{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,15]],"date-time":"2026-06-15T00:01:13Z","timestamp":1781481673031,"version":"3.54.1"},"reference-count":35,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2025,7,2]],"date-time":"2025-07-02T00:00:00Z","timestamp":1751414400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/"},{"start":{"date-parts":[[2025,7,2]],"date-time":"2025-07-02T00:00:00Z","timestamp":1751414400000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J. pediatr. gastroenterol. nutr."],"published-print":{"date-parts":[[2025,9]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Objectives<\/jats:title>\n                    <jats:p>Pediatric acute pancreatitis (AP) is associated with gut dysbiosis. We aimed to determine if dysbiosis persisted during follow\u2010up and whether it is associated with clinical outcomes.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      Prospective enrollment of participants &lt;21 years with first AP. Stool samples were obtained at baseline (\n                      <jats:italic>n<\/jats:italic>\n                      \u2009=\u200941), 3 months (\n                      <jats:italic>n<\/jats:italic>\n                      \u2009=\u200919), and 12 months (\n                      <jats:italic>n<\/jats:italic>\n                      \u2009=\u200912) and in healthy controls (HC;\n                      <jats:italic>n<\/jats:italic>\n                      \u2009=\u200934). Evaluation for diabetes (DM) or prediabetes (pre\u2010DM) was performed. At 12\u2010month follow\u2010up gastrointestinal (GI) symptom surveys were completed and AP recurrence\u2010acute recurrent pancreatitis (ARP) recorded. Shotgun metagenomic sequencing was performed on extracted microbial DNA.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Microbial alpha diversity was lower for AP versus HC at all three time points (\n                      <jats:italic>p\u2009<\/jats:italic>\n                      &lt;\u20090.008). Bray\u2010Curtis ordinations showed the AP cohort did not cluster by time point, highlighting similarity in microbial composition over time. Within 12\u2010month follow\u2010up: 7\/44 participants developed pre\u2010DM\/DM, 7\/42 developed ARP, 16 had zero or one while 15 had multiple GI symptoms. Distinct clustering of samples was observed in the baseline samples of the group that developed ARP (\n                      <jats:italic>p\u2009<\/jats:italic>\n                      =\u20090.023) and in follow\u2010up samples with multiple GI symptoms,\n                      <jats:italic>p<\/jats:italic>\n                      \u2009&lt;\u20090.05. Relative abundance of most species was lower in AP samples when compared to HC at all time points with enrichment in\n                      <jats:italic>Ruminococcus gnavus<\/jats:italic>\n                      and\n                      <jats:italic>Clostridium innocuum<\/jats:italic>\n                      (AQ) (False Discovery Rate\n                      <jats:italic>p<\/jats:italic>\n                      \u2009&lt;\u20090.05). Several pathways involved in protein biosynthesis were depleted in the AP cohort at all time points.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Gut dysbiosis persisted following AP in children at 3 and 12 months follow\u2010up compared to HC. Microbiome signatures differed in the ARP cohort and those with multiple GI symptoms.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/jpn3.70135","type":"journal-article","created":{"date-parts":[[2025,7,2]],"date-time":"2025-07-02T10:37:51Z","timestamp":1751452671000},"page":"690-698","source":"Crossref","is-referenced-by-count":1,"title":["Acute pancreatitis gut dysbiosis persists at 1\u2010year follow\u2010up and is associated with clinical outcomes"],"prefix":"10.1002","volume":"81","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-2435-3655","authenticated-orcid":false,"given":"Chinenye R.","family":"Dike","sequence":"first","affiliation":[{"name":"Department of Pediatrics, Division of Pediatric Gastroenterology, Hepatology and Nutrition University of Alabama at Birmingham Birmingham Alabama USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Qing","family":"Duan","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, Division of Biostatistics and Epidemiology Cincinnati Children's Hospital Medical Center Cincinnati Ohio USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Faizan","family":"Ahmed","sequence":"additional","affiliation":[{"name":"Division of Pediatric Gastroenterology, Hepatology and Nutrition Cincinnati Children's Hospital Medical Center Cincinnati Ohio USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lee A.","family":"Denson","sequence":"additional","affiliation":[{"name":"Division of Pediatric Gastroenterology, Hepatology and Nutrition Cincinnati Children's Hospital Medical Center Cincinnati Ohio USA"},{"name":"Department of Pediatrics, College of Medicine University of Cincinnati Cincinnati Ohio USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"David","family":"Haslam","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, College of Medicine University of Cincinnati Cincinnati Ohio USA"},{"name":"Division of Pediatric Infectious Diseases Cincinnati Children's Hospital Medical Center Cincinnati Ohio USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Philip","family":"Minar","sequence":"additional","affiliation":[{"name":"Division of Pediatric Gastroenterology, Hepatology and Nutrition Cincinnati Children's Hospital Medical Center Cincinnati Ohio USA"},{"name":"Department of Pediatrics, College of Medicine University of Cincinnati Cincinnati Ohio USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nicholas J.","family":"Ollberding","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, Division of Biostatistics and Epidemiology Cincinnati Children's Hospital Medical Center Cincinnati Ohio USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Georgios I.","family":"Papachristou","sequence":"additional","affiliation":[{"name":"Division of Gastroenterology, Hepatology, and Nutrition Ohio State University Wexner Medical Center Columbus Ohio USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kenneth D. R.","family":"Setchell","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, College of Medicine University of Cincinnati Cincinnati Ohio USA"},{"name":"Division of Pathology and Laboratory Medicine Cincinnati Children's Hospital Medical Center Cincinnati Ohio USA"},{"name":"Department of Pathology and Laboratory Medicine, College of Medicine University of Cincinnati Cincinnati Ohio USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tyler","family":"Thompson","sequence":"additional","affiliation":[{"name":"Division of Pediatric Gastroenterology, Hepatology and Nutrition Cincinnati Children's Hospital Medical Center Cincinnati Ohio USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"David S.","family":"Vitale","sequence":"additional","affiliation":[{"name":"Division of Pediatric Gastroenterology, Hepatology and Nutrition Cincinnati Children's Hospital Medical Center Cincinnati Ohio USA"},{"name":"Department of Pediatrics, College 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