Duodenal bacterial overgrowth during treatment in outpatients with omeprazole

M Fried, H Siegrist, R Frei, F Froehlich, P Duroux, J Thorens, A Blum, J Bille, J J Gonvers, K Gyr, M Fried, H Siegrist, R Frei, F Froehlich, P Duroux, J Thorens, A Blum, J Bille, J J Gonvers, K Gyr

Abstract

The extent of duodenal bacterial overgrowth during the pronounced inhibition of acid secretion that occurs with omeprazole treatment is unknown. The bacterial content of duodenal juice of patients treated with omeprazole was therefore examined in a controlled prospective study. Duodenal juice was obtained under sterile conditions during diagnostic upper endoscopy. Aspirates were plated quantitatively for anaerobic and aerobic organisms. Twenty five outpatients with peptic ulcer disease were investigated after a 5.7 (0.5) weeks (mean (SEM)) treatment course with 20 mg (nine patients) or 40 mg (16 patients). The control group consisted of 15 outpatients referred for diagnostic endoscopy without prior antisecretory treatment. No patient in the control group had duodenal bacterial overgrowth. In the omeprazole group bacterial overgrowth (> or = 10(5) cfu/ml) was found in 14 (56%) patients (p = 0.0003). The number of bacteria (log10) in duodenal juice in patients treated with omeprazole was distinctly higher (median 5.7; range < 2-8.7) when compared with the control group (median < 2; range < 2-5.0; p = 0.0004). As well as orally derived bacteria, faecal type bacteria were found in seven of 14 and anaerobic bacteria in three of 14 patients. Bacterial overgrowth was similar with the two doses of omeprazole. These results indicate that duodenal bacterial overgrowth of both oral and faecal type bacteria occurs often in ambulatory patients treated with omeprazole. Further studies are needed to determine the clinical significance of these findings, particularly in high risk groups during long term treatment with omeprazole.

References

    1. Gastroenterology. 1988 Jun;94(6):1308-14
    1. Nouv Presse Med. 1982 Jun 26;11(30):2281-3
    1. Br Med J. 1980 Jul 26;281(6235):273
    1. J Infect Dis. 1989 Sep;160(3):414-21
    1. Lancet. 1982 Jul 3;2(8288):45
    1. Lancet. 1982 Jan 30;1(8266):242-5
    1. Scand J Gastroenterol Suppl. 1989;166:27-32; discussion 41-2
    1. Lancet. 1990 Jan 27;335(8683):222
    1. Crit Care Med. 1989 Mar;17(3):211-6
    1. Gastroenterology. 1990 Dec;99(6):1593-8
    1. Gastroenterology. 1969 Jan;56(1):71-9
    1. Infect Immun. 1982 May;36(2):518-24
    1. Lancet. 1982 May 15;1(8281):1091-5
    1. Lancet. 1980 Mar 29;1(8170):672-4
    1. Gut. 1982 Dec;23(12):1048-54
    1. Gut. 1987 Jun;28(6):726-38
    1. Z Gastroenterol. 1988 Nov;26(11):685-8
    1. Gut. 1983 Dec;24(12):1148-51
    1. Gastroenterology. 1991 Apr;100(4):873-7
    1. Gut. 1967 Dec;8(6):574-81
    1. J Infect Dis. 1982 Sep;146(3):322-7
    1. Br J Surg. 1982 Nov;69(11):644-5
    1. Dig Dis. 1987;5(3):157-71
    1. Lancet. 1981 Feb 21;1(8217):408-10
    1. N Engl J Med. 1987 Nov 26;317(22):1376-82
    1. Scand J Gastroenterol. 1982 Sep;17(6):715-20
    1. Gut. 1969 Oct;10(10):812-9
    1. Crit Care Med. 1982 Jul;10(7):444-7
    1. Gut. 1992 Jul;33(7):987-93
    1. J Clin Microbiol. 1990 Mar;28(3):603-4
    1. Gastroenterology. 1984 Jan;86(1):174-93
    1. Scand J Gastroenterol. 1987 Dec;22(10):1211-6
    1. Postgrad Med J. 1984 Jul;60(705):464-6
    1. Br Med J (Clin Res Ed). 1984 Nov 10;289(6454):1272
    1. Gut. 1987 Jan;28(1):96-107
    1. Gastroenterology. 1990 Feb;98(2):302-9
    1. Br Med J (Clin Res Ed). 1984 Sep 22;289(6447):717-9
    1. Scand J Gastroenterol. 1992;27(3):253-6

Source: PubMed

3
Předplatit