[Role of Helicobacter pylori infection and use of NSAIDs in the etiopathogenesis of upper gastrointestinal bleeding].

INTRODUCTION

Non-steroid antiinflammatory drugs (NSAIDs) and Helicobacter pylori (Hp) infection are two most important independent risk factors involved in the etiopathogenesis of gastroduodenal mucosal injury with a clear and critical role in both uncomplicated and complicated peptic ulcer disease. It is estimated that upto 90% of all peptic ulcers result from the effect of one or both of these factors.

AIM

To determine the frequency of NSAIDs use and Hp infection in patients with acute upper gastrointestinal bleeding.

PATIENTS AND METHODS

Study evaluated data from 500 patients in whom esophagogastroduodenoscopy was performed following presentation in emergency unit with acute upper gastrointestinal bleeding. Anamnestic data was collected together with detailed information on previous salicilates and/or NSAIDs use. Hp status was determined and anatomic localisation of bleeding lesion was also registered.

RESULTS

Acute upper GIT bleading was caused solely by NSAIDs in 55 (11%), by aspirin in 66 (13.2%), while combined NSAID/aspirin therapy was identified in 19 (3.8%) of patients. In total NSAID and/or aspirin use were diagnosed in 139 (27.8%). while in 122 (24.4%) only Hp infection was diagnosed. Both risk factors were identified in 144 (28.8%) patients (Hp+NSAIDs in 12.2%, Hp+aspirin in 10.8% and Hp+aspirin+NSAIDs in 5.8%). In 19.8% of the cases (14% of males and 27% of females) neither NSAID/aspirin use nor presence of Hp infection was noted. Out of 500 patients enrolled, 63% were mails. In females, bleeding lesion was most frequently localized in gastric mucosa, while males had equal chance of bleeding from either gastric or duodenal mucosa. Fortunatelly, only 5 to 7% of patients were bleeding from both gastric and duodenal lesion.

CONCLUSION

Prevention of acute upper gastrointestinal bleeding can be achieved trough strict and limited use of aspirin and NSAIDs, eradication of Hp infection and use of gastroprotective therapy in well-defined risk patients that need chronic NSAIDs and/or aspirin therapy. In all patients starting long-term NSAID and/or aspirin therapy and all patients already on long-term aspirin therapy test and treat strategy for Hp infection should be used. On the other hand, only in high risk patients (more than 65 years, history of peptic ulcer disease, concomitant corticosteroid, aspirin, clopidogrel or warfarin therapy) already on chronic NSAID therapy long-term PPI therapy should be prescribed after testing and treating of Hp infection.