The relationship between Schistosoma mansoni (Sm) and hepatocellular carcinoma (HCC) has been evaluated by many studies that point towards a co-relation between schistosomal infection and HCC. While many such studies demonstrated that Sm infection in the presence of another carcinogenic factors leads to HCC, none of these studies could conclusively prove the cancer-inducing ability of Sm in humans, independent of other carcinogenic factors. The aim of this work is to present the current understanding on the association of Sm with HCC. Many epidemiological, pathological, and clinical studies have shown the role of multiple events like chronic inflammation and fibrosis as well as hepato-toxic agents like soluble egg antigens (SEAs), which help in creating a micro-environment which is suitable for HCC development. The role of Sm infection and deposited eggs in causing persistent inflammation, advanced fibrosis, and the role of SEAs, especially IPSE/alpha-1, is emphasised. This work concludes that Sm infection has the potential to induce cancer independently but the same has not been reported in humans to date. Extensive research is required to establish a causal relationship between Sm infection and HCC induction, or a complete lack thereof. However, Sm infection definitely acts along with other carcinogenic factors to induce HCC at a much faster pace and also leads to an aggressive form of liver cancer, which the other carcinogenic factor could not have achieved alone.

Patients with liver cancer or space-occupying cysts suffer from malnutrition due to compression of gastric and digestive structures, liver and cancer-mediated dysmetabolism, and impaired nutrient absorption. As proportion of these patients requires removal of lesions through hepatic resection, it is important to evaluate the effects of malnutrition on post-hepatectomy outcomes. In our study approach, 2011–2017 National Inpatient Sample was used to isolate in-hospital hepatectomy cases, which were stratified using malnutrition (composite of malnutrition, sarcopenia and weight loss/cachexia). The malnutrition-absent controls were matched to cases using nearest neighbour propensity score matching method and compared with the following endpoints: mortality, length of stay, hospitalisation costs and postoperative complications. There were 2531 patients in total who underwent hepatectomy with matched number of controls from the database; following the match, malnutrition cohort (compared with controls) was more likely to experience in-hospital death (6·60 % v. 5·25 % P < 0·049, OR 1·27, 95 % CI 1·01, 1·61) and was more likely to have higher length of stay (18·10 d v. 9·32 d, P < 0·001) and hospitalisation costs ($278 780 v. $150 812, P < 0·001). In terms of postoperative complications, malnutrition cohort was more likely to experience bleeding (6·52 % v. 3·87 %, P < 0·001, OR 1·73, 95 % CI 1·34, 2·24), infection (6·64 % v. 2·49 %, P < 0·001, OR 2·79, 95 % CI 2·07, 3·74), wound complications (4·5 % v. 1·38 %, P < 0·001, OR 3·36, 95 % CI 2·29, 4·93) and respiratory failure (9·40 % v. 4·11 %, P < 0·001, OR 2·42, 95 % CI 1·91, 3·07). In multivariate analysis, malnutrition was associated with higher mortality (P < 0·028, adjusted OR 1·3, 95 % CI 1·03, 1·65). Thus, we conclude that malnutrition is a risk factor of postoperative mortality in patients undergoing hepatectomy.

Primary liver cancer is the third leading cause of cancer-related death worldwide. Most patients are diagnosed at late stages with poor prognosis; thus, identification of modifiable risk factors for primary prevention of liver cancer is urgently needed. The well-established risk factors of liver cancer include chronic infection with hepatitis B virus (HBV) or hepatitis C virus (HCV), heavy alcohol consumption, metabolic diseases such as obesity and diabetes, and aflatoxin exposure. However, a large proportion of cancer cases worldwide cannot be explained by current known risk factors. Dietary factors have been suspected as important, but dietary aetiology of liver cancer remains poorly understood. In this review, we summarised and evaluated the observational studies of diet including single nutrients, food and food groups, as well as dietary patterns with the risk of developing liver cancer. Although there are large knowledge gaps between diet and liver cancer risk, current epidemiological evidence supports an important role of diet in liver cancer development. For example, exposure to aflatoxin, heavy alcohol drinking and possibly dairy product (not including yogurt) intake increase, while intake of coffee, fish and tea, light-to-moderate alcohol drinking and several healthy dietary patterns (e.g. Alternative Healthy Eating Index) may decrease liver cancer risk. Future studies with large sample size and accurate diet measurement are warranted and need to consider issues such as the possible aetiological heterogeneity between liver cancer subtypes, the influence of chronic HBV or HCV infection, the high-risk populations (e.g. cirrhosis) and a potential interplay with host gut microbiota or genetic variations.

Objectives: There is a growing need for efficient procedures for identification of emerging technologies by horizon scanning systems. We demonstrate the value of best-worst scaling (BWS) in exploring clinicians’ views on emerging technologies that will impact outcomes in hepatocellular carcinoma (HCC) in the next 5 to 10 years.

Methods: Clinicians in Asia, Europe, and the United States were surveyed and their views about eleven emerging technologies relevant to HCC were explored using BWS (case 1). This involved systematically presenting respondents with subsets of five technologies and asking them to identify those that will have the most and least impact on HCC within 5 to 10 years. Statistical analysis was based on sequential best-worst and analyzed using conditional logistic regression.

Results: A total of 120 clinicians uniformly distributed across ten countries completed the survey (37 percent response rate). Respondents were predominately hepatologist (41 percent) who focused on HCC (65 percent) and had national influence in this field (39 percent). Respondents viewed molecular targeted therapy (p < .001) and early detection of HCC (p < .001) as having most potential, while improved surgical techniques (p < .001) and biopsy free HCC diagnostics (p < .001) were viewed upon negatively.

Conclusions: We demonstrate that BWS could be an important research tool to facilitate horizon scanning and HTA more broadly. Our research demonstrates the value of including clinicians’ preferences as a source of data in horizon scanning, but such methods could be used to incorporate the opinions of a broad array of stakeholders, including those in advocacy and public policy.

The present investigation was carried out to evaluate the hepatoprotective effect of probiotic fermented milk (FM) containing Lactobacillus rhamnosus GG and Lactobacillus casei strain Shirota, alone as well as in combination with chlorophyllin (CHL) as an antioxidant agent in male Wistar rats administered aflatoxin-B1 (AFB1). AFB1 was injected intraperitoneally at the rate of 450 μg/kg body weight per animal twice a week for 6 weeks, maintaining an equal time interval between the two consecutive AFB1 administrations. A total of 125 male Wistar rats were randomly allocated to five groups, each group having twenty-five animals. Group I was offered FM containing L. rhamnosus GG and L. casei strain Shirota. Group II was administered AFB1 and served as the control group; group III was administered FM-AFB1, in which besides administering AFB1, FM was also offered. Group IV was offered CHL and AFB1, and group V was offered both FM and CHL along with AFB1. The rats were euthanised at the 15th and 25th week of the experiment and examined for the biochemical and hepatopathological profile. A significant reduction in thiobarbituric acid-reactive substances (TBARS) was observed in the FM–CHL–AFB1 group compared with the AFB1 control group. FM alone or in combination with CHL was found to show a significant (P < 0·05) hepatoprotective effect by lowering the levels of TBARS and by enhancing the activities of antioxidant enzymes such as glutathione peroxidase, superoxide dismutase, catalase and glutathione-S-transferase, indicating that probiotic FM alone or in combination with CHL possesses a potent protective effect against AFB1-induced hepatic damage.