Eradication of Helicobacter pylori by a 1-week course of famotidine, amoxicillin and clarithromycin.
OBJECTIVE
The combination of a proton pump inhibitor (PPI) such as omeprazole with amoxicillin and clarithromycin constitutes one of the most effective treatments for the eradication of Helicobacter pylori. Nevertheless, the mechanisms of interaction between these drugs remain unclear. It has been shown that minimal inhibitory concentration values of both antibiotics are considerably lower at neutral pH levels than in an acid environment. Further, omeprazole possesses bacteriostatic activity. To evaluate the significance of these mechanisms we replaced omeprazole with famotidine, a drug which only suppresses acid production, but has no intrinsic antimicrobial activity.


METHODS
We evaluated the efficacy of a 1-week course of famotidine 80 mg b.i.d., amoxicillin 1000 mg b.i.d. and clarithromycin 500 mg b.i.d. in a pilot study (20 patients), and then confirmed our results in a larger replication study (87 patients). A total of 107 patients with H. pylori-associated duodenal ulcer (n = 54), gastric ulcer (n = 14) or non-ulcer dyspepsia (n = 39) were included. Endoscopy was performed at baseline and 4-6 weeks after discontinuation of treatment. H. pylori status was assessed by the urease test and histology.


RESULTS
H. pylori was successfully eradicated in 94 of 104 patients who completed the study (90.4%; CI 95%, 83.0-95.3%). By intention-to-treat analysis, the eradication rate was 87.9% (CI 95%, 80.1-93.4%). Ulcer healing was observed in 98.1% of duodenal ulcers and 92.9% of gastric ulcers (based on per-protocol analysis). Mild side effects that did not require termination of treatment were reported by seven patients (6.7%).


CONCLUSIONS
A 1-week course of famotidine, amoxicillin and clarithromycin is a highly effective, simple and safe eradication regimen. Our data indicate that acid suppression is the crucial mechanism by which the activity of amoxicillin and clarithromycin against H. pylori is enhanced, whereas additional antimicrobial activity or other specific effects of PPIs seem to be less important.
Gschwantler
M
M
4th Department of Internal Medicine, KA Rudolfstiftung, Vienna, Austria.
Dragosics
B
B
Wurzer
H
H
Brandstätter
G
G
Weiss
W
W
D000328:Adult; D000368:Aged; D000658:Amoxicillin / Q000627:therapeutic use*; D000900:Anti-Bacterial Agents / Q000627:therapeutic use*; D004359:Drug Therapy, Combination; D004381:Duodenal Ulcer / Q000188:drug therapy / Q000382:microbiology; D015738:Famotidine / Q000627:therapeutic use*; D005260:Female; D016481:Helicobacter Infections / Q000188:drug therapy*; D016480:Helicobacter pylori; D006635:Histamine H2 Antagonists / Q000627:therapeutic use*; D006801:Humans; D018942:Macrolides; D008297:Male; D008875:Middle Aged; D010406:Penicillins / Q000627:therapeutic use*; D010865:Pilot Projects; D011446:Prospective Studies; D013276:Stomach Ulcer / Q000188:drug therapy / Q000382:microbiology; D016896:Treatment Outcome
D000900:Anti-Bacterial Agents; D006635:Histamine H2 Antagonists; D018942:Macrolides; D010406:Penicillins; D015738:Famotidine; D000658:Amoxicillin