Eradicating Helicobacter pylori reduces hypergastrinaemia during long-term omeprazole treatment.
BACKGROUND
Both proton pump inhibitor drug treatment and Helicobacter pylori infection cause hypergastrinaemia in man.


OBJECTIVE
To determine whether eradicating H pylori is a means of reducing hypergastrinaemia during subsequent proton pump inhibitor treatment.


METHODS
Patients with H pylori were randomised to treatment with either anti-H pylori or symptomatic treatment. One month later, all received four weeks treatment with omeprazole 40 mg/day for one month followed by 20 mg/day for six months. Serum gastrin concentrations were measured before and following each treatment.


RESULTS
In the patients randomised to anti-H pylori treatment, eradication of the infection lowered median fasting gastrin by 48% and meal stimulated gastrin by 46%. When gastrin concentrations one month following anti-H pylori/symptomatic treatment were used as baseline, omeprazole treatment produced a similar percentage increase in serum gastrin in the H pylori infected and H pylori eradicated patients. Consequently, in the patients in which H pylori was not eradicated, median fasting gastrin concentration was 38 ng/l (range 26-86) at initial presentation and increased to 64 ng/l (range 29-271) after seven months omeprazole, representing a median increase of 68% (p < 0.005). In contrast, in the patients randomised to H pylori eradication, median fasting gastrin at initial presentation was 54 ng/l (range 17-226) and was unchanged after seven months omeprazole at 38 ng/l (range 17-95).


CONCLUSIONS
Eradicating H pylori is a means of reducing the rise in gastrin during subsequent long term omeprazole treatment. In view of the potential deleterious effects of hypergastrinaemia it may be appropriate to render patients H pylori negative prior to commencing long-term proton pump inhibitor treatment.
el-Nujumi
A
A
University Department of Medicine and Therapeutics, Western Infirmary, Glasgow, UK.
Williams
C
C
Ardill
J E
JE
Oien
K
K
McColl
K E
KE
D000328:Adult; D000464:Alginates / Q000627:therapeutic use; D000536:Aluminum Hydroxide / Q000627:therapeutic use; D000658:Amoxicillin / Q000627:therapeutic use; D000863:Antacids / Q000627:therapeutic use; D000897:Anti-Ulcer Agents / Q000627:therapeutic use*; D004338:Drug Combinations; D004359:Drug Therapy, Combination; D004941:Esophagitis / Q000097:blood* / Q000188:drug therapy / Q000382:microbiology; D005260:Female; D005755:Gastrins / Q000097:blood*; D005773:Gastroscopy; D016481:Helicobacter Infections / Q000097:blood / Q000150:complications / Q000188:drug therapy*; D016480:Helicobacter pylori; D006801:Humans; D008297:Male; D008795:Metronidazole / Q000627:therapeutic use; D008875:Middle Aged; D009853:Omeprazole / Q000627:therapeutic use*; D009942:Organometallic Compounds / Q000627:therapeutic use; D010437:Peptic Ulcer / Q000097:blood* / Q000188:drug therapy / Q000382:microbiology; D012824:Silicic Acid / Q000627:therapeutic use; D017693:Sodium Bicarbonate / Q000627:therapeutic use
D000464:Alginates; D000863:Antacids; D000897:Anti-Ulcer Agents; D004338:Drug Combinations; D005755:Gastrins; D009942:Organometallic Compounds; D012824:Silicic Acid; D008795:Metronidazole; D000536:Aluminum Hydroxide; C007829:alginate, aluminium hydroxide, magnesium trisilicate, sodium bicarbonate drug combination; D000658:Amoxicillin; D017693:Sodium Bicarbonate; C002791:bismuth tripotassium dicitrate; D009853:Omeprazole