Jie Zhou, Danni Ye, Shenli Ren, Jiawei Ding, Tao Zhang, Siyao Zhang, Zheng Chen, Fangshen Xu, Yu Zhang, Huilin Zheng, Zhenhua Hu
Background/aims: Liver transplantation is the most effective treatment for the sickest patients with acute-on-chronic liver failure (ACLF). However, the influence of donor age on liver transplantation, especially in ACLF patients, is still unclear.
Methods: In this study, we used the data of the Scientific Registry of Transplant Recipients. We included patients with ACLF who received liver transplantation from January 1, 2007, to December 31, 2017, and the total number was 13,857. We allocated the ACLF recipients by age into group I (donor age ≤17 years, n=647); group II (donor age 18-59 years, n=11,423); and group III (donor age ≥60 years, n=1,787). Overall survival (OS), graft survival, and mortality were compared among the three age groups and the four ACLF grades. Cox regression was also analyzed.
Results: The 1-, 3-, and 5-year OS rates were 89.6%, 85.5%, and 82.0% in group I; 89.4%, 83.4%, and 78.2% in group II; and 86.8%, 78.4%, and 71.4% in group III, respectively (p<0.001). When we analyzed the different effects of donor age on OS with different ACLF grades, in groups II and III, we observed statistical differences. Finally, the cubic spline curve told us that the relative death rate changed linearly with increasing donor age.
Conclusions: Donor age is related to OS and graft survival of ACLF patients after transplantation, and poorer results were associated with elderly donors. In addition, different donor ages have different effects on recipients with different ACLF grades.
{"title":"Impact of Donor Age on Liver Transplant Outcomes in Patients with Acute-on-Chronic Liver Failure: A Cohort Study.","authors":"Jie Zhou, Danni Ye, Shenli Ren, Jiawei Ding, Tao Zhang, Siyao Zhang, Zheng Chen, Fangshen Xu, Yu Zhang, Huilin Zheng, Zhenhua Hu","doi":"10.5009/gnl230143","DOIUrl":"10.5009/gnl230143","url":null,"abstract":"<p><strong>Background/aims: </strong>Liver transplantation is the most effective treatment for the sickest patients with acute-on-chronic liver failure (ACLF). However, the influence of donor age on liver transplantation, especially in ACLF patients, is still unclear.</p><p><strong>Methods: </strong>In this study, we used the data of the Scientific Registry of Transplant Recipients. We included patients with ACLF who received liver transplantation from January 1, 2007, to December 31, 2017, and the total number was 13,857. We allocated the ACLF recipients by age into group I (donor age ≤17 years, n=647); group II (donor age 18-59 years, n=11,423); and group III (donor age ≥60 years, n=1,787). Overall survival (OS), graft survival, and mortality were compared among the three age groups and the four ACLF grades. Cox regression was also analyzed.</p><p><strong>Results: </strong>The 1-, 3-, and 5-year OS rates were 89.6%, 85.5%, and 82.0% in group I; 89.4%, 83.4%, and 78.2% in group II; and 86.8%, 78.4%, and 71.4% in group III, respectively (p<0.001). When we analyzed the different effects of donor age on OS with different ACLF grades, in groups II and III, we observed statistical differences. Finally, the cubic spline curve told us that the relative death rate changed linearly with increasing donor age.</p><p><strong>Conclusions: </strong>Donor age is related to OS and graft survival of ACLF patients after transplantation, and poorer results were associated with elderly donors. In addition, different donor ages have different effects on recipients with different ACLF grades.</p>","PeriodicalId":12885,"journal":{"name":"Gut and Liver","volume":null,"pages":null},"PeriodicalIF":3.4,"publicationDate":"2024-06-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141431837","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Hoonsub So, Hyun Don Joo, Tae Jun Song, Sung Woo Ko, Ho Seung Lee, Sung Hyun Cho, Dongwook Oh, Sung Yong Han, Dong Uk Kim, Dong-Wan Seo
Background/aims: Malignant duodenal obstruction has become more common with the development of palliative therapies.The outcomes of endoscopic ultrasound-guided gastrojejunostomy (EUS-GJ) are comparable to those of surgical gastrojejunostomy or duodenal stenting. However, EUS-GJ is technically challenging. Duodenal self-expandable metallic stent (SEMS) placement is popular; however, obstructions are common. Duodenal SEMS obstruction can be managed with the insertion of a second SEMS in a stent-in-stent manner. Therefore, we aimed to analyze the clinical outcomes of secondary duodenal SEMS placement in patients with malignant duodenal obstruction.
Methods: We retrospectively analyzed the data of patients who underwent secondary duodenal stent insertion for duodenal stent dysfunction between January 2016 and December 2021. The primary outcome was stent patency. The secondary outcomes were clinical success, factors associated with dysfunction, patient survival, and adverse events.
Results: A total of 109 patients were included. The mean age was 64.4±11.2 years, and 63 patients (57.8%) were male. Ninety-two patients (84.4%) had pancreaticobiliary cancer. Clinical success was achieved in 94 cases (86.2%). Twenty-three patients experienced stent dysfunction with 231 days of median stent patency (95% confidence interval [CI], 169 to not available). After a multivariable Cox hazard analysis of stent patency, the Eastern Cooperative Oncology Group performance status (hazard ratio [HR], 2.13; 95% CI, 1.20 to 3.81; p=0.010) and the first stent patency ≥6 months (HR, 0.33; 95% CI, 0.11 to 0.95; p=0.050) remained significant associated factors. Adverse events occurred in five patients (4.6%).
Conclusions: Secondary duodenal stent insertion is a viable option for first duodenal stent obstruction. Further comparative studies involving surgery or EUS-GJ for obstructed duodenal stents are warranted.
{"title":"Clinical Outcomes of Secondary Duodenal Self-Expandable Metallic Stenting for Duodenal Stent Dysfunction in Patients with Malignant Duodenal Obstruction: A Retrospective Multicenter Study.","authors":"Hoonsub So, Hyun Don Joo, Tae Jun Song, Sung Woo Ko, Ho Seung Lee, Sung Hyun Cho, Dongwook Oh, Sung Yong Han, Dong Uk Kim, Dong-Wan Seo","doi":"10.5009/gnl240014","DOIUrl":"https://doi.org/10.5009/gnl240014","url":null,"abstract":"<p><strong>Background/aims: </strong>Malignant duodenal obstruction has become more common with the development of palliative therapies.The outcomes of endoscopic ultrasound-guided gastrojejunostomy (EUS-GJ) are comparable to those of surgical gastrojejunostomy or duodenal stenting. However, EUS-GJ is technically challenging. Duodenal self-expandable metallic stent (SEMS) placement is popular; however, obstructions are common. Duodenal SEMS obstruction can be managed with the insertion of a second SEMS in a stent-in-stent manner. Therefore, we aimed to analyze the clinical outcomes of secondary duodenal SEMS placement in patients with malignant duodenal obstruction.</p><p><strong>Methods: </strong>We retrospectively analyzed the data of patients who underwent secondary duodenal stent insertion for duodenal stent dysfunction between January 2016 and December 2021. The primary outcome was stent patency. The secondary outcomes were clinical success, factors associated with dysfunction, patient survival, and adverse events.</p><p><strong>Results: </strong>A total of 109 patients were included. The mean age was 64.4±11.2 years, and 63 patients (57.8%) were male. Ninety-two patients (84.4%) had pancreaticobiliary cancer. Clinical success was achieved in 94 cases (86.2%). Twenty-three patients experienced stent dysfunction with 231 days of median stent patency (95% confidence interval [CI], 169 to not available). After a multivariable Cox hazard analysis of stent patency, the Eastern Cooperative Oncology Group performance status (hazard ratio [HR], 2.13; 95% CI, 1.20 to 3.81; p=0.010) and the first stent patency ≥6 months (HR, 0.33; 95% CI, 0.11 to 0.95; p=0.050) remained significant associated factors. Adverse events occurred in five patients (4.6%).</p><p><strong>Conclusions: </strong>Secondary duodenal stent insertion is a viable option for first duodenal stent obstruction. Further comparative studies involving surgery or EUS-GJ for obstructed duodenal stents are warranted.</p>","PeriodicalId":12885,"journal":{"name":"Gut and Liver","volume":null,"pages":null},"PeriodicalIF":3.4,"publicationDate":"2024-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141075639","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-05-15Epub Date: 2023-06-15DOI: 10.5009/gnl220449
Jia Yao, Yaqiu Ji, Tian Liu, Jinjia Bai, Han Wang, Ruoyu Yao, Juan Wang, Xiaoshuang Zhou
Background/aims: The occurrence and development of hepatitis B virus-associated acute-on-chronic liver failure (HBV-ACLF) is closely related to the immune pathway. We explored the heterogeneity of peripheral blood T cell subsets and the characteristics of exhausted T lymphocytes, in an attempt to identify potential therapeutic target molecules for immune dysfunction in ACLF patients.
Methods: A total of 83,577 T cells from HBV-ACLF patients and healthy controls were screened for heterogeneity by single-cell RNA sequencing. In addition, exhausted T-lymphocyte subsets were screened to analyze their gene expression profiles, and their developmental trajectories were investigated. Subsequently, the expression of exhausted T cells and their capacity in secreting cytokines (interleukin 2, interferon γ, and tumor necrosis factor α) were validated by flow cytometry.
Results: A total of eight stable clusters were identified, among which CD4+ TIGIT+ subset and CD8+ LAG-3+ subset, with high expression of exhaust genes, were significantly higher in the HBV-ACLF patients than in normal controls. As shown by pseudotime analysis, T cells experienced a transition from naïve T cells to effector T cells and then exhausted T cells. Flow cytometry confirmed that the CD4+TIGIT+ subset and CD8+LAG-3+ subset in the peripheral blood of the ACLF patients were significantly higher than those in the healthy controls. Moreover, in vitro cultured CD8+LAG-3+ T cells were significantly fewer capable of secreting cytokines than CD8+LAG-3- subset.
Conclusions: Peripheral blood T cells are heterogeneous in HBV-ACLF. The exhausted T cells markedly increase during the pathogenesis of ACLF, suggesting that T-cell exhaustion is involved in the immune dysfunction of HBV-ACLF patients.
背景/目的:乙型肝炎病毒相关急性慢性肝衰竭(HBV-ACLF)的发生和发展与免疫途径密切相关。我们探讨了外周血 T 细胞亚群的异质性和衰竭 T 淋巴细胞的特征,试图找出 ACLF 患者免疫功能障碍的潜在治疗靶分子:通过单细胞 RNA 测序筛选了来自 HBV-ACLF 患者和健康对照组的 83,577 个 T 细胞的异质性。此外,还筛选了衰竭的 T 淋巴细胞亚群,分析其基因表达谱,并研究其发育轨迹。随后,通过流式细胞术验证了衰竭 T 细胞的表达及其分泌细胞因子(白细胞介素 2、干扰素 γ 和肿瘤坏死因子 α)的能力:结果:HBV-ACLF 患者共发现了 8 个稳定集群,其中 CD4+ TIGIT+ 亚群和 CD8+ LAG-3+ 亚群的排气基因表达量明显高于正常对照组。伪时间分析表明,T细胞经历了从幼稚T细胞到效应T细胞再到衰竭T细胞的转变。流式细胞术证实,ACLF 患者外周血中的 CD4+TIGIT+ 亚群和 CD8+LAG-3+ 亚群明显高于健康对照组。此外,体外培养的 CD8+LAG-3+ T 细胞分泌细胞因子的能力明显低于 CD8+LAG-3- 亚群:结论:在 HBV-ACLF 中,外周血 T 细胞具有异质性。结论:HBV-ACLF 患者的外周血 T 细胞具有异质性,在 ACLF 的发病过程中,衰竭的 T 细胞明显增加,这表明 T 细胞衰竭与 HBV-ACLF 患者的免疫功能障碍有关。
{"title":"Single-Cell RNA Sequencing Shows T-Cell Exhaustion Landscape in the Peripheral Blood of Patients with Hepatitis B Virus-Associated Acute-on-Chronic Liver Failure.","authors":"Jia Yao, Yaqiu Ji, Tian Liu, Jinjia Bai, Han Wang, Ruoyu Yao, Juan Wang, Xiaoshuang Zhou","doi":"10.5009/gnl220449","DOIUrl":"10.5009/gnl220449","url":null,"abstract":"<p><strong>Background/aims: </strong>The occurrence and development of hepatitis B virus-associated acute-on-chronic liver failure (HBV-ACLF) is closely related to the immune pathway. We explored the heterogeneity of peripheral blood T cell subsets and the characteristics of exhausted T lymphocytes, in an attempt to identify potential therapeutic target molecules for immune dysfunction in ACLF patients.</p><p><strong>Methods: </strong>A total of 83,577 T cells from HBV-ACLF patients and healthy controls were screened for heterogeneity by single-cell RNA sequencing. In addition, exhausted T-lymphocyte subsets were screened to analyze their gene expression profiles, and their developmental trajectories were investigated. Subsequently, the expression of exhausted T cells and their capacity in secreting cytokines (interleukin 2, interferon γ, and tumor necrosis factor α) were validated by flow cytometry.</p><p><strong>Results: </strong>A total of eight stable clusters were identified, among which CD4<sup>+</sup> TIGIT<sup>+</sup> subset and CD8<sup>+</sup> LAG-3<sup>+</sup> subset, with high expression of exhaust genes, were significantly higher in the HBV-ACLF patients than in normal controls. As shown by pseudotime analysis, T cells experienced a transition from naïve T cells to effector T cells and then exhausted T cells. Flow cytometry confirmed that the CD4<sup>+</sup>TIGIT<sup>+</sup> subset and CD8<sup>+</sup>LAG-3<sup>+</sup> subset in the peripheral blood of the ACLF patients were significantly higher than those in the healthy controls. Moreover, <i>in vitro</i> cultured CD8<sup>+</sup>LAG-3<sup>+</sup> T cells were significantly fewer capable of secreting cytokines than CD8<sup>+</sup>LAG-3- subset.</p><p><strong>Conclusions: </strong>Peripheral blood T cells are heterogeneous in HBV-ACLF. The exhausted T cells markedly increase during the pathogenesis of ACLF, suggesting that T-cell exhaustion is involved in the immune dysfunction of HBV-ACLF patients.</p>","PeriodicalId":12885,"journal":{"name":"Gut and Liver","volume":null,"pages":null},"PeriodicalIF":3.4,"publicationDate":"2024-05-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11096905/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10005883","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-05-15Epub Date: 2023-10-06DOI: 10.5009/gnl230244
Jae Gon Lee, In Kyung Yoo, Abdullah Ozgur Yeniova, Sang Pyo Lee
Background/aims: Recognizing Helicobacter pylori infection during endoscopy is important because it can lead to the performance of confirmatory testing. Linked color imaging (LCI) is an image enhancement technique that can improve the detection of gastrointestinal lesions. The purpose of this study was to compare LCI to conventional white light imaging (WLI) in the endoscopic diagnosis of H. pylori infection.
Methods: We conducted a comprehensive literature search using PubMed, Embase, and the Cochrane Library. All studies evaluating the diagnostic performance of LCI or WLI in the endoscopic diagnosis of H. pylori were eligible. Studies on magnifying endoscopy, chromoendoscopy, and artificial intelligence were excluded.
Results: Thirty-four studies were included in this meta-analysis, of which 32 reported the performance of WLI and eight reported the performance of LCI in diagnosing H. pylori infection. The pooled sensitivity and specificity of WLI in the diagnosis of H. pylori infection were 0.528 (95% confidence interval [CI], 0.517 to 0.540) and 0.821 (95% CI, 0.811 to 0.830), respectively. The pooled sensitivity and specificity of LCI in the diagnosis of H. pylori were 0.816 (95% CI, 0.790 to 0.841) and 0.868 (95% CI, 0.850 to 0.884), respectively. The pooled diagnostic odds ratios of WLI and LCI were 15.447 (95% CI, 8.225 to 29.013) and 31.838 (95% CI, 15.576 to 65.078), respectively. The areas under the summary receiver operating characteristic curves of WLI and LCI were 0.870 and 0.911, respectively.
Conclusions: LCI showed higher sensitivity in the endoscopic diagnosis of H. pylori infection than standard WLI.
{"title":"The Diagnostic Performance of Linked Color Imaging Compared to White Light Imaging in Endoscopic Diagnosis of <i>Helicobacter pylori</i> Infection: A Systematic Review and Meta-Analysis.","authors":"Jae Gon Lee, In Kyung Yoo, Abdullah Ozgur Yeniova, Sang Pyo Lee","doi":"10.5009/gnl230244","DOIUrl":"10.5009/gnl230244","url":null,"abstract":"<p><strong>Background/aims: </strong>Recognizing <i>Helicobacter pylori</i> infection during endoscopy is important because it can lead to the performance of confirmatory testing. Linked color imaging (LCI) is an image enhancement technique that can improve the detection of gastrointestinal lesions. The purpose of this study was to compare LCI to conventional white light imaging (WLI) in the endoscopic diagnosis of <i>H. pylori</i> infection.</p><p><strong>Methods: </strong>We conducted a comprehensive literature search using PubMed, Embase, and the Cochrane Library. All studies evaluating the diagnostic performance of LCI or WLI in the endoscopic diagnosis of <i>H. pylori</i> were eligible. Studies on magnifying endoscopy, chromoendoscopy, and artificial intelligence were excluded.</p><p><strong>Results: </strong>Thirty-four studies were included in this meta-analysis, of which 32 reported the performance of WLI and eight reported the performance of LCI in diagnosing <i>H. pylori</i> infection. The pooled sensitivity and specificity of WLI in the diagnosis of <i>H. pylori</i> infection were 0.528 (95% confidence interval [CI], 0.517 to 0.540) and 0.821 (95% CI, 0.811 to 0.830), respectively. The pooled sensitivity and specificity of LCI in the diagnosis of <i>H. pylori</i> were 0.816 (95% CI, 0.790 to 0.841) and 0.868 (95% CI, 0.850 to 0.884), respectively. The pooled diagnostic odds ratios of WLI and LCI were 15.447 (95% CI, 8.225 to 29.013) and 31.838 (95% CI, 15.576 to 65.078), respectively. The areas under the summary receiver operating characteristic curves of WLI and LCI were 0.870 and 0.911, respectively.</p><p><strong>Conclusions: </strong>LCI showed higher sensitivity in the endoscopic diagnosis of <i>H. pylori</i> infection than standard WLI.</p>","PeriodicalId":12885,"journal":{"name":"Gut and Liver","volume":null,"pages":null},"PeriodicalIF":3.4,"publicationDate":"2024-05-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11096912/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41111279","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-05-15Epub Date: 2023-10-16DOI: 10.5009/gnl230093
Duo Xu, Ziheng Peng, Yong Li, Qian Hou, Yu Peng, Xiaowei Liu
Crohn's disease is a chronic intestinal inflammatory disorder of unknown etiology. Although the pharmacotherapies for Crohn's disease are constantly updating, nutritional support and adjuvant therapies have recently gained more attention. Due to advancements in clinical nutrition, various clinical nutritional therapies are used to treat Crohn's disease. Doctors treating inflammatory bowel disease can now offer several diets with more flexibility than ever. The Crohn's disease exclusion diet is a widely used diet for patients with active Crohn's disease. The Crohn's disease exclusion diet requires both exclusion and inclusion. Periodic exclusion of harmful foods and inclusion of wholesome foods gradually improves a patient's nutritional status. This article reviews the Crohn's disease exclusion diet, including its structure, mechanisms, research findings, and clinical applications.
{"title":"Progress and Clinical Applications of Crohn's Disease Exclusion Diet in Crohn's Disease.","authors":"Duo Xu, Ziheng Peng, Yong Li, Qian Hou, Yu Peng, Xiaowei Liu","doi":"10.5009/gnl230093","DOIUrl":"10.5009/gnl230093","url":null,"abstract":"<p><p>Crohn's disease is a chronic intestinal inflammatory disorder of unknown etiology. Although the pharmacotherapies for Crohn's disease are constantly updating, nutritional support and adjuvant therapies have recently gained more attention. Due to advancements in clinical nutrition, various clinical nutritional therapies are used to treat Crohn's disease. Doctors treating inflammatory bowel disease can now offer several diets with more flexibility than ever. The Crohn's disease exclusion diet is a widely used diet for patients with active Crohn's disease. The Crohn's disease exclusion diet requires both exclusion and inclusion. Periodic exclusion of harmful foods and inclusion of wholesome foods gradually improves a patient's nutritional status. This article reviews the Crohn's disease exclusion diet, including its structure, mechanisms, research findings, and clinical applications.</p>","PeriodicalId":12885,"journal":{"name":"Gut and Liver","volume":null,"pages":null},"PeriodicalIF":3.4,"publicationDate":"2024-05-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11096903/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41234630","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-05-15Epub Date: 2023-11-29DOI: 10.5009/gnl230211
Jong Hwa Na, Sun-Young Lee, Jeong Hwan Kim, In-Kyung Sung, Hyung Seok Park
Background/aims: : The prevalence of Helicobacter pylori-naive status is increasing. Nonetheless, biennial gastroscopy is recommended for all Koreans aged 40 to 75 years. This study aimed to determine whether gastric cancer screening guidelines could be changed according to H. pylori infection status and year of birth.
Methods: : Koreans who underwent serum assays and gastroscopy for gastric cancer screening between 2010 and 2016 were included if screening tests were followed up for ≥3 times. H. pylori infection was confirmed when invasive tests or 13C-urea breath tests were positive. In the case of negative test findings, eradication history, serologically detected atrophy, and intestinal metaplasia/atrophy were checked for past infection. If all were absent, H. pylori-naive status was confirmed.
Results: : Two-thousand and two (256 H. pylori-naive, 743 past-infected, and 1,003 infected) Koreans underwent screening tests for 95.5±28.4 months. The mean year of birth in the naive group (1969±7) differed from those of the past-infected (1957±10, p<0.001) and infected (1958±10, p<0.001) groups. H. pylori-naive status was correlated with recent year of birth (r=0.368, p<0.001). No gastric tumors were observed among the naive participants (p=0.007), whereas 23 adenomas, 18 adenocarcinomas, and two neuroendocrine tumors were detected in 1.9% (14/743) of past-infected and 2.5% (25/1,003) of infected participants, including four infected participants with metachronous tumors.
Conclusions: : The prevalence of H. pylori-naive status is increasing in young Koreans, and gastric tumors are rare in this population. Hence, biennial gastroscopy could be waived after the confirmation of naive status.
{"title":"<i>Helicobacter pylori</i> Infection Status and Gastric Tumor Incidence According to the Year of Birth.","authors":"Jong Hwa Na, Sun-Young Lee, Jeong Hwan Kim, In-Kyung Sung, Hyung Seok Park","doi":"10.5009/gnl230211","DOIUrl":"10.5009/gnl230211","url":null,"abstract":"<p><strong>Background/aims: </strong>: The prevalence of <i>Helicobacter pylori</i>-naive status is increasing. Nonetheless, biennial gastroscopy is recommended for all Koreans aged 40 to 75 years. This study aimed to determine whether gastric cancer screening guidelines could be changed according to <i>H. pylori</i> infection status and year of birth.</p><p><strong>Methods: </strong>: Koreans who underwent serum assays and gastroscopy for gastric cancer screening between 2010 and 2016 were included if screening tests were followed up for ≥3 times. <i>H. pylori</i> infection was confirmed when invasive tests or <sup>13</sup>C-urea breath tests were positive. In the case of negative test findings, eradication history, serologically detected atrophy, and intestinal metaplasia/atrophy were checked for past infection. If all were absent, <i>H. pylori</i>-naive status was confirmed.</p><p><strong>Results: </strong>: Two-thousand and two (256 <i>H. pylori</i>-naive, 743 past-infected, and 1,003 infected) Koreans underwent screening tests for 95.5±28.4 months. The mean year of birth in the naive group (1969±7) differed from those of the past-infected (1957±10, p<0.001) and infected (1958±10, p<0.001) groups. <i>H. pylori</i>-naive status was correlated with recent year of birth (r=0.368, p<0.001). No gastric tumors were observed among the naive participants (p=0.007), whereas 23 adenomas, 18 adenocarcinomas, and two neuroendocrine tumors were detected in 1.9% (14/743) of past-infected and 2.5% (25/1,003) of infected participants, including four infected participants with metachronous tumors.</p><p><strong>Conclusions: </strong>: The prevalence of <i>H. pylori</i>-naive status is increasing in young Koreans, and gastric tumors are rare in this population. Hence, biennial gastroscopy could be waived after the confirmation of naive status.</p>","PeriodicalId":12885,"journal":{"name":"Gut and Liver","volume":null,"pages":null},"PeriodicalIF":3.4,"publicationDate":"2024-05-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11096908/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138451366","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-05-15Epub Date: 2023-08-08DOI: 10.5009/gnl220346
Yi Feng Liang, Xiao Qi Chen, Meng Ting Zhang, He Yong Tang, Guo Ming Shen
Irritable bowel syndrome (IBS) is considered a stress disorder characterized by psychological and gastrointestinal dysfunction. IBS patients not only suffer from intestinal symptoms such as abdominal pain, diarrhea, or constipation but also, experience dysthymic disorders such as anxiety and depression. Studies have found that corticotropin-releasing hormone plays a key role in IBS with comorbid dysthymic disorders. Next, we will summarize the effects of corticotropin-releasing hormone from the central nervous system and periphery on IBS with comorbid dysthymic disorders and relevant treatments based on published literatures in recent years.
{"title":"Research Progress of Central and Peripheral Corticotropin-Releasing Hormone in Irritable Bowel Syndrome with Comorbid Dysthymic Disorders.","authors":"Yi Feng Liang, Xiao Qi Chen, Meng Ting Zhang, He Yong Tang, Guo Ming Shen","doi":"10.5009/gnl220346","DOIUrl":"10.5009/gnl220346","url":null,"abstract":"<p><p>Irritable bowel syndrome (IBS) is considered a stress disorder characterized by psychological and gastrointestinal dysfunction. IBS patients not only suffer from intestinal symptoms such as abdominal pain, diarrhea, or constipation but also, experience dysthymic disorders such as anxiety and depression. Studies have found that corticotropin-releasing hormone plays a key role in IBS with comorbid dysthymic disorders. Next, we will summarize the effects of corticotropin-releasing hormone from the central nervous system and periphery on IBS with comorbid dysthymic disorders and relevant treatments based on published literatures in recent years.</p>","PeriodicalId":12885,"journal":{"name":"Gut and Liver","volume":null,"pages":null},"PeriodicalIF":3.4,"publicationDate":"2024-05-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11096901/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10325986","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-05-15Epub Date: 2023-10-10DOI: 10.5009/gnl230179
Zesheng Lin, Wenjing Luo, Kaijun Zhang, Shixue Dai
Inflammatory bowel disease (IBD) is a complex condition resulting from environmental, microbial, immunologic, and genetic factors. With the advancement of Mendelian randomization research in IBD, we have gained new insights into the relationship between these factors and IBD. Many animal models of IBD have been developed using different methods, but few studies have attempted to model IBD by combining environmental factors and microbial factors. In this review, we examine how environmental factors and microbial factors affect the development and progression of IBD, and how they interact with each other and with the intestinal microbiota. We also summarize the current methods for creating animal models of IBD and compare their advantages and disadvantages. Based on the latest findings from Mendelian randomization studies on the role of environmental factors in IBD, we discuss which environmental and microbial factors could be used to construct a more realistic and reliable IBD experimental model. We propose that animal models of IBD should consider both environmental and microbial factors to better mimic human IBD pathogenesis and to reveal the underlying mechanisms of IBD at the immune and genetic levels. We highlight the importance of environmental and microbial factors in IBD pathogenesis and offer new perspectives and suggestions for improving experimental animal modeling. Our goal is to create a model that closely resembles the clinical picture of IBD.
{"title":"Environmental and Microbial Factors in Inflammatory Bowel Disease Model Establishment: A Review Partly through Mendelian Randomization.","authors":"Zesheng Lin, Wenjing Luo, Kaijun Zhang, Shixue Dai","doi":"10.5009/gnl230179","DOIUrl":"10.5009/gnl230179","url":null,"abstract":"<p><p>Inflammatory bowel disease (IBD) is a complex condition resulting from environmental, microbial, immunologic, and genetic factors. With the advancement of Mendelian randomization research in IBD, we have gained new insights into the relationship between these factors and IBD. Many animal models of IBD have been developed using different methods, but few studies have attempted to model IBD by combining environmental factors and microbial factors. In this review, we examine how environmental factors and microbial factors affect the development and progression of IBD, and how they interact with each other and with the intestinal microbiota. We also summarize the current methods for creating animal models of IBD and compare their advantages and disadvantages. Based on the latest findings from Mendelian randomization studies on the role of environmental factors in IBD, we discuss which environmental and microbial factors could be used to construct a more realistic and reliable IBD experimental model. We propose that animal models of IBD should consider both environmental and microbial factors to better mimic human IBD pathogenesis and to reveal the underlying mechanisms of IBD at the immune and genetic levels. We highlight the importance of environmental and microbial factors in IBD pathogenesis and offer new perspectives and suggestions for improving experimental animal modeling. Our goal is to create a model that closely resembles the clinical picture of IBD.</p>","PeriodicalId":12885,"journal":{"name":"Gut and Liver","volume":null,"pages":null},"PeriodicalIF":3.4,"publicationDate":"2024-05-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11096900/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41182458","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-05-15Epub Date: 2023-07-17DOI: 10.5009/gnl220531
Hong Peng, Ting Ye, Lei Deng, Xiaofang Yang, Qingling Li, Jin Tong, Jinjun Guo
Background/aims: Cancer stem cells (CSCs) are believed to drive tumor development and metastasis. Activin and hepatocyte growth factor (HGF) are important cytokines with the ability to induce cancer stemness. However, the effect of activin and HGF combination treatment on CSCs is still unclear.
Methods: In this study, we sequentially treated colorectal cancer cells with activin and HGF and examined CSC marker expression, self-renewal, tumorigenesis, and metastasis. The roles of forkhead box M1 (FOXM1) and sex-determining region Y-box 2 (SOX2), two stemness-related transcription factors, in activin/HGF-induced aggressive phenotype were explored.
Results: Activin and HGF treatment increased the expression of CSC markers and enhanced sphere formation in colorectal cancer cells. The tumorigenic and metastatic capacities of colorectal cancer cells were enhanced upon activin and HGF treatment. Activin and HGF treatment preferentially promoted stemness and metastasis of CD133+ subpopulations sorted from colorectal cancer cells. FOXM1 was upregulated by activin and HGF treatment, and the knockdown of FOXM1 blocked activin/HGF-induced stemness, tumorigenesis, and metastasis of colorectal cancer cells. Similarly, SOX2 was silencing impaired sphere formation of activin/HGF-treated colorectal cancers. Overexpression of SOX2 rescued the stem cell-like phenotype in FOXM1-depleted colorectal cancer cells with activin and HGF treatment. Additionally, the inhibition of FOXM1 via thiostrepton suppressed activin/HGF-induced stemness, tumorigenesis and metastasis.
Conclusions: Sequential treatment with activin and HGF promotes colorectal cancer stemness and metastasis through activation of the FOXM1/SOX2 signaling. FOXM1 could be a potential target for the treatment of colorectal cancer metastasis.
{"title":"Activin and Hepatocyte Growth Factor Promotes Colorectal Cancer Stemness and Metastasis through FOXM1/SOX2/CXCR4 Signaling.","authors":"Hong Peng, Ting Ye, Lei Deng, Xiaofang Yang, Qingling Li, Jin Tong, Jinjun Guo","doi":"10.5009/gnl220531","DOIUrl":"10.5009/gnl220531","url":null,"abstract":"<p><strong>Background/aims: </strong>Cancer stem cells (CSCs) are believed to drive tumor development and metastasis. Activin and hepatocyte growth factor (HGF) are important cytokines with the ability to induce cancer stemness. However, the effect of activin and HGF combination treatment on CSCs is still unclear.</p><p><strong>Methods: </strong>In this study, we sequentially treated colorectal cancer cells with activin and HGF and examined CSC marker expression, self-renewal, tumorigenesis, and metastasis. The roles of forkhead box M1 (FOXM1) and sex-determining region Y-box 2 (SOX2), two stemness-related transcription factors, in activin/HGF-induced aggressive phenotype were explored.</p><p><strong>Results: </strong>Activin and HGF treatment increased the expression of CSC markers and enhanced sphere formation in colorectal cancer cells. The tumorigenic and metastatic capacities of colorectal cancer cells were enhanced upon activin and HGF treatment. Activin and HGF treatment preferentially promoted stemness and metastasis of CD133+ subpopulations sorted from colorectal cancer cells. FOXM1 was upregulated by activin and HGF treatment, and the knockdown of FOXM1 blocked activin/HGF-induced stemness, tumorigenesis, and metastasis of colorectal cancer cells. Similarly, SOX2 was silencing impaired sphere formation of activin/HGF-treated colorectal cancers. Overexpression of SOX2 rescued the stem cell-like phenotype in FOXM1-depleted colorectal cancer cells with activin and HGF treatment. Additionally, the inhibition of FOXM1 via thiostrepton suppressed activin/HGF-induced stemness, tumorigenesis and metastasis.</p><p><strong>Conclusions: </strong>Sequential treatment with activin and HGF promotes colorectal cancer stemness and metastasis through activation of the FOXM1/SOX2 signaling. FOXM1 could be a potential target for the treatment of colorectal cancer metastasis.</p>","PeriodicalId":12885,"journal":{"name":"Gut and Liver","volume":null,"pages":null},"PeriodicalIF":3.4,"publicationDate":"2024-05-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11096902/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10139343","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-05-15Epub Date: 2023-03-02DOI: 10.5009/gnl220394
Xiaofang Yang, Ting Ye, Li Rong, Hong Peng, Jin Tong, Xiao Xiao, Xiaoqiang Wan, Jinjun Guo
Background/aims: Gastric intestinal metaplasia (GIM), a common precancerous lesion of gastric cancer, can be caused by bile acid reflux. GATA binding protein 4 (GATA4) is an intestinal transcription factor involved in the progression of gastric cancer. However, the expression and regulation of GATA4 in GIM has not been clarified.
Methods: The expression of GATA4 in bile acid-induced cell models and human specimens was examined. The transcriptional regulation of GATA4 was investigated by chromatin immunoprecipitation and luciferase reporter gene analysis. An animal model of duodenogastric reflux was used to confirm the regulation of GATA4 and its target genes by bile acids.
Results: GATA4 expression was elevated in bile acid-induced GIM and human specimens. GATA4 bound to the promoter of mucin 2 (MUC2) and stimulate its transcription. GATA4 and MUC2 expression was positively correlated in GIM tissues. Nuclear transcription factor-κB activation was required for the upregulation of GATA4 and MUC2 in bile acid-induced GIM cell models. GATA4 and caudal-related homeobox 2 (CDX2) reciprocally transactivated each other to drive the transcription of MUC2. In chenodeoxycholic acid-treated mice, MUC2, CDX2, GATA4, p50, and p65 expression levels were increased in the gastric mucosa.
Conclusions: GATA4 is upregulated and can form a positive feedback loop with CDX2 to transactivate MUC2 in GIM. NF-κB signaling is involved in the upregulation of GATA4 by chenodeoxycholic acid.
{"title":"GATA4 Forms a Positive Feedback Loop with CDX2 to Transactivate MUC2 in Bile Acids-Induced Gastric Intestinal Metaplasia.","authors":"Xiaofang Yang, Ting Ye, Li Rong, Hong Peng, Jin Tong, Xiao Xiao, Xiaoqiang Wan, Jinjun Guo","doi":"10.5009/gnl220394","DOIUrl":"10.5009/gnl220394","url":null,"abstract":"<p><strong>Background/aims: </strong>Gastric intestinal metaplasia (GIM), a common precancerous lesion of gastric cancer, can be caused by bile acid reflux. GATA binding protein 4 (GATA4) is an intestinal transcription factor involved in the progression of gastric cancer. However, the expression and regulation of GATA4 in GIM has not been clarified.</p><p><strong>Methods: </strong>The expression of GATA4 in bile acid-induced cell models and human specimens was examined. The transcriptional regulation of GATA4 was investigated by chromatin immunoprecipitation and luciferase reporter gene analysis. An animal model of duodenogastric reflux was used to confirm the regulation of GATA4 and its target genes by bile acids.</p><p><strong>Results: </strong>GATA4 expression was elevated in bile acid-induced GIM and human specimens. GATA4 bound to the promoter of mucin 2 (MUC2) and stimulate its transcription. GATA4 and MUC2 expression was positively correlated in GIM tissues. Nuclear transcription factor-κB activation was required for the upregulation of GATA4 and MUC2 in bile acid-induced GIM cell models. GATA4 and caudal-related homeobox 2 (CDX2) reciprocally transactivated each other to drive the transcription of MUC2. In chenodeoxycholic acid-treated mice, MUC2, CDX2, GATA4, p50, and p65 expression levels were increased in the gastric mucosa.</p><p><strong>Conclusions: </strong>GATA4 is upregulated and can form a positive feedback loop with CDX2 to transactivate MUC2 in GIM. NF-κB signaling is involved in the upregulation of GATA4 by chenodeoxycholic acid.</p>","PeriodicalId":12885,"journal":{"name":"Gut and Liver","volume":null,"pages":null},"PeriodicalIF":3.4,"publicationDate":"2024-05-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11096910/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9363607","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}