The 13carbon urea breath test for the diagnosis of Helicobacter pylori infection in subjects with atrophic gastritis: evaluation in a primary care setting
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Summary Background 13 Carbon urea breath testing is reliable to detect current infection with Helicobacter pylori but has been reported to be of limited value in selected patients with atrophic body gastritis or acid‐lowering medication. Aim To evaluate the accuracy of 13 carbon urea breath testing for H. pylori detection in 20 asymptomatic patients with histologically confirmed atrophic body gastritis in a primary care setting. Methods 13 Carbon urea breath testing and serology were compared with H. pylori culture of a corpus biopsy as reference test. Results All tests were in agreement in 12 patients, being all positive in six and all negative in six. One patient was positive for serology and culture but negative for 13 carbon urea breath testing, five patients had only positive serology and two patients had only positive 13 carbon urea breath testing. 13 Carbon urea breath testing showed an accuracy with culture of 85% and anti‐ H. pylori serology with culture of 75%. 13 Carbon urea breath testing carried out in patients with positive serology showed an accuracy of 92%. Receiver operating characteristic curve analysis of 13 carbon urea breath testing shows optimal discrimination at the prescribed cut‐off value. Conclusions 13 Carbon urea breath testing can be used as diagnostic H. pylori test in asymptomatic patients with atrophic body gastritis, preferably in addition to serology, to select subjects for anti‐ H. pylori therapy.Keywords:
Urea breath test
Atrophic gastritis
Objective To observe the effect of interleukin-1β(IL-1β) in atrophic gastritis and to identify the relationship between IL-1β level and helicobacter pylori(HP) infection.Methods 52 cases of superficial gastritis and 50 cases of atrophic gastritis were investigated.The trail has four groups: group A: superficial gastritis with HP negative subjects;group B: superficial gastritis with HP positive subjects;group C: atrophic gastritis with HP negative subjects;groups D: atrophic gastritis with HP positive subjects.Serum IL-1β level was examined by enzyme-linked immunosorbent assay.HP infection was determined by 14C-urea breath test(14C-uBT).Results Serum IL-1β levels in atrophic gastritis were higher than those in superficial gastritis.Especially serum IL-1β in atrophic gastritis with HP positive subjects(P0.01)and atrophic gastritis with HP negative subjects(P0.05).In superficial gastritis with HP infection serum IL-1β were higher than HP negative subjects,but there was no significance(P0.05).Conclusion IL-1β may contribute to the pathogenesis of atrophic gastritis.Inducible generation of IL-1β may one of the mechanisms to explain the link between HP infection and atrophic gastritis.
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The recent discussions about the relationship between helicobacter-pylori-infection, gastritis and the occurrence of stomach cancer caused us to analyse blood sera of 543 participants randomly selected from the general population in the age of 25 to 34 and of 55 to 64 years from Mosbach (Neckar-Odenwald-Kreis), the county of Deggendorf (Lower-Bavaria) and Augsburg (Upper-Bavaria) regarding IgG-antibodies against helicobacter pylori and the concentrations of the pepsinogens A and C. The latter were used as markers for the presence of chronic gastritis without atrophy and with severe atrophy. The prevalence of helicobacter pylori infection and of forms of gastritis showed no particular differences regarding region or gender. Notable differences in the prevalences were observed with respect to the two age strata. The helicobacter pylori prevalence of the regions being studied ranged for males from 13% to 75% and for females from 22% to 76%. The prevalences of chronic gastritis without atrophy in the investigated areas, derived from the pepsinogen titers, were found to be for males between 24% and 70% and for females between 28% and 61%. Chronic gastritis with severe atrophy appeared mainly in the age group of 55 to 64 years, ranging from 2% to 11% in males and 4% to 10% in females, depending upon region. The helicobacter pylori prevalence and the prevalence of chronic gastritis without atrophy were found to be highly correlated. Chronic gastritis with severe atrophy was also found to be associated with helicobacter pylori prevalence. However, this association did not reach statistical significance.(ABSTRACT TRUNCATED AT 250 WORDS)
Chronic gastritis
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Helicobacter
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Helicobacter Infections
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To determine the utility of the [13C]urea breath test in confirming the eradication of Helicobacter pylori.We reviewed our H. pylori database for patients who underwent [13C]urea breath test at baseline and 6 wk after triple therapy with tetracycline, metronidazole, and bismuth subsalicylate. Baseline infection was defined by the identification of the organism on antral biopsies or a reactive CLO test. Eradication was defined as a negative Warthin-Starry stain and a non-reactive CLO test at 24 h. All patients had a positive baseline [13C]urea breath test defined as [13C] enrichment > 6% at 60 min.One hundred eighteen H. pylori-infected patients (mean age 58.3 +/- 13.9 yr) met the review criteria (61 duodenal ulcers, 24 gastric ulcers, 33 non-ulcer dyspepsia). In 101/118 patients (86%), H. pylori was successfully eradicated (mean baseline breath test value 25.8 +/- 1.6). Of 101 patients, 95 had a negative 6-wk follow-up breath test (mean 2.2 +/- 0.2, p < 0.001). Of the 6/101 patients in whom treatment was successful, and who remained breath test positive at 6 wk, 4/6 were breath test negative when retested at 3 months. The remaining two patients were lost to follow-up. In 17/118 (14%) patients, H. pylori failed to be eradicated (mean baseline breath test 22.4 +/- 3.6). Fifteen of 17 patients had a positive breath test at 6 wk (mean 19.9 +/- 3.7). Two of 17 with a negative breath test at 6 wk tested positive when the breath test was repeated at 3 months. The sensitivity and specificity of [13C]urea breath test at 6 wk posttreatment are 97% and 71%, respectively. The positive and negative predictive values are 94% and 88%, respectively.[13C]urea breath test is a sensitive indicator of H. pylori eradication 6 wk after treatment. Antral biopsies are unnecessary to confirm eradication of H. pylori after completion of treatment.
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Background: Helicobacter pylori-infection associated gastritis is known to be a significant risk factor of gastric cancer. Serum levels of Gastrin-17 and Pepsinogen1which are respectively biomarkers of gastric antral and corpus mucosal activity are well known parameters of atrophic gastritis.Objectives: To determine the prevalence of Helicobacter pylori and atrophic gastritis amongst dyspeptic patients and to compare the production of PGI and G-17 in the various atrophic stages.Methods: A total of 139 dyspeptic patients aged 46.68±15.50 years [females 106 aged47.23±15.51years, males 33 aged 44.48±14.62] were included during the one year period, March 2008-april 2009 at the district hospital Tombel. The degree of atrophy was determined by the levels of serum pepsinogen1, and gastrin-17 and the presence of Helicobacter pylori antibodies detected by an enzyme immunoassay.Results: The prevalence of Helicobacter pylori was 79.82% and that for atrophic gastritis was 6.6%. A decrease in mean serum levels of gastin-17 along with increasing antral atrophy was observed; the mean serum levels of pepsinogen1 were reduced during progression of corpus atrophy.Conclusion: A weak reverse correlation(r =-0.036) was found between Gastrin-17 and Helicobacter pylori antibodies.Key words: Helicobacter pylori, atrophic gastritis, gastrin, pepsinogen
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Helicobacter pylori eradication therapy is useful and requires more precise determination of actual eradication. Patients often become positive for Helicobacter pylori again after presumed eradication. Reinfection is thought rare and patients with positive reconversion may be false-negative at determination. After a year, positive reconversion was 26.8% in our work after determination by culture and histopathological methods and 4.3% after these were combined with urea breath test (UBT). The positive reconversion rate is significantly lower after combination with UBT, suggesting the usefulness of UBT in determining Helicobacter pylori eradication. This may be because UBT includes no biopsy, eliminating sampling error, and highly sensitive UBT detects traces of Helicobacter pylori. The UBT is thus expected to become widely used to determine Helicobacter pylori eradication.
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This was a descriptive study carried out from January to December 2021, at Quanzhou First Hospital, an affiliated hospital of Fujian Medical University, to investigate the efficacy of the urea breath test in detecting Helicobacter pylori infection in patients with peptic ulcer bleeding affected with proton pump inhibitors. A total of 77 patients with peptic ulcer bleeding, who underwent urea breath testing after active bleeding, were divided into two groups. The Helicobacter pylori infection positivity rate in patients with peptic ulcer bleeding was 66.2%. The time from bleeding to detection and from admission to detection was not significantly different between the Helicobacter pylori-positive and -negative groups (p=0.840 and 0.285, respectively). Even with high-dose proton pump inhibitor treatment, a urea breath test can be performed after peptic ulcer bleeding ceases and results in an acceptable positivity rate. There was no significant difference in the accuracy of Helicobacter pylori detection between the time from bleeding to testing and from admission to testing. Key Words: Peptic ulcer, Helicobacter pylori, Upper gastrointestinal bleeding, Urea breath test, Proton pump inhibitor.
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A simple method for grading gastritis is to assess the severity of round cell infiltration and the loss of normal glands, and this may be applied to both antral and body changes. However, there is, as yet, no satisfactory classification of gastritis.In population samples, gastritis shows a linear increase in age-specific prevalence so that the annual increase in the body atrophic gastritis pool up to geriatric age is constant (1.5%). In the elderly, there appears to be a retardation of the process, particularly in the antral mucosa, where some healing trend is demonstrable. This dynamic behaviour is qualitatively similar in all population samples collected in Finland and Estonia. On the other hand, the dynamic behaviour of gastritis in different subpopulations differs markedly from that in the population at large.In pernicious anemia patients and their first-degree relatives, the progression of body atrophic gastritis in its final stages is about 20 times more rapid than in a general population, while, simultaneously, antral gastritis displays a distinct healing tendency. A behaviour opposite to that in pernicious anemia is seen in patients with active or healed duodenal ulcer disease and in duodenitis: antral gastritis behaves, on the whole, similarly to that in the general population, but in the body mucosa there occurs virtually no progression with age, and the mucosa generally remains normal or at the stage of superficial gastritis. However, after antrectomy body gastritis progresses rapidly in the remnant at first, but it slows down later and then closely resembles that in the general population. Gastric ulcer shows a variable behaviour so that most juxtapyloric ulcers behave dynamically like duodenal ulcers, while the angular ulcers indicate a rapid progression of body gastritis associated with a markedly slower progression of antral gastritis.It seems that the characteristics of, and variations in, antral body gastritis in the different subpopulations are related to age, the only distinct dynamic feature in common being the dissimilar and poorly co-ordinated dynamic behaviour of these stomach areas.Despite significant association with clinically important diseases, chronic gastritis shows poor correlation with different kinds of upper abdominal complaints, and it is probable that complaints which are found in connection with chronic gastritis are due to other concomitant diseases or unrelated functional disturbances.
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Objective To explore the relationship between different types of gastritis and gastric cancer.Methods The expression of p21 and p16 proteins in varioliform gastritis, non-atrophic gastritis, atrophic gastritis,and gastric cancer was detected by immunohistochemistry. The results were compared. Results The positive rate of p21 protein expression in non-atrophic gastritis, atrophic gastritis, varioliform gastritis, gastric cancer was 0, 22.5%,35.0%, 60.0%, respectively, which was significantly higher in varioliform gastritis than non-atrophic gastritis, but significantly lower than gastric cancer(P0.05). The positive rate of p16 protein expression in non-atrophic gastritis, atrophic gastritis, varioliform gastritis, gastric cancer was 90.0%, 50.0%, 45.0%, 17.5%, respectively, which was significantly lower in varioliform gastritis than non-atrophic gastritis, but significantly higher than gastric cancer(P0.01).No significant differences were noted between varioliform gastritis and atrophic gastritis. Conclusion Both p21 and p16 proteins may be involved in the evolution of varioliform gastritis to gastric cancer.
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