Obstructive sleep apnoea syndrome (OSAS) is a common sleep disorder, affecting over 4% of the general population, and is associated with metabolic syndrome and cardiovascular disease, independent of obesity and traditional risk factors. OSAS has been recently connected to nonalcoholic fatty liver disease (NAFLD), the most common chronic liver disease in the world, which can be found in 30% of the general adult population. Several studies suggest that the chronic intermittent hypoxia (CIH) of OSAS patients may per se trigger liver injury, inflammation, and fibrogenesis, promoting NAFLD development and the progression from steatosis to steatohepatitis, cirrhosis, and hepatocellular carcinoma. In NAFLD patients, liver disease may be caused by hypoxia both indirectly by promoting inflammation and insulin resistance and directly by enhancing proinflammatory cytokine production and metabolic dysregulation in liver cells. In this review, we focus on molecular mechanisms linking OSAS to NAFLD, including hypoxia inducible factor (HIF), nuclear factor kappa B (NF-κB), YKL-40, unfolded protein response, and hypoxic adipose tissue inflammation, which all could provide novel potential therapeutic approaches for the management of NAFLD patients with OSAS.

Nonalcoholic fatty liver disease (NAFLD) is the most common chronic liver disease in the Western world (it affects 30% of the general adult population). The NAFLD encompasses a histological spectrum ranging from simple steatosis to nonalcoholic steatohepatitis (NASH), defined by steatosis, hepatocellular damage, and lobular inflammation in individuals without significant alcohol consumption and negative viral, congenital, and autoimmune liver disease markers. Currently, NAFLD is considered an emerging epidemic in light of the dramatic increase in obesity rates. With the progressive nature of NASH and its rising prevalence there is a significant need for a specific and targeted treatments since to date there has not been any validated therapies for NAFLD other than weight loss, which is well known to have a poor long-term success rate. In recent years, visceral adipose tissue has taken an important role in NAFLD pathogenesis, and current therapeutic approaches aim at reducing visceral obesity and free fatty acid overflow to the liver. This paper is focused on the treatments used for NAFLD and the potential new therapy.

The headword "overlap syndromes" of liver diseases includes the coexistence of autoimmune hepatitis, primary biliary cirrhosis, and primary sclerosing cholangitis. These syndromes often represent a diagnostic and therapeutic challenge for hepatologists; it remains unclear whether these overlap syndromes form distinct entities or they are only variants of the major autoimmune liver diseases. The most frequent reported association occurs between autoimmune hepatitis and primary biliary cirrhosis, whereas the overlap between autoimmune hepatitis and primary sclerosing cholangitis is less frequent, typically at young age and often attendant with an inflammatory bowel disease. The choice therapy is based on ursodeoxycholic acid and immunosuppressive drugs, used at the same time or consecutively, according to the course of disease. The diagnostic scores for autoimmune hepatitis can help for diagnosis, even though their definitive soundness is lacking.

Aim:The liver is a sexually dimorphic organ presenting gender differences in its metabolism, functions, enzyme activity, membrane lipid composition and immune response. This paper aimed to assess whether gender may predict virological response to standard antiviral therapy in subjects with chronic hepatitis C (CHC). Methods: The authors retrospectively analyzed 100 patients with genotype 1 CHC (55 men, 45 women), who performed standard antiviral therapy (interferon and ribavirin for 12 months) in the period 2002-2012, evaluated with blood tests and abdominal ultrasound to compare different virological and biochemical response in both gender. Results: Rate of substained virological response (SVR) was higher, but not significant, in women than men (46.7% vs. 34.5%, P = 0.05); difference became significant after stratification by age (< 50 and ≥ 50 years). Specifically in the group aged under 50 years, rate of SVR was significantly higher in women than in men (66.7% vs. 38.2%, P < 0.05). Conclusion: Female gender may predict virological response to standard antiviral therapy in subjects with CHC aged below 50 years. Considering new potent and more expensive antiviral drugs actually available for HCV treatment, it could be useful to identify candidates firstly eligible to therapy.

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