title: Do changes in visceral sensory function determine the development of dyspepsia during treatment with aspirin?
abstract: OBJECTIVE
  We hypothesized that the development of dyspeptic symptoms during treatment with nonsteroidal anti-inflammatory drugs (NSAIDs) would be linked to alterations in gastric mechanosensory function and gastric emptying.
  
  
  METHODS
  In the first study, gastric mechanosensory thresholds (barostat technique) and gastric emptying ((13)C-octanoic breath test) were measured and endoscopy was performed at entry and after 5 days of treatment with aspirin (500 mg 3 times daily) in 8 patients with functional dyspepsia (initially without symptoms) and 8 healthy controls. In a second, double-blind, placebo-controlled, cross-over study, 6 new patients with functional dyspepsia and 6 controls were started with either placebo or aspirin for 5 days. Sensory thresholds were tested after the fifth day of aspirin or placebo treatment. Abdominal symptoms were assessed daily.
  
  
  RESULTS
  In the first study, 6 of 8 patients and 3 of 8 controls, and in the second trial 6 of 6 patients and 1 of 6 healthy subjects, developed dyspepsia on aspirin (P < 0.005 patients vs. healthy subjects). No symptoms occurred during placebo treatment. Lanza scores were not associated with symptoms. After aspirin, sensory thresholds increased in both studies in subjects without development of symptoms (by 25.9% +/- 7.9%, and 31.0% +/- 4.1%, respectively, all P < 0.05), whereas there was no significant increase in subjects who developed symptoms (-11.2% +/- 5.3% and -3.4% +/- 13.4%, all P > 0.4). Neither thresholds nor symptoms were linked with the severity of mucosal damage, baseline gastric emptying (t1/2), or changes of gastric emptying (all P > 0.4).
  
  
  CONCLUSIONS
  Failure to increase sensory thresholds during treatment with aspirin is associated with the development of dyspepsia.
authors.affiliation: Division of Gastroenterology and Hepatology, University of Essen, Essen, Germany. g.holtmann@uni-essen.de
authors.forename: Gerald
authors.initials: G
authors.lastname: Holtmann
authors.forename: Juergen
authors.initials: J
authors.lastname: Gschossmann
authors.forename: Lydia
authors.initials: L
authors.lastname: Buenger
authors.forename: Guido
authors.initials: G
authors.lastname: Gerken
authors.forename: Nicholas J
authors.initials: NJ
authors.lastname: Talley
mesh_terms: D000328:Adult; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000009:adverse effects*; D001241:Aspirin / Q000009:adverse effects*; D001760:Bleeding Time; D018592:Cross-Over Studies; D004311:Double-Blind Method; D004415:Dyspepsia / Q000139:chemically induced* / Q000503:physiopathology; D005260:Female; D005753:Gastric Mucosa / Q000187:drug effects / Q000473:pathology; D006801:Humans; D008297:Male; D008465:Mechanoreceptors / Q000503:physiopathology; D009129:Muscle Tonus; D011312:Pressure; D012016:Reference Values; D012677:Sensation / Q000502:physiology*; D012684:Sensory Thresholds; D016037:Single-Blind Method; D013270:Stomach / Q000294:innervation / Q000503:physiopathology; D014781:Viscera / Q000503:physiopathology*
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; D001241:Aspirin