JGH OpenPub Date : 2026-05-20eCollection Date: 2026-05-01DOI: 10.1002/jgh3.70418
Umar Hayat, Azhar Hussain, Hassam Ali, Karan J Yagnik, Pranav Patel, Ali A Siddiqui, Sumant Inamdar, Kamran Qureshi, Harshit S Khara, Bradley Confer, David L Diehl
{"title":"Post-ERCP Outcomes in Cirrhotic Patients With Thrombocytopenia: A Propensity-Matched Retrospective Comparative Analysis on TriNetX Health Research Database.","authors":"Umar Hayat, Azhar Hussain, Hassam Ali, Karan J Yagnik, Pranav Patel, Ali A Siddiqui, Sumant Inamdar, Kamran Qureshi, Harshit S Khara, Bradley Confer, David L Diehl","doi":"10.1002/jgh3.70418","DOIUrl":"10.1002/jgh3.70418","url":null,"abstract":"<p><strong>Background: </strong>Patients with cirrhosis have an increased risk of developing complications secondary to thrombocytopenia. This study aims to investigate post-ERCP outcomes in patients with liver cirrhosis and concomitant low platelet count who undergo endoscopic retrograde cholangiopancreatography (ERCP) for choledocholithiasis in a large, matched cohort with cirrhosis.</p><p><strong>Methods: </strong>A retrospective cohort study was conducted using data from the TriNetX research network. Patients aged 18 years or older with cirrhosis undergoing ERCP for choledocholithiasis were included. Cohorts were categorized by platelet count into mild or moderate thrombocytopenia groups, with 5097 patients in each cohort after propensity score matching, yielding a total of 10 194 patients. Univariate regression analysis was used to assess the primary outcome, namely, all-cause mortality. Secondary outcomes included post-ERCP bleeding, post-ERCP pancreatitis, need for blood transfusion, and other adverse events such as sepsis and acute kidney injury (AKI). Odds ratios (ORs) and 95% confidence intervals (CIs) were then calculated.</p><p><strong>Results: </strong>All-cause mortality [OR 1.54 (95% CI): (1.32-1.80)] and need for blood transfusion (OR 1.37; 95% CI 1.17-1.61) were higher among patients with moderate thrombocytopenia. However, adverse events, including post-ERCP bleeding (OR 0.96; 95% CI 0.72-1.3), post-ERCP pancreatitis (OR 0.81; 95% CI 0.69-1.02), sepsis (OR 1.04; 95% CI 0.93-1.16), and AKI (OR 1.11; 95% CI 1.00-1.23), were statistically not significant between the two groups.</p><p><strong>Conclusion: </strong>The cirrhotic population with moderate thrombocytopenia undergoing ERCP for choledocholithiasis experiences significantly worse outcomes compared to those with mild thrombocytopenia.</p>","PeriodicalId":45861,"journal":{"name":"JGH Open","volume":"10 5","pages":"e70418"},"PeriodicalIF":1.6,"publicationDate":"2026-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13240326/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148200550","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
JGH OpenPub Date : 2026-05-18eCollection Date: 2026-05-01DOI: 10.1002/jgh3.70401
Kiran Josy Kanjamala, Prakash Zacharias, Shibi Mathew, Hasim Ahamed, Remya R Pai, Anvin Kurian Thomas, Arjun R Gupta, Mathew Philip
{"title":"Stricturing Phenotype Predisposes to Small Bowel and Colorectal Malignancy in Crohn's Disease.","authors":"Kiran Josy Kanjamala, Prakash Zacharias, Shibi Mathew, Hasim Ahamed, Remya R Pai, Anvin Kurian Thomas, Arjun R Gupta, Mathew Philip","doi":"10.1002/jgh3.70401","DOIUrl":"10.1002/jgh3.70401","url":null,"abstract":"<p><strong>Background: </strong>Carcinogenesis is a major complication in patients with inflammatory bowel disease (IBD). We report the data of Crohn's disease (CD)-associated intestinal malignancy in our IBD cohort.</p><p><strong>Methods: </strong>Retrospective analysis of data from prospectively maintained medical records of 1416 CD patients diagnosed or under follow up from January 1st 2013 to December 31st 2023.</p><p><strong>Results: </strong>A total of 1416 patients were included (13037.9 person-years of follow-up with mean age at diagnosis 27.62 ± 11.8 years, 64.1% males, disease duration: 9.2 ± 6.7 years). Eighteen patients (1.27%) developed intestinal malignancy at a mean age of 46.7 ± 14.2 years after 15.9 ± 10.3 years of disease. Colorectal carcinoma (10/1416) was most frequent, followed by jejunal (4/1416), anal canal (3/1416), and ileal (1/1416) cancers. All luminal malignancies occurred in stricturing disease, while anal canal carcinoma occurred in chronic perianal fistulizing disease with anal stricture. The cumulative risk of malignancy in stricturing disease was 1.5%, 8.3%, and 25.1% in the first, second, and third decades of disease, respectively. Independent risk factors included older age at CD diagnosis, longer disease duration, stricturing phenotype, and active smoking. The standardized incidence ratio (SIR) for intestinal malignancy was 95.36 (95% CI: 52.98-143.04), nearly 95-fold higher than the general population.</p><p><strong>Conclusion: </strong>The incidence rate of intestinal malignancy was 1.27% in our CD cohort with standardized incidence rate of 95.3. Stricturing disease predisposed to small bowel and colorectal carcinoma. Carcinoma in anal canal was seen in chronic perianal fistulizing disease with anal canal stricture.</p>","PeriodicalId":45861,"journal":{"name":"JGH Open","volume":"10 ","pages":"e70401"},"PeriodicalIF":1.6,"publicationDate":"2026-05-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13181914/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147976108","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
JGH OpenPub Date : 2026-05-18eCollection Date: 2026-05-01DOI: 10.1002/jgh3.70417
Neda Rehan, Jubilee Benedict, Rehan Qayyum
{"title":"Selenium and Liver Steatosis and Fibrosis: Opposing Direct and Steatosis-Mediated Associations in a Large Cohort.","authors":"Neda Rehan, Jubilee Benedict, Rehan Qayyum","doi":"10.1002/jgh3.70417","DOIUrl":"10.1002/jgh3.70417","url":null,"abstract":"<p><strong>Background and aims: </strong>Epidemiologic studies have reported conflicting associations between selenium exposure and liver disease. Whether selenium exerts opposing direct and steatosis-mediated effects on liver fibrosis is unknown. To evaluate the associations of blood selenium with elastography-defined hepatic steatosis and fibrosis and to determine whether hepatic steatosis mediates the relationship between selenium and fibrosis.</p><p><strong>Methods: </strong>We conducted a cross-sectional analysis of adults aged ≥ 18 years in NHANES 2017-2023. Hepatic steatosis was assessed using the controlled attenuation parameter (CAP) and fibrosis using liver stiffness measurement (LSM). Blood selenium was categorized into quartiles. Survey-weighted multivariable linear regression and structural equation modeling were used, adjusting for demographic, behavioral, and metabolic covariates.</p><p><strong>Results: </strong>Among 13 241 adults (52.4% women; mean age 51.3 years), higher selenium was associated with lower liver stiffness and greater hepatic steatosis. In fully adjusted models, participants in the highest selenium quartile had lower LSM compared with the lowest quartile (<i>β</i> = -0.54 kPa; 95% CI: -0.86 to -0.22; <i>p</i> = 0.002) and higher CAP (<i>β</i> = 9.17 dB/m; 95% CI: 5.87-12.47; <i>p</i> < 0.001). Mediation analysis demonstrated a positive indirect effect of selenium on fibrosis through steatosis (β_indirect = 0.04; 95% CI: 0.02-0.07; <i>p</i> = 0.001) and a stronger negative direct association with fibrosis (β_direct = -0.59 kPa; 95% CI: -0.90 to -0.27; <i>p</i> < 0.001). The total effect of selenium on fibrosis remained protective (β_total = -0.54; 95% CI: -0.85 to -0.23; <i>p</i> = 0.001).</p><p><strong>Conclusions: </strong>Higher blood selenium is associated with increased hepatic steatosis yet lower liver stiffness, reflecting opposing steatosis-mediated and direct antifibrotic pathways. Longitudinal studies are needed to clarify causal mechanisms and define optimal selenium exposure in metabolic liver disease.</p>","PeriodicalId":45861,"journal":{"name":"JGH Open","volume":"10 ","pages":"e70417"},"PeriodicalIF":1.6,"publicationDate":"2026-05-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13184169/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147983849","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
JGH OpenPub Date : 2026-05-15eCollection Date: 2026-05-01DOI: 10.1002/jgh3.70419
Ayesha Shah, Gerald Holtmann, Peter R Gibson
{"title":"Critical Review: The Past, Present, and Future of Small Intestinal Bacterial Overgrowth (SIBO).","authors":"Ayesha Shah, Gerald Holtmann, Peter R Gibson","doi":"10.1002/jgh3.70419","DOIUrl":"10.1002/jgh3.70419","url":null,"abstract":"<p><p>Small intestinal bacterial overgrowth (SIBO) has evolved from a severe debilitating illness to a clinical spectrum associated with abnormalities of microbial populations in the small intestine. It is best described as a pathophysiological state that may contribute to symptoms or other pathology in a wide range of gastrointestinal conditions that include disorders of gut-brain interaction, inflammatory bowel disease, and chronic liver disease. The controversy surrounding SIBO largely rests on diagnostic limitations of currently widely used diagnostic tests. The gold standard test of bacterial culture of proximal small intestinal fluid will miss the majority of bacteria, has severe methodological limitations, and is clinically uncommonly used. Breath-hydrogen testing after oral glucose or lactulose ingestion is associated with falsely positive and negative results, due largely to the inability to accurately define where in the gastrointestinal tract the hydrogen is being generated. Such performance characteristics raise concerns regarding its application to clinical decision-making in the individual patient. Therapies such as antibiotics can normalize breath test findings and ameliorate symptoms, but whether this is due to an action on the small intestinal microbiota is uncertain. It is proposed that conceptual modifications that include the assessment of the mucosa-associated microbiota in biopsies obtained with minimal contamination, molecular and functional characterization of the microbiota, rather than purely culture-based density of bacteria, and expansion of the definition of SIBO to small intestinal dysbiosis will facilitate more precision and resolve the controversial place of SIBO in clinical practice.</p>","PeriodicalId":45861,"journal":{"name":"JGH Open","volume":"10 ","pages":"e70419"},"PeriodicalIF":1.6,"publicationDate":"2026-05-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13179449/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147964507","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
JGH OpenPub Date : 2026-05-12eCollection Date: 2026-05-01DOI: 10.1002/jgh3.70410
R Gilmore, T Pham, R G Fernandes, S Lo, E K Wright, O Rosella, P De Cruz, B Andrew, A Vasudevan, K Gazelakis, G T Moore, L Thin, K Au, S Ghaly, C Chen, W Mohsen, T Goodwin, M P Sparrow, M G Ward, M Chew, M Garg, E Shelton, I C Lawrance, A Thorat, C da Fonseca Pereira, J Begun, Y K An
{"title":"Extended High-Dose Tofacitinib Induction Improves Clinical Response in Ulcerative Colitis: A Multicenter Cohort Study.","authors":"R Gilmore, T Pham, R G Fernandes, S Lo, E K Wright, O Rosella, P De Cruz, B Andrew, A Vasudevan, K Gazelakis, G T Moore, L Thin, K Au, S Ghaly, C Chen, W Mohsen, T Goodwin, M P Sparrow, M G Ward, M Chew, M Garg, E Shelton, I C Lawrance, A Thorat, C da Fonseca Pereira, J Begun, Y K An","doi":"10.1002/jgh3.70410","DOIUrl":"10.1002/jgh3.70410","url":null,"abstract":"<p><strong>Background and aims: </strong>Tofacitinib, an oral Janus Kinase (JAK) inhibitor, has demonstrated efficacy for ulcerative colitis (UC) in clinical trials, but the optimal dosing regimen remains unclear. This study aims to assess the effectiveness and safety of tofacitinib for UC in a real-world Australian cohort focusing on outcomes of standard 8-week induction with 10 mg twice daily compared with extended 16-week induction.</p><p><strong>Methods: </strong>This multicenter study included patients with moderate-to-severe UC initiating tofacitinib between October 2020 and March 2021 across 13 Australian Inflammatory Bowel Disease centers. Clinical, biochemical, endoscopic, and adverse event (AE) outcomes were collected at baseline, week 8, week 16, and week 52, and stratified by duration of induction therapy.</p><p><strong>Results: </strong>A total of 124 patients (41% female; median age 41 [IQR 29-49] years) were identified, with 40% receiving standard induction and 60% receiving extended induction. Overall clinical response was achieved by 70% at week 8, 60% at week 16 and 68% at week 52. A significantly higher proportion of patients who received extended induction achieved clinical response by week 16 (69% vs. 45%, <i>p</i> = 0.02) and week 52 (75% vs. 54%, <i>p</i> = 0.03) compared with standard induction. Over 52 weeks, AEs and serious AEs were seen in 17% and 7% of patients, respectively. AEs of special interest occurred in 6% of patients (herpes zoster in 6/8 patients).</p><p><strong>Conclusions: </strong>Tofacitinib was effective in an UC real-world Australian population and safety was consistent with its known profile. Clinical response at 16 and 52 weeks was significantly higher with extended induction dosing of tofacitinib.</p>","PeriodicalId":45861,"journal":{"name":"JGH Open","volume":"10 ","pages":"e70410"},"PeriodicalIF":1.6,"publicationDate":"2026-05-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13167392/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147943218","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}