Kaur Avneet, Azeez Gibran A, Thirunagari Mounika, Fatima Nazeefa, Anand Abhinav, Palvia Aadi R, Yu Ann Kashmer
Internal Medicine, California Institute of Behavioral Neurosciences & Psychology, Fairfield, USA.
Cureus. 2024 Dec 20;16(12):e76079. doi: 10.7759/cureus.76079. eCollection 2024 Dec.
Viral hepatitis B is infamous for being contracted in young adulthood and adolescence, as high-risk behaviors like unprotected sexual intercourse and intravenous drug abuse are common. Most infections caused by the hepatitis B virus (HBV) are cleared without any long-term sequelae, but some may persist and cause chronic hepatitis B (CHB). This chronicity may produce a state of prolonged inflammation and significantly increase the risk of developing colorectal adenomas (CRA) and colorectal carcinomas (CRC). The aim of this review is to deep-dive into the mechanisms by which CHB may predispose a patient to develop CRA and, more grimly, CRC. It also focuses on studying the influence of CHB on colorectal cancer liver metastases (CRLM). We conducted a comprehensive literature search using databases like PubMed and Google Scholar, focusing on studies that investigate the role of HBV in colorectal carcinogenesis and CRLM rates in patients suffering from CHB. Chronic inflammation, viral protein interactions with tumor suppressor genes, alteration of cellular pathways such as wingless-related integration site (Wnt) signaling, and extrahepatic accumulation of hepatitis B surface antigen (HBsAg) were the key mechanisms identified. Quite peculiarly, CHB, which is thought to increase the risk for CRA, seemed to protect against CRLM probably due to its sclerosing effect on the liver parenchyma and due to certain immune-mediated mechanisms that suppress tumor growth. Nonetheless, high viral count or the presence of hepatitis B envelope antigen (HBeAg) was found to increase the risk for CRLM, potentially due to increased angiogenesis in the liver. These findings provide convincing evidence that enhanced colonoscopic screening and stronger management protocols for patients suffering from it have the potential to reduce the risk of developing CRC and CRLM.
乙型病毒性肝炎因在青壮年和青少年时期易感染而声名狼藉，因为无保护性行为和静脉注射吸毒等高风险行为很常见。大多数由乙型肝炎病毒（HBV）引起的感染可自行清除，不会留下任何长期后遗症，但有些感染可能会持续存在并导致慢性乙型肝炎（CHB）。这种慢性状态可能会导致长期炎症状态，并显著增加患结直肠腺瘤（CRA）和结直肠癌（CRC）的风险。本综述的目的是深入探讨CHB可能使患者易患CRA以及更严重的CRC的机制。它还侧重于研究CHB对结直肠癌肝转移（CRLM）的影响。我们使用PubMed和谷歌学术等数据库进行了全面的文献检索，重点关注研究HBV在结直肠癌发生中的作用以及CHB患者CRLM发生率的研究。慢性炎症、病毒蛋白与肿瘤抑制基因的相互作用、细胞途径的改变，如无翅相关整合位点（Wnt）信号传导，以及乙型肝炎表面抗原（HBsAg）的肝外积累是确定的关键机制。非常特别的是，被认为会增加CRA风险的CHB似乎对CRLM有保护作用，这可能是由于其对肝实质的硬化作用以及某些抑制肿瘤生长的免疫介导机制。尽管如此，发现高病毒载量或乙型肝炎包膜抗原（HBeAg）的存在会增加CRLM的风险，这可能是由于肝脏中血管生成增加所致。这些发现提供了令人信服的证据，即加强结肠镜筛查以及对CHB患者采取更强有力的管理方案有可能降低患CRC和CRLM的风险。
