title: Gastrointestinal bleeding in the setting of anticoagulation and antiplatelet therapy.
abstract: OBJECTIVE
  To review the literature on the significance, risk factors, and management of occult and gross gastrointestinal (GI) bleeding in patients on antiplatelets and/or anticoagulants.
  
  
  METHODS
  Relevant original and review articles and their bibliographies were analyzed. Estimates of risks and therapeutic outcomes were obtained from randomized trials, whereas risk factor identification was gathered from cross-control and prospective cohort studies.
  
  
  RESULTS
  Antiplatelets and anticoagulants do not diminish the positive predictive value of fecal occult blood testing to find GI pathology. They increase the risk of gross GI bleeding, and predictors of hemorrhage include history of GI bleeding or ulcer disease, higher intensity of anticoagulation, combination therapy, and presence of comorbid conditions. A bleeding site is identified in most patients with peptic ulcer being the most common. In case of significant bleeding, complete or partial reversal of anticoagulation is undertaken on the basis of the balance of risks between bleeding and thromboembolic events. Early endoscopy can reveal lesions requiring endoscopic hemostasis, which can be performed in the setting of low-intensity anticoagulation. In patients with history of peptic disease or bleeding from an acid-related lesion, proton-pump inhibitors and Helicobacter pylori eradication reduce the risk of upper GI bleeding even when antiplatelet therapy is continued.
  
  
  CONCLUSIONS
  Predictors of bleeding on antiplatelets and/or antithrombotics therapy have been identified, but formulation and validation of a GI bleeding index for stratification of risk in individual patients is suggested. Reversal of anticoagulation in bleeding patients is associated with a low risk of thromboembolic events and permits the performance of diagnostic and therapeutic endoscopy. Proton-pump inhibitors and H. pylori eradication reduce the risk of rebleeding in those with acid-related disease.
authors.affiliation: Department of Internal Medicine, American University of Beirut, Lebanon. kb02@aub.edu.lb
authors.forename: Kassem
authors.initials: K
authors.lastname: Barada
authors.forename: Heitham
authors.initials: H
authors.lastname: Abdul-Baki
authors.forename: Ihab I
authors.initials: II
authors.lastname: El Hajj
authors.forename: Jana G
authors.initials: JG
authors.lastname: Hashash
authors.forename: Peter H
authors.initials: PH
authors.lastname: Green
mesh_terms: D000925:Anticoagulants / Q000009:adverse effects*; D002986:Clinical Trials as Topic; D004724:Endoscopy / Q000379:methods; D006471:Gastrointestinal Hemorrhage / Q000139:chemically induced* / Q000209:etiology / Q000628:therapy; D016481:Helicobacter Infections / Q000188:drug therapy / Q000382:microbiology; D016480:Helicobacter pylori / Q000187:drug effects / Q000302:isolation & purification; D006801:Humans; D010975:Platelet Aggregation Inhibitors / Q000009:adverse effects*; D054328:Proton Pump Inhibitors / Q000627:therapeutic use; D012307:Risk Factors
chemical_list: D000925:Anticoagulants; D010975:Platelet Aggregation Inhibitors; D054328:Proton Pump Inhibitors