{"title":"Estimating cancer risk in immune-mediated inflammatory diseases exposed to varying doses of tumour necrosis factor inhibitors.","authors":"Shinji Okabayashi, Takahiro Itaya, Hajime Yamazaki, Ryo Yanai, Masaaki Isshiki, Yosuke Yamamoto","doi":"10.1007/s00535-024-02190-z","DOIUrl":"10.1007/s00535-024-02190-z","url":null,"abstract":"<p><strong>Background: </strong>The safety profile of high doses of tumour necrosis factor inhibitors (TNFi) therapy for cancer risk in immune-mediated inflammatory diseases (IMIDs) remains uncertain. We evaluated the risk of cancer development in patients with IMIDs exposed to standard and high doses of TNFi compared with those never exposed to TNFi.</p><p><strong>Methods: </strong>A cohort study was conducted using the Japanese claims database encompassing over 4.6 million individuals from 2013 to 2021. The study included patients aged 16 years or older with new-onset IMIDs, such as inflammatory bowel disease, rheumatoid arthritis, or psoriasis, who had no cancer history. The subdistribution hazard ratios (SHR) for cancer risk in TNFi standard and high dose groups comparing with TNFi unexposed group were estimated using a Fine and Gray model that accounted for the competing risk of death unrelated to cancer. The high dose of TNFi was defined as either a dose escalation or shortening of the intervals during administrations from the standard dose treatment.</p><p><strong>Results: </strong>We identified a total of 42,006 patients with new-onset IMIDs (40,573 in TNFi unexposed, 876 in TNFi standard dose, and 557 in TNFi high dose) and 1211 (2.8%) patients developed cancer, yielding an incidence rate of 787.8 (739.9-828.1) per 100,000 person-years. Neither the standard nor high doses of TNFi significantly increased the cancer risk (TNFi standard dose vs. TNFi unexposed, adjusted SHR, 0.65 [0.40-1.08]; TNF high dose vs. TNFi unexposed, adjusted SHR, 1.12 [0.67-1.87]).</p><p><strong>Conclusions: </strong>There is no association between varying doses of TNFi therapy and cancer risk in IMIDs.</p>","PeriodicalId":16059,"journal":{"name":"Journal of Gastroenterology","volume":" ","pages":"285-293"},"PeriodicalIF":6.9,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142785951","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Tadakazu Hisamatsu, Makoto Naganuma, Philippe Pinton, Mitsuhiro Takeno
{"title":"Behçet's disease: incidence, prevalence, and real-word data on the use of biologic agents in Japan.","authors":"Tadakazu Hisamatsu, Makoto Naganuma, Philippe Pinton, Mitsuhiro Takeno","doi":"10.1007/s00535-024-02191-y","DOIUrl":"10.1007/s00535-024-02191-y","url":null,"abstract":"<p><strong>Background: </strong>Behçet's disease (BD) is an autoinflammatory disease that can affect multiple organs, including the gastrointestinal tract. Conventional management comprises anti-inflammatory drugs such as glucocorticoids (GCs) and/or immunomodulators that alleviate symptoms. The introduction of biological agents that target tumor necrosis factor α (TNF-α) has improved disease management. The goal of this work was to analyze the current prevalence and incidence of total BD and gastrointestinal Behçet's disease (GIBD) in Japan, and examine treatment trends, especially regarding the use of TNF-α inhibitors (TNFαi).</p><p><strong>Methods: </strong>We performed a retrospective descriptive observational study in which BD and GIBD demographic trends, medical treatment patterns, and reported adverse events (AEs) were assessed among patients with data recorded between 2017 and 2021 in the Japan Medical Data Center Claims Database (now JMDC Inc.).</p><p><strong>Results: </strong>Prevalence of BD and GIBD in Japan during the observation period increased at an annual rate of + 3% and + 4%, respectively, while incidence decreased by - 5% and - 2%, with a more prominent decline in confirmed GIBD cases (- 15%). Although GCs were the most common initial treatment administered, use of TNFαi for BD and GIBD management increased by + 5.6% and + 8.1%, respectively. Severe AEs (mainly pneumonia and GI-associated AEs) were reported in 40% of patients receiving TNFαi; however, a high retention rate (of up to 80%) was observed 3 years after treatment initiation.</p><p><strong>Conclusion: </strong>The use of TNFαi for GIBD treatment has increased in Japan in recent years. Additional research is necessary to further evaluate TNFαi effectiveness in GIBD and other BD subtypes.</p>","PeriodicalId":16059,"journal":{"name":"Journal of Gastroenterology","volume":" ","pages":"294-305"},"PeriodicalIF":6.9,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11880103/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142791984","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"WWP1 inhibition suppresses the proliferation of pancreatic cancer cells by regulating the PI3K-AKT pathway.","authors":"Genso Notoya, Takahiro Kishikawa, Kengo Yasugi, Takuma Iwata, Takahiro Seimiya, Koji Miyabayashi, Ryota Takahashi, Keisuke Yamamoto, Hideaki Ijichi, Motoyuki Otsuka, Mitsuhiro Fujishiro","doi":"10.1007/s00535-024-02192-x","DOIUrl":"10.1007/s00535-024-02192-x","url":null,"abstract":"<p><strong>Background: </strong>The proto-oncogene WWP1 is overexpressed in various cancers and contributes to tumor growth and poor prognosis. Recently, WWP1 inhibition was reported to suppress tumor development and cell proliferation by activating the PTEN function. However, the expression profiles and clinical significance of WWP1 in pancreatic ductal adenocarcinoma (PDAC) tissues remain undetermined. Therefore, this study aimed to evaluate the WWP1 expression in PDAC and investigate the therapeutic potential of WWP1 inhibition.</p><p><strong>Methods: </strong>Cellular proliferation assays were performed using a doxycycline-inducible shWWP1 expression system. Transcriptome analyses were conducted to identify the altered pathways in WWP1-depleted cells. PTEN ubiquitination by WWP1 was confirmed using immunoprecipitation assays. In vivo xenograft and drug screening assays were performed to evaluate the clinical significance of WWP1 inhibition.</p><p><strong>Results: </strong>WWP1 was significantly upregulated in PDAC tissues and associated with poor prognosis. WWP1 depletion significantly reduced the proliferation of PDAC cell lines, correlating with the suppression of the PI3K-AKT pathway. Mechanistically, as reported in other cancer types, PTEN is a target of WWP1 in PDAC cells. PTEN silencing abrogated the growth-inhibitory effects in WWP1-depleted cells, suggesting that the anti-tumor effects of WWP1 inhibition are mediated through PTEN activation. In vivo xenograft studies confirmed that WWP1 depletion substantially inhibited tumor growth. Moreover, drug screening assays revealed that WWP1 depletion had an additive effect with the PI3K-AKT pathway inhibitors on hindering tumor growth.</p><p><strong>Conclusion: </strong>WWP1 inhibition enhances the anti-tumor effects of PI3K-AKT pathway inhibitors through PTEN activation. Thus, WWP1 could be a potential therapeutic target in PDAC.</p>","PeriodicalId":16059,"journal":{"name":"Journal of Gastroenterology","volume":" ","pages":"370-384"},"PeriodicalIF":6.9,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11880106/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142801099","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Fungal mycobiome dysbiosis in choledocholithiasis concurrent with cholangitis.","authors":"Zhiyuan Hao, Yiting Lu, Yarong Hao, Yuanyuan Luo, Kaiming Wu, Changpeng Zhu, Peimei Shi, Feng Zhu, Yong Lin, Xin Zeng","doi":"10.1007/s00535-024-02183-y","DOIUrl":"10.1007/s00535-024-02183-y","url":null,"abstract":"<p><strong>Background: </strong>The gut mycobiome might have an important influence on the pathogenesis of choledocholithiasis concurrent with cholangitis (CC). The aim of this study was to characterize the fungal mycobiome profiles, explore the correlation and equilibrium of gut interkingdom network among bacteria-fungi-metabolites triangle in CCs.</p><p><strong>Methods: </strong>In a retrospective case-control study, we recruited patients with CC (n = 25) and healthy controls (HCs) (n = 25) respectively to analyze the gut fungal dysbiosis. Metagenomic sequencing was employed to characterize the gut mycobiome profiles, and liquid chromatography/mass spectrometry (LC/MS) analysis was used to quantify the metabolites composition.</p><p><strong>Results: </strong>The Shannon index displayed a reduction in fungal α-diversity in CCs compared to HCs (p = 0.041), and the overall fungal composition differed significantly between two groups. The dominant 7 fungi species with the remarkable altered abundance were identified (LDA score > 3.0, p < 0.05), including CC-enriched Aspergillus_niger and CC-depleted fungi Saccharomyces_boulardii. In addition, the correlations between CC-related fungi and clinical variables in CCs were analyzed. Moreover, the increased abundance ratio of Basidiomycota-to-Ascomycota and a dense linkage of bacteria-fungi interkingdom network in CCs were demonstrated. Finally, we identified 30 markedly altered metabolites in CCs (VIP > 1.0 and p < 0.05), including low level of acetate and butyrate, and the deeper understanding on the complexity of bacteria-fungi-metabolites triangle involving bile inflammation was verified.</p><p><strong>Conclusion: </strong>Our investigation demonstrated a distinct gut fungal dysbiosis in CCs and proposed that, beyond bacteria, the more attention should be paid to significantly potential influence of fungi and bacteria-fungi-metabolites triangle interkingdom interactions on pathogenesis of CC.</p>","PeriodicalId":16059,"journal":{"name":"Journal of Gastroenterology","volume":" ","pages":"340-355"},"PeriodicalIF":6.9,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142739644","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Ryoichi Miura, Atsushi Ono, Hikaru Nakahara, Yuki Shirane, Kenji Yamaoka, Yasutoshi Fujii, Shinsuke Uchikawa, Hatsue Fujino, Eisuke Murakami, Tomokazu Kawaoka, Daiki Miki, Masataka Tsuge, Takeshi Kishi, Waka Ohishi, Naoya Sakamoto, Koji Arihiro, Clair Nelson Hayes, Shiro Oka
{"title":"Serum IL-6 concentration is a useful biomarker to predict the efficacy of atezolizumab plus bevacizumab in patients with hepatocellular carcinoma.","authors":"Ryoichi Miura, Atsushi Ono, Hikaru Nakahara, Yuki Shirane, Kenji Yamaoka, Yasutoshi Fujii, Shinsuke Uchikawa, Hatsue Fujino, Eisuke Murakami, Tomokazu Kawaoka, Daiki Miki, Masataka Tsuge, Takeshi Kishi, Waka Ohishi, Naoya Sakamoto, Koji Arihiro, Clair Nelson Hayes, Shiro Oka","doi":"10.1007/s00535-024-02185-w","DOIUrl":"10.1007/s00535-024-02185-w","url":null,"abstract":"<p><strong>Background: </strong>This study aims to identify biomarkers for treatment response of atezolizumab plus bevacizumab (Atezo+Bev) in patients with hepatocellular carcinoma (HCC).</p><p><strong>Methods: </strong>96 patients who received Atezo+Bev or lenvatinib as a first-line systemic therapy were enrolled as the training group after propensity score matching (PSM), and 42 patients treated with Atezo+Bev were enrolled as the validation group. 17 serum cytokines were measured by Luminex multiplex assay at the start of treatment. For further assessment of the association between cytokine levels and the tumor microenvironment (TME), immunohistochemistry (IHC) was performed on pre-treatment liver biopsy specimens.</p><p><strong>Results: </strong>In the derivation set, multivariate analysis identified elevated IL-6 as an independent risk factor in the Atezo+Bev group (HR 5.80: p<0.01), but not in the lenvatinib group; in a subset analysis of patients with low IL-6, PFS was longer in the Atezo+Bev training group than in the lenvatinib group (p = 0.02). A validation study also showed a significantly longer prognosis in the low IL-6 group for both PFS (p = 0.0001) and OS (p = 0.03). Serum IL-6 had a positive correlation with tumor IL-6 expression (ρ = 0.56, p < 0.0001) and an inverse correlation with the CD8/CD163-positive cell count ratio (ρ = -0.4, p < 0.01).</p><p><strong>Conclusion: </strong>Serum IL-6 levels are thought to be involved in the suppression of tumor immunity and are useful in predicting the therapeutic effect of Atezo+Bev treatment.</p>","PeriodicalId":16059,"journal":{"name":"Journal of Gastroenterology","volume":" ","pages":"328-339"},"PeriodicalIF":6.9,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11880141/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142801089","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Efficacy of liposomal irinotecan + 5-FU/LV vs. S-1 in gemcitabine-refractory metastatic pancreatic cancer: a real-world study using inverse probability of treatment weighting.","authors":"Hiroshi Imaoka, Masafumi Ikeda, Satoshi Kobayashi, Akihiro Ohba, Masayuki Ueno, Yuko Suzuki, Hidetaka Tsumura, Nana Kimura, Shinya Kawaguchi, Yasuyuki Kawamoto, Kohei Nakachi, Kunihiro Tsuji, Noritoshi Kobayashi, Reiko Ashida, Naohiro Okano, Kumiko Umemoto, Gou Murohisa, Ayumu Hosokawa, Akinori Asagi, Hiroko Nebiki, Rei Suzuki, Takeshi Terashima, Ryusuke Shibata, Kazuhito Kawata, Toshifumi Doi, Hiroshi Ohyama, Yohei Kitano, Kazuhiko Shioji, Hiroyuki Okuyama, Atsushi Naganuma, Yuji Negoro, Yasunari Sakamoto, Satoshi Shimizu, Chigusa Morizane, Makoto Ueno, Junji Furuse, Hiroaki Nagano","doi":"10.1007/s00535-024-02186-9","DOIUrl":"10.1007/s00535-024-02186-9","url":null,"abstract":"<p><strong>Background: </strong>S-1 monotherapy had previously been widely used as a second-line treatment for pancreatic cancer (PC) after gemcitabine-based chemotherapy mainly in Japan. Based on the results of the NAPOLI-1 trial, the recommended second-line therapy is now liposomal irinotecan plus fluorouracil/folinic acid (nal-IRI + 5-FU/LV). However, there have been no studies comparing nal-IRI + 5-FU/LV therapy with S-1 monotherapy.</p><p><strong>Methods: </strong>The main objective of this study was to compare overall survival (OS) in patients treated with nal-IRI + 5-FU/LV and those treated with S-1 monotherapy as second-line treatments, using the inverse probability of treatment weighting (IPTW) method. This study was conducted in 31 institutions participating in Japan Oncology Network in Hepatobiliary and Pancreas. To minimize potential biases due to the retrospective design, IPTW analysis was performed with multiple imputation, and imputed IPTW-adjusted hazard ratios and corresponding 95% confidence intervals (CIs) were estimated using a Cox proportional hazards model and combined into pooled estimates.</p><p><strong>Results: </strong>A total of 463 metastatic PC patients were enrolled in this study (257 in the S-1 monotherapy group and 206 in the nal-IRI + 5-FU/LV group). The median OS was 7.50 months (95% CI 4.18-12.69 months) in the nal-IRI + 5-FU/LV group and 5.72 months (95% CI 2.76-10.79 months) in the S-1 monotherapy group. In the IPTW-adjusted Cox proportional hazards model, nal-IRI + 5-FU/LV was associated with a significant OS benefit (pooled IPTW-adjusted hazard ratio, 0.779; 95% CI 0.399-0.941; p = 0.025).</p><p><strong>Conclusion: </strong>These findings support the use of nal-IRI + 5-FU/LV as standard second-line treatment for PC patients after gemcitabine-based chemotherapy.</p>","PeriodicalId":16059,"journal":{"name":"Journal of Gastroenterology","volume":" ","pages":"356-367"},"PeriodicalIF":6.9,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11880175/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142769671","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Inhibition of liver cancer cell growth by metabolites S-adenosylmethionine and nicotinic acid originating from liver progenitor cells.","authors":"Wen-Ming Liu, Cai-Yang Chen, Hong-Qian Ma, Qiu-Qiu Zhang, Xu Zhou, Yu-Ling Wu, Wei-Jian Huang, Xiao-Shu Qi, Yu-Xin Zhang, Dan Tang, Han-Yong Sun, Hong-Ping Wu, Ying-Fu Jiao, Zhi-Ying He, Wei-Feng Yu, He-Xin Yan","doi":"10.1007/s00535-025-02226-y","DOIUrl":"https://doi.org/10.1007/s00535-025-02226-y","url":null,"abstract":"<p><strong>Background: </strong>Hepatocellular carcinoma (HCC), the most common form of liver cancer, presents a challenging malignancy with scarce treatment options. Liver progenitor cells (LPCs) play a pivotal role in both liver regeneration and the progression of liver cancer, yet the specific functions of LPCs from different origins in liver cancer remain to be fully elucidated.</p><p><strong>Methods: </strong>We explored the liver progenitor-like cells derived from human hepatocytes (HepLPCs) on the proliferation of HCC both in vitro and in vivo. The mitochondrial function was assessed through electron microscopy and functional experiments. Transcriptomic sequencing and western blot unveiled the fundamental mechanisms at play, whereas metabolomic sequencing pinpointed crucial effector molecules involved in the paracrine secretion of HepLPCs.</p><p><strong>Results: </strong>By employing a co-culture system of HepLPCs and HCC cells, we found that HepLPCs markedly inhibited HCC growth by prompting mitochondrial dysfunction, which further led to the co-inhibition of the Notch1 and JAK1/STAT3 signaling pathways through paracrine actions involving S-adenosylmethionine (SAM) and Nicotinic acid (NA).</p><p><strong>Conclusions: </strong>This study has uncovered that HepLPCs have a suppressive influence on the proliferation of HCC cells. This is achieved through the impairment of mitochondrial function and the inhibition of key signaling pathways, namely, Notch1 and JAK1/STAT3, which are critical drivers of cancer progression. The secretion of the metabolites SAM and NA by HepLPCs appears to be instrumental in mediating these effects. These findings provide a solid foundation for identifying new therapeutic targets and clarifying the mechanisms through which HepLPCs can be harnessed to effectively treat HCC.</p>","PeriodicalId":16059,"journal":{"name":"Journal of Gastroenterology","volume":" ","pages":""},"PeriodicalIF":6.9,"publicationDate":"2025-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143523281","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Min Kyu Kim, Seung Hwan Shin, Cheol-Hyung Lee, Soyoung Kim, Jong Whan Kim, Songhyun Lee, Seung Wook Hong, Sang Hyoung Park, Dong-Hoon Yang, Byong Duk Ye, Jeong-Sik Byeon, Seung-Jae Myung, Suk-Kyun Yang, Sung Wook Hwang
{"title":"Temporal trends in obesity and its prognostic impact in Korean patients with inflammatory bowel disease.","authors":"Min Kyu Kim, Seung Hwan Shin, Cheol-Hyung Lee, Soyoung Kim, Jong Whan Kim, Songhyun Lee, Seung Wook Hong, Sang Hyoung Park, Dong-Hoon Yang, Byong Duk Ye, Jeong-Sik Byeon, Seung-Jae Myung, Suk-Kyun Yang, Sung Wook Hwang","doi":"10.1007/s00535-025-02230-2","DOIUrl":"https://doi.org/10.1007/s00535-025-02230-2","url":null,"abstract":"<p><strong>Background: </strong>To assess the changes in body mass index (BMI) among Korean patients with inflammatory bowel disease (IBD) over a 14-year period and to explore how BMI at diagnosis impacts prognosis.</p><p><strong>Methods: </strong>We retrospectively collected BMI and laboratory data from patients with IBD who visited the Asan Medical Center between 2008 and 2021 (Cohort 1). Clinical outcomes, including intestinal resection and medication use, were analyzed in patients with a recorded BMI at diagnosis who were followed up in a prospectively maintained cohort (Cohort 2).</p><p><strong>Results: </strong>Among 11,216 IBD patients (Cohort 1), the median BMI increased over the study period, and the disparity in the prevalence of obese individuals (BMI ≥ 25 kg/m<sup>2</sup>) between those with IBD and the general population narrowed. Serum glucose and lipid profiles showed an upward trend during the study period. In patients with recorded BMI at the time of diagnosis (Cohort 2), the odds of intestinal resection and the use of biologics/small molecules were comparable or even lower in Crohn's disease (CD) and ulcerative colitis patients who were obese compared to patients with a normal BMI. Obesity (≥ 25 kg/m<sup>2</sup>) was inversely associated with the risk of thiopurine use in CD patients (adjusted hazard ratio: 0.61, 95% confidence interval: 0.48-0.78, p < 0.001).</p><p><strong>Conclusions: </strong>During a 14-year period, Korean IBD patients showed increasing trends in the prevalence of obese individuals and metabolic syndrome-associated laboratory results. CD patients with high BMI at diagnosis exhibited a similar or lower likelihood of undergoing intestinal resection and medication use compared to those with a normal BMI.</p>","PeriodicalId":16059,"journal":{"name":"Journal of Gastroenterology","volume":" ","pages":""},"PeriodicalIF":6.9,"publicationDate":"2025-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143501868","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"The external validation of Dallas Steatosis Index among Asian population: a useful tool for metabolic dysfunction-associated steatotic liver disease identification and prevention.","authors":"Mengyang Xia, Yixuan Lu, Feiyang Yin, Zhiqiang Cao, Ping Yao, Hongxia Li","doi":"10.1007/s00535-025-02220-4","DOIUrl":"https://doi.org/10.1007/s00535-025-02220-4","url":null,"abstract":"<p><strong>Background: </strong>The Dallas Steatosis Index (DSI) is a non-invasive tool (NIT) developed to detect the risk of metabolic dysfunction-associated steatotic liver disease (MASLD) in multi-ethnic populations, external validation in Asians has yet to be conducted. Therefore, we evaluated the ability of the DSI with the BMI classification of WPRO (DSI_WPRO) to identify MASLD in the Chinese population. In addition, we investigated the associations between the DSI_WPRO and the risk of MASLD in a longitudinal study.</p><p><strong>Methods: </strong>Baseline data from the Dongfeng-Tongji cohort were collected to investigate the ability of the DSI_WPRO to identify MASLD patients by ROC analysis. Furthermore, multivariate logistic regressions were performed to investigate the associations of the DSI_WPRO and MASLD risks in a 5-year follow-up of the DFTJ cohort study.</p><p><strong>Results: </strong>Among a total of 9,376 MASLD participants and 25,974 non-MASLD participants, the area under the curve (AUC) of the DSI_WPRO reached 0.777 after adjusting BMI classification, which is higher than other NITs in this study. In addition, we redefined the risk category and the screening proposal of MASLD in Asians with the DSI_WPRO. We found that the cutoff point of 0 has the best ability to recognize the presence or absence of MASLD. Furthermore, compared with the low DSI_WPRO (DSI_WPRO < 0), OR (95% CIs) of higher DSI_WPRO (DSI_WPRO ≥ 0) was 3.048 (2.827 ~ 3.285) for MASLD.</p><p><strong>Conclusion: </strong>The DSI is a useful tool for MASLD identification and prevention. After more validation studies, DSI can be generalized in the Asian population.</p>","PeriodicalId":16059,"journal":{"name":"Journal of Gastroenterology","volume":" ","pages":""},"PeriodicalIF":6.9,"publicationDate":"2025-02-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143492344","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}