Postinfectious irritable bowel syndrome may occur after non-gastrointestinal and intestinal infection

Abstract

Postinfectious functional gastrointestinal disorders (FGIDs) may not be specific to gastroenteritis. This pilot study aimed to ascertain the 3- and 6-month incidence of functional gut disorders in people with non-gastrointestinal (GI) infection, gastroenteritis and healthy controls. This was a prospective study of three cohorts recruited from hospital (non-GI infections) and the community (others). FGIDs were diagnosed using self-completed Rome II modular questionnaires administered at baseline, 3 and 6 months. Thirty-six subjects with non-GI infection, 219 healthy subjects and 108 with bacterial gastroenteritis participated. No difference in incidence of FGID was detected between the GI and non-GI infection cohorts. Any FGID was more frequent in people who had a non-GI infection than in controls at both 3 [odds ratio: 4.34 (95% CI: 3.60-16.45)] and 6 months [4.76 (4.42-27.92)]. Irritable bowel syndrome (IBS) alone was more frequent in people with non-GI infections than in controls at 3 months (6.12 [1.30-29.12]) but did not quite reach statistical significance at 6 months (4.58 [0.79-26.46]). Our findings were unexpected. Postinfectious FGIDs may be related to non-GI and GI infection, although not all potential biases were controlled in study design. Further studies need to explore these preliminary findings and, if confirmed, the underlying mechanisms.

Discrepancies between the responses to skin prick test to food and respiratory antigens in two subtypes of patients with irritable bowel syndrome

“…Various mechanisms, including gastrointestinal dismotility and visceral hypersensitivity, have been extensively studied in IBS [8][9][10] , but recent interest has also been associated with, or directed to the possible participation of the intestinal mucosa in the pathophysiology of IBS [11][12][13]17] . Several lines of evidence suggest that IBS may be associated with inflammation in the ileal or colonic mucosa, and at least in a subset of patients with IBS, the mucosal immune system seems to be activated [11,[15][16][17] .…”

“…Clinically, the frequency of IBS is associated with psychological stress, food intolerance (adverse reaction to a specific food or ingredient that is not immune mediated or associated with psychological phenomena), intestinal infections, and even previous abdominal surgery [3,7,12,[20][21][22][23][24][25] . Dunlop et al [16] have reported that patients with subtype D-IBS (pos-infectious and non-infectious origin) have a more pronounced permeability increase in the proximal intestine compared with controls and those with C-IBS.…”

“…The exact pathophysiology of IBS remains unknown, although various mechanisms including gastrointestinal dismotility and visceral hypersensitivity have been well studied in IBS [8][9][10] . Recent interest has also been directed to the possible participation of the mucosa in the pathophysiology of IBS [11][12][13] . Inflammatory mediators cause intestinal dysfunction and a consequent increase in permeability [14][15][16][17] .…”

Relative risk of irritable bowel syndrome following acute gastroenteritis and associated risk factors

“…There is increasing evidence that acute infectious gastroenteritis (GE) can increase the risk of IBS, with several studies demonstrating that a significant number of GE patients develop PI-IBS [1,2,[18][19][20][21][22][23]. Campylobacter, Shigella, Salmonella and Escherichia coli infections as well as viral agents, including norovirus, and parasites have been associated with PI-IBS [5,21,[23][24][25].…”

Disease burden of post-infectious irritable bowel syndrome in The Netherlands

“…042. For the duration of PI-IBS, several long-term follow-up studies were assessed [15,16,[22][23][24][25]. Based on these studies, we assumed for PI-IBS provoked by bacteria an average duration of 5 years [14].…”