Gastric electrical activity and gastrointestinal hormones in dyspeptic patients

AIMS: To explore the patterns of gastric electrical activity, gastric emptying and gastrointestinal hormones in dyspeptic patients and relate them to Helicobacter pylori status. METHODS: Twenty-two patients with functional dyspepsia and 29 healthy volunteers underwent cutaneous electrogastrography and dynamic ultrasound before and after a test meal. All dyspeptic patients underwent endoscopy and biopsy; all subjects were examined for the presence of antibodies to H. pylori, and the plasma levels of gastrin, neurotensin, cholecystokinin, and pancreatic polypeptide were measured. RESULTS: The area under the curve (AUC) of the normal slow wave percentage was lower in dyspeptic patients than controls (Kruskal-Wallis p = 0.016; Dunn's test: H. pylori-positive patients: 21,235.5 [19,101.0-22,688.8] vs. H. pylori-negative controls: 22,532.0 [20,133.0-23,755.0], p < 0.05). The AUC of the tachygastria percentage was higher in dyspeptic patients than controls (p = 0.0001; H. pylori-positive patients: 2,173.5 [325.8-3,055.3] vs. H. pylori-negative controls: 682.0 [118.5-1,902.4], p < 0.05; H. pylori-negative patients: 1,843.0 [1,107.0-4,277.0] vs. H. pylori-negative controls: 682.0 [118.5-1,902.4], p < 0.05). The AUC of gastrin was higher in H. pylori-positive than H. pylori-negative subjects (p = 0.0002; H. pylori-positive patients: 16,146.5 [11,368.8-33,141.7] vs. H. pylori-negative controls: 11,250.0 [5,674.0-17,448.0], p < 0.05; H. pylori-positive controls: 20,250.0 [12,070.0-64,430.0] vs. H. pylori-negative controls: 11,250.0 [5,674.0-17,448.0], p < 0.05). In the total group of dyspeptic patients and in the H. pylori-positive patients, a negative correlation was found between the AUC of neurotensin and the total score for postprandial fullness (dyspeptic patients r = -0.51, p = 0.01; H. pylori-positive patients r = -0.66, p = 0.02). CONCLUSIONS: In dyspeptic patients, alterations in gastric electrical activity were not related to H. pylori infection. Nevertheless, H. pylori infection induces higher gastrin levels in both patients and asymptomatic subjects.     

Helicobacter pylori: Evidence for spouse-to-spouse transmission

BACKGROUND: Spouse-to-spouse transmission of Helicobacter pylori infection still remains controversial. METHODS: We studied the prevalence of H. pylori infection among spouses of H. pylori-positive or -negative individuals and looked for intraspousal transmission. Twenty-five couples were studied. Initially, one individual per couple was selected as the index subject. Spouses of these H. pylori-positive or -negative index individuals underwent screening for H. pylori by serology, the rapid urease test and histology. Those couples in whom only one spouse was positive were followed up and H. pylori status was re-evaluated using the above tests after approximately 1 year in the H. pylori-negative spouse. RESULTS: Of 25 randomly selected index subjects, 18 were H. pylori positive and seven were negative. There was no significant difference in age, sex, socioeconomic status, presence of dyspeptic symptoms, duration of marriage and number of children in these index subjects. Spouses of H. pylori-infected index subjects had a significantly higher prevalence of H. pylori infection than the spouses of H. pylori-negative index subjects (83.3 vs 28.5%; P < 0.01). Age, sex, socioeconomic status, dyspeptic symptoms, duration of marriage and number of children were not different in H. pylori-positive or -negative spouses of H. pylori-positive index subjects. There were five such couples in whom only one spouse was H. pylori positive initially. At follow up, three of these H. pylori-negative spouses became positive. These findings suggest person-to-person transmission or common source exposure within couples.     

Effect of age and Helicobacter pylori infection on gastric acid secretion

BACKGROUND: Whether gastric acid secretion decreases with age is still controversial. With the discovery of Helicobacter pylori, the association of this bacterium with gastric acid secretion has also been discussed. The aim of this study was to investigate the relationship between gastric acid secretion, age and H. pylori infection. METHODS: The presence of H. pylori infection, the grade of fundic atrophic gastritis (FAG), and gastric acid secretion were investigated in 280 subjects without localized lesions in the upper gastrointestinal tract. Helicobacter pylori infection was confirmed by Giemsa and immunohistochemical staining, and FAG of biopsy specimens was graded on a scale of 0-4. RESULTS: Both basal and maximal acid output decreased with age in H. pylori-positive subjects, while they did not change with age in H. pylori-negative subjects. Gastric acid secretion decreased with the progression of FAG. An age-correlated decrease in gastric acid secretion in H. pylori-positive subjects depended on an increasing prevalence of FAG with age. CONCLUSIONS: In the population studied, advancing age had no influence on gastric acid secretion in H. pylori-negative subjects. Gastric acid secretion decreases with age in H. pylori-positive subjects because of the increasing prevalence of FAG with age.     

Helicobacter pylori and gastrointestinal symptoms in school children in Russia

BACKGROUND AND AIMS: Helicobacter pylori is considered to be the major cause of chronic gastritis and duodenal ulcer disease recurrence in childhood. However, the association between H. pylori and recurrent abdominal pain (RAP) syndrome is still controversial. Therefore, the spectrum of clinical variants of gastrointestinal symptoms associated with H. pylori-positive status was studied in consecutive symptomatic children who were undergoing diagnostic endoscopy. METHODS: A consecutive series of 225 school children from the Ural area of Russia (mean age 11.1 + 1.4 years, age range 7-15 years) who presented with RAP were investigated using esophagogastroduodenoscopy, including three antral biopsies for histology and polymerase chain reaction. Helicobacter pylori immunoglobulin G antibodies were found using a second-generation enzyme immunoassay. Information about the clinical symptoms was collected using a special questionnaire. RESULTS: The authors found a high incidence of H. pylori infection (80%) and peptic ulcers (16%) in 225 school children from the Ural area of Russia who were referred for upper gastrointestinal (UGI) endoscopy for chronic abdominal pain. Of the overall 225 symptomatic children who underwent endoscopy, 182 (80,8%) were found to be H. pylori-positive. Duodenal ulcers were detected in 36 H. pylori-positive children. A family history of peptic ulcers was significantly more frequent in the children infected with H. pylori (P < 0.001). Symptom score and duration of symptoms were similar, but night-time pain (P < 0.0001) and fasting pain relieved by food (P < 0.001) were more frequent in the H. pylori-positive children as compared with the H. pylori-negative children. CONCLUSIONS: The present results provide further evidence for a significant association between H. pylori and some patterns of gastrointestinal symptoms in children who underwent UGI endoscopy in order to exclude an organic cause of severe chronic gastrointestinal disorders.     

Clinical usefulness of serum pepsinogen II in the management of Helicobacter pylori infection

BACKGROUND: Serum pepsinogen II (sPGII) levels are known to increase during Helicobacter pylori infection. AIM: To assess H. pylori infection and success of H. pylori therapy by means of sPGII levels. METHODS: sPGII levels were determined in 156 H. pylori-positive and 157 H. pylori-negative consecutive patients with dyspeptic symptoms. Additionally, sPGII determination was performed in 70 H. pylori-positive patients 2 months after H. pylori eradication therapy. In 29 of these 70 patients, gastroscopy was performed to evaluate the effect of H. pylori therapy on gastric activity. RESULTS: H. pylori-positive subjects demonstrated a significantly higher mean of sPGII levels than H. pylori-negative subjects (16.8 +/- 7.4 vs. 8.6 +/- 3.7 microg/l; p < 0.001). The best sPGII cut-off for predicting H. pylori infection was 9.93 microg/l (sensitivity 83%, specificity 73%). The best cut-off values to evaluate success of therapy were: sPGII of 9.47 microg/l, a sPGII variation level (difference between baseline and after therapy) of 4.54 microg/l, and a sPGII Deltavalue (sPGII variation divided by sPGII before therapy) of 25% (sensitivity 93%, specificity 91%). CONCLUSIONS: sPGII levels may be used as a reliable marker of H. pylori infection in the initial diagnosis as well as to evaluate H. pylori eradication and subsequent changes in gastric inflammation.     

Helicobacter pylori infection in diabetic patients: prevalence and endoscopic findings

BACKGROUND: In patients with diabetes mellitus, chronic infections are frequent and severe, due to the impairment of their immune status. However, data on the prevalence of Helicobacter pylori (H. pylori) infection in diabetics are scanty and contradictory. The aim of our study was to assess the prevalence of H. pylori infection in diabetic patients and to evaluate the association between endoscopic features and H. pylori colonization of the gastric mucosa in diabetes mellitus. METHODS: A cross-sectional study of 172 dyspeptic patients (67 diabetics and 105 nondiabetic subjects) was designed. In all cases, an upper gastrointestinal endoscopy was performed, gastroduodenal lesions were noted, and the presence of gastritis and H. pylori was assessed by histopathological examination. Differences between diabetic patients and nondiabetic subjects were evaluated. RESULTS: The difference of H. pylori prevalence between diabetics (37.3%) and nondiabetics (35.2%) was not significant (P=0.78). Nor did the prevalence of gastritis and peptic ulcer differ significantly between the two groups (59.7% vs. 49.5%, P=0.19; and 32.8% vs. 40.9%, P=0.08, respectively). Studying only H. pylori-positive patients, we found no difference between diabetics and nondiabetics with regard to the prevalence of either gastritis (80% vs. 72.9%, P=0.71) or peptic ulcer (91.8% vs. 76%, P=0.09). CONCLUSIONS: Our data do not support an association between H. pylori infection and diabetes mellitus. This is confirmed by the lack of difference between diabetics and nondiabetics with regard to the prevalence of both H. pylori infection and H. pylori-related gastroduodenal disorders.     

Helicobacter pylori infection and the prevention of peptic ulcer with proton pump inhibitors in elderly subjects taking low-dose aspirin

INTRODUCTION: The role of Helicobacter pylori infection on the risk of low-dose aspirin-related gastroduodenal damage and on the efficacy of the prevention therapy in elderly chronic users of low-dose aspirin is still controversial. AIM: To evaluate in symptomatic elderly chronic users of low-dose aspirin: (1) the association between H. pylori infection and the prevalence of upper gastrointestinal lesions; and (2) the effect of H. pylori infection on the efficacy of proton pump inhibitors in the prevention of aspirin-related gastroduodenal lesions. PATIENTS AND METHODS: Two hundred and forty-five symptomatic elderly who were taking aspirin 75-300 mg daily, at least during the last 3 months, were evaluated by endoscopy. A structured interview was carried out to evaluate gastrointestinal symptoms and the use of proton pump inhibitors. H. pylori infection was diagnosed according to histology and the rapid urease test on gastric biopsies. RESULTS: One hundred and twelve patients were H. pylori-positive and 133 patients were H. pylori-negative. A significantly higher prevalence of peptic ulcers was observed in H. pylori-positive than in H. pylori-negative subjects (36.6% versus 15.8%, P = 0.0002). The use of proton pump inhibitors was associated with a significant decreased risk of peptic ulcer both in H. pylori-positive (absolute risk reduction, ARR = -36.2, 95% confidence interval: -51.2 to -21.3, P < 0.001) and H. pylori-negative patients (ARR = -12.6, 95% confidence interval: -23.9 to -1.2, P = 0.03). However, the number of patients who needed to be treated in order to gain a reduction of one peptic ulcer (number needed to treat, NnT) was lower in H. pylori-positive than in H. pylori-negative patients (NnT = 3 versus 8). CONCLUSIONS: In symptomatic elderly chronic users of low-dose aspirin, H. pylori infection may influence the prevalence of peptic ulcers and the cost-effectiveness of the proton pump inhibitor prevention therapy.     

Direct measurement of gastric H^＋／K^＋-ATPase activities in patients with or without Helicobacterpylori-associated chronic gastritis

AIM: The role of Helicobacter pylori (H pylori) infection in gastric acid secretion of patients with chronic gastritis remains controversial. This study was designed to elucidate the effect of H pylori on H+/K+-ATPase activities in gastric biopsy specimens. METHODS: Eighty-two patients with chronic gastritis who had undergone upper endoscopy were included in this study. H pylori infection was confirmed by rapid urease test and histology. Gastric H+/K+-ATPase activities and serum gastrin concentrations were measured by an enzymatic method and radioimmunoassay, respectively. For those patients who received triple therapy for eradicating H pylori, changes in the activity of gastric H+/K+-ATPase and serum gastrin levels were also measured. RESULTS: The mean gastric H+/K+-ATPase activity in Hpylori-positive group (42 patients) was slightly higher than that in Hpylori-negative group (29 patients) (169.65±52.9 and 161.38±43.85nmol P/(mg·h),respectively, P=0.301). After eradication of H pylori, the gastric H+/K+-ATPase activities slightly decreased compared to prior therapy (165.03±59.50 and 158.42±38.93 nmol P/(mg·h), respectively, P=0.805). The mean basal gastrin concentration was slightly higher in H pylori-positive patients than in H pylori-negative patients (87.92±39.65 pg/mL vs75.04±42.57 pg/mL, P= 0.228). The gastrin levels fell significantly after the eradication of H pylori. (Before treatment 87.00±30.78 pg/mL, after treatment 64.73±18.96 pg/mL, P=0.015). CONCLUSION: Gastric H+/K+-ATPase activities are not associated with H pylori status in patients with chronic gastritis.     

In Dyspeptic Patients without Gastric Phase III of the Migrating Motor Complex,Helicobacter pylori Eradication Produces no Short-term Changes in Interdigestive Motility Pattern

Background: The relationship between Helicobacter pylori infection and interdigestive gastroduodenal motility in functional dyspepsia is still uncertain. Recent data from a large series documented that in dyspeptic patients without gastric phase III of the interdigestive migrating motor complex (MMC), the prevalence of bacterial infection was significantly higher. Since most H. pylori-positive dyspeptic patients have coexisting chronic gastritis, whether or not dyspepsia per se rather than bacterial colonization or chronic inflammation of the gastric mucosa may account for the observed interdigestive motility pattern is unknown. Our aim was to compare the interdigestive gastroduodenal motility pattern and dyspeptic symptoms before and 1 month after bacterial eradication in 20 H. pylori-positive dyspeptic subjects with chronic non-atrophic gastritis and without gastric phase III of the MMC, who were randomly allocated to receive eradication treatment (n = 10) or not (n = 10). Methods: Upper GI endoscopy with duplicate biopsies in antrum and corpus, 240-min interdigestive gastroduodenal manometric recording and symptoms assessment were performed before and 1 month after the treatments; bacterial eradication was confirmed by 13C-urea breath test. Results: After H. pylori eradication, neither in the incidence of antral and duodenal phase III of MMC nor in the phase II motility index values were any changes observed. Symptomatic improvement was recorded in both groups, with no significant differences between eradicated patients and controls. Conclusions: In dyspeptic patients with chronic non-atrophic gastritis and without gastric phase III of MMC, H. pylori eradication influences neither the interdigestive motility pattern nor the symptoms in the short-term period.     

Alteration of sister chromatid exchange frequencies in gastric cancer and chronic atrophic gastritis patients with and without H. pylori infection

AIM： To determine, by counting sister chromatid exchange （SCE） frequencies, whether genetic impairment and DNA damage have an effect on the pathogenesis of gastric cancer （GC）. METHODS： Analysis of SCE is a cytogenetic technique used to show DNA damage as a result of an exchange of DNA fragments between sister chromatids. We analyzed SCE frequency in 24 patients with GC, 26 patients with chronic atrophic gastritis （CAG）, and 15 normal controls. The presence of H pylori was confirmed by urease test, toluidine-blue stain and hematoxylin-eosin stain. RESULTS： SCE was significantly increased in H pylori- negative GC patients, and in H pylori-negative CAG patients compared with controls （7.41 ± 1.36 and 6.92 ± 1.20, respectively, vs 5.54 ± 0.8, P 〈 0.001）. There was no difference in the SCE frequency between H pylori- negative GC patients and H pylori-negative CAG patients （P 〉 0.05）. On other hand, the SCE frequencies in H pylori-positive GC patients were higher than those in H pylori-positive CAG patients （9.20 ± 0.94 vs 7.93 ± 0.81, P 〈 0.01）. Furthermore, H pylori-positive GC patients had a higher SCE frequency than H pylori- negative GC patients （9.20 ± 0.94 vs 7.41 ± 1.36, P 〈 0.001）. Similarly, a significant difference was detected between H pylori-positive CAG patients and H pylori-negative CAG patients （7.93 ± 0.81 vs 6.92 ± 1.20, P 〈 0.05）. CONCLUSION： We suggest the increased SCE in patients reflects a genomic instability that may be operative in gastric carcinogenesis.     

Comparison of clinical, serological and histological findings between non-ulcer dyspepsia patients with and without Helicobacter pylori infection

BACKGROUND AND AIMS: The role of Helicobacter pylori (H. pylori) infection in non-ulcer dyspepsia (NUD) remains controversial. This study investigates the clinical, serological and histological differences between patients with H. pylori-positive and -negative NUD. METHODS: One hundred and eighty consecutive patients with NUD were enrolled from January to December 1998. The severity of symptoms was evaluated by the Tucci's scoring system. The histological changes of gastric mucosa were assessed according to the Updated Sydney System, and a fasting blood sample was obtained to test the serum gastrin and pepsinogen I levels. RESULTS: The H. pylori-positive NUD patients were notably older than H. pylori-negative NUD patients (48.2 +/- 15.9 vs 39.8 +/- 15.7 years, P= 0.001). There were no differences in other clinical factors between the two NUD groups. The serum pepsinogen I levels were considerably higher in H. pylori-positive NUD patients than in H. pylori-negative NUD patients (78.9 +/- 42.2 vs 61.5 +/- 43.3 ng/mL, P<0.01). However, no significant differences in serum gastrin levels were discovered between the two groups. The antrum histological scores for chronic inflammation, acute inflammation, gland atrophy and lymphoid follicles were higher in H. pylori-positive NUD patients than in H. pylori-negative NUD patients (2.09 vs 1.01, P<0.001; 1.22 vs 0.36, P<0.001; 0.76 vs 0.36, P<0.01; 0.33 vs 0.13, P<0.01, respectively). CONCLUSIONS: The present study discovered marked differences in age, serum pepsinogen I levels, histological grades of acute inflammation, chronic inflammation, gland atrophy and lymphoid tissue formation between H. pylori-positive and H. pylori-negative NUD patients. Further investigation of the clinical prognosis of the two groups of patients is necessary.     

Helicobacter pylori infection, pattern of gastritis, and symptoms in erosive and nonerosive gastroesophageal reflux disease.

BACKGROUND: The aim of this study was to evaluate the prevalence of Helicobacter pylori infection and the characteristics of gastritis and symptoms of patients with erosive and nonerosive gastroesophageal reflux disease (GERD). METHODS: We studied 202 consecutive patients with a diagnosis of GERD (symptoms score and endoscopy): group A (n = 110), erosive GERD; group B (n = 92), nonerosive GERD; 200 patients with upper abdominal complaints without abnormalities at endoscopy (functional dyspepsia, group C); and 200 asymptomatic controls tested for H. pylori serum antibody (group D). Antral and body biopsy specimens were taken for histology and the rapid urease test in groups A, B, and C. RESULTS: The prevalence of H. pylori infection was higher in groups B and C (62% and 55%, respectively) than in A and D (36% and 40%) (P < 0.05). In positive patients H. pylori colonization and gastritis grade scores in the gastric body were higher in nonerosive than in erosive GERD and functional dyspepsia (P < 0.05). No differences in H. pylori colonization or gastritis grades were found in the antrum. Fifty-nine patients with nonerosive GERD (64%) and 42 with erosive GERD (38%) showed other dyspeptic symptoms associated with reflux symptoms (P < 0.05). CONCLUSIONS: H. pylori prevalence is higher in patients with nonerosive GERD than in normal subjects and in patients with erosive GERD and similar to that of patients with dyspepsia. Patients with nonerosive GERD often show dyspeptic symptoms and higher H. pylori colonization and inflammation grades in the proximal stomach. Our data support the hypothesis that in GERD H. pylori gastritis may, on the one hand, protect against the development of esophageal erosions and, on the other, contribute to the esophageal hypersensitivity to acid which is a feature of GERD.     

Helicobacterpylori infection and gastropathy： A comparison between Indonesian and Japanese patients

AIM: To compare the effects of Helicobacter pylori ( H pylori) infection on gastropathy between Indonesian and Japanese patients.METHODS: Biopsy specimens were obtained during upper gastrointestinal endoscopy from 167 subjects (125 Indonesians and 42 Japanese) with uninvestigated symptoms of dyspepsia. The specimens were analyzed for the presence of H pylori using urease analysis, histopathology, and cell culture. The grade and activity of gastritis was assessed using the updated Sydney system.RESULTS: The percentages of Indonesian and Japanese patients who were H pylori-positive at the antrum or body of the stomach were similar (68% and 59.5%, respectively; P = 0.316). Of those who were H pylori-positive, more Japanese patients than Indonesian patients had high levels of polymorphonuclear cells ( P = 0.001), mononuclear cells ( P = 0.013), glandular atrophy ( P = 0.000), and intestinal metaplasia ( P = 0.011) in both the antrum and body of the stomach.CONCLUSION: The grade of gastritis and prevalence of mucosal atrophy and intestinal metaplasia were higher in Japanese patients. The difference between Indonesian and Japanese patients was significant.     

In dyspeptic patients without gastric phase III of the migrating motor complex, Helicobacter pylori eradication produces no short-term changes in interdigestive motility pattern

BACKGROUND: The relationship between Helicobacter pylori infection and interdigestive gastroduodenal motility in functional dyspepsia is still uncertain. Recent data from a large series documented that in dyspeptic patients without gastric phase III of the interdigestive migrating motor complex (MMC), the prevalence of bacterial infection was significantly higher. Since most H. pylori-positive dyspeptic patients have coexisting chronic gastritis, whether or not dyspepsia per se rather than bacterial colonization or chronic inflammation of the gastric mucosa may account for the observed interdigestive motility pattern is unknown. Our aim was to compare the interdigestive gastroduodenal motility pattern and dyspeptic symptoms before and 1 month after bacterial eradication in 20 H. pylori-positive dyspeptic subjects with chronic non-atrophic gastritis and without gastric phase III of the MMC, who were randomly allocated to receive eradication treatment (n = 10) or not (n = 10). METHODS: Upper GI endoscopy with duplicate biopsies in antrum and corpus, 240-min interdigestive gastroduodenal manometric recording and symptoms assessment were performed before and 1 month after the treatments; bacterial eradication was confirmed by 13C-urea breath test. RESULTS: After H. pylori eradication, neither in the incidence of antral and duodenal phase III of MMC nor in the phase II motility index values were any changes observed. Symptomatic improvement was recorded in both groups, with no significant differences between eradicated patients and controls. CONCLUSIONS: In dyspeptic patients with chronic non-atrophic gastritis and without gastric phase III of MMC, H. pylori eradication influences neither the interdigestive motility pattern nor the symptoms in the short-term period.     

Nodular Gastritis: An Endoscopic Indicator of <Emphasis Type="Italic">Helicobacter Pylori</Emphasis> Infection

We prospectively assessed the relationship between nodular gastritis and Helicobacter pylori infection. Of 1409 adults who underwent endoscopy for persistent dyspepsia between June 2004 and August 2005, 41 (2.9%) patients were diagnosed with nodular gastritis (11 [27%] men and 30 [73%] women). The mean age was 45.9 years. A control group of 65 patients without nodular gastritis was also evaluated. The prevalence of H. pylori infection was higher in patients with nodular gastritis than in controls (38/41 [93%] vs. 33/65 [51%]). Of 21 patients treated to eradicate H. pylori, the nodular gastritis pattern resolved or improved in 16 patients on subsequent endoscopy. This study suggests that a nodular pattern of the gastric mucosa on endocscopy is a good indicator for H. pylori infection in adults, with the high positive predictive value of 92.7%.     

Prophylactic placement of gastrostomy feeding tubes before radiotherapy in patients with head and neck cancer: is it worthwhile?

As available data on Helicobacter pylori infection in patients with diabetes are scattered and discordant, we evaluated the prevalence of H. pylori and its relationship to dyspeptic symptoms in adult patients with diabetes and subjects with dyspepsia. H. pylori infection (evaluated using the 13C urea breath test) and dyspeptic symptoms (nausea, bloating, and epigastric distress) were investigated in 71 consecutive diabetic outpatients; the presence of gross lesions, histologic gastritis, and Helicobacter was verified in the patients with a positive urea test who agreed to undergo upper gastrointestinal tract endoscopy. Seventy-one age- and gender-matched subjects with dyspepsia were used as controls. Helicobacter pylori infection was detected in 49 (69%) patients with diabetes and in 33 (46%) subject with dyspepsia (p = 0.007). Helicobacter pylori was present in 27 (77%) of 35 patients with diabetes with dyspeptic symptoms and in 22 (61%) of 36 patients without dyspeptic symptoms. Endoscopy revealed peptic ulcers in 13 of 23 patients; H. pylori infection was histologically confirmed in the gastric antrum of all patients with diabetes, and in the body of the stomach in 74%. The significantly higher prevalence of H. pylori infection in the patients with diabetes may partially explain their dyspeptic symptoms. The high prevalence of H. pylori infection, esophagitis, and peptic ulcers found in our patients with diabetes (with or without dyspepsia) suggests that this population should be considered "at risk" for H. pylori infection and suitable candidates for treatment.     

Bleeding duodenal ulcer: comparison between Helicobacter pylori positive and Helicobacter pylori negative bleeders

BACKGROUND AND AIMS: To provide a direct comparison of Helicobacter pylori-positive subjects bleeding from duodenal ulcer with H. pylori-negative ones, in terms of severity of bleeding and outcome. PATIENTS AND METHODS: A case-control study was prospectively conducted in 105 H. pylori-negative duodenal ulcer bleeders and same number of sex- and age-matched H. pylori-positive ones. RESULTS: NSAID consumption was more common among H. pylori-negative subjects (81%) compared to their H. pylori-positive counterparts (58.1%, P < 0.001). H. pylori-negative bleeders were found to need more often haemostasis (55.2% versus 31.4%, P < 0.001) or surgical intervention (15.2% versus 4.8%, P = 0.011) and to have a greater proportion of rebleeding (32.4% versus 13.3%, P = 0.001), a more prolonged hospitalisation (11.6 +/- 4.1 versus 6.2 +/- 1.5 days, P < 0.001) and a higher rate of in-hospital mortality (15.2% versus 3.8%, P = 0.005). In the overall population (N = 210), H. pylori negativity, among other known risk factors, emerged as independent predictor (odds ratio: 3.2; 95% CI: 1.5, 11.2; P = 0.004) of an unfavourable outcome (surgery or death). CONCLUSIONS: Duodenal ulcer bleeding in H. pylori-negative subjects appears to be more severe, to have a higher rate of rebleeding, and to lead more often to surgery or fatality compared to the vast majority of H. pylori-positive duodenal ulcer bleeders.     

Clinical features of cardiac nodularity-like appearance induced by Helicobacter pylori infection

BACKGROUND We have previously reported that Helicobacter pylori(H. pylori)-associated nodular gastritis could occur in both the antrum and the cardia. Cardiac nodularity-like appearance(hereafter, called as cardiac nodularity) had a high predictive accuracy for the diagnosis of H. pylori infection. In the previous study, we included only the patients who were evaluated for H. pylori infection for the first time, and excluded patients with a history of eradication. Therefore, the prevalence and clinical features of cardiac nodularity remains unknown.AIM To perform this cross-sectional study to explore the characteristics of cardiac nodularity.METHODS Consecutive patients who underwent esophagogastroduodenoscopy between May, 2017 and August, 2019 in the Toyoshima Endoscopy Clinic were enrolled in this study. We included H. pylori-negative, H. pylori-positive, and H. pylorieradicated patients, and excluded patients with unclear H. pylori status and eradication failure. H. pylori infection was diagnosed according to serum anti-H. pylori antibody and the urea breath test or histology. Cardiac nodularity was defined as a miliary nodular appearance or the presence of scattered whitish circular small colorations within 2 cm of the esophagogastric junction. Nodularity was visualized as whitish in the narrow-band imaging mode. We collected data on the patients' baseline characteristics.RESULTS A total of 1078 patients were finally included. Among H. pylori-negative patients, cardiac nodularity and antral nodularity were recognized in 0.14% each. Among H. pylori-positive patients, cardiac nodularity and antral nodularity were recognized in 54.5% and 29.5%, respectively. Among H. pylori-eradicated patients, cardiac nodularity and antral nodularity were recognized in 4.5% and 0.6%, respectively. The frequency of cardiac nodularity was significantly higher than that of antral nodularity in H. pylori-positive and-eradicated patients. The frequencies of cardiac nodularity and antral nodularity in H. pylori-eradicated patients were significantly lower than those in H. pylori-positive patients(P 0.001). The patients with cardiac nodularity were significantly younger than those without cardiac nodularity(P = 0.0013). Intestinal metaplasia score of the patients with cardiac nodularity were significantly lower than those without cardiac nodularity(P = 0.0216). Among H. pylori-eradicated patients, the patients with cardiac nodularity underwent eradication significantly more recently compared with those without cardiac nodularity(P 0.0001).CONCLUSION This report outlines the prevalence and clinical features of cardiac nodularity, and confirm its close association with active H. pylori infection.     

Clinical presentation of Helicobacter pylori-positive and -negative functional dyspepsia

BACKGROUND: A questionnaire was used to record the clinical presentation of functional dyspepsia in relation to Helicobacter pylori infection in a consecutive series of patients sent for upper gastrointestinal endoscopy. Only patients without macroscopic abnormalities in their oesophagus, stomach and duodenum were included. METHODS: The study questionnaire included two questions related to daily life, and the calculation of a symptom score. Biopsy specimens were taken from all patients for histological and microbiological examination, and immunoglobulin G antibodies were also determined. RESULTS: Two hundred and twenty-two patients were H. pylori positive and 182 patients were H. pylori negative. Loss of weight was significantly more common in the H. pylori positive group (P<0.001). Patients with H. pylori infection had a significantly higher overall symptom score compared with H. pylori-negative subjects (P<0.05). In addition, the severity of epigastric and nocturnal pain, heartburn, retrosternal heartburn, and vomiting was significantly higher in H. pylori-positive functional dyspeptic patients, and the influence on daily life and activities was significantly worse. CONCLUSIONS: The combination of retrosternal pain, weight loss, food intolerance and the absence of halitosis signified a 64% accuracy in predicting H. pylori infection. It is not possible to differentiate between H. pylori-positive and H. pylori-negative functional dyspeptics on the basis of clinical presentation and the number of complaints. However, overall symptom score and severity of several symptoms was significantly higher in the H. pylori-positive group.     

Relationship among serum pepsinogens, serum gastrin, gastric mucosal histology and H. pylori virulence factors in a paediatric population

OBJECTIVE: Serum pepsinogens and gastrin have been proposed as markers of gastritis, but have seldom been studied in children. In this study the aim was to identify host- and Helicobacter pylori-related factors linked to variations in serum gastrin, PGI, PGII, and to evaluate the potential of these biomarkers for diagnosing gastritis, whether H. pylori-associated or not. MATERIAL AND METHODS: Ninety-two dyspeptic children referred for endoscopy (peptic ulcer exclusion) were included in the study. H. pylori status (urease, culture, histology) was assessed, and genotype determined (PCR) in H. pylori-positive subjects. Serum gastrin, PGI and PGII levels were measured by standard radioimmunoassay (RIA). RESULTS: PGI and PGII levels were significantly higher in H. pylori-positive subjects (p=0.007; p=0.012, respectively). Gastrin levels were significantly higher in H. pylori-negative subjects (p=0.035). PGI and PGII were associated significantly with higher antrum inflammation scores (p=0.002; p=0.016, respectively); only PGI was associated with age, after controlling for inflammation (p=0.033) and for activity (p=0.037). The contribution of virulence factors could not be assessed owing to the low number of virulent strains. After multivariate analysis, only antrum inflammation was independently associated with PGI level (p=0.012). Receiver operating characteristic (ROC) analysis showed a low PGI and PGII discriminant power for predicting antrum inflammation. CONCLUSIONS: Pepsinogen levels as measured in this study seem predominantly to reflect antral inflammation, but they are not an effective screening test for gastritis (H. pylori-positive or -negative) in dyspeptic children.