Non-alcoholic liver disease (NAFLD) defines liver abnormalities ranging from simple steatosis to nonalcoholic steatohepatitis with or without cirrhosis development, occurring in the absence of significant alcohol consumption, use of teratogenic medication, or hereditary disorders. The association between NAFLD and metabolic syndrome is well documented and widely recognized. Obesity, type 2 diabetes mellitus (T2DM), and dyslipidemia are the most common metabolic risk factors associated with NAFLD. Among the components of metabolic syndrome, current evidence strongly indicates obesity and diabetes as hepatocellular carcinoma (HCC) risk factors. There is also growing evidence that suggests an increased risk of HCC in NAFLD patients, even surpassing other etiologies in some high-income countries. Epidemiologic data demonstrate a parallel rise in prevalence of obesity, diabetes, NAFLD, and HCC. As obesity and its related diseases have steadily afflicted larger populations, HCC incidence is expected to increase in the future. Pathophysiologic mechanisms that underlie NAFLD development and subsequent progression to nonalcoholic steatohepatitis and cirrhosis (insulin resistance and hyperinsulinemia, oxidative stress, hepatic stellate cell activation, cytokine/adipocytokine signaling pathways, and genetic and environmental factors) appear to play a significant role in the development of NAFLD-related HCC. However, a comprehensive view of molecular mechanisms linking obesity, T2DM, and NAFLD-related HCC, as well as the exact sequence of molecular events, is still not understood in its entirety. Good-quality data are still necessary, and efforts should continue towards better understanding the underlying carcinogenic mechanisms of NAFLD-related HCC. In this paper, we aimed to centralize the most important links supporting these relationships, focusing on obesity, T2DM, and NAFLD-related HCC, as well as point out the major gaps in knowledge regarding the underlying molecular mechanisms behind them.

Background and Aims. Hepatocellular carcinoma (HCC) remains a leading cause of death by cancer worldwide. Computerized diagnosis systems relying on novel imaging markers gained significant importance in recent years. Our aim was to integrate a novel morphometric measurement—the fractal dimension (FD)—into an artificial neural network (ANN) designed to diagnose HCC. Material and Methods. The study included 21 HCC and 28 liver metastases (LM) patients scheduled for surgery. We performed hematoxylin staining for cell nuclei and CD31/34 immunostaining for vascular elements. We captured digital images and used an in-house application to segment elements of interest; FDs were calculated and fed to an ANN which classified them as malignant or benign, further identifying HCC and LM cases. Results. User intervention corrected segmentation errors and fractal dimensions were calculated. ANNs correctly classified 947/1050 HCC images (90.2%), 1021/1050 normal tissue images (97.23%), 1215/1400 LM (86.78%), and 1372/1400 normal tissues (98%). We obtained excellent interobserver agreement between human operators and the system. Conclusion. We successfully implemented FD as a morphometric marker in a decision system, an ensemble of ANNs designed to differentiate histological images of normal parenchyma from malignancy and classify HCCs and LMs.

Liver innervation comprises sympathetic, parasympathetic and peptidergic nerve fibers, organized as either afferent or efferent nerves with different origins and roles. Their anatomy and physiology have been studied in the past 30 years, with different results published over time. Hepatocytes are the main cell population of the liver, making up almost 80% of the total liver volume. The interaction between hepatocytes and nerve fibers is accomplished through a wealth of neurotransmitters and signaling pathways. In this short review, we have taken the task of condensing the most important data related to how the nervous system interacts with the liver and especially with the hepatocyte population, how it influences their metabolism and functions, and how different receptors and transmitters are involved in this complex process.

Abusive alcohol intake currently ranks as a major cause of liver disease, and is associated with significant mortality worldwide. Alcoholic liver disease (ALD) generically defines liver abnormalities ranging from liver steatosis to the end-stages of disease such as liver cirrhosis. Information regarding the precise incidence and prevalence of ALD is still limited by a lack of large population-based studies and by the absence of large systematic reviews of all epidemiological data available. However, existing collected data show an overall increase in the number of alcohol abusers and alcohol-related liver disease. The burden exerted on medical systems worldwide is significant, with hospitalization and management costs rising constantly over the years. A great number of all cirrhosis-related deaths in Europe and a significant percentage worldwide are associated with alcohol consumption. The main possible risk factors for ALD are the amount and duration of alcohol abuse, patterns of drinking and the type of alcoholic beverage consumed. However, ALD does not progress to cirrhosis in all patients, therefore a series of additional factors are implicated. Even though insufficiently studied, genetic factors are generally regarded as highly important, and the presence of comorbidities and dietary habits seem to play a role in disease onset and progression. This lack of clear pathophysiological data further translates in the absence of definite treatment for ALD and shall prove challenging in the coming years. In this article, we aimed to briefly review epidemiologic data on the burden of ALD, risk factors, clinical and nosographic as well as therapeutic aspects of this disease. Without attempting to be exhaustive, this short topic highlight emphasizes each point and may serve as a general guidance tool in the complicated literature related to ALD.

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Hepatitis B virus (HBV) infection remains a major health problem worldwide and a major risk factor for end-stage liver disease and hepatocellular carcinoma. Notable differences of chronic hepatitis B prevalence were observed in geographic area. In highly endemic areas, at least 50 % of HBV infections are most commonly acquired either perinatally or in early childhood, during the first 5 years of life. The prevalence of chronic HBV infection in pregnant women is expected to mirror those in the general populations of each geographic area. Chronic hepatitis B during pregnancy is associated with high risk of maternal complications and an increased risk of mother-to-child transmission (MTCT). Thus, chronic hepatitis B during pregnancy can now be considered an important contributor to new HBV infections and to the global burden of disease. As a result, HBV infection during pregnancy requires management strategies for both the mother and the fetus/neonate, including prevention/elimination of MTCT and lessening the HBV effects on maternal and fetal health. This chapter will review current management strategies for hepatitis B in the pregnancy and the postpartum period, including special considerations on the effects of pregnancy on the course of HBV infection, MTCT, and antiviral therapy during the pregnancy.

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