Chronic Gastritis : Diagnosis, natural history and consequences
Abstract: Background & alms: The main cause of chronic gastritis is Helicobacter pylori (H. pylori). Clinical manifestations of chronic gastritis are ulcer disease, gastric cancer and mucosa-associated lymphoma tissue (MALT) lymphoma in the stomach. It is uncertain whether gastritis can be diagnosed macroscopically at endoscopy. H. pylori infection may be diagnosed by several different methods, the accuracy of which needs to be explored. Some individuals with H. pylori related chronic gastritis will develop atrophy of the gastric mucosa. This condition is the main risk factor for cancer development and may also be associated with vitamin B12 deficiency leading to hyperhomocysteinaemia. The natural history of chronic gastritis in terms of development of atrophy and ulcer disease in the adult general population is largely unknown.Material & methods: A sample of 50 I volunteers from the general population in the municipality of Linköping was examined with esophago-gastro-duodenoscopy (EGD) with biopsy. Blood samples were collected in the fasting state and the subjects answered a questionnaire about lifestyle factors, medications and disease history. In-hospital diagnoses and causes of death during follow-up of the population were extracted from local and national patient files. Re-examination was done in 314 subjects after a median follow-up interval of 8.4 years. Five diagnostic tests (serology UBT, RUT, culture and microscopic examination) for H. pylori infection were used at re-examination.Results: The best values of sensitivity and specificity were for visible vessels in relation to microscopic presence of severe atrophy in the gastric corpus mucosa (80% and 87%, respectively). There was a positive relation of S-homocysteine to male gender, age, S-cystatin C (renal function), methylenetetrahydrofolate reductase 677TT genotype and atrophic gastritis. Logistic regression analysis showed an association of S-homocysteine higher than 14.5 Ilmol/L to cardiovascular diseases (OR 2.05), but not to dementia overall.The incidence ofulcer was 0.45 per 100 person years and was associated with weekly NSAID use, weekly alcohol consumption (OR 19.4) and smoking (OR 31.0), but not with H. pylori status. Among subjects with chronic gastritis, the incidence of atrophy of the corpus mucosa was 1.4 per 100 person years. Considering diagnostic test for H. pylori infection the accuracy was 0.86 for serology, 0.94 for UBT, 0.94 for RUT, 0.93 for culture, and 0.93 for histological examination. There was a strong correlation between the results of UBT and the histological scores of H. pylori colonisation as well as between the results of UBT and scores of RUT.Conclusions: The occurrence of chronic gastritis or H. pylori infection is not evaluable macroscopically at gastroscopy, except for the absence of rugae or visible vessels in the gastric corpus mucosa. Serum Hcy concentrations are dependent on gender, age, the levels of vitamin B12 and folate, renal function, the occurrence of atrophic gastritis and the MTHFR 677 TT genotype. Elevated S-Hcy is a risk factor for cardiovascular disease. The incidence of atrophy of the corpus mucosa is 1.4 per 100 person years for chronic gastritis overall. Chronic gastritis with or without H. pylori infection is a variable process in which milder degrees of atrophy of the corpus mucosa may appear or disappear. In contrast, moderate-to-severe atrophy of the corpus mucosa rarely regresses. Age and the degree of chronic inflammation in the gastric corpus mucosa are major risk factors for the development of atrophy. The incidence of ulcer was 0.45 per 100 person years. There are only minor differences in accuracy between the three invasive tests for H. pylori infection. The UBT is recommended for situations where endoscopy is not required. RUT may be recommended as the first non-invasive method of choice in the diagnosis of H. pylori infection.
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