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Jordi Llaneras (1), Mar Riveiro-Barciela (1)(2), Sabela Lens (2)(3), Moisés Diago (4), Alba Cachero (5), Javier García-Samaniego (2)(6), Isabel Conde (7), Ana Arencibia (8), Juan Arenas (9), Francisco Gea (10), Xavier Torras (2)(11), José Luis Calleja (12), José Antonio Carrión (13), Inmaculada Fernández (14), Rosa María Morillas (2)(15), José Miguel Rosales (16), Isabel Carmona (17), Conrado Fernández-Rodríguez (18), Manuel Hernández-Guerra (19), Susana Llerena (20), Vanesa Bernal (21), Juan Turnes (22), Jesús M. González-Santiago (23), Silvia Montoliu (24), Blanca Figueruela (25), Ester Badia (26), Manuel Delgado (27), Miguel Fernández-Bermejo (28), Mercedes Iñarrairaegui (2)(29), Juan Manuel Pascasio (2)(30), Rafael Esteban (1)(2), Zoe Mariño (2)(3), Maria Buti (1)(2).

Non-alcoholic fatty liver disease (NAFLD), which affects about a quarter of the global population, poses a substantial health and economic burden in all countries, yet there is no approved pharmacotherapy to treat this entity, nor well-established strategies for its diagnosis. Its prevalence has been rapidly driven by increased physical inactivity, in addition to excessive calorie intake compared to energy expenditure, affecting both adults and children. The increase in the number of cases, together with the higher morbimortality that this disease entails with respect to the general population, makes NAFLD a serious public health problem. Closely related to the development of this disease, there is a hormone derived from adipocytes, leptin, which is involved in energy homeostasis and lipid metabolism. Numerous studies have verified the relationship between persistent hyperleptinemia and the development of steatosis, fibrinogenesis and liver carcinogenesis. Therefore, further studies of the role of leptin in the NAFLD spectrum could represent an advance in the management of this set of diseases.

Fibrosis progression is common in hepatitis C. Both host and viral factors influence its natural history. Liver fibrosis is a key predictive factor for advanced disease including endpoints such as liver failure, cirrhosis and hepatocellular carcinoma (HCC). METAVIR fibrosis stages F3-F4 have been considered as the threshold for antiviral therapy. However, this aspect is controversial after the advent of new direct-acting antivirals (DAAs) because they show an excellent efficacy and safety profile. Moreover, in the DAA era, fibrosis stage seems not to be a predictive factor of a sustained virological response (SVR). Viral eradication decreases liver damage by improving the inflammation, as well as by regressing fibrosis irrespective of the treatment regimen. Non-invasive methods are useful in the assessment of liver fibrosis, replacing liver biopsy in clinical practice; but their usefulness for monitoring fibrosis after SVR needs to be demonstrated. Fibrosis regression has been demonstrated after the eradication of hepatitis C virus infection and is associated with a lower risk of hepatic cirrhosis and liver cancer. However, patients showing advanced fibrosis and cirrhosis must be followed-up after SVR, as risks of portal hypertension and HCC remain.

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