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False Negative Urea Breath Tests with H 2 ‐Receptor Antagonists: Interactions Between Helicobacter pylori Density and pH

2004; Wiley; Volume: 9; Issue: 1 Linguagem: Inglês

10.1111/j.1083-4389.2004.00191.x

1523-5378

David Y. Graham, Antone R. Opekun, Medhavi Jogi, Yoshio Yamaoka, Hong Lü, Rita Reddy, H. M. T. EL‐ZIMAITY,

Mycobacterium research and diagnosis

ABSTRACT Background. We studied the effects of famotidine, sodium bicarbonate, and citric acid on the 13 C‐urea breath test (UBT). Methods. Helicobacter pylori ‐infected volunteers received a UBT, 40 mg of famotidine at bedtime, and a second UBT (pudding test meal, 648 mg NaHCO 3 tablet then 125 mg of urea in 200 ml of water containing 650 mg of NaHCO 3 ). Experiment 2 consisted of four UBTs. Two were standard citric acid UBTs with 75 mg of urea and 2 g citric acid and two were sequential bicarbonate‐citric acid UBTs. Sequential UBTs consisted of administration of a 648 mg bicarbonate tablet with 50 g of Polycose in 200 ml of water. Five minutes later, 125 mg of 13 C‐urea was given in 75 ml of water containing 650 mg of NaHCO 3 . Breath samples were collected after 15 minutes. Then, to acutely acidify the stomach, 4 g of citric acid was given in 200 ml of water. A second breath sample was collected 15 minutes after the citric acid. The standard UBTs were done before and after 6 days of famotidine (40 mg b.i.d.). Sequential UBTs were done after 1 and 6 days of famotidine therapy. Gastric biopsies for histology, culture, and mucosal cytokines were assessed before and after 6 days of famotidine. Results. Eighteen subjects participated, 10 in each experiment; seven had endoscopy with biopsy. Famotidine/bicarbonate resulted an ∼50% fall in UBT values ( p = .021) with 10% becoming negative. The gastric pH increased from 5.1 ± 0.5 to 6.7 ± 0.2 ( p = .03) although no pH value predicted the occurrence of false negative results. Under famotidine acid suppression, NaHCO 3 reduced the delta over baseline (DOB) by 63% ( p = .021). This was reversed with citric acid. Histology showed a H 2 ‐receptor antagonist‐associated increase in the depth of gastric corpus inflammation. Conclusions. H 2 ‐receptor antagonists differ from proton pump inhibitors as high intragastric pH may cause a reduction in urease activity, unrelated to a reduced bacterial load and reversed by citric acid.