[The assessment of nitric oxide metabolites in gastric juice in Helicobacter pylori infected subjects in compliance with grade of inflammatory lesions in gastric mucosa].

UNLABELLED

The infection of H. pylori causes inflammatory lesions in gastric mucosa--until atrophic gastritis, intestinal metaplasia, dysplasia (precancerous states) and finally to gastric cancer or lymphoma. The mechanism of mentioned disturbances is complicated, no doubt that nitric oxide plays here very important role. It is proved, that H. pylori causes essential oxygen metabolism disturbances by activation of inflammatory infiltration's cells to oxide reactive forms as nitric oxide formation. Nitric oxide as oxide radical could react with other free radicals and contribute to oxidative lesions of gastric mucosa and alterations of its structure. The aim of the study was try to answer the question: 1. Is this the relationship between NO metabolites concentrations in gastric juice and morphological state of gastric mucosa? 2. Does H. pylori eradication influence on NO metabolites concentrations in gastric juice? 3. Does H. pylori eradication influence on grade of inflammatory lesions in gastric mucosa?

MATERIAL AND METHODS

The study included 75 subjects between of 21 to 60 years, infected with H. pylori with diagnosed (according to the Sydney system) different stages of chronic gastritis progression. The type of inflammation, activity, the presence of atrophy, intestinal metaplasia and H. pylori infection were assessed. The study group was divided into 3 subgroups: group I--25 subjects with chronic active gastritis, group II--25 subjects with chronic atrophic gastritis without intestinal metaplasia, group III--25 subjects with chronic atrophic gastritis with intestinal metaplasia. Control group comprised 20 healthy subjects, without H. pylori infection. In each patient during gastroscopy 5 biopsy specimens for histopathologic examination and for urea test and 3 ml gastric juice were collected. The concentration of nitric oxide metabolites in gastric juice was determined with spectrophotometric method, based on Griess reaction. H. pylori infection was detected using fast urea test (CLO--test), confirmed by histopathological examination (stained Giemsa method) and non-invasive urea breath test (UBT-13C). In H. pylori--infected patients the above mentioned investigations were performed three times -before, in 8 weeks and in 12 months after antibacterial treatment's finish. In antibacterial therapy we use 7-days three-drugs therapy (omeprasole, amoksycillin and clarythromycin).

RESULTS

The concentration of nitric oxide metabolites in gastric juice in healthy subjects was 6.81 +/- 2.23 micromol. In patients with chronic gastritis, H. pylori infected was significantly higher--in patients with chronic active gastritis was 9.29 +/- 2.19 micromol/l, in patients with chronic atrophic gastritis--10.25 +/- 2.31 micromol/l (p < 0.01), in patients with intestinal metaplasia--11.89 +/- 2.46 micromol/l (p < 0.01). 8 weeks after antibacterial treatment's finish the concentration of nitric oxide metabolites in gastric juice in each group decreased and were: in patients with chronic active gastritis was 8.18 +/- 1.63 micromol/l, in patients with chronic atrophic gastritis--10.02 +/- 2.28 micromol/l, in patients with intestinal metaplasia--10.83 +/- 2.32 micromol/l. The differences were not statistically significant. 12 months after antibacterial treatment's finish the concentration of nitric oxide metabolites in gastric juice in each group decreased and were: in patients with chronic active gastritis was 6.90 +/- 1.43 micromol/l, in patients with chronic atrophic gastritis--7.22 +/- 2.01 micromol/l, in patients with intestinal metaplasia--7.56 +/- 1.98 micromol/l. The differences were statistically significant--p < 0.05, p < 0.01. 8 weeks after antibacterial treatment's finish in each patient also the gastroscopy was performed and another biopsy specimen for histopathologic examination were collected. Only in group I in microscopic image the decreased of inflammation intensity was find (both in antrum and in corpus)--however the differences were not statistically significant. In the other groups the alterations in gastric mucosa do not improve significantly. The gastroscopy was performed again in 12 months after antibacterial treatment's finish. In group I the significant decrease or regression of inflammatory infiltration (in corpus and in antrum) was found. Also in group II the significant decrease of the grade of atrophy and similarly in III group the improvement of histopathological state were observed.

CONCLUSIONS

1. The increase of NO metabolites concentration demonstrates positive correlation with grade of inflammatory lesions in gastric mucosa. 2. The effective antibacterial therapy causes the decrease of NO metabolites concentration in gastric juice, especially in patients with chronic active gastritis. 3. Eradication influence on decrease of grade of lesions' progression in gastric mucosa just in 12 months after effective antibacterial therapy.