Influence of a diet meal plan on pepsinogen I and II,gastrin-17,and nutritional status in gastric ulcer patients

BACKGROUND Gastric ulcers(GUs)have a high risk of clinical morbidity and recurrence,and further exploration is needed for the prevention,diagnosis,and treatment of the disease.AIM To investigated the effects of a diet plan on pepsinogen(PG)I,PG II,gastrin-17(G-17)levels and nutritional status in patients with GUs.METHODS A total of 100 patients with GUs treated between May 2022 and May 2023 were enrolled,with 47 patients in the control group receiving routine nursing and 53 patients in the experimental group receiving dietary nursing intervention based on a diet plan.The study compared the two groups in terms of nursing efficacy,adverse events(vomiting,acid reflux,and celialgia),time to symptom improvement(burning sensation,acid reflux,and celialgia),gastric function(PG I,PG II,and G-17 levels),and nutritional status[prealbumin(PA)and albumin(ALB)levels].RESULTS The experimental group showed a markedly higher total effective rate of nursing,a significantly lower incidence of adverse events,and a shorter time to symptom improvement than the control group.Additionally,the experimental group’s post-intervention PG I,PG II,and G-17 levels were significantly lower than preintervention or control group levels,whereas PA and ALB levels were significantly higher.CONCLUSION The diet plan significantly reduced PG I,PG II,and G-17 levels in patients with GUs and significantly improved their nutritional status.

Helicobacter pylori infection alters gastric microbiota structure and biological functions in patients with gastric ulcer or duodenal ulcer

BACKGROUND Helicobacter pylori(H.pylori)infection is closely associated with gastrointestinal diseases.Our preliminary studies have indicated that H.pylori infection had a significant impact on the mucosal microbiome structure in patients with gastric ulcer(GU)or duodenal ulcer(DU).AIM To investigate the contributions of H.pylori infection and the mucosal microbiome to the pathogenesis and progression of ulcerative diseases.METHODS Patients with H.pylori infection and either GU or DU,and healthy individuals without H.pylori infection were included.Gastric or duodenal mucosal samples was obtained and subjected to metagenomic sequencing.The compositions of the microbial communities and their metabolic functions in the mucosal tissues were analyzed.RESULTS Compared with that in the healthy individuals,the gastric mucosal microbiota in the H.pylori-positive patients with GU was dominated by H.pylori,with signi-ficantly reduced biodiversity.The intergroup differential functions,which were enriched in the H.pylori-positive GU patients,were all derived from H.pylori,particularly those concerning transfer RNA queuosine-modification and the synthesis of demethylmenaquinones or menaquinones.A significant enrichment of the uibE gene was detected in the synthesis pathway.There was no significant difference in microbial diversity between the H.pylori-positive DU patients and healthy controls.CONCLUSION H.pylori infection significantly alters the gastric microbiota structure,diversity,and biological functions,which may be important contributing factors for GU.

Assay of gastrin and somatostatin in gastric antrum tissues of children with chronic gastritis and duodenal ulcer

AIM： To study the expressions of gastrin （GAS） and somatostatin （SS） in gastric antrum tissues of children with chronic gastritis and duodenal ulcer and their role in pathogenic mechanism. METHODS： Specimens of gastric antrum mucosa from 83 children were retrospectively analyzed. Expressions of GAS and SS in gastric antrum tissues were assayed by the immunohistochemical Fn Vision method. RESULTS： The expressions of GAS in chronic gastritis Hp＋ group （group A）, chronic gastritis Hp-group （group B）, the duodenal ulcer Hp＋group （group C）, duodenal ulcer Hp group （group D）, and normal control group （group E） were 28.50＋4.55, 19.60＋2.49, 22.69＋2.71, 25.33 ＋ 4.76, and 18.80 ＋ 2.36, respectively. The value in groups A-D was higher than that in group F. The difference was not statistically significant. The expressions of SS in groups A-E were 15.47＋ 1.44, 17.29＋ 2.04, 15.30＋ 1.38, 13.11 ＋0.93 and 12.14＋ 1.68, respectively. The value in groups A-D was higher than that in group F. The difference was also not statistically significant. CONCLUSION： The expressions of GAS and SS are increased in children with chronic gastritis and duodenal ulcer.

History of Helicobacter pylori,duodenal ulcer,gastric ulcer and gastric cancer

Helicobacter pylori (H. pylori) infection underlies gastric ulcer disease, gastric cancer and duodenal ulcer disease. The disease expression reflects the pattern and extent of gastritis/gastric atrophy (i.e., duodenal ulcer with non-atrophic and gastric ulcer and gastric cancer with atrophic gastritis). Gastric and duodenal ulcers and gastric cancer have been known for thousands of years. Ulcers are generally non-fatal and until the 20th century were difficult to diagnose. However, the presence and pattern of gastritis in past civilizations can be deduced based on the diseases present. It has been suggested that gastric ulcer and duodenal ulcer both arose or became more frequent in Europe in the 19th century. Here, we show that gastric cancer and gastric ulcer were present throughout the 17th to 19th centuries consistent with atrophic gastritis being the predominant pattern, as it proved to be when it could be examined directly in the late 19th century. The environment before the 20th century favored acquisition of H. pylori infection and atrophic gastritis (e.g., poor sanitation and standards of living, seasonal diets poor in fresh fruits and vegetables, especially in winter, vitamin deficiencies, and frequent febrile infections in childhood). The latter part of the 19th century saw improvements in standards of living, sanitation, and diets with a corresponding decrease in rate of development of atrophic gastritis allowing duodenal ulcers to become more prominent. In the early 20th century physician’s believed they could diagnose ulcers clinically and that the diagnosis required hospitalization for “surgical disease” or for “Sippy” diets. We show that while H. pylori remained common and virulent in Europe and the United States, environmental changes resulted in changes of the pattern of gastritis producing a change in the manifestations of H. pylori infections and subsequently to a rapid decline in transmission and a rapid decline in all H. pylori-related diseases.

Reduced secretion of epidermal growth factor in duodenal ulcer patients with Helicobacter pylori infection

AIM To investigate the concentration changes of epidermal growth factor (EGF) in duodenal ulcer patients with H. pylori infection.

Gastrin,somatostatin,G and D cells of gastric ulcer in rats

AIM: To investigate the relationship among gastrin, somatostatin, G and D cells in gastric ulcer and in its healing process in rats. METHODS: Fourty-nine Wistar rats were divided into 7 groups. The gastric ulcer model was induced by acetic acid successfully. The gastrin and the somatostatin in rat plasma, gastric fluid and antral tissue were measured by radioimmunoassay(RIA). G and D cells in antral mucosa were analyzed with polyclonal antibody of gastrin and somatostatin by immunohistochemical method and Quantimet 500 image analysis system. RESULTS: In gastric ulcer, the level of gastrin in plasma, gastric fluid, and antral tissue increased, that of somatostatin declined, and the disorder gradually recovered to the normal level in the healing process. Immunohistochemical technique of G and D cells in antral mucosa demonstrated that the number of G cells increased and that of D cells decreased, both areas of G and D cells declined, the ratio of number and area of G/D increased in gastric ulcer, and the disorder gradually recovered in the healing process. CONCLUSION: In gastric ulcer, the increased gastrin secreted by G cells, the declined somatostatin secreted by D cells, and the disordered G/D cell ratio can lead to gastrointestinal dysfunction.

Life threatening bleeding from duodenal ulcer after Roux-en-Y gastric bypass: Case report and review of the literature

Acute upper gastrointestinal bleeding is a rare, but serious complication of gastric bypass surgery. The inaccessibility of the excluded stomach restrains postoperative examination and treatment of the gastric remnant and duodenum, and represents a major challenge, especially in the emergency setting. A 59-year-old patient with previous history of peptic ulcer disease had an upper gastrointestinal bleeding from a duodenal ulcer two years after having a gastric bypass procedure for morbid obesity. After negative upper endoscopy finding, he was urgently evaluated for gastrointestinal bleeding. At emergency laparotomy, the bleeding duodenal ulcer was identified by intraoperative endoscopy through gastrotomy. The patient recovered well after surgical hemostasis, excision of the duodenal ulcer and completion of the remnant gastrectomy. Every general practitioner, gastroenterologist and general surgeon should be aware of growing incidenceof bariatric operations and coherently possible complications after such procedures, which modify patient's anatomy and physiology.

Hemorrhagic gastric and duodenal ulcers after the Great East Japan Earthquake Disaster

AIM:To elucidate the characteristics of hemorrhagic gastric/duodenal ulcers in a post-earthquake period within one medical district.METHODS:Hemorrhagic gastric/duodenal ulcers in the Iwate Prefectural Kamaishi Hospital during the 6-mo period after the Great East Japan Earthquake Disaster were reviewed retrospectively.The subjects were 27patients who visited our hospital with a chief complaint of hematemesis or hemorrhagic stool and were diagnosed as having hemorrhagic gastric/duodenal ulcers by upper gastrointestinal endoscopy during a 6-mo period starting on March 11,2011.This period was divided into two phases:the acute stress phase,comprising the first month after the earthquake disaster,and the chronic stress phase,from the second through the sixth month.The following items were analyzed according to these phases:age,sex,sites and number of ulcers,peptic ulcer history,status of Helicobacter pylori(H.pylori)infection,intake of non-steroidal anti-inflammatory drugs,and degree of impact of the earthquake disaster.RESULTS:In the acute stress phase from 10 d to 1mo after the disaster,the number of patients increased rapidly,with a nearly equal male-to-female ratio,and the rate of multiple ulcers was significantly higher than in the previous year(88.9%vs 25%,P<0.005).In the chronic stress phase starting 1 mo after the earthquake disaster,the number of patients decreased to a level similar to that of the previous year.There were more male patients during this period,and many patients tended to have a solitary ulcer.All patients with duodenal ulcers found in the acute stress phase were negative for serum H.pylori antibodies,and this was significantly different from the previous year’s positive rate of 75%(P<0.05).CONCLUSION:Severe stress caused by an earthquake disaster may have affected the characteristics of hemorrhagic gastric/duodenal ulcers.

Changes of G cells and D cells in the antral mucosa in rat experimental gastric ulcer

Objective: To investigate the association of changes in G and D cells in the antral mucosa with the production of gastrin and somatostatin during gastric ulcer and the healing process. Methods: Experimental gastric ulcer was induced with acetic acid in 42 Wistar rats and another 7 normal rats served as control. Changes in the production of gastrin and somatostatin in the plasma, gastric fluid and the antral tissues of the rats were measured by radio immunoassay, and the number and distribution of G and D cells were respectively determined by immunochemistry and Quantimet500 image analysis system. Results: In rats with gastric ulcer, the gastrin levels in the plasma, gastric fluid and the antral tissues increased while somatostatin levels were reduced, which were corrected in the healing process. Immunochemistry demonstrated the increase in the number of G cells in the antral tissues with decrease in D cell number, and the area covered by both cells shrank. The G cell to D cell number and area ratios were both decreased after the onset of the ulcer and returned to the normal when the healing process took place. Conclusion; Secretion of gastrin by G cells increases and that of somatostatin by D cells declines during gastric ulcer in rats, and imbalance of G and D cells may be responsible for gastrointestinal dysfunction.

Mechanisms involved in Helicobacter pylori induced duodenal ulcer disease:an overview

Duodenal ulcer (DU) can be developed viaseveral different mechanisms.Hypersecretion ofgastric acid is,however,a common denominator.Amassive hypersecretion of acid can by itself evoke aDU,e.g.in the Zollinger-Ellison syndrome.Irrespective of the mechanism behind thedevelopment of a DU,powerful antisecretorytreatment will heal the ulcer and preventrecurrence.

Serum gastrin-17 concentration for prediction of upper gastrointestinal tract bleeding risk among peptic ulcer patients

BACKGROUND Serum gastrin-17(G-17),pepsinogen I(PGI),and pepsinogen II(PGII)concentrations regulate gastric acid secretion,and hypersecretion of gastric acid increases the risks of peptic ulcer and upper gastrointestinal bleeding.These associations suggest that serum G-17,PGI,and(or)PGII may predict gastrointestinal bleeding risk among peptic ulcer patients.AIM To evaluate the efficacies of serum G-17,PGI,PGII,and PGI/PGII ratio(PGR)for predicting upper gastrointestinal bleeding among peptic ulcer patients.METHODS A total of 199 patients diagnosed with peptic ulcer confirmed by gastroscopy and positivity for Helicobacter pylori by the 14C-urea breath test were recruited,including 107 patients with simple peptic ulcer and 92 cases complicated by upper gastrointestinal bleeding.Serum PGI,PGII,G-17,and PGR were measured by immune methods and compared between bleeding and non-bleeding groups by univariate analysis.The specificity and sensitivity of PGs and G-17 for evaluating upper gastrointestinal bleeding risk were then assessed by constructing receiver operating characteristic(ROC)curves.RESULTS Serum G-17 was significantly higher among peptic ulcer patients with upper gastrointestinal bleeding compared to simple peptic ulcer patients(25.34±14.29 vs 8.84±8.03 pmol/L,t=9.822,P<0.01),whereas serum PGI,PGII,and PGR did not differ significantly between bleeding and non-bleeding groups(all P>0.05).The risk of bleeding was significantly higher among peptic ulcer patients with elevated serum G-17(>15 pmol/L)compared to patients with normal or low serum G-17(73.2%vs 27.4%,χ2=40.72,P<0.01).The area under the ROC curve for serum G-17 was 0.866±0.024,and a cut-off of 9.86 pmol/L yielded 90.2%sensitivity and 68.2%specificity for distinguishing peptic ulcer with and without upper gastrointestinal bleeding.CONCLUSION Serum G-17 is significantly upregulated in peptic ulcer patients and higher levels are predictive of upper gastrointestinal bleeding.Conversely,serum PGI,PGII,and PGR have no predictive value.Further prospective studies are warranted to examine if high G-17 can be used to assess risk of bleeding prior to onset.

Lipoma of the Stomach Prolapsing into the Duodenal Bulb and Causing a Duodenal Ulcer: A Case Report

We report a case of lipoma in the antum of the stomach which prolapsed into the duodenal bulb and caused a duodenal ulcer, speculated to have been induced by the friction of its top against the duodenal mucosa. Although the ulcer healed after the administration of a proton pump inhibitor, the symptom of epigastric discomfort continued, suggested to be due to prolapsing. Therefore, a laparoscopic operation was conducted. The incidence of lipoma of the stomach is rare, and cases of its prolapse into the duodenum are very few. Furthermore, it is extremely rare for it to cause a duodenal ulcer. Because these features made this case clinically interesting, we report it here.

Helicobacter pylori infection and gastric microbiota:Insights into gastric and duodenal ulcer development

Helicobacter pylori(H.pylori)infection plays a critical role in gastric diseases,impacting the microbiota structure in gastric and duodenal ulcers.In their study,Jin et al utilized metagenomic sequencing to analyze mucosal samples from patients with ulcers and healthy controls,revealing significant changes in microbial diversity and composition.This article reviews their findings,emphasizing H.pylori’s role in gastric ulcers and the need for further research on its impact on duodenal ulcers.We evaluate the study’s strengths and limitations,suggesting future research directions to enhance our understanding of H.pylori’s contribution to ulcerative diseases.

Evidence for the role of gastric mucosa at the secretion of soluble triggering receptor expressed on myeloid cells(strem-1) in peptic ulcer disease

AIM： To investigate the role of gastric mucosa at the secretion of sTREM-1 in peptic ulcer.METHODS： Seventy two patients were enrolled; 35 with duodenal, 22 with gastric ulcer and 26 with chronic gastritis. Patients were endoscoped and gastric juice was aspirated. Patients with duodenal and gastric ulcer underwent a second endoscopy post-treatment. Biopsies were incubated in the absence/presence of endotoxins or gastric juice. Supernatants were collected and sTREM-2 and TNF~ were measured by enzyme immunoabsorbent assays. Scoring of gastritis was performed before and after treatment according to updated Sydney score.RESULTS： Patients with duodenal and gastric ulcer and those with chronic gastritis had similar scores of gastritis, sTREM-1 was higher in supernatants of tissue samples of H pylori-positive than of H pylori-negative patients with gastric ulcer. Median （± SE） sTREM-1 was found increased in supernatants of patients with gastric ulcer before treatment （203.21 ± 88.91 pg/1000 cells） compared to supernatants either from the same patients post-treatment （8.23 ± 5.79 pg/1000 cells） or from patients with chronic gastritis （6.21 ± 0.71 pg/1000 cells） （P 〈 0.001 and 〈 0.001, respectively）. Similar differences for sTREM-1 were recorded among LPS-stimulated tissue samples of patients （P = 0.001）. Similar differences were not found for TNFα. Positive correlations were found between sTREM-1 of supernatants from patients with both duodenal and gastric ulcer before treatment and the degree of infiltration of neutrophils and monocytes.CONCLUSION： sTREM-1 secreted by the gastric mucosa is an independent mechanism connected to the pathogenesis of peptic ulcer, sTREM-1 was released at the presence of H pylori from the inflamed gastric mucosa in the field of gastric ulcer.

Association of Helicobacter pylori IgA antibodies with the risk of peptic ulcer disease and gastric cancer

AIM: To compare the prevalence of Helicobacter pylori (Hpylori) IgG and IgA antibodies between adult subjects,with defined gastric diseases, nondefined gastric disorders and those representing the population.METHODS: Data on H pylori IgG and IgA antibodies,determined by enzyme immunoassay, were analyzed in 3 252 subjects with DGD including 482 patients with gastric ulcer, 882 patients with duodenal ulcer, 1 525patients with chronic gastritis only and 363 subjects with subsequent gastric cancer, 19 145 patients with NoDg and4 854 POPUL subjects. The age-adjusted prevalences were calculated for 1- and 20-year age cohorts.RESULTS: The prevalences of IgG antibodies were equally high (89-96%) in all 20-year age cohorts of the DGD groups, whereas the prevalences of IgG antibodies were lower and increased by age in the POPUL and NoDg groups. The prevalences of IgA antibodies were also higher in the DGD groups; among them CA (84-89%) and GU groups (78-91%) showed significantly higher prevalences than DU (68-77%) and CG patients (59-74%) (OR 2.49, 95%CI 1.86-3.34 between the GU and DU groups). In the CA, GU, and DU groups, the IgA prevalences showed only minor variation according to age, while they increased by age in the CG, POPUL, and NoDg groups (P≤0.0001). The IgA response, but not the IgG response, was associated with an increased risk of CA (OR 2.41, 95%CI 1.79-3.53) and GU (OR 2.57,95%CI 1.95-3.39) in comparison with CG patients.CONCLUSION: An IgA antibody response during H pylori infection is significantly more common in CA and GU patients as compared with CG patients.

Bromophenacyl bromide,a phospholipase A_2 inhibitor attenuates chemically induced gastroduodenal ulcers in rats

AIM: To study the effect of bromophenacyl bromide (BPB), a phospholipase A2 inhibitor on gastric secretion and to protect chemically induced gastric and duodenal ulcers in rats. METHODS: Acid secretion studies were undertaken in pylorus-ligated rats with BPB treatment (0, 5, 15 and 45 mg/kg). Gastric and duodenal lesions in the rats were induced by ethanol and cysteamine respectively. The levels of gastric wall mucus, nonprotein sulfhydryls (NP- SH) and myeloperoxidase (MPO) were also measured in the glandular stomach of rats following ethanol induced gastric lesions. RESULTS: BPB produced a dose-dependent inhibition of gastric acid secretion and acidity in rats. Pretreatment with BPB significantly attenuated the formation of etha- nol induced gastric lesion. BPB also protected intestinal mucosa against cysteamine-induced duodenal ulcers. The antiulcer activity of BPB was associated with signifi- cant inhibition of ethanol-induced depletion of gastric wall mucus, NP-SH and MPO. These findings pointed towards the mediation of sulfhydryls in BPB induced gas- trointestinal cytoprotection. CONCLUSION: BPB possesses significant antiulcer and cytoprotective activity against experimentally induced gastroduodenal lesions.

Characteristics of gastric cancer in peptic ulcer patients with Helicobacter pylori infection

AIM:To evaluate the incidence and clinical characteristics of gastric cancer(GC) in peptic ulcer patients with Helicobacter pylori(H.pylori) infection.METHODS:Between January 2003 and December 2013, the medical records of patients diagnosed with GC were retrospectively reviewed.Those with previous gastric ulcer(GU) and H.pylori infection were assigned to the Hp GU-GC group(n = 86) and those with previous duodenal ulcer(DU) disease and H.pylori infection were assigned to the Hp DUGC group(n = 35).The incidence rates of GC in the Hp GU-GC and Hp DU-GC groups were analyzed.Data on demographics(age, gender, peptic ulcer complications and cancer treatment), GC clinical characteristics [location, pathological diagnosis, differentiation, T stage, Lauren's classification, atrophy of surrounding mucosa and intestinal metaplasia(IM)], outcome of eradication therapy for H.pylori infection, esophagogastroduodenoscopy number and the duration until GC onset were reviewed.Univariate and multivariate analyses were performed to identify factors influencing GC development.The relative risk of GC was evaluated using a Cox proportional hazards model.RESULTS:The incidence rates of GC were 3.60%(86/2387) in the Hp GU-GC group and 1.66%(35/2098) in the Hp DU-GC group.The annual incidence was 0.41% in the Hp GU-GC group and 0.11% in the Hp DUGC group.The rates of moderate-to-severe atrophy of the surrounding mucosa and IM were higher in the Hp GU-GC group than in the Hp DU-GC group(86% vs 34.3%, respectively, and 61.6% vs 14.3%, respectively, P < 0.05).In the univariate analysis, atrophy of surrounding mucosa, IM and eradication therapy for H.pylori infection were significantly associated with the development of GC(P < 0.05).There was no significant difference in the prognosis of GC patients between the Hp GU-GC and Hp DU-GC groups(P = 0.347).The relative risk of GC development in the Hp GUGC group compared to that of the Hp DU-GC group,after correction for age and gender,was 1.71(95%CI:1.09-2.70;P=0.02).CONCLUSION:GU patients with H.pylori infection had higher GC incidence rates and relative risks.Atrophy of surrounding mucosa,IM and eradication therapy were associated with GC.

Pathogenetic factors affecting gastroesophageal refluxin patients with esophagitis and concomitant duodenal ulcer:a multivariate analysis

AIM To assess the relationship between gastric acid output (GAO) and both pattern of gastroesophageal reflux (GER) and esophageal lesions, and to evaluate the role of GAO and other potential pathogenetic factors in the development of esophagitis. METHODS Gastric acid secretory testing and 24 h intraesophageal pH monitoring were performed in 31 patients with esophagitis and concomitant duodenal ulcer (E+DU) and compared with those of 72 patients with esophagitis (E) alone. RESULTS The GAO in patients with E+DU was significantly higher than in patients with E ( P <0 05). There was no significant difference between the two groups of patients as to endoscopicl findings and parameters of GER ( P >0 05). A multiple regression analysis with stepwise deletion showed that the pre sence of hiatal hernia (HH), GER in upright position and age appeared to correlate significantly with the presence of esophagitis. CONCLUSIONS No parallel relationship between GAO and severity of GER or esophageal lesions exists in patients with E+DU, and that GAO is not a major pathogenetic factor in GER disease.

Perforations of Gastro-Duodenal Ulcers in the Surgery Department “A” at the University Hospital Point G Bamako

The purpose of this study was to investigate the clinical and therapeutic aspects of peritonitis by perforation of gastric and duodenal ulcer. This was a retrospective and descriptive study over 8 years (2010-2018) which allowed to collect 54 cases of peptic ulcer. Included in the study were all patients with confirmed gastroduodenal perforation on histology or laparotomy. We collected 54 cases of peptic ulcer perforated s. The age group of 30 - 49 years was the majority. The male sex was dominant with 90.7% of cases;the clinical picture was dominated by abdominal contracture associated with pain in 74.07% of cases. X-ray of the abdomen without preparation (AWP) revealed in 87.03% of cases of pneumoperitoneum. The perforation was in 68.52% of cases on the gastric antrum and in 31.48% on the duodenum. The surgical procedure used was the bank of excision, and a suture reinforcement epiploic in 68.52% of cases, a simple suture made in 31.48% of cases, the disease was marked by a fistula (1.90%) and mortality was 5.55% of cases. The gastroduodenal ulcer perforation is potentially serious and responsible peritonitis whose surgical treatment involves the peritoneal toilet and sutures the puncture.

Different risk factors influence peptic ulcer disease development in a Brazilian population

AIM: To investigate age, sex, histopathology and Helicobacter pylori (H. pylori) status, as risk factors for gastroduodenal disease outcome in Brazilian dyspeptic patients.tients submitted to upper gastroscopy at Hospital das Clinicas of Marilia, antral biopsy specimens were obtained and subjected to histopathology and H. pylori diagnosis. All patients presenting chronic gastritis (CG) and peptic ulcer (PU) disease localized in the stomach, gastric ulcer (GU) and/or duodenal ulcer (DU) were included in the study. Gastric biopsies (n = 668) positive for H. pylori by rapid urease test were investigated for vacuolating cytotoxin A (vacA ) medium (m) region mosaicism by polymerase chain reaction. Logistic regression analysis was performed to verify the association of age, sex, histopathologic alterations, H. pylori diagnosis and vacA m region mosaicism with the incidence of DU, GU and CG in patients. RESULTS: Of 1466 patients submitted to endoscopy, 1060 (72.3%) presented CG [male/female = 506/554; mean age (year) ± SD = 51.2 ± 17.81], 88 (6.0%) presented DU [male/female = 54/34; mean age (year) ± SD = 51.4 ± 17.14], and 75 (5.1%) presented GU [male/female = 54/21; mean age (year) ± SD = 51.3 ± 17.12] and were included in the comparative analysis. Sex and age showed no detectable effect on CG incidence (overall c 2 = 2.1, P = 0.3423). Sex [Odds ratios (OR) = 1.8631, P = 0.0058] but not age (OR = 0.9929, P = 0.2699) was associated with DU and both parameters had a highly significant effect on GU (overall c 2 = 30.5, P < 0.0001). The histopathological results showed a significant contribution of ageing for both atrophy (OR = 1.0297, P < 0.0001) and intestinal metaplasia (OR = 1.0520, P < 0.0001). Presence of H. pylori was significantly associated with decreasing age (OR = 0.9827, P < 0.0001) and with the incidence of DU (OR = 3.6077, P < 0.0001). The prevalence of m1 in DU was statistically significant (OR = 2.3563, P = 0.0018) but not in CG (OR = 2.678, P = 0.0863) and GU (OR = 1.520, P = 0.2863). CONCLUSION: In our population, male gender was a risk factor for PU; ageing for GU, atrophy and metapla-sia; and H. pylori of vacA m1 genotype for DU.