SPINK1 can be used to differentiate between a WD-HCC and a HGDN with high diagnostic validity.

Deletion in the 3p21 region, the chromosomal location of BAP1, has been reported in a subset of hepatocellular carcinoma (HCC), biliary and pancreatic cancers. This suggests that BAP1 could play a role in the pathogenesis of these tumors. We assessed the frequency of BAP1 loss by immunohistochemistry in 103 hepatic, biliary and pancreatic cancers. We also assessed chromosomal alterations in the BAP1 region in the same tumors by genotyping. We identified high frequency 4/8 (50%) of BAP1 loss in intrahepatic cholangicarcinoma (ICC). However the frequency was lower in HCC 9/51 (17.6%), pancreatic 1/42(2.4%) and extrahepatic biliary cancers (0/2). Loss of heterozygosity of at least one marker from the 3p21 region was observed in 75% of ICC, 52.9% of HCC and 45.2% of pancreatic cancers. Expression of hepatocytic (HepPar1) and bile duct (cytokeratin 7) markers were common (7/9, 77.8%) in the HCC tumors with loss or decrease of BAP1 compared with those with preserved BAP1 (18/42, 42.9%), (Fisher exact p = 0.0751). Our results confirm the high frequency of BAP1 alterations in ICC and low frequency in pancreatic cancers. It also suggests that BAP1 is commonly altered in a subtype of HCC with both hepatocytic and biliary differentiation. Further studies of the therapeutic implications of our findings are warranted.

Background The pandemic of COVID19 which is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) was first described in China as an unexplained pneumonia transmitted by respiratory droplets. Gastrointestinal (GI) and liver injury associated with SARS-CoV-2 infection were reported as an early or sole disease manifestation, mainly outside China. The exact mechanism and incidence of GI and liver involvement are not well elucidated. Main body We conducted a PubMed search for all articles written in the English language about SARS-CoV-2 affecting the GI and liver. Following data extraction, 590 articles were selected. In addition to respiratory droplets, SARS-CoV-2 may reach the GI system through the fecal-oral route, saliva, and swallowing of nasopharyngeal fluids, while breastmilk and blood transmission were not implicated. Moreover, GI infection may act as a septic focus for viral persistence and transmission to the liver, appendix, and brain. In addition to the direct viral cytopathic effect, the mechanism of injury is multifactorial and is related to genetic and demographic variations. The most frequently reported GI symptoms are diarrhea, nausea, vomiting, abdominal pain, and bleeding. However, liver infection is generally discovered during laboratory testing or a post-mortem. Radiological imaging is the gold standard in diagnosing COVID-19 patients and contributes to understanding the mechanism of extra-thoracic involvement. Medications should be prescribed with caution, especially in chronic GI and liver patients. Conclusion GI manifestations are common in COVID-19 patients. Special care should be paid for high-risk patients, older males, and those with background liver disease.

Background The rapidly developing era of direct-acting antiviral regimens (DAAs) for more than one hepatitis C virus (HCV) genotype had certainly alleviated HCV burden all over the world. Liver fibrosis is the major dramatic complication of HCV infection, and its progression leads to cirrhosis, liver failure, and hepatocellular carcinoma. The impact of DAAs on liver fibrosis had been debatably evaluated with undetermined resolution. Main body The aim of this review is to accurately revise the effects of DAA regimens on liver fibrosis which can either be regression, progression, or non-significant association. Liver fibrosis regression is a genuine fact assured by many retrospective and prospective clinical studies. Evaluation could be concluded early post-therapy reflecting the dynamic nature of the process. Conclusions The ideal application of DAA regimens in treating HCV has to be accomplished with efficient non-invasive markers in differentiating proper fibrosis evaluation from necroinflammation consequences. Liver biopsy is the gold standard that visualizes the dynamic of fibrosis regression.

Background Periampullary adenocarcinoma (PAAC) had a poor prognosis, and pancreaticoduodenectomy (PD) remains the only potentially curative treatment. The study aimed to identify the impact of different clinicopathological factors on long-term survival following PD for PAAC. Patients and methods This study is a retrospective cohort study for the patients who underwent PD for pathologically proven PAAC from January 2010 to January 2019. Statistical analysis was done using Cox regression multivariate analyses for independent risk factors for survival. Result There were 137 patients with PAAC who underwent PD, 79 patients (57.7%) underwent pylorus-preserving PD. Pancreatico-jejunostomy was done in 108 patients (78.8%). The primary analysis showed that risk factors for poor long-term survival include patients with co-morbidities like hypertension or ischemic heart disease, Carbohydrate Antigen 19-9 > 400U/ml, tumor size > 3 cm, poor tumor differentiation, positive lymph nodes invasion, lymphovascular invasion, and Perineural invasion. Multivariate analysis demonstrated that large tumor size > 3 cm (HR: 0.177, 95%CI: 0.084–0.374, P = 0.002), poorly differentiated tumor (HR: 0.059, 95%CI: 0.020–0.0174, P = 0.016), and perineural invasion in the pathological study (HR: 0.101, 95%CI: 0.046–0.224, P = 0.006) were independent risk factors for poor 5-years survival. The prognosis was better in ampullary adenocarcinoma (5-year survival was 42.1%) than pancreatic adenocarcinoma (5-year survival was 24.3%). The 1, 3, 5 and 7-year overall survival rates were 84.5%, 57.4%, 35.9% and 20.1% respectively. Conclusion It seems from the current study that Tumor size > 3 cm, poor tumor differentiation, and Perineural invasion were independent predictors of poor survival in patients with PAAC.