stepwise increase in mean fibrosis in the cohort overall (Table 3), and if alcohol use was dichotomized into 50 g/day vs. 50 g/day, there was a difference in mean fibrosis between the two groups (P .01).
- Genes or environment to determine alcoholic liver disease and non-alcoholic fatty liver disease Abstract: While the vast majority of heavy drinkers and individuals with obesity, insulin resistance, and the metabolic syndrome will have steatosis, only a minority will ever develop steatohepatitis, fibrosis, and cirrhosis. Genetic and environmental risk factors for advanced alcoholic liver disease (ALD) and non-alcoholic fatty liver disease (NAFLD) seem likely to include factors that influence the severity of steatosis and oxidative stress, the cytokine milieu, the magnitude of the immune response, and/or the severity of fibrosis . For ALD, the dose and pattern of alcohol intake, along with obesity are the most important environmental factors determining disease risk. For NAFLD, dietary saturated fat and antioxidant intake and small bowel bacterial overgrowth may play a role. Family studies and interethnic variations in susceptibility suggest that genetic factors are important in determining disease risk. For ALD, functional polymorphisms in the alcohol dehydrogenases and aldehyde dehydrogenase alcohol metabolising genes play a role in determining susceptibility in Oriental populations. No genetic associations with advanced NAFLD have been replicated in large studies. Preliminary data suggest that polymorphisms in the genes encoding microsomal triglyceride transfer protein, superoxide dismutase 2, the CD14 endotoxin receptor, TNF-a, transforming growth factor-b, and angiotensinogen may be associated with steatohepatitis and/or fibrosis
- Cohen SM, et al. Review article: the diagnosis and management of alcoholic Hepatitis. Aliment Pharmacol Ther , 2009, NUTRICION: It has been recommended to provide B-vitamins (especially thiamine: B1; B6:piridoxina), folic acid and vitamin K at several times the minimum daily allowance. 53 It is common to provide these intravenously for the first few days. Daily oral multimineral supplementation (without iron) should also be provided. Most patients are deficient in zinc, probably due to decreased oral intake and increased urinary loss.56, 57 In animal models of alcoholic liver disease, zinc replacement prevents apoptosis and translocation of bacteria across the small intestines.58 Thus, zinc replacement at a dose of approximately 200 mg⁄ day should also be considered. The optimal duration of vitamin and mineral support is not established, but it is reasonable to continue these for at least 6 months, with oral zinc continuing for 12 months or longer. The general consensus is that nutritional support results in a more rapid improvement in liver disease, but does not improve survival Nutritional support consists of 1.2–1.5 g of protein and an energy intake of 35–40 kcal ⁄ kg of ideal body
- Existen varios scores pronósticos de mortalidad que en la practica clinica se utilizan para discriminar la mayor o menor severidad. Se ha recomendado el uso del score de Maddrey y el MELD, puntajes altos serian indicadores de mayor severidad, asociandose a mal pronostico un puntaje > 32 Maddrey y en el caso del MELD un valor > 18 EL TRATAMEINTO DE LA HA DEPENDERA DE LA GRAVEDAD DE LA ENFERMEDAD
- PREDNISOLONA: The drug is given orally in a dose of 40-60 mg/d for a total duration of 4 wk. The treatment is then tapered over next 2-3 wk. If the patient is unable to take it orally due to nausea, vomiting or altered sensorium, an intravenous preparation such as methylprednisolone may be used until the patient is capable to take medication by mouth. It is prudent to screen patients for any contraindication prior to starting steroids. One of the most important contraindications is the presence of infection which is fairly common among patients with severe AH. This Other contra-indications are an active gastrointestinal bleeding, renal failure, acute pancreatitis, active tuberculosis, uncontrolled diabetes and psychosis Patients should be assessed for response to steroids. It has been shown that a decrease in bilirubin at 1 wk (early change in bilirubin, ECBL) is a reliable and specific marker for response. Existe un score que evalua la respuesta a la 1 semana post esteroides, (score de lille) , Patients with a Lille score of ≥ 0.45 are defined as non-responders to steroids (NRS). De todos los tratamientoa para HA los corticoides shan sido los framacos mas extensaemente estudiados, aunque su eficacia es controvertida. No todos los estudios han demostrado la superioridad del farmaco frente a placebo (5 si, 8, era igual)
- De todos los tratamientoa para HA los corticoides shan sido los framacos mas extensaemente estudiados, aunque su eficacia es controvertida. No todos los estudios han demostrado la superioridad del farmaco frente a placebo (5 si, 8, era igual)
- UN METANALISIS RECIENTE HA EVALUADO LA SEGURIDAD Y EFICACIA DEL USO DE LA PENTOXIFILINA EN LA H.A. 5 ESTUDIOS, EN TODOS LOS CASOS SE DEMOSTRO MENOR MORTALIDAD AL COMPARAR p VS CONTROL. OBSERVACIONES: I) POCOS PACIENTES, 2) DOSIS DE PENTOXIFILINA NO SIMILAR EN TODOS LOS ESTUDIOS, 3) METODOLOGIA NO CLARA EN ALGUNOS DE ELLOS. 1.- Akriviadis: Pentoxifina – placebo (P:400 mg c /8h, por 28 dias) Primary outcome measure(s): 28-day survival and progression to hepatorenal syndrome. 12/50 (24%) in pentoxifylline group died. 24/52 (46%) in control group died. Hepatorenal syndrome developed in 6/50 (21%) in pentoxifylline group and 22/52 (42%) in control group. 2.- Lebrec: Pentoxifilina – placebo (P:400 mg c /8h, no duracion en el estudio) Primary outcome measure(s): death at 2 months. In the subgroup with severe alcoholic hepatitis of those who received pentoxifylline 14% died, and of those who received; control 46% died within 2 months. No claro en el resto de cosas… llamadas al autor para aclarar … 3.- Mc Hutchinson, 10 / 12 pac) Intervention: pentoxifylline 1200 mg once a day, orally, 10 days.Control: standard treatment. Thirty day mortality was higher in controls compared to treated patients (1 vs 3, p = not significant)” 4.- Padalagu: Intervention: dose and regimen of pentoxifylline not described, duration 4 weeks. Control: placebo. Primary outcome measure(s): end-of-study survival or hepatorenal syndrome. 4/14 in the pentoxifylline group died, and 7/16 in the control group died. 5.- Sidhu: Intervention: pentoxifylline 400 mg three times a day, orally, 28 days. Control: placebo. short-term survival. 6/25 in the pentoxifylline group died, and 10/25 in the control group died.
- PENTOXIFILINA: Recently, pentoxifylline, a non-specific phosphodiesterase inhibitor, with combined anti-inflammatory ( TNF-α inhibition ) and antifibrogenic properties, has been found to be useful in patients with acute alcoholic hepatitis with DF ≥ 32[15-17]. The beneficial effects are believed to occur through various mechanisms such as inhibition of phosphodiesterases, increased cAMP levels and downregulation of TNF-α, IL-1, IL-6, transforming growth factor-beta (TGF-β), interferon-gamma (IFN-γ), stellate cell activation and procollagen-Ⅰ mRNA expression[ 18 Patients in group Ⅰ received pentoxifylline (Trental tablets, Sanofi Aventis, Mumbai, India) at a dose of 400 mg thrice daily orally and a placebo tablet in the place of prednisolone for the first 4 wk. Patients in group Ⅱ received prednisolone tablet (Wysolone, Wreath, Mumbai, India) at a dose of 40 mg once daily for 4 wk and a placebo tablet taken thrice daily in place of pentoxifylline for the same duration.
- Cirrosis Debe exitir depósito en el hígado de fibras de colágeno, pero para que se pueda hacer el diagnóstico anatomopatológico de cirrosis, este acúmulo de fibras ha de delimitar nódulos, es decir, ha de aislar áreas de tejido hepático, alterando la arquitectura del órgano y dificultando la relación entre los hepatocitos y los finos vasos sanguíneos a través de los cuales ejercen su función de síntesis y depuración y a través de los cuales se nutren La cirrosis hepática es una enfermedad que se caracteriza por una distorsión irreversible de la arquitectura hepática y una exacerbada acumulación de fibrosis con formacion de NR; incremento en los depósitos de proteínas de matriz extracelular (MEC), fundamentalmente colágenas tipo I, III y IV en el espacio perisinusoidal o «de Disse», lo que dificulta el intercambio de substancias entre el sinusoide y los hepatocitos (Figura 2)1-4. Las manifestaciones clínicas se atribuyen a la disfunción hepatocelular progresiva e hipertensión portal5. .
- La cirrosis es la fibrosis que ha progresado provocando una distorsión generalizada de la arquitectura hepática normal con intentos de regeneración de los hepatocitos para reemplazar la pérdida. VER PASO DE FIBROSIS A CIRROSIS !!!!
- JEPSEN, HEPATOLOGY 2010 The clinical course of alcoholic cirrhosis, a condition with a high mortality, has not been well described. We examined prevalence, risk, chronology, and mortality associated with three complications of cirrhosis: ascites, variceal bleeding, and hepatic encephalopathy We followed a population-based cohort of 466 Danish patients diagnosed with alcoholic cirrhosis in 1993-2005, At diagnosis of alcoholic cirrhosis, 24% of patients had no complications, 55% had ascites alone, 6% had variceal bleeding alone, 4% had ascites and variceal bleeding, and 11% had hepatic encephalopathy. One-year mortality was 17% among patients with no initial complications, 20% following variceal bleeding alone, 29% following ascites alone, 49% following ascites and variceal bleeding (from the onset of the later of the two complications), and 64% following hepatic encephalopathy. Five-year mortality ranged from 58% to 85%. The risk of complications was about 25% after 1 year and 50% after 5 years for all patients without hepatic encephalopathy. Although patients initially without complications usually developed ascites first (12% within 1 year), many developed either variceal bleeding first (6% within 1 year) or hepatic encephalopathy first (4% within 1 year). Subsequent complications occurred in an unpredictable order among patients with ascites or variceal bleeding. Conclusion: Patients with alcoholic cirrhosis had a high prevalence of complications at the time of cirrhosis diagnosis. The presence and type of complications at diagnosis were predictors of mortality, but not of the risk of subsequent complications.
- Contraindicaciones de TH Las habituales para todos los T Las especificas del OH… Vibha Varma, et al. Liver transplantation for alcoholic liver disease World J Gastroenterol. 2010 The contraindications to listing were those factors , which would result in poor outcome for the graft. (1) Alcoholic, hepatitis (AH) which is a clinical syndrome of jaundice and coagulopathy in the presence of active alcohol intake and not a histological diagnosis is a contraindication for listing; (2) Repetitive episodes (more than 2) of noncompliance with medical care where there was no satisfactory explanation. This should not be confined to management of their liver disease; (3) Return to drinking following full professional assessment and advice (this includes permanent removal from the list if found drinking while listed); and (4) Concurrent or consecutive illicit drug use
- 6 meses: Valorar la funcion hepatica despues de un periodo de abstienecia Identificar a pacientes con riesgo de recidiva post TH
- VARMA: Alcoholic liver disease (ALD) is the second commonest indication for liver transplantation after viral hepatitis in the United States and Europe It is the main indication for orthotopic liver transplantation (OLT) in males and after viral hepatitis, is the second commonest indication overall in the United States and Europe[2] (Figures 1-4). ALD accounts for approximately 17%-25% of all transplants performed in the United States and Europe[3,4]. Without transplant 5-year survival in patients with ALD is as low as 23% which improves to 88% with OLT[1,5].