Natural history of abdominal pain in family practice: Longitudinal study of electronic medical record data in southwestern Ontario.

OBJECTIVE: To examine the frequency, natural history, and outcomes of 3 subtypes of abdominal pain (general abdominal pain, epigastric pain, localized abdominal pain) among patients visiting Canadian family practices. DESIGN: Retrospective cohort study with a 4-year longitudinal analysis. SETTING: Southwestern Ontario. PARTICIPANTS: A total of 1790 eligible patients with International Classification of Primary Care codes for abdominal pain from 18 family physicians in 8 group practices. MAIN OUTCOME MEASURES: The symptom pathways, the length of an episode, and the number of visits. RESULTS: Abdominal pain accounted for 2.4% of the 15,149 patient visits and involved 14.0% of the 1790 eligible patients. The frequencies of each of the 3 subtypes were as follows: localized abdominal pain, 89 patients, 1.0% of visits, and 5.0% of patients; general abdominal pain, 79 patients, 0.8% of visits, and 4.4% of patients; and epigastric pain, 65 patients, 0.7% of visits, and 3.6% of patients. Those with epigastric pain received more medications, and patients with localized abdominal pain underwent more investigations. Three longitudinal outcome pathways were identified. Pathway 1, in which the symptom remains at the end of the visit with no diagnosis, was the most common among patients with all subtypes of abdominal symptoms at 52.8%, 54.4%, and 50.8% for localized, general, and epigastric pain, respectively, and the symptom episodes were relatively short. Less than 15% of patients followed pathway 2, in which a diagnosis is made and the symptom persists, and yet the episodes were long with 8.75 to 16.80 months' mean duration and 2.70 to 4.00 mean number of visits. Pathway 3, in which a diagnosis is made and there are no further visits for that symptom, occurred approximately one-third of the time, with about 1 visit over about 2 months. Prior chronic conditions were common across all 3 subtypes of abdominal pain ranging from 72.2% to 80.0%. Psychological symptoms consistently occurred at a rate of approximately one-third. CONCLUSION: The 3 subtypes of abdominal pain differed in clinically important ways. The most frequent pathway was that the symptom remained with no diagnosis, suggesting a need for clinical approaches and education programs for care of symptoms themselves, not merely in the service of coming to a diagnosis. The importance of prior chronic conditions and psychological conditions was highlighted by the results.

Alterations to enteric neural signaling underlie secretory abnormalities of the ileum in experimental colitis in the guinea pig.

Inflammatory bowel diseases (IBD) can involve widespread gastrointestinal dysfunction, even in cases in which inflammation is localized to a single site. The underlying pathophysiology of dysfunction in noninflamed regions is unclear. We examined whether colitis is associated with altered electrogenic ion transport in the ileal mucosa and/or changes in the properties of ileal submucosal neurons. Colitis was induced by administration of trinitrobenzene sulfonic acid (TNBS), and the uninflamed ileum from animals was examined 3, 7, and 28 days later. Electrogenic ion transport was assessed in Ussing chambers. Intracellular microelectrode recordings were used to examine the neurophysiology of the submucosal plexus of the ileum in animals with colitis. Noncholinergic secretion was reduced by 33% in the ileum from animals 7 days after the induction of colitis. The epithelial response to vasoactive intestinal peptide (VIP) was unaltered in animals with colitis, but the response to carbachol was enhanced. Slow excitatory synaptic transmission was dramatically reduced in VIP-expressing, noncholinergic secretomotor neurons. This change was detected as early as 3 days following TNBS treatment. No changes to fast synaptic transmission or the number of VIP neurons were observed. In addition, cholinergic secretomotor neurons fired more action potentials during a given stimulus, and intrinsic primary afferent neurons had broader action potentials in animals with colitis. These findings implicate changes to enteric neural circuits as contributing factors in inflammation-induced secretory dysfunction at sites proximal to a localized inflammatory insult.