Nonalcoholic fatty liver disease and nonalcoholic steatohepatitis in HIV infection: a metabolic approach of an infectious disease.

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.

Current trends of liver cirrhosis in Mexico: Similitudes and differences with other world regions.

AIM: To investigate the main current etiologies of cirrhosis in Mexico. METHODS: We performed a cross-sectional retrospective multicenter study that included eight hospitals in different areas of Mexico. These hospitals provide health care to people of diverse social classes. The inclusion criteria were a histological, clinical, biochemical, endoscopic, or imaging diagnosis of liver cirrhosis. Data were obtained during a 5-year period (January 2012-December 2017). RESULTS: A total of 1210 patients were included. The mean age was 62.5 years (SD = 12.1), and the percentages of men and women were similar (52.0% vs 48.0%). The most frequent causes of liver cirrhosis were hepatitis C virus (HCV) (36.2%), alcoholic liver disease (ALD) (31.2%), and nonalcoholic steatohepatitis (23.2%), and the least frequent were hepatitis B virus (1.1%), autoimmune disorders (7.3%), and other conditions (1.0%). CONCLUSION: HCV and ALD are the most frequent causes of cirrhosis in Mexico. However, we note that non-alcoholic fatty liver disease (NAFLD) as an etiology of cirrhosis increased by 100% compared with the rate noted previously. We conclude that NAFLD will soon become one of the most frequent etiologies of liver cirrhosis in Mexico.

New Aspects of Lipotoxicity in Nonalcoholic Steatohepatitis.

NASH is becoming increasingly common worldwide because of the growing global prevalence of obesity and consequently NAFLD. Unfortunately, the mechanism of progression of NAFLD to NASH and then cirrhosis is not completely understood. Several factors, including insulin resistance, inflammation, oxidative stress, lipotoxicity, and bile acid (BA) toxicity, have been reported to be associated with NASH progression. The release of fatty acids from dysfunctional and insulin-resistant adipocytes results in lipotoxicity, which is caused by the ectopic accumulation of triglyceride-derived toxic metabolites and the subsequent activation of inflammatory pathways, cellular dysfunction, and lipoapoptosis. Adipose tissue (AT), especially visceral AT, comprises multiple cell populations that produce adipokines and insulin-like growth factor, plus macrophages and other immune cells that stimulate the development of lipotoxic liver disease. These biomolecules have been recently linked with many digestive diseases and gastrointestinal malignancies such as hepatocellular carcinoma. This made us question what role lipotoxicity has in the natural history of liver fibrosis. Therefore, this review focuses on the close relationship between AT and NASH. A good comprehension of the pathways that are related to dysregulated AT, metabolic dysfunction, and hepatic lipotoxicity will result in the development of prevention strategies and promising therapeutics for patients with NASH.