title: Upper gastrointestinal hemorrhage: have new therapeutics made a difference?
abstract: BACKGROUND
  To explore the distribution of etiologies and risk factors of upper gastrointestinal hemorrhage (UGH) in the context of new pharmacologic therapies that may alter the risk of UGH.
  
  
  METHODS
  Retrospective study performed on eligible UGH inpatients at 2 academic medical centers, between July 1, 2001 and June 30, 2003. Administrative data and chart review were used to identify demographics, UGH risk factors, and UGH etiologies. Bivariate and multivariate analyses were performed to describe distributions and associations of risk factors and etiologies.
  
  
  RESULTS
  UGH was identified in 227 subjects, with ED (n = 99; 44%), peptic ulcer disease (PUD) (n = 75; 33%), and variceal bleeds (n = 39; 17%) accounting for the majority of bleeds. Known risk factors for UGH occurred in 70% (n = 156) of subjects (prior UGH 43% [n = 90], nonsteroidal anti-inflammatory drug (NSAID) use 23% [n = 52], aspirin [ASA] use 25% [n = 57], NSAID + ASA use 6.6% [n = 15]), while 19% (n = 42) were using a proton-pump inhibitor (PPI) and 5% (n = 11) a cyclooxygenase-2 (COX-2) inhibitor. Subjects at site 1 were more likely to have ED (odds ratio [OR], 7.1; P < 0.001) and less likely to have variceal bleeding (OR, 0.12; P = 0.009) in multivariate analyses. Preventive therapy did not differ between sites.
  
  
  CONCLUSIONS
  Unlike older studies, PUD was not the most common etiology, suggesting that advances in Helicobacter pylori (H. pylori) eradication may affect the epidemiology of UGH. Despite advances in therapeutics of acid-related disease, ED accounted for the majority of UGH. Most subjects had risk factors for UGH and most were not receiving protective therapy. Large between site-differences in the distribution of etiologies existed.
authors.affiliation: Department of Internal Medicine, University of Chicago, Chicago, Illinois 60637, USA. cwhelan@uchicago.edu
authors.forename: Chad T
authors.initials: CT
authors.lastname: Whelan
authors.forename: Peter
authors.initials: P
authors.lastname: Kaboli
authors.forename: Qi
authors.initials: Q
authors.lastname: Zhang
authors.forename: Juned
authors.initials: J
authors.lastname: Siddique
authors.forename: Siqin
authors.initials: S
authors.lastname: Ye
authors.forename: David O
authors.initials: DO
authors.lastname: Meltzer
mesh_terms: D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000009:adverse effects; D001241:Aspirin / Q000009:adverse effects; D016009:Chi-Square Distribution; D052246:Cyclooxygenase 2 Inhibitors / Q000009:adverse effects / Q000627:therapeutic use*; D005260:Female; D006471:Gastrointestinal Hemorrhage / Q000188:drug therapy* / Q000209:etiology; D006801:Humans; D016015:Logistic Models; D008297:Male; D008875:Middle Aged; D010438:Peptic Ulcer Hemorrhage / Q000188:drug therapy / Q000209:etiology; D054328:Proton Pump Inhibitors / Q000009:adverse effects / Q000627:therapeutic use*; D012189:Retrospective Studies; D012307:Risk Factors; D016896:Treatment Outcome; D041742:Upper Gastrointestinal Tract / Q000187:drug effects*
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; D052246:Cyclooxygenase 2 Inhibitors; D054328:Proton Pump Inhibitors; D001241:Aspirin