Background and Aims: Endoscopic resection of lesions involving the appendiceal orifice (AO) remains a challenge. We aim to report the outcomes of full-thickness resection device (FTRD) for the resection of appendiceal lesions and identify factors associated with the occurrence of appendicitis. Methods: This is a retrospective study at 18 tertiary-care centers (12 U.S., Canada 1, 5 Europe) between 11/2016 and 8/2020. Consecutive patients who underwent resection of AO lesions using the FTRD were included. The primary outcome was the rate of R0 margin resection in neoplastic lesions, defined as negative lateral and deep margins on post-resection histologic evaluation. Secondary outcomes included the rates of; technical success (en bloc resection), clinical success (technical success without need for further surgical interventions), post-resection appendicitis, and polyp recurrence. Results: A total of 66 patients (mean age 64 yr., 29 F) underwent resection of colonic lesions (mean size 14.5 (6.2) mm) involving the AO, with 40 (61%) deep extending into the appendiceal lumen. Technical success was achieved in 59/66 (89%) cases, out of which, 56 were found to be neoplastic lesions on post-resection pathology. Clinical success was achieved in 53/66 (80%). R0 resection was achieved in 52/56 (93%) cases. Out of the 58 patients of whom EFTR was completed and had no prior history of appendectomy, appendicitis was reported in 10 (17%) cases, with 6 (60%) requiring surgical appendectomies. Follow-up colonoscopy was completed in 41 cases with evidence of recurrence in 5 (12.2%). Conclusions: FTRD is a promising non-surgical alternative for resecting appendiceal lesions but appendicitis occurs in 1 out of 6 cases.

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Hepatitis B virus (HBV) is one of the most significant hepatocarcinogens. The ultimate goal of anti-HBV treatment is to prevent the development of hepatocellular carcinoma (HCC). During the last two decades, with the use of currently available anti-HBV therapies (lamivudine, entecavir and tenofovir disoproxil fumatate), there has been a decrease in the incidence of HBV-associated HCC (HBV-HCC). Furthermore, several studies have demonstrated a reduction in recurrent or new HCC development after initial HCC tumor ablation. However, during an observation period spanning 10 to 20 years, several case reports have demonstrated the development of new, subsequent new and recurrent HCC even in patients with undetectable serum HBV DNA. The persistent risk for HCC is attributed to the presence of covalently closed circular DNA (cccDNA) in the hepatocyte nucleus which continues to work as a template for HBV replication. While a functional cure (loss of hepatitis B surface antigen and undetectable viral DNA) can be attained with nucleos(t)ide analogues, these therapies do not eliminate cccDNA. Of utmost importance is successful eradication of the transcriptionally active HBV cccDNA from hepatocyte nuclei which would be considered a complete cure. The unpredictable nature of HCC development in patients with chronic HBV infection shows the need for a complete cure. Continued support and encouragement for research efforts aimed at developing curative therapies is imperative. The aims of this minireview are to highlight these observations and emphasize the need for a cure for HBV.

: The hepatitis B virus (HBV) is one of the leading causes of hepatocellular carcinoma (HCC) worldwide. In the endemic region the infection is commonly spread through vertical transmission in which mother and child possess genetically identical viral genotypes in the setting of similar host genomes. Despite these genetic similarities, clinical outcomes from chronic hepatitis B (CHB) can vary widely, ranging from lifelong asymptomatic infection to terminal HCC. Presented here are the longitudinal observations over multiple decades of three family clusters, including monozygotic twins with non-discordant HCC, that demonstrate the heterogeneity of HBV-related outcomes. These findings emphasize the important need to untangle the role of genetic and non-genetic host factors in the development of HBV-related HCC, as well as highlight novel research avenues that can clarify the contributions of such factors in HBV-related HCC.

Chronic hepatitis B virus (HBV) infection is a major public health challenge on the global scale. Affecting hundreds of millions worldwide, HBV is a leading risk factor for hepatocellular carcinoma (HCC). Clinical outcomes from chronic HBV infection are varied and appear to be influenced by a complex and dysregulated host immune response. In turn, much attention has been given to the immunologic response to HBV in an effort to identify host factors that lead to the development of HCC. However, the role of nonimmunologic host factors, such as chronic stress, in HBV-related HCC is poorly defined. Indeed, a growing appreciation for the effects of stress on chronic liver diseases raises the question of its role in chronic HBV infection. In this light, the present review will untangle the roles of key host factors in HBV-related HCC with an emphasis on chronic stress as a viable contributor. First discussed is the interplay of stress, inflammation and chronic liver disease. The host immune response’s role as a driver of HBV-related HCC is then reviewed, allowing for a close exploration of the effects of stress on immune function in chronic hepatitis B and as a potential risk factor for HBV-related HCC.

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