Short-term/low-dose aspirin-induced duodenal erosions are not dependent on Helicobacter pylori infection, cyclooxygenase expression and prostaglandin E2 levels.
OBJECTIVE
The mechanisms of interaction between Helicobacter pylori infection and low-dose aspirin in the induction of duodenal erosions are not fully understood. The aim of this study was to investigate the effects of low-dose aspirin on the induction of duodenal erosions, the expression of cyclooxygenases and prostaglandin (PG)-E(2) levels in healthy subjects according to their H. pylori status.


METHODS
Twenty healthy volunteers (H. pylori-negative n=10, H. pylori-positive n=10) received 100 mg aspirin/day for 1 week. During esophagogastroduodenoscopy, duodenal biopsies were taken before and at days 1, 3, and 7 of medication. COX-1 and -2 expressions were analyzed by reverse transcriptase-polymerase chain reaction (RT-PCR), and immunohistochemistry; mucosal PGE(2) levels were determined by ELISA. Three months after successful eradication of infection, nine H. pylori-positive subjects repeated the protocol.


RESULTS
Aspirin-induced duodenal erosions occurred independently of whether H. pylori infection was present or not. There was no difference in duodenal COX-1 and COX-2 expression among the groups and expression was not affected by aspirin. Basal duodenal PGE(2) levels were similar among the different groups (H. pylori-negative 4.3+/-4.2, H. pylori-positive 5.2+/-1.3, following H. pylori eradication 5.2+/-1.4 ng/microg protein) and were not affected by low-dose aspirin.


CONCLUSIONS
In healthy subjects, low-dose aspirin-induced duodenal erosions are not influenced by H. pylori status. Low-dose aspirin medication for one week does not affect either cyclooxygenase expression or duodenal PGE(2) levels and therefore is likely to induce duodenal damage mainly through topical toxicity.
Venerito
Marino
M
Department of Gastroenterology, Hepatology and Infectious Diseases, Otto-von-Guericke University, Magdeburg, Germany.
Treiber
Gerhard
G
Wex
Thomas
T
Kuester
Doerthe
D
Roessner
Albert
A
Mönkemüller
Klaus
K
Malfertheiner
Peter
P
D000328:Adult; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000008:administration & dosage / Q000009:adverse effects*; D001241:Aspirin / Q000008:administration & dosage / Q000009:adverse effects*; D016861:Cyclooxygenase Inhibitors / Q000008:administration & dosage / Q000009:adverse effects*; D015232:Dinoprostone / Q000378:metabolism*; D004381:Duodenal Ulcer / Q000139:chemically induced* / Q000378:metabolism / Q000382:microbiology*; D004386:Duodenum / Q000378:metabolism; D005260:Female; D016481:Helicobacter Infections / Q000139:chemically induced* / Q000378:metabolism / Q000382:microbiology*; D016480:Helicobacter pylori; D006801:Humans; D007150:Immunohistochemistry; D007413:Intestinal Mucosa / Q000378:metabolism; D008297:Male; D011451:Prostaglandin-Endoperoxide Synthases / Q000378:metabolism*
D000894:Anti-Inflammatory Agents, Non-Steroidal; D016861:Cyclooxygenase Inhibitors; D011451:Prostaglandin-Endoperoxide Synthases; D015232:Dinoprostone; D001241:Aspirin