Upper gastrointestinal hemorrhage: Have new therapeutics made a difference?

• Published in: Journal of hospital medicine Vol. 4; no. 7; pp. E6 - E10
• Main Authors: Whelan, Chad T., Kaboli, Peter, Zhang, Qi, Siddique, Juned, Ye, Siqin, Meltzer, David O.
• Format: Journal Article
• Language: English
• Published: Hoboken Wiley Subscription Services, Inc., A Wiley Company 01.09.2009
• Subjects: Anti-Inflammatory Agents, Non-Steroidal - adverse effects; Aspirin - adverse effects; Chi-Square Distribution; Cyclooxygenase 2 Inhibitors - adverse effects; Cyclooxygenase 2 Inhibitors - therapeutic use; epidemiology; Female; gastrointestinal hemorrhage; Gastrointestinal Hemorrhage - drug therapy; Gastrointestinal Hemorrhage - etiology; Humans; Logistic Models; Male; Middle Aged; Peptic Ulcer Hemorrhage - drug therapy; Peptic Ulcer Hemorrhage - etiology; Proton Pump Inhibitors - adverse effects; Proton Pump Inhibitors - therapeutic use; Retrospective Studies; Risk Factors; Treatment Outcome; Upper Gastrointestinal Tract - drug effects
• ISSN: 1553-5592; 1553-5606; 1553-5606
• DOI: 10.1002/jhm.443

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. Journal of Hospital Medicine 2009;4:E6–E10. © 2009 Society of Hospital Medicine.