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1.
Dig Liver Dis ; 54(12): 1630-1638, 2022 12.
Article in English | MEDLINE | ID: mdl-35382973

ABSTRACT

BACKGROUND: The endoscopic diagnosis of Helicobacter-pylori(H.pylori) infection and gastric precancerous lesions(GPL), namely atrophic-gastritis and intestinal-metaplasia, still remains challenging. Artificial intelligence(AI) may represent a powerful resource for the endoscopic recognition of these conditions. AIMS: To explore the diagnostic performance(DP) of AI in the diagnosis of GPL and H.pylori infection. METHODS: A systematic-review was performed by two independent authors up to September 2021. Inclusion criteria were studies focusing on the DP of AI-system in the diagnosis of GPL and H.pylori infection. The pooled accuracy of studies included was reported. RESULTS: Overall, 128 studies were found (PubMed-Embase-Cochrane Library) and four and nine studies were finally included regarding GPL and H.pylori infection, respectively. The pooled-accuracy(random effects model) was 90.3%(95%CI 84.3-94.9) and 79.6%(95%CI 66.7-90.0) with a significant heterogeneity[I2=90.4%(95%CI 78.5-95.7);I2=97.9%(97.2-98.6)] for GPL and H.pylori infection, respectively. The Begg's-test showed a significant publication-bias(p = 0.0371) only among studies regarding H.pylori infection. The pooled-accuracy(random-effects-model) was similar considering only studies using CNN-model for the diagnosis of H.pylori infection: 74.1%[(95%CI 51.6-91.3);I2=98.9%(95%CI 98.5-99.3)], Begg's-test(p = 0.1416) did not show publication-bias. CONCLUSION: AI-system seems to be a good resource for an easier diagnosis of GPL and H.pylori infection, showing a pooled-diagnostic-accuracy of 90% and 80%, respectively. However, considering the high heterogeneity, these promising data need an external validation by randomized control trials and prospective real-time studies.


Subject(s)
Helicobacter Infections , Helicobacter pylori , Precancerous Conditions , Stomach Neoplasms , Humans , Artificial Intelligence , Helicobacter Infections/diagnosis , Precancerous Conditions/diagnosis , Precancerous Conditions/pathology , Prospective Studies , Stomach Neoplasms/diagnosis , Stomach Neoplasms/pathology
2.
Gastroenterol Res Pract ; 2021: 6616334, 2021.
Article in English | MEDLINE | ID: mdl-33824659

ABSTRACT

BACKGROUND: EndoFaster® analyzes gastric juice in real time during gastroscopy allowing the detection of hypo-achlorhydric conditions, like corpus atrophic gastritis. Narrow-band imaging (NBI) endoscopy allows to accurately detect and perform target biopsies in areas of intestinal metaplasia, a histological change often associated to corpus atrophic gastritis. AIMS: To compare the diagnostic accuracy of EndoFaster® with histological evaluation for corpus atrophic gastritis through high-resolution (HR) NBI targeted biopsies. METHODS: Prospective study on consecutive adult patients undergoing gastroscopy between April and November 2018. Patients in therapy with proton pump inhibitors, previous gastric surgery, and/or known gastric neoplasia were excluded. At the beginning of gastroscopy, gastric juice was aspirated and analyzed by EndoFaster® in 15 seconds. Endoscopists were blinded to the report of EndoFaster®. Evaluation of gastric mucosa in HR-white light was firstly performed, then with HR-NBI allowing to perform targeted biopsies on areas suspected for intestinal metaplasia; otherwise, biopsies were performed according to the updated Sydney System protocol and sent for histopathological evaluation. RESULTS: Overall, 124 patients were included [64% F; 56 (18-85) years]. Corpus atrophic gastritis was present in 41.9% of patients. EndoFaster® showed an accuracy for corpus atrophic gastritis diagnosis, compared to histopathological evaluation as gold standard, of 87.1% and a sensitivity, specificity, PPV, and NPV of 78.8%, 93.1%, 89.1%, and 85.9%, respectively. pH showed a positive correlation with the severity score of atrophy (r = 0.67, 95% CI: 0.73-0.81, and p < 0.0001). EndoFaster® allowed to diagnose corpus atrophic gastritis in 3.7% of patients negative to NBI (corpus atrophic gastritis without intestinal metaplasia). CONCLUSION: EndoFaster® seems a promising tool to diagnose corpus atrophic gastritis. The evaluation of hypo-achlorhydria during gastroscopy can address bioptic sampling in corpus atrophic gastritis patients without intestinal metaplasia.

4.
Clin Res Hepatol Gastroenterol ; 42(6): 604-609, 2018 12.
Article in English | MEDLINE | ID: mdl-29910147

ABSTRACT

Cameron lesions are erosive-ulcerative alterations of gastric mucosa occurring in patients with large hiatal hernia, potentially causing gastrointestinal bleeding and iron deficiency anaemia. Diagnosis may be challenging, and not infrequently erosions are overlooked at endoscopy, so that repeated and unnecessary diagnostic procedures are performed, particularly in those patients with chronic anaemia. We described two peculiar cases of patients with iron deficiency anaemia in whom Cameron lesions were either overlooked or misinterpreted. By reviewing data of 22publications reporting endoscopic and clinical data of 140patients, we noted a large prevalence of females (75%). The most frequent presenting symptoms were anaemia (62%) and overt gastrointestinal bleeding (36%). Noteworthy, as many as 69% of patients underwent one or more previous upper endoscopy before diagnosis of Cameron lesion was achieved. Patients were mainly treated with proton pump inhibitor (PPI) therapy and iron supplementation. Moreover, endoscopic haemostasis was performed in 10% of case, blood transfusion was required in one third of cases, and a similar quote of patients underwent a surgical approach for hiatal hernia repair. The observation that as many as 60% patients were already receiving standard PPI therapy when diagnosis was performed would suggest that either long-term treatment with adequate dose PPI or surgical approach for hiatal hernia repair is required. In conclusion, Cameron lesion is still an overlooked diagnosis in patients with iron deficiency anaemia in whom a 5-9.2% prevalence has been reported.


Subject(s)
Gastric Mucosa/pathology , Aged , Aged, 80 and over , Anemia, Iron-Deficiency/complications , Capsule Endoscopy , Endoscopy, Gastrointestinal , Female , Hernia, Hiatal/complications , Humans
7.
Aliment Pharmacol Ther ; 40(6): 639-47, 2014 Sep.
Article in English | MEDLINE | ID: mdl-25066096

ABSTRACT

BACKGROUND: Adequate gluten-free diet (GFD) is the only treatment for coeliac disease (CD). However, no agreement has been reached on either how and when to assess patient adherence to GFD or its effectiveness on villous atrophy. AIM: To assess, in a prospective study, patient adherence to and efficacy of GFD on histological recovery after 1-year of GFD. METHODS: Between 2009 and 2012, we enrolled 65 consecutive newly-diagnosed adult patients (median age 38 years, 18-70) with biopsy-proven atrophic CD. Patients were re-evaluated after 1 year of GFD with duodenal histology, serological assays, symptoms and a dietary interview based on a validated questionnaire. Complete histological recovery was defined as the absence of villous atrophy and ≤30/100 intraepithelial lymphocytes. RESULTS: Overall, 81.5% of patients had adequate adherence (ADA) to GFD, whereas 18.5% had an inadequate adherence (IADA); 66% of ADA patients and no IADA patients achieved complete histological recovery (P < 0.00001). Among ADA patients, antibody seroconversion and symptoms were not significantly different between patients who achieved complete histological recovery and those who achieved partial histological recovery with P = 0.309 and P = 0.197, respectively. Multivariate analysis showed that Marsh 3C was a risk factor for incomplete histological recovery in ADA patients (OR 8.74, 95% CI: 1.87-40.83). CONCLUSIONS: This study shows that complete histological recovery after 1-year of GFD in adult patients, who are assessed as adherent to the GFD, can be obtained in 66% of patients. Patients with severe histological damage at diagnosis are at risk for incomplete histological recovery 1 year later.


Subject(s)
Celiac Disease/diet therapy , Diet, Gluten-Free , Duodenum/pathology , Adult , Atrophy/diet therapy , Atrophy/pathology , Biopsy , Celiac Disease/pathology , Female , Follow-Up Studies , Humans , Male , Middle Aged , Patient Compliance , Prospective Studies , Surveys and Questionnaires
9.
Aliment Pharmacol Ther ; 37(4): 375-82, 2013 Feb.
Article in English | MEDLINE | ID: mdl-23216458

ABSTRACT

BACKGROUND: Pernicious anaemia (PA) has an increased risk for gastric cancer (GC). It is not established whether PA patients need to undergo endoscopic/histological follow-up. AIM: To provide a systematic overview of the literature on PA and the development of gastric cancer, to estimate the gastric cancer incidence-rate. METHODS: According to PRISMA, we identified studies on PA patients reporting the incidence of gastric cancer. Quality of studies was evaluated using the Newcastle-Ottawa Quality Assessment Scale. Meta-analysis on annual gastric cancer incidence rates was performed. RESULTS: Twenty-seven studies met eligibility criteria. 7 studies were of high, 6 of medium, 10 of low and 4 of very low quality. Gastric cancer incidence-rates ranged from 0% to 0.2% per person-years in 7 American, from 0% to 0.5% in 2 Asiatic, from 0% to 1.2% in 11 Northern European studies and from 0% to 0.9% in 7 studies from other European countries. The incidence-rates of gastric cancer ranged from 0% to 1.2% per person-years in studies which used gastroscopy, from 0.1% to 0.9% in those based on International Classification of Disease. Heterogeneity between studies was not statistically significant at the 5% level (Chi-squared test = 17.9, P = 0.08). The calculated pooled gastric cancer incidence-rate was 0.27% per person-years. Meta-analysis showed overall gastric cancer relative risk in PA as 6.8 (95% CI: 2.6-18.1). CONCLUSIONS: This systematic review shows a pooled gastric cancer incidence-rate in pernicious anaemia of 0.27% per person-years and an estimated nearly sevenfold relative risk of gastric cancer in pernicious anaemia patients. Further high quality studies are needed to confirm this higher risk.


Subject(s)
Anemia, Pernicious/complications , Stomach Neoplasms/etiology , Gastroscopy/methods , Humans , Incidence , Risk Factors
10.
Aliment Pharmacol Ther ; 33(12): 1361-9, 2011 Jun.
Article in English | MEDLINE | ID: mdl-21492197

ABSTRACT

BACKGROUND: Long-term observational studies assessing the incidence of type I gastric carcinoid (typeIGC) in patients with chronic atrophic gastritis are few. AIM: To evaluate the occurrence of typeIGC at diagnosis and during follow-up and to identify patient features associated with the presence of typeIGC in a cohort of chronic atrophic gastritis patients. METHODS: Three hundred and sixty-seven chronic atrophic gastritis patients [245 women, age 54 (18-79) years] underwent regular follow-up by gastroscopy. The incidence of typeIGC was determined in chronic atrophic gastritis patients with at least 2 years of follow-up (n = 214). Baseline clinical and histological features were analysed as factors associated with the presence of typeIGC by univariate analysis. RESULTS: Type I gastric carcinoid was diagnosed in nine (2.4%) patients at the moment when chronic atrophic gastritis was diagnosed. After 1463 person-years, six patients developed typeIGC with an annual incidence rate (person-year) of 0.4%. Patients with typeIGC had significantly higher levels of gastrin, chromogranin A and more frequently the presence of body polyps and ECL-dysplasia compared with chronic atrophic gastritis patients without typeIGC. CONCLUSIONS: This cohort study shows that typeIGC is a rare complication in patients with chronic atrophic gastritis, and the presence of body polyps and ECL-dysplasia at gastroscopic/histologic evaluation is strongly associated with the presence of typeIGC.


Subject(s)
Carcinoid Tumor/pathology , Gastritis, Atrophic/pathology , Precancerous Conditions/pathology , Stomach Neoplasms/pathology , Adolescent , Adult , Aged , Carcinoid Tumor/classification , Cohort Studies , Female , Gastric Mucosa/pathology , Gastroscopy/methods , Humans , Immunohistochemistry , Incidence , Male , Middle Aged , Precancerous Conditions/classification , Young Adult
11.
Minerva Gastroenterol Dietol ; 57(1): 13-22, 2011 Mar.
Article in English | MEDLINE | ID: mdl-21372765

ABSTRACT

AIM: The standard therapeutic approach for symptomatic uncomplicated diverticular disease (DD) remains to be defined, and only a few studies have tested the efficacy of probiotics in these patients. METHODS: Patients with symptomatic uncomplicated DD were randomized to a control arm, i.e., (group A, [N.=16], high-fibre diet alone), or to Group B ([n=18], twice daily 1 sachet of probiotic + high-fibre diet), or group C ([N.=16], twice daily 2 sachets of probiotic + high-fibre diet). The probiotic Genefilus F19© containing Lactobacillus paracasei sub. paracasei F19 was administered for 14 days/month for 6 months. The primary endpoint under consideration was a decrease in abdominal pain and bloating intensity after treatment. RESULTS: Bloating decreased significantly in Groups B and C VAS score group B: 4.6 ± 2.6 vs. 2.3 ± 2.0, P<0.05, group C: 3.9 ± 2.9 vs. 1.8 ± 2.1, P<0.05). The decrease in abdominal pain within 24 hours in these groups did not reach statistical significance. During treatment, none of the group B (N.=4) or group C patients (N=3) with abdominal pain >24 hours reported the recurrence of this symptom, while the 3 group A patients reported at least one episode (P=0.016). No significant difference regarding abdominal pain <24 hours and bloating was observed between the two groups of patients treated with a low or high probiotic dose. CONCLUSION: Lactobacillus paracasei F19, in association with a high-fibre diet, is effective in reducing abdominal bloating and prolonged abdominal pain in symptomatic uncomplicated diverticular disease, and could thus be a promising option in the treatment of these patients.


Subject(s)
Diverticulitis/therapy , Diverticulum , Lacticaseibacillus casei , Probiotics/therapeutic use , Abdominal Pain/drug therapy , Abdominal Pain/etiology , Aged , Dietary Fiber/administration & dosage , Diverticulitis/complications , Female , Flatulence/drug therapy , Flatulence/etiology , Humans , Male , Middle Aged , Pilot Projects , Treatment Outcome
12.
Minerva Gastroenterol Dietol ; 56(4): 397-404, 2010 Dec.
Article in English | MEDLINE | ID: mdl-21139539

ABSTRACT

AIM: In the elderly, prevalence of bleeding- and/or iron malabsorption-related gastrointestinal (GI) causes of iron deficiency anemia (IDA) has not been addressed yet. The aim of this study was to assess the occurrence of malabsorptive diseases and bleeding lesions of the upper and lower GI tract in early (65-74 year-old) and late (over 75 year-old) elderly group compared with adult (50-64 year-old) outpatients. METHODS: The study enrolled 136 consecutive adult (N.=31), early (N.=48) and late elderly (N.=57) IDA outpatients who were referred to the Gastroenterology Department for IDA evaluation and underwent gastroscopy/histology and colonoscopy. RESULTS: Bleeding lesions were significantly less frequent in adult patients than in elderly patients (29% vs. 49.5%, P=0.0252). The most common bleeding lesions were large hiatal hernia (14.7%) and colon cancer (12.5%). Iron malabsorption diseases (Hp-related pangastritis, atrophic body gastritis and celiac disease) were more frequent in the adult group than in the early elderly group (80.6% vs. 56.2%, P=0.0367). In elderly patients, the observed prevalence of bleeding and iron malabsorption IDA causes was similar, whereas in adult patients iron malabsoptive diseases were more frequently detected (P<0.0001). The occurrence of concomitant IDA causes was not different among the three age-groups. CONCLUSION: In the early and late elderly, almost half of GI IDA causes are related to bleeding lesions which are more frequently observed respect to the adult patients. Iron malabsorption diseases affect almost 60% of early and late elderly groups. As for adult patients, an accurate upper and lower endoscopical/histological evaluation diagnoses IDA causes in the vast majority of the elderly outpatients.


Subject(s)
Anemia, Iron-Deficiency/diagnosis , Anemia, Iron-Deficiency/etiology , Gastrointestinal Hemorrhage/diagnosis , Gastrointestinal Hemorrhage/etiology , Lower Gastrointestinal Tract/pathology , Outpatients , Upper Gastrointestinal Tract/pathology , Adult , Aged , Aged, 80 and over , Anemia, Iron-Deficiency/complications , Anemia, Iron-Deficiency/epidemiology , Female , Humans , Italy/epidemiology , Malabsorption Syndromes/complications , Malabsorption Syndromes/etiology , Male , Middle Aged , Outpatients/statistics & numerical data , Prevalence , Prospective Studies , Risk Factors , Surveys and Questionnaires
13.
Aliment Pharmacol Ther ; 31(9): 1042-50, 2010 May.
Article in English | MEDLINE | ID: mdl-20175768

ABSTRACT

BACKGROUND: Atrophic gastritis, involving the gastric body mucosa, predisposes to gastric neoplastic lesions (GNL). However, regular gastroscopic-histological follow-up for GNL is not recommended for patients with atrophic gastritis. AIM: To evaluate risk factors for the progression to GNL in a cohort of patients with atrophic gastritis. METHODS: A total of 300 patients with atrophic gastritis [205 women, aged 54 (18-78) years] underwent gastroscopy with six gastric antrum and body biopsies. All patients had at least one follow-up gastroscopy/histology at an interval of at least 1 year after the atrophic gastritis diagnosis. Baseline clinical and histological features were analysed as risk factors for the development of GNL by Cox-regression. RESULTS: During a median follow-up of 4.3 (1-16.5) years, 15 GNL were detected in 14 of the 300 patients with atrophic gastritis: three were gastric cancer, whereas 12 were non-invasive neoplasia. The annual incidence for GNL was 1%. Cox-regression analysis identified the following risk factors: age over 50 years (HR 8.8, 95%CI 1.2-68.4), atrophic pangastritis (HR 4.5, 95% CI 1.5-14.1) and severe intestinal metaplasia in the gastric body (HR 4.0, 95% CI 1.3-11.8). CONCLUSIONS: Atrophic pangastritis, severe body intestinal metaplasia and/or age over 50 years increase the risk for developing GNL in patients with atrophic gastritis. In this subset of patients, an endoscopic-histological follow-up for GNL surveillance may be worthwhile.


Subject(s)
Adenocarcinoma/pathology , Gastric Mucosa/pathology , Gastritis, Atrophic/pathology , Precancerous Conditions/pathology , Stomach Neoplasms/pathology , Adolescent , Adult , Aged , Epidemiologic Methods , Female , Gastroscopy , Humans , Male , Middle Aged , Risk Factors , Young Adult
14.
Aliment Pharmacol Ther ; 29(12): 1219-29, 2009 Jun 15.
Article in English | MEDLINE | ID: mdl-19302263

ABSTRACT

BACKGROUND: Due to suppression of gastric acidity during antisecretory therapy, an impaired absorption of co-administered drugs may occur. AIM: To review evidence of impaired drug absorption related to the use of co-administered PPIs or H2RAs. METHODS: Systematic search of MEDLINE/EMBASE/SCOPUS databases (1980-September 2008) for English articles with keywords: drug malabsorption and absorption, stomach, anti-secretory/acid inhibitory drugs, histamine H2 antagonists, PPIs, gastric acid, pH, hypochlorhydria, gastric hypoacidity. From 2126 retrieved articles, 16 randomized crossover studies were identified investigating impaired absorption of nine different drugs in association with co-administration of PPIs or H2RAs. Information on investigated drug, study type, features of investigated subjects, study design, type of intervention, and study results were extracted. RESULTS: The identified studies investigated the absorption kinetics of nine drugs. Acid suppression reduced absorption of ketoconazole, itraconazole, atazanavir, cefpodoxime, enoxacin and dipyridamole (median C(max) reduction by 66.5%). An increased absorption of nifedipine and digoxin (median AUC increase by 10%) and a 2-fold-increase in alendronate bioavailability were observed. CONCLUSIONS: Gastric pH appears relevant for absorption of some cardiovascular or infectious disease agents. Antisecretory treatment may significantly modify the absorption of co-administered drugs.


Subject(s)
Anti-Ulcer Agents/administration & dosage , Gastric Mucosa/drug effects , Gastrointestinal Diseases/drug therapy , Histamine H2 Antagonists/administration & dosage , Intestinal Absorption/drug effects , Proton Pump Inhibitors/administration & dosage , Drug Administration Schedule , Gastric Acid/metabolism , Humans , Randomized Controlled Trials as Topic
15.
Aliment Pharmacol Ther ; 29(4): 379-86, 2009 Feb 15.
Article in English | MEDLINE | ID: mdl-19053985

ABSTRACT

BACKGROUND: Impaired acid secretion may affect drug absorption and may be consequent to corporal Helicobacter pylori-gastritis, which may affect the absorption of orally administered drugs. AIM: To focus on the evidence of impaired drug absorption associated with H. pylori infection. METHODS: Data sources were the systematic search of MEDLINE/EMBASE/SCOPUS databases (1980-April 2008) for English articles using the keywords: drug malabsorption/absorption, stomach, Helicobacter pylori, gastritis, gastric acid, gastric pH, hypochlorhydria, gastric hypoacidity. Study selection was made from 2099 retrieved articles, five studies were identified. Data were extracted from selected papers, investigated drugs, study type, main features of subjects, study design, intervention type and results were extracted. RESULTS: In all, five studies investigated impaired absorption of l-dopa, thyroxine and delavirdine in H. pylori infection. Eradication treatment led to 21-54% increase in l-dopa in Parkinson's disease. Thyroxine requirement was higher in hypochlorhydric goitre with H. pylori-gastritis and thyrotropin levels decreased by 94% after treatment. In H. pylori- and HIV-positive hypochlorhydric subjects, delavirdine absorption increased by 57% with orange juice administration and by 150% after eradication. CONCLUSIONS: A plausible mechanism of impaired drug absorption is decreased acid secretion in H. pylori-gastritis patients. Helicobacter pylori infection and hypochlorhydria should be considered in prescribing drugs the absorption of which is potentially affected by intragastric pH.


Subject(s)
Anti-Ulcer Agents/pharmacokinetics , Helicobacter Infections/metabolism , Helicobacter pylori , Intestinal Absorption/drug effects , Delavirdine/pharmacokinetics , Gastritis/drug therapy , Gastritis/microbiology , Humans , Reverse Transcriptase Inhibitors/pharmacokinetics , Thyroxine/pharmacokinetics
16.
Aliment Pharmacol Ther ; 27(4): 355-65, 2008 Feb 15.
Article in English | MEDLINE | ID: mdl-18047563

ABSTRACT

BACKGROUND: Atrophic body gastritis patients are at increased risk for gastric cancer. IL-1B/IL-1RN polymorphisms have been associated with gastric cancer susceptibility. The relationship between these polymorphisms and the long-term outcome of atrophic body gastritis patients is not known. AIM: To investigate whether the genotyping of IL-1B-511/IL-1RN polymorphisms is useful to characterize atrophic body gastritis patients at increased risk for gastric neoplasms. METHODS: IL-1B-511/IL-1RN polymorphisms were compared between 110 atrophic body gastritis patients and 110 age- and gender-matched controls, and patients were followed up (median 4.1 years) according to a cohort study design. RESULTS: Genotype frequencies of IL-1B-511/IL-1RN were similar between patients and controls. Atrophic body gastritis patients harbouring the wild type of IL-1B-511/IL-1RN polymorphisms were not different from those harbouring the proinflammatory pattern as far as regards gender, age, gastric cancer family history and metaplastic atrophy. Sixteen atrophic body gastritis patients developed a gastric neoplastic lesion at follow-up: eight were IL-1B-511-T carriers and eight were IL-1RN-allele-2 carriers. Harbouring the proinflammatory genotypes was not significantly associated with developing gastric neoplastic lesions. CONCLUSIONS: In atrophic body gastritis patients, IL-1B-511 and IL-1RN polymorphisms do not appear to be associated either with specific clinical, biochemical or histological features or with the development of gastric neoplastic lesions at long-term follow-up.


Subject(s)
Gastritis, Atrophic/genetics , Interleukin 1 Receptor Antagonist Protein/genetics , Interleukin-1beta/genetics , Polymorphism, Genetic , Stomach Neoplasms/genetics , Adult , Aged , Case-Control Studies , Cohort Studies , DNA/genetics , Female , Follow-Up Studies , Gastritis, Atrophic/complications , Gastritis, Atrophic/pathology , Gastritis, Atrophic/therapy , Gastroscopy , Genotype , Humans , Male , Middle Aged , Stomach Neoplasms/etiology , Stomach Neoplasms/pathology
18.
Aliment Pharmacol Ther ; 24(10): 1453-60, 2006 Nov 15.
Article in English | MEDLINE | ID: mdl-17032284

ABSTRACT

BACKGROUND: Urea breath test sensitivity seems affected by increased intragastric acidity during therapy with antisecretory drugs. Intragastric pH is increased in patients with corpus gastritis with/without atrophy. AIM: To test the hypothesis that urea breath test results may also be affected by this gastritis phenotype. METHODS: 123 untreated patients underwent gastroscopy plus biopsies and intragastric pH measurement. The study included 82 endoscopically proven Helicobacter pylori-positive patients who were offered urea breath test with an acidic meal. Histological findings, urea breath test results and intragastric pH were compared in 66 of the subjects. RESULTS: 21 of 66 (31.8%) patients had a false-negative urea breath test. In these patients corpus-predominant gastritis (85.7% vs. 37.7%; P = 0.0004) and fundic atrophy (66.6% vs. 17.7%; P = 0.0001) were more frequent than in patients with true-positive urea breath test. Intragastric pH was higher in false-negative patients (mean 6.3 vs. 4.4; P = 0.001). In a multivariate analysis, the only risk factor for a false-negative urea breath test was the presence of corpus-predominant gastritis (OR = 5.6; 95% CI: 1.1-27). There was a negative correlation between the intragastric pH and the delta over baseline values (r = -0.378; P = 0.0023). CONCLUSIONS: Our results support the hypothesis that the pattern of gastritis can affect the sensitivity of urea breath test, and suggest that patients with corpus-predominant gastritis have a high risk of false-negative urea breath test results.


Subject(s)
Gastritis/diagnosis , Helicobacter Infections/diagnosis , Helicobacter pylori , Urea/analysis , Adult , Aged , Breath Tests , False Negative Reactions , Female , Humans , Male , Middle Aged , Predictive Value of Tests , Risk Factors
19.
Aliment Pharmacol Ther ; 22(5): 471-81, 2005 Sep 01.
Article in English | MEDLINE | ID: mdl-16128686

ABSTRACT

BACKGROUND: Long-term outcome of atrophic body gastritis has not yet been defined. AIM: To investigate at long-term follow-up the behaviour of atrophy and intestinal metaplasia and the occurrence of neoplastic lesions in atrophic body gastritis patients. METHODS: Overall 106 atrophic body gastritis patients with > or = 4-year follow-up were studied; 38 were Helicobacter pylori-positive at histology + serology and cured of infection (group A), 36 were positive at serology and not treated (group B) and 32 were H. pylori-negative (group C). Patients underwent gastroscopy with antral (n = 3) and body (n = 3) biopsies for histology according to the Sydney System. RESULTS: At 6.7-year follow-up body atrophy and intestinal metaplasia remained unchanged in all 106 patients irrespective of H. pylori status. Antral atrophy was significantly increased at follow-up only in group C, whereas antral intestinal metaplasia was unchanged in all three groups. During follow-up eight (8%) patients developed neoplastic lesions (one adenocarcinoma, one adenoma with low-grade dysplasia and six low-grade dysplasia without endoscopic lesions). Antral atrophic gastritis was present at baseline in all but one (88%) of the eight patients with neoplastic lesions, but only in 15 (15%) of the 98 patients without (P < 0.0001, RR = 26.7). CONCLUSIONS: Atrophy and intestinal metaplasia persist at 6.7-year follow-up and atrophic body gastritis patients with panatrophic gastritis are at increased risk of developing neoplastic lesions.


Subject(s)
Gastritis, Atrophic/etiology , Helicobacter Infections , Helicobacter pylori , Intestinal Neoplasms/etiology , Adult , Aged , Endoscopy, Gastrointestinal , Female , Follow-Up Studies , Humans , Male , Middle Aged , Prognosis , Prospective Studies
20.
Aliment Pharmacol Ther ; 21(5): 567-74, 2005 Mar 01.
Article in English | MEDLINE | ID: mdl-15740540

ABSTRACT

BACKGROUND: Benign epithelial gastric polyps have been reported to be more common in atrophic body gastritis. The role of Helicobacter pylori infection in the induction of gastric atrophy is well-known. The development of hyperplastic polyps may be in relation to H. pylori infection. AIM: To investigate occurrence of benign epithelial gastric polyps in atrophic body gastritis patients at diagnosis and follow-up, and the role of H. pylori and other risk factors for the development of benign epithelial gastric polyps. METHODS: A total of 259 consecutive atrophic body gastritis patients included in a follow-up programme, of whom 202 were followed up for median period of 4 years (range: 2-11). At baseline and follow-up gastroscopies, the presence of benign epithelial gastric polyps was evaluated. Biopsies for histology were obtained from all detected benign epithelial gastric polyps. RESULTS: Frequency of benign epithelial gastric polyps in atrophic body gastritis patients were 4.6% at baseline and 5.9% at follow-up. About 91.7% were hyperplastic polyps. H. pylori infection was detected in 79.2% atrophic body gastritis patients with benign epithelial gastric polyps, and in 70.8% without benign epithelial gastric polyps. Smoking was more frequent among patients with benign epithelial gastric polyps [42% vs. 20%, OR 2.8 (95% CI: 1.2-6.9)]. CONCLUSIONS: Benign epithelial gastric polyps occur in about 5% of atrophic body gastritis patients, and the vast majority are hyperplastic polyps. Smoking habit, but not H. pylori infection, increases the risk for benign epithelial gastric polyps in atrophic body gastritis patients.


Subject(s)
Gastritis, Atrophic/pathology , Helicobacter Infections , Helicobacter pylori , Intestinal Polyps/etiology , Stomach Diseases/etiology , Adolescent , Adult , Aged , Female , Follow-Up Studies , Humans , Intestinal Polyps/pathology , Male , Middle Aged , Risk Factors , Stomach Diseases/pathology
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