Minimal hepatic encephalopathy identifies patients at risk of faster cirrhosis progression.

BACKGROUND AND AIM: Minimal hepatic encephalopathy (MHE) predicts poor prognosis and could reflect an advanced liver disease. We aimed to assess whether MHE could be a surrogate marker of a further liver disease. METHODS: Prospective multicenter study including 320 cirrhotic patients, followed for up to 5 years, which were classified at baseline in compensated cirrhosis without (stage 1) and with varices (stage 2), one decompensating event (stage 3), and any second decompensating event (stage 4). Cirrhosis progression was defined by a transition towards a different stage (competing events: liver transplant due to hepatocellular carcinoma and non-liver-related death). MHE was detected by critical flicker frequency and psychometric tests. RESULTS: Minimal hepatic encephalopathy was diagnosed in 18.2% (57/314) of patients. Cirrhosis progression occurred in 38.1% (122/320) of patients, while liver transplant was required in 10.9% (35/320), and 19.1% (61/320) died. In competing risk regression, MHE was associated with disease progression: model 1 {subhazard ratio [sHR] 2.34 [95%confidence interval (CI) 1.58-3.46]; P = 0.0001}; model 2 [sHR 2.18 (95%CI 1.43-3.33); P = 0.0001]; model 3 [sHR 2.48 (95%CI 1.63-3.76); P = 0.0001]. The annual incidence rate of progression was higher in MHE patients: stage 1 (19.4 vs 5.6 cases per 100 person-years); stage 2 (26.8 vs 15.6); stage 3 (45.7 vs 16.5); and stage 4 (40.7 vs 12.8). MHE showed a higher cumulative incidence of disease progression from the first year in decompensated and the third year in compensated cirrhosis. CONCLUSION: Minimal hepatic encephalopathy was associated with cirrhosis progression and showed a higher cumulative and annual incidence rate of disease progression. MHE could be a surrogate marker of disease progression, irrespective of cirrhosis status, identifying patients at risk of suffering a more aggressive cirrhosis form.

Hepatitis B and NAFLD: Lives Crossed.

Hepatitis B virus infection seems to protect against steatosis and insulin resistance decreasing NAFLD. Metabolic syndrome has been associated with increased risk of disease progression to cirrhosis and liver cancer in hepatitis B. HBsAg seroclearance increased over time and it could be a confounding factor when analysing NAFLD and hepatitis B prevalence.

Case Report: Acute-on-Chronic Liver Failure: Making the Diagnosis between Infection and Acute Alcoholic Hepatitis.

Acute-on-chronic liver failure (ACLF) represents a reversible syndrome associated with high short-term mortality, characterized by acute decompensation in patients with chronic liver disease and extrahepatic organ failure. Diagnosis and prognosis assessment is based on a newly developed diagnostic score, the Chronic Liver Failure Consortium Organ Failure score. Susceptibility to infections and systemic inflammation are typical triggers. The authors report a case in which a patient with alcohol-related cirrhosis was admitted to the hospital with acute decompensation and developed ACLF during hospitalization. This case led to an evaluation of the underlying process causing ACLF: infection versus acute alcoholic hepatitis.

Hepatopulmonary Syndrome and Portopulmonary Hypertension: Management in Liver Transplantation in the Horizon 2020.

Hepatopulmonary syndrome (HPS) is characterized by intrapulmonary microvasculature dilatation that causes intrapulmonary shunting and leads to a gas exchange abnormality in the presence of liver diseases, which is the most common cause of respiratory insufficiency in these patients. HPS doubles the risk of death, and liver transplantation (LT) is the only curative therapeutic option so it should be considered in patients with severe HPS, with excellent survival rates post-LT. However, pretransplant Pao2 <45 mm Hg has been associated with an increase in post-transplant morbidity and mortality, but it does not imply a contraindication for LT. The resolution of HPS usually occurs within 6 months post-LT, but it can take 1 year. Portopulmonary hypertension (PoPH) is defined as pulmonary arterial hypertension (PAH) that develops in the setting of portal hypertension with or without liver disease in the absence of other causes of PAH. The prevalence of PoPH is 5% to 10% among liver transplant (LT) candidates. The impact of LT on PoPH is unpredictable. Therefore, despite conferring a high morbidity and mortality, PoPH itself is not an indication for liver transplantation. It may be considered a contraindication for LT in severe cases.

El impacto del tratamiento de la encefalopatía hepática mínima en el pronóstico a largo plazo / The impact of minimal hepatic encephalopathy treatment in long-term prognosis

La encefalopatía hepática mínima (EHm) afecta del 30% al 50% de los pacientes cirróticos. Su detección es esencial por su relación con la encefalopatía hepática clínica, la alteración de la habilidad para conducir, el mayor riesgo de caídas, la alteración de la calidad de vida, la progresión más acelerada de la cirrosis y la supervivencia. A pesar de la información fidedigna de su relevancia clínica, pronóstica y social, la detección de EHm no está generalizada en la práctica clínica. El espectro de la encefalopatía hepática engloba diversas alteraciones de las funciones cerebrales, por lo que se requiere realizar más de un test para su diagnóstico. Además, las alteraciones iniciales difieren de un paciente a otro. Esto ha dificultado el desarrollo de una estrategia diagnóstica universal. Como resultado, no disponemos de datos suficientes para generar recomendaciones basadas en la evidencia del impacto del tratamiento de la EHm en la calidad de vida y la supervivencia, así como de su rentabilidad. Por lo tanto, las guías clínicas actuales sugieren que se evalúe la EHm cuando se afecta la calidad de vida de los pacientes, ya que no se conocen las consecuencias del tamizaje. Las terapias reductoras de amonio se consideran la piedra angular del tratamiento de la EHm. Los disacáridos no absorbibles, la rifaximina y, más recientemente, los probióticos, han mostrado efectos beneficiosos. Se necesitan más ensayos controlados con placebo para evaluar la eficacia, seguridad y rentabilidad de los regímenes de tratamiento disponibles para evaluar el impacto del tratamiento de la EHm en el pronóstico a largo plazo de estos pacientes.

Minimal hepatic encephalopathy (MHE) affects up to 30-50% of cirrhotic patients. The detection of MHE is essential because of its relationship with overt hepatic encephalopathy, impairment of motor vehicle driving abilities, higher risk of falls, quality of life impairment, faster cirrhosis progression and survival. Despite the robust evidence regarding its clinical, prognostic and social relevance, MHE testing is not widespread in routine clinical care. Hepatic encephalopathy spectrum covers various alterations in complex brain functions, requiring more than one test to be quantified. In addition, initial disturbances differ from one patient to another. All this has made it difficult to develop a universal diagnostic strategy. As a consequence, there is a lack of available robust data in the literature to generate evidence-based recommendations related to the impact of MHE treatment on quality of life and survival of these patients, as well as on cost-effectiveness. Therefore, current clinical guidelines suggest MHE testing only when patients have problems with their quality of life, since consequences of the screening procedure are still unclear. Ammonia lowering therapies have been considered the cornerstone of MHE treatment. Beneficial effects of non-absorbable disaccharides (lactulose or lactitol), rifaximin and more recently, probiotics have been reported. Further placebo-controlled trials are needed to assess the efficacy, safety, and cost-effectiveness of available treatment regimes to evaluate the impact of MHE treatment on the long-term prognosis of these patients.