title: Antiplatelet drugs are a risk factor for esophageal mucosal injury.
abstract: BACKGROUND
  In esophagus whether antiplatelet drugs, such as low-dose aspirin (LDA) and clopidogrel, induce mucosal injury by pH changes or by acid reflux is unclear. We designed to clarify which mechanism was responsible.
  
  
  METHODS
  In study 1, 80 patients taking LDA and 80 age- and sex-matched subjects who underwent endoscopy for dyspeptic symptoms or for a health check-up were evaluated the endoscopic incidence of esophageal mucosal injury and severity. In study 2, 35 healthy subjects were treated with LDA 100 mg (regimen A), and then 20 randomly selected subjects were dosed clopidogrel 75 mg (regimen C), LDA/clopidogrel (regimen AC), or LDA/clopidogrel/rabeprazole 10 mg for 7 days. Subjects underwent endoscopy and 24-hour pH measurements on day 7.
  
  
  RESULTS
  In study 1, the prevalence of esophageal injury in LDA patients was 40.0%, significantly higher than in non-LDA subjects (25.0%, p = 0.042). In study 2, significant increases in incidence of injury were observed with regimens A (45.8%) and AC (50.0%), but not with C (20.0%), on day 7. Among subjects in whom pH was >5.0 and <4.0 for less than 40% of time, none developed esophageal injury.
  
  
  CONCLUSIONS
  LDA caused esophageal injury in half of patients and volunteers. Acid-inhibitory drugs effectively prevented the development of LDA-induced, not clopidogrel, esophageal injury.
authors.affiliation: First Department of Medicine, Hamamatsu University School of Medicine, Hamamatsu, Japan. mitsu@hama-med.ac.jp
authors.forename: Mitsushige
authors.initials: M
authors.lastname: Sugimoto
authors.forename: Takahiro
authors.initials: T
authors.lastname: Uotani
authors.forename: Masafumi
authors.initials: M
authors.lastname: Nishino
authors.forename: Mihoko
authors.initials: M
authors.lastname: Yamade
authors.forename: Shu
authors.initials: S
authors.lastname: Sahara
authors.forename: Takanori
authors.initials: T
authors.lastname: Yamada
authors.forename: Satoshi
authors.initials: S
authors.lastname: Osawa
authors.forename: Ken
authors.initials: K
authors.lastname: Sugimoto
authors.forename: Kazuo
authors.initials: K
authors.lastname: Umemura
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Watanabe
authors.forename: Hiroaki
authors.initials: H
authors.lastname: Miyajima
authors.forename: Takahisa
authors.initials: T
authors.lastname: Furuta
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D001189:Aryl Hydrocarbon Hydroxylases / Q000235:genetics; D001241:Aspirin / Q000009:adverse effects*; D016022:Case-Control Studies; D000077144:Clopidogrel; D065731:Cytochrome P-450 CYP2C19; D004939:Esophageal Perforation / Q000139:chemically induced* / Q000235:genetics / Q000517:prevention & control; D050782:Esophageal pH Monitoring; D005764:Gastroesophageal Reflux / Q000150:complications*; D005838:Genotype; D006801:Humans; D008875:Middle Aged; D010975:Platelet Aggregation Inhibitors / Q000009:adverse effects*; D054328:Proton Pump Inhibitors / Q000627:therapeutic use; D016032:Randomized Controlled Trials as Topic; D012307:Risk Factors; D013988:Ticlopidine / Q000009:adverse effects / Q000031:analogs & derivatives*
chemical_list: D010975:Platelet Aggregation Inhibitors; D054328:Proton Pump Inhibitors; D000077144:Clopidogrel; D001189:Aryl Hydrocarbon Hydroxylases; C045793:CYP2C19 protein, human; D065731:Cytochrome P-450 CYP2C19; D013988:Ticlopidine; D001241:Aspirin