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Query: UMLS:C0038358 (gastric ulcer)
 5,179 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Helicobacter pylori (Hp) is considered to be one of the causes of gastric mucosal injury. Using biopsy specimens from the gastric mucosa of patients with gastritis or gastric ulcer, the intramucosal mucus was quantified by computer image analysis to evaluate its relationship with Hp. In gastric mucosa positive for Hp, the mucus content within the gastric mucosa was significantly decreased. Ammonia was administered based on its assumed role in decreasing the mucus content of the gastric mucosa, and resulted in a decrease in rats to whom it was administered. Based on these results, cases of intractable gastric ulcer were studied. In these intractable cases, Hp was present significantly more often than in other cases and the intramucosal mucus content was significantly lower. These findings suggest that Hp may be a factor in the resistance of gastric ulcer to treatment.
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PMID:[Relation between Helicobacter pylori and intractable gastric ulcer--PAS positive intramucosal mucus as an index]. 157 1

Ammonia, released in the gastric mucosa by the action of Helicobacter pylori urease on transuded plasma urea, curtails the biosynthesis of mucus and/or causes the mucus to be disassembled at the mucosal surface. These changes facilitate colonisation by H pylori and may promote gastric ulcer formation.
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PMID:Hypothesis: Helicobacter pylori, urease, mucus, and gastric ulcer. 196 87

The in vitro effect of urea and hydrolysis of urea by urease on mucus H+ permeability is reported here. The effective DHCl values indicate a strong pH dependence for H+ diffusion in both water and mucus layers, with no apparent trend at concentrations between 1 and 50 mM urea. However, the estimated DHCl at near-neutral and alkaline pH are 4- to 10-fold lower through mucus than through aqueous films. Moreover, the pKa values of HCO3- and NH3 (generated by urease action on urea) had a profound effect on measured DHCl. These in vitro studies suggest that a high local concentration of NH3 and HCO3- within the mucus layer, generated by the action of Helicobacter pylori urease on endogenous intragastric urea, could greatly accelerate proton flux to the surface epithelium by operation of a buffer shuttle. This results in enhanced H+ permeability, particularly at pKa values of HCO3- and NH3, and in extreme circumstances it may result in gastric ulcer formation.
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PMID:An in vitro study of enhanced H+ diffusion by urease action on urea. Implications for Helicobacter pylori-associated peptic ulceration. 826 22

The in vitro effect of ammonium bicarbonate buffer on mucus H+ permeability is reported here. The diffusional resistance of mucus and water was demonstrated to be dependent on buffer concentration, and the contrast between the two types of layers was most pronounced for low buffer concentration near neutrality. Moreover, the pKa values of HCO3- and NH3 had a profound effect on measured DHCl. These in vitro studies suggest that a potentially damaging high local concentration of NH3 and HCO3- within the mucus layer generated by the action of Helicobacter pylori urease on endogenous intragastric urea could greatly accelerate proton flux to the surface epithelium by operation of a buffer shuttle. This results in enhanced H+ permeability, particularly at pKa values of HCO3- and NH3, and that in extreme circumstances this may result in gastric ulcer formation.
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PMID:Enhanced H+ diffusion by NH4+/HCO3-: implications for Helicobacter-pylori-associated peptic ulceration. 851 85