Roleofammonia inthepathogenesis ofthegastritis, hypergastrinaemia, andhyperpepsinogenaemia I caused byHelicobacter pylori infection

Studies wereperformed inpatients withand without renal failure toinvestigate therole of bacterial ammoniaproduction inthepathogenesis ofthemucosal abnormalities caused byHelicobacter pylori. Thehighrateof H pylonammoniaproduction inuraemic patients shouldaccentuate anyammonia induced effects. Themedian(range) gastric juice ammoniumconcentration intheH pylori positive patients withrenal failure was19 mmol/l (1I-43) compared with5mmoIl(1-11) intheH pylonpositive patients without renal failure (p<0005). IntheH pylori negative patients thevalues were3 mmol/l (0.5-11) and0.7mmol/l(0.1-1.4) respectively in thepatients withandwithout renal failure (p<O.Ol). Despite themuchhigher ammonia production intheH pylonpositive uraemic patients, thenatureandseverity oftheir gastritis wasthesameasthat intheH pylori positive non-uraemic patients. Themedian (range) fasting serumgastrin concentration wasraised intheuraemic patients compared withthenon-uraemic patients butwassimilar intheuraemic patients with(95pmoIl (52-333)) orwithout (114pmoIIl (47-533)) H pylori infection. Themedian (range) serum pepsinogen Iconcentration wasalsohighin theuraemic compared withthenon-uraemic patients andwas significantly higher in uraemic patients withH pylon(352ng/ml, range280-653) thaninthose without H pylori infection (165ng/ml, range86-337) (p<0.01). Thesefindings indicate that thegastritis and hypergastrinaemia associated withH pylori infection arenottheresult ofmucosal damage induced bytheorganism's ammonia production. (Gut 1992; 33:1612-1616)