Prospective study evaluating immune‐mediated mechanisms and predisposing factors underlying persistent postinfectious abdominal complaints

• Published in: Neurogastroenterology and motility Vol. 31; no. 4; pp. e13542 - n/a
• Main Authors: Florens, Morgane V., Van Wanrooy, Sander, Dooley, James, Aguilera‐Lizarraga, Javier, Vanbrabant, Winde, Wouters, Mira M., Van Oudenhove, Lukas, Peetermans, Willy E., Liston, Adrian, Boeckxstaens, Guy E.
• Format: Journal Article
• Language: English
• Published: England Wiley Subscription Services, Inc 01.04.2019
• Subjects: Abdomen; Abdominal Pain - complications; Adult; Anxiety; Anxiety - complications; Diarrhea; Diarrhea - complications; Female; Gastroenteritis; Gastroenteritis - complications; Gene expression; Humans; Immunoglobulin E; Infections; Intestine; Irritable bowel syndrome; Irritable Bowel Syndrome - diagnosis; Irritable Bowel Syndrome - etiology; Lymphocytes B; Male; Middle Aged; Pain; Peripheral blood mononuclear cells; Prospective Studies; Rectum; Risk Factors; Surveys and Questionnaires; Travel
• DOI: 10.1111/nmo.13542
• ISSN: 1350-1925; 1365-2982

Background The role of persistent immune activation in postinfectious irritable bowel syndrome (PI‐IBS) remains controversial. Here, we prospectively studied healthy subjects traveling to destinations with a high‐risk to develop infectious gastroenteritis (IGE) in order to identify immune‐mediated mechanisms and risk factors of PI‐IBS. Methods One hundred and one travelers were asked to complete questionnaires on psychological profile and gastrointestinal (GI) symptoms before travel, 2 weeks, 6 months and 1 year after travel. At each visit, blood was collected for PBMC isolation and rectal biopsies were taken. PI‐IBS was diagnosed using the Rome III criteria and subjects with persistent postinfectious abdominal complaints (PI‐AC) were identified using 3 GSRS symptoms (ie, loose stools, urgency and abdominal pain). Results Forty‐seven of the 101 subjects reported IGE during travel. After 1 year, two subjects were diagnosed with PI‐IBS and eight subjects were presented with PI‐AC versus two subjects with IBS and two with abdominal complaints in the non‐infected group. PBMC analysis showed no differences in T and B cell populations in subjects with PI‐AC vs healthy. Additionally, no differences in gene expression were observed in the early postinfectious phase or after 1 year. Regression analysis identified looser stools, higher anxiety and somatization before infection and several postinfectious GI symptoms as risk factors for PI‐AC. Conclusions The incidence of PI‐IBS is low following travelers’ diarrhea and there is need for larger studies investigating the role of immune activation in PI‐IBS. Psychological factors before infection and the severity of symptoms shortly after infection are risk factors for the persistence of PI‐AC. In this study, we prospectively studied healthy subjects traveling to destinations with a high risk to develop infectious gastroenteritis in order to identify immune‐mediated mechanisms and risk factors of PI‐IBS. We demonstrated that the incidence of PI‐IBS is low after TD compared to outbreak studies. As the number of patients who developed PI‐IBS or persistent abdominal complaints was low, no firm conclusions could be drawn with respect to the role of immune activation. Nonetheless, our study confirms the importance of psychological factors prior to infection and the severity of abdominal symptoms in the early post‐infectious period as risk factors for persistent post‐infectious abdominal complaints.