Severe ICP was associated with adverse fetal outcomes, including stillbirth (1.5% vs. 0.5% in the control group). There was a significant positive correlation between nonfasting maternal serum bile acid levels and perinatal complications, such as preterm delivery and meconium-stained

amniotic fluid. The researchers speculate that bile acids may affect the contractility of muscle cells. In any case, this study, which is unique for its large size, emphasizes the importance of measuring maternal bile acid levels in ICP. (Hepatology 2014;59:1482-1491.) learn more In nonalcoholic steatohepatitis (NASH), is fibrosis risk the same in men and women? This sounds like a simple question, and thus far the literature has not been unambiguous. Yang et al. tried to answer this question with a group of 541 patients with histologically proven NASH. They analyzed their cohort comparing men to pre- and postmenopausal women. They found that men and postmenopausal women

have comparable severity of fibrosis, whereas premenopausal women have a lower risk for severe fibrosis. The researchers took age into account and tried to Selleckchem GSK3 inhibitor adjust for several confounders, but it remains possible that behavior characteristics differ (degree of physical activity, alcohol intake), which could, in part, explain the difference. Nevertheless, the researchers interpret their results by suggesting that premenopausal women might be at lower risk for fibrosis: They mention estrogen, and we can now add relaxin. (Hepatology 2014;59:1406-1414.) Often, patients with liver disease think they should renounce alcohol, fast food, and coffee. If there is one piece of dietary advice we can give them, it is not to stop drinking coffee. According to numerous epidemiologic studies, coffee is good for the liver. But how? This is the question. Sinha et al. describe how caffeine decreases steatosis. They found that caffeine induces the formation of autophagosomes Thiamine-diphosphate kinase in HepG2 cells. Knocking down ATG5 or blocking lysosomes with chloroquine prevented caffeine-induced reduction in intracellular lipids. They complement these in vitro studies

with in vivo experiments administering caffeine to mice. Caffeine induced hepatic β-oxidation, increased autophagy, and, interestingly, decreased mammalian target of rapamycin (mTOR) signaling. Then, the researchers fed the mice a high-fat diet. Caffeine decreased weight gain and prevented intrahepatic lipid accumulation. These effects were obtained at concentrations that are reached after drinking coffee. No reason for our patients to give up this “drug,” on the contrary! (Hepatology 2014;59:1366-1380.) Intrahepatic cholangiocarcinoma (CCC) shares a rising incidence and poor prognosis with hepatocellular carcinoma (HCC). Systemic targeted therapy with the potential to prolong the survival of patients affected by this type of tumor is urgently needed.