Abstract
Helicobacter pylori (H. pylon) infection of the stomach may be harmful both to the mucus layer and the underlying cells which might impair defence against noxious agents such as NSAIDs. The aim of this study was to evaluate the prevalence of H. pylori and gastric lesions in NSAID-treated patients.
Methods: In 132 patients treated with NSAID and upper gastrointestinal symptoms (63 males, 69 females, mean age 49 years, range 28-59), endoscopic investigation of the antral and corporal mucosa, including H. pylori testing (urease and histology) was performed.
Results:
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1
H. pylori was found in 95 patients (72%);
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2
In this group, ulcers were found in 73 cases (77%), 33 in the duodenal bulb (35%), 27 in the prepyloric region (29%) and 13 (13%) in the gastric body.
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3
In the H. pylori-negative group (37), ulcers were found in 19 patients (51%), 7 (19%) in the duodenal bulb, 8 (21.6%) in the prepyloric region and 4 (10.8%) in the gastric body.
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4
In the H. pylori-positive group, a predominant finding was chronic superficial active gastritis, with focal intestinal metaplasia (mostly complete) and atrophy in 25 (24%) of ulcer and in 26 (23%) of non-ulcer cases; in 33 (29%) in prepyloric and in 38 (53%) in gastric body ulcer.
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Chronic superficial gastritis was not found in the H. pylori-negative group.
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6
Endoscopie findings in non-ulcer cases showed a higher proportion of more-severe lesions — bleeding areas — in the H. pylori-positive group, whereas less-severe lesions (erosions, bleeding, spots) were more often present in the H. pylori-negative group. Frank bleeding occurred in 20% of the H. pylori-positive and in 19% of the H. pylori-negative group, in the first group predominantly due to ulcer.
Conclusions: NSAID-related ulcers occur more frequently in H. pylori-positive cases, probably due to impaired defence. This seems to justify H. pylori testing and adequate treatment of positive cases in NSAID gastropathy.
Correspondence
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References
Development Panel on Helicobacter pylori in Peptic Ulcer Disease. J Am Med Assoc. 1994;272(1):659.
Marshall BJ. Helicobacter pylori. Am J Gastroenterol. 1994;89(8):S116–28.
Marshall BJ, Barrett LJ, Prakasch C et al. Urea protects Helicobacter (Campylobacter) pylori from the bactericidal effects of acid. Gastroenterology. 1990;99:697–702.
Murakami M, Yod JK, Teramura S et al. Generation of ammonia and mucosal lesion formation following hydrolysis of urea by urease in the stomach. J Clin Gastroenterol. 1990;12:5104–9.
Goggin PM, Northfield TC, Spychal RT. Factors affecting gastric mucosal hydrophobicity in man. Scand J Gastroenterol. 1991; 181(Suppl):65–73
Tummura MX, Cover TL, Blaser MJ. Cloning and expression of a high-molecular mass major antigen of Helicobacter pylori: Evidence of linkage to cytotoxin production. Infect Immun. 1993;61:1799–809.
Salim AS. The relationship between Helicobacter pylori and oxygen-derived free radicals in the mechanism of duodenal ulceration. Intern Med. 1993;32:359–64.
Xiang Z, Bugnoli M, Rappuoli R et al. Helicobacter pylori host responses in peptic ulceration. Lancet. 1993;341:900–1.
Hirschl AM, Brandstatter RG, Dragosics B et al. Kinetics of specific IgG antibodies for monitoring the effect of anti-Helicobacter pylori chemo-therapy. J Infect Dis. 1993;168:763–6.
Crabtree JE, Wyatt JH, Sobala GM et al. Systemic and mucosal humoral responses to Helicobacter pylori in gastric cancer. Gut. 1993;34(10):1339–43.
Sobala GM, Pignatelli B, Schorah CJ et al. Levels of nitrite, nitrate, N-nitrose compounds, ascorbic acid and total bile acids in gastric juice of patients with and without precancerous conditions of the stomach. Carcinogenesis. 1991;12:193–8.
Correa P. Human gastric carcinogenesis: A multistep and multifactorial process. Cancer Res. 1992;52:6735–40.
Sobola GM, Schorah GJ, Pilnatell B et al. High gastric juice ascorbic acid concentrations in members of a gastric cancer family. Carcinogenesis. 1993;14:291–2.
Langmann MJS, Brooks P, Hawkey F et al. Management of non-steroidal anti-inflammatory drug gastroduodenopathy: Epidemiology, causation and treatment. Working party reports, World Congress of Gastroenterology, Sydney. 1990:11–16.
Flemstroem G, Garner A, Nylander O et al. Surface epithelial bicarbonate transport by mammalian duodenum in vivo. Am J Physiol. 1982;243:G348–58.
Robert A, Nezamis J, Lancaster C et al. Cytoprotection by prostaglandin in rats. Prevention of gastric necrosis produced by alcohol, HC1, NaOH, hypertonic NaHC1 and thermal injury. Gastroenterology. 1979;77:433–43.
Cullen DJE, Collins J, Christiansen HJ et al. Long term risk of peptic ulcer disease in people with Helicobacter pylori infection — a community based study. Abstr. Gastroenterology. 1993;104(Suppl 2):60.
Fries JF, Miller SR, Spitz FW et al. Towards an epidemiology of gastropathy associated with non-steroidal anti-inflammatory drug use. Gastroenterology. 1989;96:647–55.
Tytgat GNJ, Axon ATR, Dixon MF et al. Helicobacter pylori: causal agent in peptic ulcer disease? Working party reports of the World Congress of Gastroenterology, Sydney. 1990:36–45.
Adamek RJ, Wegeler M, Opferkuch W et al. Successful Helicobacter pylori eradication: A systemic effect of antibiotic? Am J Gastroenterol. 1993;88:792–3.
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Jablonska, M., Chlumská, A. (1997). Impaired Gastric Mucosal Defence in Helicobacter Pylori-Related Conditions. In: Mózsik, G., Nagy, L., Pár, A., Rainsford, K.D. (eds) Cell Injury and Protection in the Gastrointestinal Tract. Springer, Dordrecht. https://doi.org/10.1007/978-94-011-5392-8_17
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DOI: https://doi.org/10.1007/978-94-011-5392-8_17
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