World Journal of Hepatology最新文献

{"title":"Liver cell cancer surveillance practice in Nigeria: Pitfalls and future prospects.","authors":"Yusuf Musa, Ijeoma M Ifeorah, Abubakar Sadiq Maiyaki, Rahama Mohammad Almustapha, Yussuf Abdulkadir Maisuna, Habib Tijjani Saleh, Abdulmumini Yakubu","doi":"10.4254/wjh.v16.i10.1132","DOIUrl":"https://doi.org/10.4254/wjh.v16.i10.1132","url":null,"abstract":"<p><p>Hepatocellular carcinoma (HCC) is a disease of public health concern in Nigeria, with chronic hepatitis B and C infections contributing most to the disease burden. Despite the increasing incidence of HCC, surveillance practices for early diagnosis and possible cure are not deeply rooted in the country. This article aims to review the current status of HCC surveillance in Nigeria, stressing the encounters, breaches, and potential prospects. Several factors, such as limited tools for screening and diagnostics, insufficient infrastructure, and low cognizance among the doctors, and the general public affect the surveillance practices for HCC in Nigeria. Moreover, the lack of standardized guidelines and protocols for HCC surveillance further intensifies the suboptimal diagnosis and treatment. Nevertheless, there are opportunities for refining surveillance practices in the country. This would be achieved through boosted public health sensitization campaigns, integrating HCC screening into routine clinical services, and leveraging technological developments for early detection and monitoring. Furthermore, collaboration between government agencies, healthcare providers, and international organizations can facilitate the development of comprehensive HCC surveillance programs personalized to the Nigerian setting. Thus, HCC surveillance practice faces substantial challenges. By addressing the drawbacks and leveraging prospects, Nigeria can improve HCC surveillance, with subsequent improved outcomes for individuals at risk of developing the disease.</p>","PeriodicalId":23687,"journal":{"name":"World Journal of Hepatology","volume":null,"pages":null},"PeriodicalIF":2.5,"publicationDate":"2024-10-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11514613/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142547760","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hepatitis B surface antigen-negative but hepatitis B envelope antigen-positive false occult hepatitis B virus infection: A case report.","authors":"Shu-Sheng Yang, Fei Fu, Qian-Kun Xuan, Zhou-Xiang Zhang, Zhi-Jun Li, Guang-Bo Li, Xiao-Yu Yu","doi":"10.4254/wjh.v16.i10.1199","DOIUrl":"https://doi.org/10.4254/wjh.v16.i10.1199","url":null,"abstract":"<p><strong>Background: </strong>Occult hepatitis B infection (OBI) is characterized by the detection of hepatitis B virus (HBV) DNA in serum (usually HBV DNA < 200 IU/mL) or the liver but negativity for hepatitis B surface antigen (HBsAg). The diagnosis of OBI relies on the sensitivity of assays used in the detection of HBV DNA and HBsAg. HBsAg assays with inadequate sensitivity or inability to detect HBV S variants may lead to misdiagnosis of OBI in people with overt HBV infection.</p><p><strong>Case summary: </strong>We report a HBsAg-negative but hepatitis B envelope antigen-positive patient who had a significant HBV DNA level. The patient was initially diagnosed as having OBI. However, sequence analysis revealed a unique insertion of amino acid residues at positions 120-124 in the S protein, which affects the formation of a disulfide bond that is associated with the formation of a loop. It is well known that there is an overlap between the S protein and Pol protein. We found that this new insertion site occurred in polymerase/reverse transcriptase domain, indicating that this insertion might be involved in HBV pathogenicity. The patient was finally diagnosed with a false OBI.</p><p><strong>Conclusion: </strong>An insertion of amino acid residues at positions 120-124 of the S protein affects the formation of immunodominant epitopes and results in negative HBsAg levels.</p>","PeriodicalId":23687,"journal":{"name":"World Journal of Hepatology","volume":null,"pages":null},"PeriodicalIF":2.5,"publicationDate":"2024-10-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11514620/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142547759","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Complement activation targeted inhibitor C2-FH ameliorates acetaminophen-induced liver injury in mice.","authors":"Chun-Mei Li, Tian Sun, Mou-Jie Yang, Zhi Yang, Qing Li, Jia-Lin Shi, Chong Zhang, Jun-Fei Jin","doi":"10.4254/wjh.v16.i10.1188","DOIUrl":"https://doi.org/10.4254/wjh.v16.i10.1188","url":null,"abstract":"<p><strong>Background: </strong>Complement activation is recognized as an important factor in the progression of liver damage caused by acetaminophen (APAP). However, the role of the complement inhibitor C2-FH in APAP-induced liver injury remains unclear.</p><p><strong>Aim: </strong>To explore C2-FH in protecting against APAP-induced liver injury by inhibiting complement activation.</p><p><strong>Methods: </strong>A model of APAP-induced liver injury was used to study the protective effect of C2-FH on liver injury. C2-FH was administered through intraperitoneal injection 30 minutes after APAP treatment. We detected the effects of C2-FH on liver function, inflammatory response and complement activation. Additionally, RNA-sequencing (RNA-Seq) analysis was conducted to understand the mechanism through which C2-FH provides protection against APAP-induced liver injury.</p><p><strong>Results: </strong>C2-FH inhibited the increase in serum alanine aminotransferase activity, aspartate aminotransferase activity and lactate dehydrogenase, and reduced liver tissue necrosis caused by APAP. Moreover, it attenuated the inflammatory response and inhibited complement activation in APAP-induced liver injury. RNA-Seq analysis provided additional explanations for the protective role of C2-FH against APAP-induced liver injury.</p><p><strong>Conclusion: </strong>C2-FH attenuates APAP-induced liver injury by inhibiting complement activation.</p>","PeriodicalId":23687,"journal":{"name":"World Journal of Hepatology","volume":null,"pages":null},"PeriodicalIF":2.5,"publicationDate":"2024-10-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11514617/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142547758","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Suppression of hepatic steatosis in non-alcoholic steatohepatitis model by modified Xiaoyao San formula: Evidence, mechanisms and perspective.","authors":"Nabil Eid, Payal Bhatnagar, Li-Li Chan, Marina Garcia-Macia","doi":"10.4254/wjh.v16.i10.1208","DOIUrl":"https://doi.org/10.4254/wjh.v16.i10.1208","url":null,"abstract":"<p><p>In this letter, we comment on a recent publication by Mei <i>et al</i>, in the <i>World Journal of Hepatology</i>, investigating the hepatoprotective effects of the modified Xiaoyao San (MXS) formula in a male rat model of non-alcoholic steatohepatitis (NASH). The authors found that MXS treatment mitigated hepatic steatosis and inflammation in the NASH model, as evidenced by the reduction in lipid droplets (LDs), fibrosis markers and lipogenic factors. Interestingly, these hepatoprotective effects were associated with androgen upregulation (based on metabolomics analysis of male steroid hormone metabolites), adenosine 5'-monophosphate-activated protein kinase (AMPK) activation, and restoration of phosphatase and tensin homolog (PTEN) expression. However, the authors did not clearly discuss the relationships between MXS-induced hepatic steatosis reduction in the NASH model, and androgen upregulation, AMPK activation, and restoration of PTEN expression. This editorial emphasizes the reported mechanisms and explains how they act or interact with each other to reduce hepatic steatosis and inflammation in the NASH model. As a perspective, we propose additional mechanisms (such as autophagy/lipophagy activation in hepatocytes) for the clearance of LDs and suppression of hepatic steatosis by MXS in the NASH model. A proper understanding of the mechanisms of MXS-induced reduction of hepatic steatosis might help in the treatment of NASH and related diseases.</p>","PeriodicalId":23687,"journal":{"name":"World Journal of Hepatology","volume":null,"pages":null},"PeriodicalIF":2.5,"publicationDate":"2024-10-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11514612/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142547764","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Prevalence and risk factors associated with metabolic dysfunction-associated steatohepatitis in patients with <i>Helicobacter pylori</i> infection: A population-based study.","authors":"Rashid Abdel-Razeq, Lynn Bitar, Elio R Bitar, Chidera Onwuzo, Mohamad-Noor Abu-Hammour, Barish Eren, Islam Mohamed, Adejoke Johnson, Antoine Boustany, Somtochukwu Onwuzo, Imad Asaad","doi":"10.4254/wjh.v16.i10.1169","DOIUrl":"https://doi.org/10.4254/wjh.v16.i10.1169","url":null,"abstract":"<p><strong>Background: </strong><i>Helicobacter pylori</i> (<i>H. pylori</i>) is associated with the development of gastrointestinal disorders ranging from gastritis to gastric cancer. The evidence of the association between metabolic dysfunction-associated steatohepatitis (MASH) and <i>H. pylori</i> infection in the literature is scarce. Therefore, we aim to evaluate the risk of developing MASH in patients who have had a diagnosis of <i>H. pylori</i> infection independently of any confounding variables.</p><p><strong>Aim: </strong>To evaluate the risk of developing MASH in patients who have had a diagnosis of <i>H. pylori</i> infection.</p><p><strong>Methods: </strong>This study used a validated multicenter research database of over 360 hospitals across 26 healthcare systems across the United States from 1999 to 2022. Multivariate regression analysis assessed the risk of developing MASH, adjusting for confounders including <i>H. pylori</i> infection, obesity, type 2 diabetes, hypertension, dyslipidemia, and male gender. A two-sided <i>P</i> value < 0.05 was considered as statistically significant, and all statistical analyses were performed using R version 4.0.2 (R Foundation for Statistical Computing, Vienna, Austria, 2008).</p><p><strong>Results: </strong>A total of 79476132 individuals were screened in the database and 69232620 were selected in the final analysis after accounting for inclusion and exclusion criteria. Smokers (14.30%), patients with hyperlipidemia (70.35%), hypertension (73.86%), diabetes mellitus type 2 (56.46%), and obese patients (58.15%) were more common in patients with MASH compared to control. Using a multivariate regression analysis, the risk of MASH was increased in diabetics [odds ratio (OR): 3.55; 95%CI: 3.48-3.62], obese (OR: 5.93; 95%CI: 5.81-6.04), males (OR: 1.49; 95%CI: 1.46-1.52), individuals with hyperlipidemia (OR: 2.43; 95%CI: 2.38-2.49) and <i>H. pylori</i> infection (OR: 2.51; 95%CI: 2.31-2.73).</p><p><strong>Conclusion: </strong>This is the largest population-based study in the United States illustrating an increased prevalence and odds of developing MASH in patients with <i>H. pylori</i> infection after adjusting for risk factors.</p>","PeriodicalId":23687,"journal":{"name":"World Journal of Hepatology","volume":null,"pages":null},"PeriodicalIF":2.5,"publicationDate":"2024-10-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11514611/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142547763","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Bioactive constituents and action mechanism of Xiaoyao San for treatment of non-alcoholic fatty liver disease.","authors":"Xiao-Xia Qiu, Zheng Li","doi":"10.4254/wjh.v16.i10.1213","DOIUrl":"https://doi.org/10.4254/wjh.v16.i10.1213","url":null,"abstract":"<p><p>Xiaoyao San (XYS) is a classic Chinese medicine prescription. It is traditionally used to relieve syndrome of \"liver stagnation and spleen deficiency\", a common syndrome type in traditional Chinese medicine, through soothing liver, tonifying spleen, and nourishing blood. Correspondingly, XYS has long application in the treatment of depression, dyspepsia and liver diseases. Given the rising of cutting-edge researches on XYS, there's a significant need to diligently uncover the bioactive constituents and action mechanisms of XYS for treating non-alcoholic fatty liver disease accordingly.</p>","PeriodicalId":23687,"journal":{"name":"World Journal of Hepatology","volume":null,"pages":null},"PeriodicalIF":2.5,"publicationDate":"2024-10-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11514614/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142547837","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Platelet counts to spleen diameter ratio: A promising noninvasive tool for predicting esophageal varices in cirrhosis patients.","authors":"Getnet Yigzaw Mossie, Abdulsemed Mohammed Nur, Zekarias Seifu Ayalew, Gebeyehu Tessema Azibte, Kaleb Assefa Berhane","doi":"10.4254/wjh.v16.i10.1177","DOIUrl":"https://doi.org/10.4254/wjh.v16.i10.1177","url":null,"abstract":"<p><strong>Background: </strong>Liver cirrhosis is the end stage of progressive liver fibrosis as a consequence of chronic liver inflammation, wherein the standard hepatic architecture is replaced by regenerative hepatic nodules, which eventually lead to liver failure. Cirrhosis without any symptoms is referred to as compensated cirrhosis. Complications such as ascites, variceal bleeding, and hepatic encephalopathy indicate the onset of decompensated cirrhosis. Gastroesophageal varices are the hallmark of clinically significant portal hypertension.</p><p><strong>Aim: </strong>To determine the accuracy of the platelet count-to-spleen diameter (PC/SD) ratio to evaluate esophageal varices (EV) in patients with cirrhosis.</p><p><strong>Methods: </strong>This retrospective observational study was conducted at Tikur Anbessa Specialized Hospital and Adera Medical Center from January 1, 2019, to December 30, 2023. Data were collected <i>via</i> chart review and direct patient interviews using structured questionnaires. The data were exported to the SPSS software version 26 for analysis and clearance. A receiver operating characteristic curve was plotted for splenic diameter, platelet count, and PC/SD ratio to obtain sensitivity, specificity, positive predictive value, negative predictive value, positive likelihood ratio, and negative likelihood ratio.</p><p><strong>Results: </strong>Of the 140 participants, 67% were men. Hepatitis B (38%) was the most common cause of cirrhosis, followed by cryptogenic cirrhosis (28%) and hepatitis C (16%). Approximately 83.6% of the participants had endoscopic evidence of EV, whereas 51.1% had gastric varices. Decompensated cirrhosis and PC were associated with the presence of EV with adjusted odds ratios of 12.63 (95%CI: 3.16-67.58, <i>P</i> = 0.001) and 0.14 (95%CI: 0.037-0.52, <i>P</i> = 0.004), respectively. A PC/SD ratio < 1119 had a sensitivity of 86.32% and specificity of 70% with area under the curve of 0.835 (95%CI: 0.736-0.934, <i>P</i> < 0.001).</p><p><strong>Conclusion: </strong>A PC/SD ratio < 1119 predicts EV in patients with cirrhosis. It is a valuable, noninvasive tool for EV risk assessment in resource-limited settings.</p>","PeriodicalId":23687,"journal":{"name":"World Journal of Hepatology","volume":null,"pages":null},"PeriodicalIF":2.5,"publicationDate":"2024-10-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11514619/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142547762","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Advances in immunotherapy for hepatitis B virus associated hepatocellular carcinoma patients.","authors":"Wei-Hua Cao, Ya-Qin Zhang, Xin-Xin Li, Zi-Yu Zhang, Ming-Hui Li","doi":"10.4254/wjh.v16.i10.1158","DOIUrl":"https://doi.org/10.4254/wjh.v16.i10.1158","url":null,"abstract":"<p><p>Hepatitis B virus (HBV) infection plays an important role in the occurrence and development of hepatocellular carcinoma (HCC), and the rate of HBV infection in liver cancer patients in China is as high as 92.05%. Due to long-term exposure to chronic antigens from the gut, the liver needs to maintain a certain level of immune tolerance, both to avoid severe inflammation caused by non-pathogenic antigens and to maintain the possibility of rapid and violent responses to infection and tumors. Therefore, HBV infection interacts with the tumor microenvironment (TME) through a highly complex and intertwined signaling pathway, which results in a special TME in HCC. Due to changes in the TME, tumor cells can evade immune surveillance by inhibiting tumor-specific T cell function through cytotoxic T-lymphocy-associated protein-4 (CTLA-4) and programmed cell death 1 (PD-1)/programmed cell death ligand 1 (PD-L1). Interferons, as a class of immune factors with strong biological activity, can improve the TME of HBV-HCC through various pathways. In recent years, the systematic treatment of HCC has gradually come out of the dilemma. In addition to the continuous emergence of new multi-target anti-vascular tyrosine kinase inhibitor drugs, immune checkpoint inhibitors have opened up a new avenue for the systematic treatment of HCC. At present, immunotherapy based on PD-1/L1 inhibitors has gradually become a new direction of systematic treatment for HCC, and the disease characteristics of patients included in global clinical studies are different from those of Chinese patients. Therefore, whether a group of HCC patients with HBV background and poor prognosis in China can also benefit from immunotherapy is an issue of wide concern. This review aims to elucidate the advances of immunotherapy for HBV related HCC patients with regard to: (1) Immunotherapy based on interferons; (2) Immunotherapy based on PD-1/L1 inhibitors; (3) Immunotherapy based on CTLA4 inhibitors; (4) Adoptive cell transfer; (5) Combination immunotherapy strategy; and (6) Shortcomings of immunotherapy.</p>","PeriodicalId":23687,"journal":{"name":"World Journal of Hepatology","volume":null,"pages":null},"PeriodicalIF":2.5,"publicationDate":"2024-10-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11514615/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142547836","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pathogenesis and research progress of nonalcoholic fatty liver disease/nonalcoholic steatohepatitis.","authors":"Guan-Yue Shan, Hui Wan, Yu-Xin Zhang, Jun-Ya Cheng, Duan-Rui Qiao, Yi-Ying Liu, Wen-Na Shi, Hai-Jun Li","doi":"10.4254/wjh.v16.i10.1142","DOIUrl":"https://doi.org/10.4254/wjh.v16.i10.1142","url":null,"abstract":"<p><p>In this editorial, we comment on the article by Mei <i>et al</i>. Nonalcoholic steatohepatitis (NASH) is a severe inflammatory subtype of nonalcoholic fatty liver disease (NAFLD) with pathological features including steatosis, hepatocellular damage, and varying degrees of fibrosis. With the epidemic of metabolic diseases and obesity, the prevalence of NAFLD in China has increased, and it is now similar to that in developed countries; thus, NAFLD has become a major chronic liver disease in China. Human epidemiological data suggest that estrogen has a protective effect on NASH in premenopausal women and that sex hormones influence the development of liver disease. This review focuses on the pathogenesis, treatment, and relationship between NASH and other diseases as well as on the relationship between NASH and sex hormone metabolism, with the aim of providing new strategies for the treatment of NASH.</p>","PeriodicalId":23687,"journal":{"name":"World Journal of Hepatology","volume":null,"pages":null},"PeriodicalIF":2.5,"publicationDate":"2024-10-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11514618/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142547761","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Chronic hepatitis B: Prevent, diagnose, and treat before the point of no return.","authors":"Sudheer Marrapu, Ramesh Kumar","doi":"10.4254/wjh.v16.i10.1151","DOIUrl":"https://doi.org/10.4254/wjh.v16.i10.1151","url":null,"abstract":"<p><p>Hepatitis B remains a significant global health challenge, contributing to substantial morbidity and mortality. Approximately 254 million people worldwide live with Chronic hepatitis B (CHB), with the majority of cases occurring in sub-Saharan Africa and the Western Pacific regions. Alarmingly, only about 13.4% of the individuals infected with this disease have been diagnosed, and awareness of hepatitis B virus (HBV) infection status is as low as 1% in sub-Saharan Africa. In 2022, CHB led to 1.1 million deaths globally. The World Health Organization (WHO) has set a target of eliminating hepatitis B as a public health concern by 2030; however, this goal appears increasingly unattainable due to multiple challenges. These challenges include low vaccination coverage; a large number of undiagnosed cases; a low proportion of patients eligible for treatment under current guidelines; limited access to healthcare; and the costs associated with lifelong treatment. Treatment of HBV can yield significant clinical benefits within a long window of opportunity. However, the benefits of therapy are markedly diminished when the disease is detected at the advanced cirrhosis stage. This editorial aim to highlight the current challenges in hepatitis care and the necessary steps to achieve the WHO's hepatitis elimination goals for 2030.</p>","PeriodicalId":23687,"journal":{"name":"World Journal of Hepatology","volume":null,"pages":null},"PeriodicalIF":2.5,"publicationDate":"2024-10-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11514616/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142547757","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}