Non-alcoholic steatohepatitis (NASH) is considered the advanced stage of non-alcoholic fatty liver disease (NAFLD). It is characterized by liver steatosis, inflammation and different degrees of fibrosis. Although the exact mechanisms by which fatty liver progresses to NASH are still not well understood, innate and adaptive immune responses seem to be essential key regulators in the establishment, progression, and chronicity of these disease. Diet-induced lipid overload of parenchymal and non-parenchymal liver cells is considered the first step for the development of fatty liver with the consequent organelle dysfunction, cellular stress and liver injury. These will generate the production of pro-inflammatory cytokines, chemokines and damage-associated molecular patterns (DAMPs) that will upregulate the activation of Kupffer cells (KCs) and monocyte-derived macrophages (MMs) favoring the polarization of the tolerogenic environment of the liver to an immunogenic phenotype with the resulting transdifferentiation of hepatic stellate cells (HSCs) into myofibroblasts developing fibrosis. In the long run, dendritic cells (DCs) will activate CD4+ T cells polarizing into the pro-inflammatory lymphocytes Th1 and Th17 worsening the liver damage and inflammation. Therefore, the objective of this review is to discuss in a systematic way the mechanisms known so far of the immune and non-proper immune liver cells in the development and progression of NASH.

Introduction: With the successes of antiretroviral therapy, patients infected with human immunodeficiency virus (HIV) living longer. Regarding this, the common diseases of HIV population (i.e., opportunistic infections) are now losing ground in front of metabolic alterations. This phenomenon is related to the delay in progression to acquired immune deficiency syndrome (AIDS), making it so that patients live in a chronic inflammatory state which, combined with other mechanisms such infectious ones, cause metabolic diseases. Areas covered: Considering a high prevalence of metabolic alterations, the relationship between metabolic syndrome (MetS) with nonalcoholic fatty liver disease (NAFLD) and nonalcoholic steatohepatitis (NASH), and liver diseases as a major cause of death in the HIV-infected population, this paper aims to overview the mechanisms and prevalence of NAFLD and NASH as they relate to the developed metabolic diseases of HIV patients. Expert opinion: The pathways underlying MetS include the effects of HIV and ART on the liver, adipose tissue, and muscle. These mechanisms result in liver damage, consequently leading to NAFLD and its more severe form NASH. These conditions have increased in HIV-infected population in recent years and since their life expectancy is improving it is important to be ready to attend their new emerging diseases.

Chronic hepatitis C virus infection is an important cause of liver cirrhosis, hepatocellular carcinoma and death. Furthermore, it is estimated that about 40–70% of patients develop non-hepatic alterations in the course of chronic infection. Such manifestations can be immune-related conditions, lymphoproliferative disorders and metabolic alterations with serious adverse events in the short and long term. The introduction of new Direct-Acting Antivirals has shown promising results, with current evidence indicating an improvement and remission of these conditions after a sustained virological response.

Cholestasis is a condition characterized by decrease in bile flow due to progressive pathological states that lead to chronic cholestatic liver diseases which affect the biliary tree at the intrahepatic level and extrahepatic level. They induce complications such as cirrhosis, liver failure, malignancies, bone disease and nutritional deficiencies that merit close follow-up and specific interventions. Furthermore, as those conditions progress to liver cirrhosis, there will be an increase in mortality but also an important impact in quality of life and economic burden due to comorbidities related with liver failure. Therefore, it is important that clinicians understand the treatment options for cholestatic liver diseases. With a general view of therapeutic options and their molecular targets, this review addresses the pathophysiology of cholangiopathies. The objective is to provide clinicians with an overview of the safety and efficacy of the treatment of cholangiopathies based on the current evidence.

Impairments in liver function lead to different complications. As chronic liver disease progresses (CLD), hypoalbuminemia and alterations in bile acid compositions lead to changes in gut microbiota and, therefore, in the host–microbiome interaction, leading to a proinflammatory state. Alterations in gut microbiota composition and permeability, known as gut dysbiosis, have important implications in CLD; alterations in the gut–liver axis are a consequence of liver disease, but also a cause of CLD. Furthermore, gut dysbiosis plays an important role in the progression of liver cirrhosis and decompensation, particularly with complications such as hepatic encephalopathy and spontaneous bacterial peritonitis. In relation to this, antibiotics play an important role in treating CLD. While certain antibiotics have specific indications, others have been subjected to continued study to determine whether or not they have a modulatory effect on gut microbiota. In contrast, the rational use of antibiotics is important, not only because of their disrupting effects on gut microbiota, but also in the context of multidrug-resistant organisms. The aim of this review is to illustrate the role of gut microbiota alterations in CLD, the use and impact of antibiotics in liver cirrhosis, and their harmful and beneficial effects.

La encefalopatía hepática (EH) es una complicación frecuente en pacientes con cirrosis hepática y se asocia a una alta tasa de mortalidad. Los costos atribuidos al manejo de pacientes con cirrosis son especialmente elevados debido a complicaciones como la EH puesto que prolongan los días de estancia hospitalaria. Actualmente para el tratamiento de la EH, existen diferentes fármacos de los cuales los principales son la lactulosa, L-ornitina, L-aspartato (LOLA) y ciertos antibióticos, especialmente la rifaximina-α (RFX). Aunque muchos de ellos han demostrado ser efectivos en mayor o menor medida, es importante contar con información que permita discernir sobre uno y otro con el objetivo de individualizar el tratamiento al paciente y elegir la mejor opción en diferentes escenarios. Por lo anterior, el objetivo de este estudio fue analizar la evidencia sobre las ventajas y desventajas del uso individual o en combinación de los 3 principales tratamientos de la EH, específicamente su eficacia en los diferentes grados, su impacto en la calidad de vida, profilaxis y reducción de costos. Hepatic encephalopathy is a frequent complication in patients with cirrhosis of the liver and is associated with a high mortality rate. Costs attributed to the management of patients with cirrhosis are especially high due to complications, such as hepatic encephalopathy, given that they increase the number of days of hospital stay. Different drugs are currently used to treat hepatic encephalopathy, and the main ones are lactulose, L-ornithine L-aspartate (LOLA), and certain antibiotics, especially rifaximin-α (RFX). Even though many of them have been shown to be effective to greater or lesser degrees, it is important to understand the differences between them, so that every patient receives individualized treatment and the best option is chosen, in accordance with the different clinical scenarios. Thus, the aim of the present study was to analyze the evidence on the advantages and disadvantages of the individual or combined use of the 3 main treatments for hepatic encephalopathy, specifically taking into consideration their different degrees of efficacy, their impact on quality of life, prophylaxis, and cost reduction.