Effect of omeprazole therapy on the survival of Helicobacter pylori, urease activity, and antral gastric histology in patients with duodenal ulcer.
BACKGROUND
Helicobacter pylori is associated with chronic active gastritis and peptic ulceration (PU). Omeprazole is a proton pump inhibitor that is effective in healing PU and reducing gastritis. Previously it has been found that omeprazole has some bacteriostatic activity against H. pylori both in vitro and in vivo and in inhibiting urease activity in vitro. Our aim was to evaluate the effect of omeprazole on H. pylori colonization of the gastric mucosa, urease activity in vivo, and the presence of associated gastritis in patients with duodenal ulcer (DU).


METHODS
We studied 12 patients (7 men and 5 women, ages 22-68 yr) with Du larger than 5 mm in diameter with a positive CLOtest (Delta West Ltd., Australia). Omeprazole, 20 mg bid, was given for 8 weeks to each patient, patients were endoscoped at the end of this period to check for healing of DU, and repeat biopsies were obtained from the gastric antrum for histological analysis, CLOtest, and culture.


RESULTS
DU healed completely in all patients. Likewise in all patients there was significant reduction in the urease activity, from 22.1 +/- 4.17 to 1.58 +/- 0.92 units/ml (p < .001; 95% confidence interval of the difference between means, 32.7-14.1), and reduced H. pylori density, from 1,403.46 +/- 128.23 to 422.5 +/- 172.39 colony-forming units (CFU) per milligram of tissue biopsy (p < .001; 95% confidence interval of the difference between means, 1,486.1-590.5). The numbers of H. pylori were reduced on the gastric mucosa after omeprazole therapy and disappeared in six patients, a result that correlated with a negative CLOtest reading after 24 hours.


CONCLUSIONS
Omeprazole, 20 mg bid, is capable of reducing H. pylori numbers and urease activity in vivo. There was no significant reduction in the severity of antral gastritis in DU patients studied.
Nakshabendi
I M
IM
Department of Gastroenterology, Royal Infirmary, Glasgow, Scotland.
Zhang
Q B
QB
Mokhashi
M
M
Gemmell
C G
CG
Lee
F D
FD
Russell
R I
RI
D000328:Adult; D000368:Aged; D000897:Anti-Ulcer Agents / Q000494:pharmacology / Q000627:therapeutic use*; D001426:Bacterial Proteins / Q000032:analysis / Q000037:antagonists & inhibitors*; D001706:Biopsy; D004341:Drug Evaluation; D004381:Duodenal Ulcer / Q000188:drug therapy* / Q000209:etiology / Q000382:microbiology; D004384:Duodenoscopy; D004791:Enzyme Inhibitors / Q000494:pharmacology / Q000627:therapeutic use*; D005260:Female; D005756:Gastritis / Q000150:complications / Q000188:drug therapy* / Q000382:microbiology / Q000473:pathology; D005773:Gastroscopy; D016481:Helicobacter Infections / Q000150:complications / Q000188:drug therapy* / Q000473:pathology; D016480:Helicobacter pylori / Q000187:drug effects* / Q000201:enzymology / Q000302:isolation & purification; D006801:Humans; D008297:Male; D008875:Middle Aged; D011706:Pyloric Antrum / Q000382:microbiology / Q000473:pathology*; D016896:Treatment Outcome; D014510:Urease / Q000032:analysis / Q000037:antagonists & inhibitors*
D000897:Anti-Ulcer Agents; D001426:Bacterial Proteins; D004791:Enzyme Inhibitors; D014510:Urease