Alimentary Pharmacology & Therapeutics最新文献

{"title":"Editorial: The Devil Is in the Detail—Interpreting the Findings of Network Meta‐Analyses. Authors' Reply","authors":"Mohammad Shehab, Amro Hassan, Talat Bessissow","doi":"10.1111/apt.70342","DOIUrl":"https://doi.org/10.1111/apt.70342","url":null,"abstract":"","PeriodicalId":121,"journal":{"name":"Alimentary Pharmacology & Therapeutics","volume":"103 1","pages":""},"PeriodicalIF":7.6,"publicationDate":"2025-09-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145003089","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Editorial: The Devil Is in the Detail—Interpreting the Findings of Network Meta‐Analyses","authors":"Christy Riggott, David J. Gracie","doi":"10.1111/apt.70324","DOIUrl":"https://doi.org/10.1111/apt.70324","url":null,"abstract":"","PeriodicalId":121,"journal":{"name":"Alimentary Pharmacology & Therapeutics","volume":"14 1","pages":""},"PeriodicalIF":7.6,"publicationDate":"2025-09-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145002795","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Letter on ‘Long-Term Dynamic Changes of Alanine Aminotransferase Levels Are Associated With Liver-Related Events in Nucleos(t)ide Analogue-Treated Chronic Hepatitis B Patients in China’—Authors' Reply","authors":"Ning Yu, Rong Fan","doi":"10.1111/apt.70363","DOIUrl":"10.1111/apt.70363","url":null,"abstract":"<p>We are grateful for the insightful letter by Drs. Dong Hyun Kim and Hye Won Lee [<span>1</span>] on our recent study regarding the prognostic significance of longitudinal alanine aminotransferase (ALT) dynamics in nucleos(t)ide analogue-treated chronic hepatitis B (CHB) patients [<span>2</span>]. We sincerely appreciate the opportunity to address the issues raised.</p><p>First, the Search-B cohort, from which the ALT thresholds were derived, originated from a well-designed prospective study with standardised follow-up protocols and systematic data collection, ensuring high data quality and reliability for threshold determination. In contrast, the Hong Kong cohort was constructed from retrospective electronic medical records, in which the frequency of patient follow-up showed significant fluctuations according to the clinical condition of patients. These characteristics make it more suitable as a real-world validation set. Moreover, the ALT thresholds were selected based on LRE risk discrimination and defined using the 95th percentile of the statistical reference range—a widely adopted approach for determining clinical cutoffs. When compared with the established ALT cutoffs [<span>3-5</span>], patients with ALT ≤ 23/16 U/L had the lowest 7-year LRE incidence (5.8%), which increased with ALT ≤ 30/19 (6.8%), or ≤ 35/25 (6.9%) (Figure 1A–C). Notably, the cutoffs of 23/16 U/L can further stratify the risk of LRE in patients with ALT below these established thresholds (Figure 1D). These findings further support the notion that lower ALT thresholds provide superior prognostic discrimination. While histologic validation would strengthen our findings, concordant findings across two independent cohorts underscore the robustness of sex-specific thresholds.</p><p>Second, we fully acknowledge that ALT levels can be influenced by various factors beyond viral activity. While accounting for these determinants would enhance precision for specific populations, it introduces great challenges and substantial complexity for widespread clinical implementation. Therefore, sex-specific ALT thresholds remain a practical and feasible strategy for risk stratification. Additionally, our analyses confirmed that the cutoffs of 23/16 U/L demonstrated consistent prognostic value across varied clinical profiles, suggesting their broad applicability. Nevertheless, as noted in the limitations, residual confounding from alcohol use, medications and lifestyle factors cannot be fully excluded in this retrospective design study. Future research should incorporate these elements to validate our findings.</p><p>Third, we fully agree that ALT fluctuations—which may reflect viral replication and host immune responses [<span>6, 7</span>]—have important clinical implications and warrant further investigation. As shown in table S5 of the original manuscript [<span>2</span>], patients with fluctuating trajectories had a higher 7-year LRE incidence (13.1% in men and 6.8% in women) than thos","PeriodicalId":121,"journal":{"name":"Alimentary Pharmacology & Therapeutics","volume":"62 9","pages":"956-958"},"PeriodicalIF":6.7,"publicationDate":"2025-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/apt.70363","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145003099","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Letter on ‘Long-Term Dynamic Changes of Alanine Aminotransferase Levels Are Associated With Liver-Related Events in Nucleos(t)ide Analogue-Treated Chronic Hepatitis B Patients in China’","authors":"Dong Hyun Kim, Hye Won Lee","doi":"10.1111/apt.70347","DOIUrl":"10.1111/apt.70347","url":null,"abstract":"<p>We read with great interest the study by Fan et al. [<span>1</span>], which demonstrated the prognostic significance of sustained alanine aminotransferase (ALT) normalization in nucleos(t)ide analogue (NA)-treated chronic hepatitis B (CHB). Their large, long-term cohorts and latent class mixed modelling (LCMM) provide strong support for sex-specific ALT thresholds (≤ 23/16 U/L in men/women) during antiviral therapy.</p><p>While the study presents significant advances, several issues merit consideration. The cut-offs were derived in the Search-B cohort from the lowest-risk trajectory group and applied unchanged to the Hong Kong cohort, which differed significantly in age, baseline virological suppression and ALT distribution. Yet the ≤ 23/16 U/L group in Hong Kong had nearly identical 7-year LRE rates to Search-B (5.9% vs. 5.5%), suggesting they may simply capture a broadly low-risk subset rather than being optimal for each population. A more rigorous approach would be to derive trajectory groups through LCMM within the Hong Kong population and test whether similar thresholds emerge, directly assessing reproducibility. Moreover, the absence of histologic validation and comparison with established cut-offs (e.g., 35/25 U/L, 40 U/L) [<span>2, 3</span>] leaves their added prognostic utility and specificity uncertain.</p><p>Second, stratification by sex alone may overlook other independent predictors of LREs and ALT fluctuation. Diabetes, cirrhosis, older age and higher FIB-4 were associated with increased LRE risk, while elevated triglycerides were inversely associated with LRE but linked to greater ALT variability. Obesity showed weaker associations and key metabolic data—including fatty liver status and triglyceride levels—were available only in the Search-B cohort, limiting validation. These findings, consistent with prior studies [<span>4, 5</span>], suggest that ALT thresholds should incorporate metabolic and fibrosis-related factors in addition to sex.</p><p>Third, the analysis did not account for factors that can lower ALT independently of disease activity. Commonly used hepatoprotective agents (e.g., ursodeoxycholic acid, silymarin, dimethyl dicarboxylate biphenyl) may reduce ALT without improving long-term outcomes [<span>6, 7</span>]. Alcohol intake, diet and physical activity can also affect ALT via inflammation and insulin resistance [<span>8</span>]. Without adjusting for these, ALT trajectories may not accurately reflect hepatic disease activity.</p><p>Lastly, excluding trajectory groups with unstable ALT (~8% of Search-B) may have omitted clinically relevant subgroups. These patterns, often indicating ALT flares, are strongly associated with hepatocellular carcinoma risk; a recent multi-country cohort reported hazard ratios of 2.55 in China and 7.62 in the US for ALT flares during NA therapy compared with stable ALT [<span>9, 10</span>]. Exploratory analyses of such groups could provide insights into immune activity, inflammation an","PeriodicalId":121,"journal":{"name":"Alimentary Pharmacology & Therapeutics","volume":"62 9","pages":"954-955"},"PeriodicalIF":6.7,"publicationDate":"2025-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/apt.70347","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145003088","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Editorial: Time to Genotype—Genetic Risk and Prognosis in Steatotic Liver Disease. Authors' Reply","authors":"Matthew Kubina, Vincent L. Chen","doi":"10.1111/apt.70361","DOIUrl":"10.1111/apt.70361","url":null,"abstract":"<p>We thank Drs. Mancina and Romeo for their comments and for highlighting the importance of genetic markers as prognostic tools in steatotic liver disease (SLD) [<span>1</span>]. We agree with their statement that early genotyping, especially for high-impact variants such as <i>PNPLA3</i> and <i>TM6SF2</i>, could meaningfully change disease trajectories in clinical practice by identifying individuals at risk for major adverse liver outcomes (MALO) [<span>2</span>]. As our meta-analysis demonstrated, genetic risk alleles are not only associated with disease onset but can stratify risk for cirrhosis, hepatocellular carcinoma, liver-related mortality and other key outcomes [<span>3</span>].</p><p>Most published studies to date have focused on hepatic outcomes, yet the field is rapidly evolving to explore broader implications of genetic variation in SLD. Genetics may help refine disease subgroups and explain heterogeneity in disease trajectory in which some patients die of liver disease while many more never develop cirrhosis but die instead of cardiovascular disease and cancer. As recent genome-wide association studies have illustrated, genetic risk variants in SLD not only influence disease severity but also define biologically distinct subgroups with different distributions of cardiometabolic comorbidities and risk of cardiovascular or hepatic outcomes [<span>4-6</span>]. For example, two recent studies studied ‘partitioned’ polygenic risk scores (PRS) based on subsets of SLD-promoting alleles [<span>5, 6</span>]. While the partitions were defined slightly differently in the two studies, across both studies one PRS group included alleles that impaired hepatic lipid export but reduced serum/plasma lipids (exemplified by alleles in <i>PNPLA3</i> and <i>TM6SF2</i>) and were associated with markedly higher risk of MALO but lower risk of cardiovascular disease, and a second group promoted <i>de novo</i> lipogenesis (exemplified by <i>GCKR</i> and <i>TRIB1</i> variants) and resulted in smaller increases in MALO but large increases in cardiovascular disease.</p><p>Genetics may eventually inform treatment selection. Recent studies have suggested that carriage of the <i>PNPLA3</i>-rs738409-G risk allele is associated with larger ALT reductions in response to semaglutide treatment [<span>7</span>] and greater reductions in liver fat content measured on magnetic resonance imaging following bariatric surgery [<span>8</span>]. In contrast, there was no association between <i>PNPLA3</i>, <i>TM6SF2</i> or <i>HSD17B13</i> genotype and histologic response to resmetirom [<span>9</span>]. In parallel, two first-in-human trials of <i>PNPLA3</i>-targeted gene therapies demonstrated that genetic variants may act not only as risk markers but also as treatment targets [<span>10</span>]. Additional real-world studies will be required to understand if genetics has a role in predicting response to non-targeted therapy and how gene therapy (if efficacious in phase 3 trials)","PeriodicalId":121,"journal":{"name":"Alimentary Pharmacology & Therapeutics","volume":"62 8","pages":"843-844"},"PeriodicalIF":6.7,"publicationDate":"2025-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/apt.70361","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144960251","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Editorial: Time to Genotype—Genetic Risk and Prognosis in Steatotic Liver Disease","authors":"Rosellina M. Mancina, Stefano Romeo","doi":"10.1111/apt.70269","DOIUrl":"10.1111/apt.70269","url":null,"abstract":"<p>As the global burden of steatotic liver disease (SLD), including metabolic dysfunction-associated steatotic liver disease (MASLD) and alcohol-associated liver disease (ALD), continues to grow, hepatology faces a critical need for better tools to predict disease progression. In the last two decades, human genetic studies on SLD identified several variants associated with this disease [<span>1, 2</span>]. The meta-analysis by Kubina et al. [<span>3</span>] provides timely evidence that common variants in key genetic determinants of SLD, namely, <i>PNPLA3</i>, <i>TM6SF2</i> and <i>MBOAT7</i>, may help address this gap. By using data from 40 independent studies for a total of more than 270,000 people, the authors demonstrate that these variants are not just risk factors for SLD onset but meaningful predictors of major adverse liver outcomes (MALO).</p><p>Among all the genetic variants studied, homozygosity for the <i>PNPLA3</i>-rs738409 minor (G) allele emerges as the most powerful and consistent marker of adverse hepatic outcomes. It increases the risk of MALO by 2.3-fold (95% CI 1.66–3.18) [<span>3</span>], hepatocellular carcinoma (HCC) by 2.18-fold (95% CI 1.46–3.27) [<span>3</span>], cirrhosis/advanced liver disease by 2.47-fold (95% CI 1.81–3.37) [<span>3</span>] and, critically, liver-related mortality by 2.83-fold (95% CI 1.58–5.06) [<span>3</span>]. These are substantial effect sizes, comparable to, and in some cases greater than, those of traditional clinical risk factors such as diabetes, highlighting that <i>PNPLA3</i> is a key driver of MASLD progression and, ultimately, liver-related mortality. Interestingly, a recent study showed that <i>PNPLA3</i> homozygosis was associated with higher liver fibrosis by age 44, with an increased impact with aging [<span>4, 5</span>].</p><p>Importantly, <i>TM6SF2</i>-rs58542926 also proved clinically meaningful, particularly for HCC. People carrying the CT or TT genotype had more than a twofold increased risk of HCC (sHR 2.12; 95% CI 1.66–2.70) [<span>3</span>]. Mechanistically, TM6SF2 stabilises APOB [<span>6</span>] and when its function is impaired, hepatocellular lipids accumulate due to reduced very low-density lipoprotein secretion [<span>6</span>]. This is consistent with prior studies showing an enrichment of <i>APOB</i> loss-of-function variants in a cohort of people with HCC [<span>7</span>].</p><p>Crucially, the utility of genetic information is highest when known early. By the time someone reaches advanced fibrosis, the effects of deleterious variants like those in <i>PNPLA3</i> and <i>TM6SF2</i> have often already played out across decades of unrecognised liver injury. Genotyping at the first signs of SLD, namely, elevated transaminases, SLD on imaging or initial fibrosis, offers a window of opportunity to change liver disease trajectory. Early identification of high-risk people may allow for targeted diet, lifestyle and pharmacological intervention.</p><p><i>MBOAT7</i> TT allele showed","PeriodicalId":121,"journal":{"name":"Alimentary Pharmacology & Therapeutics","volume":"62 8","pages":"841-842"},"PeriodicalIF":6.7,"publicationDate":"2025-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/apt.70269","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144960252","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Letter: “Tenofovir Alafenamide—The ‘Star of Potential’ for Long-Term Chronic Hepatitis B Treatment. A Deep-Dive Analysis of Phase 3 Clinical Trials.” Authors' Reply","authors":"Maria Buti, the study team","doi":"10.1111/apt.70358","DOIUrl":"10.1111/apt.70358","url":null,"abstract":"<p>We thank Drs. Dai and Zhu for their comments on our manuscript, ‘Eight-year efficacy and safety of tenofovir alafenamide for treatment of chronic hepatitis B virus infection: Final results from two randomized phase 3 trials’, and for highlighting the long-term benefits of tenofovir alafenamide (TAF) in chronic hepatitis B (CHB) management [<span>1</span>].</p><p>We agree that assessing fibrosis regression, cirrhosis reversal, and hepatocellular carcinoma (HCC) incidence is critical to understanding the full impact of long-term antiviral therapy [<span>2</span>]. While serial liver biopsies were not performed, we employed validated non-invasive markers such as FibroTest, endorsed by international guidelines [<span>3</span>]. Indeed, guidelines have shifted away from recommending invasive percutaneous biopsies. At baseline, approximately 10% of patients had compensated cirrhosis; those with decompensated disease were excluded. By Year 8, cirrhosis prevalence substantially declined across all treatment groups [<span>4</span>]. Most patients with cirrhosis at baseline shifted to lower fibrosis categories, and no patients with compensated cirrhosis experienced hepatic decompensation. The overall 8-year HCC incidence was low (1.8%), notably below predictions from established HCC risk scores [<span>5</span>]. HCC was a predefined adverse event of interest with patients screened per local standard of care. Importantly, prospective surveillance with hepatic ultrasonography was introduced at Week 96 and conducted biannually thereafter. In a recent 5-year analysis of these trials, TAF and tenofovir disoproxil fumarate (TDF) were associated with significantly lower HCC incidence than predicted for untreated patients, with a 68% and 44% reduction in the TAF and TDF-TAF groups, respectively [<span>6</span>]. An extended 8-year analysis is underway. Collectively, these findings underscore the long-term capacity of TAF to alter the natural history of HBV, supporting its role as a preferred therapeutic option for patients with CHB.</p><p>We also agree that broader inclusion of patients with co-infections, advanced liver disease, and diverse racial and ethnic backgrounds would enhance the generalisability of TAF's safety and efficacy profiles across broader patient populations [<span>2</span>]. The two phase 3 trials for TAF enrolled a global population, while subsequent studies have examined TAF in diverse populations such as in patients with renal/hepatic impairment and HIV/HBV coinfection [<span>7, 8</span>]. Future real-world studies should aim to capture underrepresented groups to inform clinical practice across diverse settings. Despite bearing a high burden of HBV, patients from Sub-Saharan Africa remain underrepresented in clinical trials [<span>9</span>]. Greater inclusion of these and other underserved groups is essential to ensure CHB treatment strategies are globally relevant and equitable.</p><p>Although economic factors were beyond our manuscript'","PeriodicalId":121,"journal":{"name":"Alimentary Pharmacology & Therapeutics","volume":"62 7","pages":"762-763"},"PeriodicalIF":6.7,"publicationDate":"2025-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/apt.70358","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144937059","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Letter: Tenofovir Alafenamide—The “Star of Potential” for Long-Term Chronic Hepatitis B Treatment. A Deep-Dive Analysis of Phase 3 Clinical Trials","authors":"YaoYao Dai, JunFeng Zhu","doi":"10.1111/apt.70343","DOIUrl":"10.1111/apt.70343","url":null,"abstract":"<p>I read with great interest the article titled “Eight - Year Efficacy and Safety of Tenofovir Alafenamide for Chronic Hepatitis B Virus Infection: Final Results of Two Randomized Phase 3 Clinical Trials [<span>1</span>].” This study provides valuable insights into the long—term management of chronic hepatitis B (CHB) using tenofovir alafenamide (TAF), which is a significant advancement in the field of hepatology.</p><p>The findings of this study are indeed remarkable. The sustained virological suppression rate over 8 years highlights the potent antiviral efficacy of TAF. Given the chronic nature of hepatitis B infection, long-term viral control is crucial for preventing disease progression to cirrhosis and hepatocellular carcinoma. Although the overall rate of hepatitis B surface antigen (HBsAg) loss is relatively low, it is still noteworthy. HBsAg loss is considered a functional cure for CHB, and any increase in this outcome represents an important step forward in managing this challenging disease.</p><p>Moreover, the safety profile of TAF is commendable. Compared with tenofovir disoproxil fumarate (TDF), TAF has a lower incidence of renal and bone adverse events, which is a major advantage. These side effects have long been a concern in long-term nucleos (t) ide analog therapy, and the improved safety of TAF offers a more favourable risk–benefit ratio for patients who require lifelong treatment. This is especially true for elderly patients or those with comorbidities that may exacerbate renal or bone issues.</p><p>However, I would like to raise some points that merit further discussion. First, although the study demonstrates impressive long-term outcomes, the long-term impact on liver histology and clinical endpoints (such as cirrhosis reversal or hepatocellular carcinoma incidence) would provide a more comprehensive understanding of the benefits of TAF. Longitudinal liver biopsies or non-invasive liver fibrosis markers could offer valuable reference for histological changes associated with long-term TAF treatment [<span>2</span>].</p><p>Second, the study population is relatively homogeneous in terms of baseline characteristics. Future research should strive to include more diverse cohorts, including patients with different racial backgrounds, stages of liver disease, and co-infections. This will help to better understand the efficacy and safety of TAF in real-world settings and its applicability in different patient subgroups [<span>3</span>].</p><p>Lastly, especially in resource–limited settings, the cost–effectiveness of TAF deserves further investigation. Although its superior safety profile may make it valuable for certain populations, the economic burden of long–term treatment needs to be considered. Cost–effectiveness analyses compared with other available treatment options can guide clinical decision–making and health policy [<span>4</span>].</p><p>In summary, the eight-year results of the Phase 3 clinical trials of TAF for CHB are ve","PeriodicalId":121,"journal":{"name":"Alimentary Pharmacology & Therapeutics","volume":"62 7","pages":"760-761"},"PeriodicalIF":6.7,"publicationDate":"2025-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/apt.70343","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144928600","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Editorial: A Step Back to Leap Forward—Strategic Nucleos(t)ide Analogue Discontinuation Towards HBV Functional Cure","authors":"Xuwen Xu, Aili Lu, Shaohang Cai","doi":"10.1111/apt.70352","DOIUrl":"https://doi.org/10.1111/apt.70352","url":null,"abstract":"","PeriodicalId":121,"journal":{"name":"Alimentary Pharmacology & Therapeutics","volume":"4 1","pages":""},"PeriodicalIF":7.6,"publicationDate":"2025-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144928255","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Letter: The Complexity of Deciphering Complex Mechanisms That Underpin Changing Trends in Complex Disease","authors":"Sasza Koczanowski, Jonathan P. Segal","doi":"10.1111/apt.70359","DOIUrl":"https://doi.org/10.1111/apt.70359","url":null,"abstract":"","PeriodicalId":121,"journal":{"name":"Alimentary Pharmacology & Therapeutics","volume":"41 1","pages":""},"PeriodicalIF":7.6,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144924066","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}