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Recent evidence suggests that the gut microbiota plays a key role in the development of insulin resistance, fatty liver, necro-inflammation and fibrosis through effects on caloric salvage, host energy metabolism, pro-inflammatory signaling and direct hepatotoxicity of bacterial products. In this respect, manipulating enteric flora may represent a potential therapeutic option in the treatment of nonalcoholic fatty liver diseases (NAFLD). Several studies reported that administration of prebiotics (oligosaccharides), probiotics (living microorganisms) and synbiotics (mixture of prebiotics and probiotics) modified the composition of intestinal flora and restored the microbial balance. This review presents a compilation of the scientific evidence found in the last years showing the results of interventions with prebiotics, probiotics or both in the treatment of NAFLD in animals and human.
Acquiring a sustained virological response (SVR) in patients with cirrhosis or advanced hepatic fibrosis reduces liver disease- related mortality and the incidence of hepatocellular carcinoma. However, the SVR rate of the current standard of care, which is combination therapy with peg-interferon-alpha and ribavirin, is significantly lower, and treatment-related complications occur more frequently in patients with cirrhosis. Thus, antiviral treatment should be individualized in this population. This review highlights the issues associated with anti-hepatitis C virus treatment in patients with compensated and decompensated cirrhosis. (Korean J Med 2015;88:643-646)
Recently, the concept of acute-on-chronic liver failure (ACLF) was introduced to describe a specific clinical form of liver failure associated with cirrhosis. The syndrome refers to an acute deterioration of liver function and a rapidly evolving multi-organ failure following a precipitating event in a patient with previously well-compensated cirrhosis. The precipitating events include an indirect (e.g., variceal bleeding, sepsis) and a direct (e.g., drug) hepatotoxin. ACLF is frequently accompanied by the development of severe inflammatory response syndrome and has a high mortality. At present, considerable efforts are ongoing to better characterize this disease entity and to gain further insight into its pathophysiology.
Hepatitis B virus (HBV) infection during pregnancy brings up unique management challenges. Varying aspects of care must be considered, including the effects of pregnancy on the course of HBV infection, effects of HBV infection on maternal and fetal health, treatment of HBV during and after pregnancy, and prevention of perinatal infection. For those with chronic HBV infection, the course of disease is usually unchanged during pregnancy. However, flares have been reported shortly after delivery. Women with high HBV DNA titer have an increased likelihood of perinatal transmission and may contribute to the failure of current passive-active immunoprophylaxis at birth. The aim of the present review is to provide a tool that may help physicians to manage correctly HBV infection in pregnancy.
Toll-like receptors are a family of pattern recognition receptors that allow the immune system to sense molecules that are present in most classes of pathogens such as bacteria and viruses, but not the host, and to coordinate defense mechanisms against these pathogens. Emerging evidence also suggests that TLRs have an important role in maintaining tissue homeostasis by regulating the inflammatory and tissue repair responses to injury. Due to the important role in inflammation, tissue regeneration and fibrogenesis, TLRs are potential candidates to mediate effects of the innate immune system on carcinogenesis. Although the role of TLRs in carcinogenesis is far from being completely understood, current data suggest a dual role of TLRs in carcinogenesis: anti-tumor effects versus tumor-promoting effects. Here we discuss how TLRs function in the context of carcinogenesis.
The address of direct-acting antivirals (DAAs) has dramatically increased the rates of sustained viral response as compared to the pegylated interferon-based therapy in chronic hepatitis C patients. However, the rates of DAA failure in daily clinical practice are not negligible, ranging from 1% to 15%. Most of these cases are due to the presence of resistance-associated substitutions (RASs), resulting from substitutions of amino acids in the viral target protein that reduce viral sensitivity to DAAs. The high genetic diversity of hepatitis C virus causes the development of RASs, sometimes even before treatment with DAAs. This lecture covers the principle of RAS development, prevalence of RASs, impact of RASs on virological failure, and clinical utility of RAS testing.