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Research and Practice"],"published-print":{"date-parts":[[2017]]},"abstract":"<jats:p>Intestinal fatty acid binding protein (I-FABP) indicates barrier integrity. Aims: determine if I-FABP is elevated in active Crohn\u2019s disease (CD) and if I-FABP parallels anti-TNF<jats:italic>\u03b1<\/jats:italic> antibody (infliximab) induced lowering of TNF<jats:italic>\u03b1<\/jats:italic> and Harvey-Bradshaw Index (HBI) as potential indicator of mucosal healing. I-FABP distribution along human gut was determined. Serum from 10 CD patients collected during first three consecutive infliximab treatments with matched pretreatment and follow-up samples one week after each treatment and corresponding HBI data were analyzed. I-FABP reference interval was established from 31 healthy subjects with normal gut permeability. I-FABP and TNF<jats:italic>\u03b1<\/jats:italic> were measured by ELISA; CRP was measured by nephelometry. Healthy tissue was used for I-FABP immunohistochemistry. Pretreatment CD patient TNF<jats:italic>\u03b1<\/jats:italic> was 1.6-fold higher than in-house reference interval, while I-FABP was 2.5-fold higher, which lowered at follow-ups. Combining all 30 infusion\/follow-up pairs also revealed changes in I-FABP. HBI followed this pattern; CRP declined gradually. I-FABP was expressed in epithelium of stomach, jejunum, ileum, and colon, with the highest expression in jejunum and ileum. I-FABP is elevated in active CD with a magnitude comparable to TNF<jats:italic>\u03b1<\/jats:italic>. Parallel infliximab effects on TNF<jats:italic>\u03b1<\/jats:italic>, HBI, and I-FABP were found. I-FABP may be useful as an intestine selective prognostic marker in CD.<\/jats:p>","DOI":"10.1155\/2017\/1745918","type":"journal-article","created":{"date-parts":[[2017,10,23]],"date-time":"2017-10-23T19:34:19Z","timestamp":1508787259000},"page":"1-8","source":"Crossref","is-referenced-by-count":18,"title":["Parallel Changes in Harvey-Bradshaw Index, TNF<i>\u03b1<\/i>, and Intestinal Fatty Acid Binding Protein in Response to Infliximab in Crohn\u2019s Disease"],"prefix":"10.1155","volume":"2017","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-4842-3227","authenticated-orcid":true,"given":"Anas Kh.","family":"Al-Saffar","sequence":"first","affiliation":[{"name":"Department of Medical Sciences, Gastroenterology and Hepatology Unit, Uppsala University, Uppsala, Sweden"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Carl Hampus","family":"Meijer","sequence":"additional","affiliation":[{"name":"Department of Medical Sciences, Gastroenterology and Hepatology Unit, 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