Role of Helicobacter pylori infection in gastroduodenal injury and gastric prostaglandin synthesis during long term/low dose aspirin therapy: a prospective placebo-controlled, double-blind randomized trial

OBJECTIVES: Whether gastric infection with Helicobacter pylori increases the risk of gastric mucosal injury during long term/low dose aspirin therapy is unknown. We examined whether H. pylori infection enhances upper GI mucosal damage, assessed endoscopically, in volunteers given low dose aspirin. We studied 61 healthy men and women, 29 with and 32 without active H. pylori infection. METHODS: We treated volunteers for 45 days with a placebo or aspirin (either 81 mg every day or 325 mg every 3 days). Gastroduodenal mucosal damage was then assessed by endoscopy, as was gastric histology and ex vivo gastric mucosal prostaglandin E2 and F2alpha synthesis rates. RESULTS: Erosive disease from low dose aspirin (erosions and/or ulcers) occurred in 50% of H. pylori-infected volunteers and in 16% of their noninfected counterparts (p = 0.02). Aspirin caused a significantly higher average mucosal injury score in the gastric antrum in H. pylori-infected participants than in noninfected subjects (p = 0.03), and two H. pylori-infected subjects developed antral gastric ulcers. Subjects with H. pylori gastritis treated with the placebo had nearly 50% higher gastric mucosal prostaglandin (E2 plus F2alpha) synthesis rates than their noninfected counterparts (108 +/- 6 ng/g/min versus 75 +/- 6 ng/g/min, p < 0.001). Aspirin reduced mucosal prostaglandin synthesis to similar levels in infected and noninfected participants. CONCLUSIONS: Long term/low dose aspirin therapy led to more gastric mucosal damage when H. pylori gastritis was present than when it was absent, despite similar degrees of gastric mucosal prostaglandin depletion.     

Effect of Helicobacter pylori colonisation on gastric mucosal eicosanoid synthesis in patients taking non-steroidal anti-inflammatory drugs.

Colonisation with Helicobacter pylori may influence susceptibility to gastroduodenal injury and ulceration in patients taking non-steroidal anti-inflammatory drugs (NSAIDs). The aim of this study was to determine if Helicobacter pylori colonisation altered eicosanoid synthesis by gastric mucosa in these patients. Sixty five patients with long-standing NSAID intake and 23 control subjects underwent endoscopy. In vitro gastric antral biopsies were stimulated by vortex mixing and eicosanoid measurements determined by radioimmunoassay. Helicobacter pylori colonisation was determined by a CLO test (a gel based rapid urease test) and histological assessment. Median prostaglandin E2 synthesis by gastric mucosa was 61.0 (interquartile range: 19.2-73.1) pg/mg in control subjects colonised with Helicobacter pylori compared with 46.5 (23.3-65.5) pg/mg in Helicobacter pylori negative subjects. This was not significantly different. Treatment with NSAIDs was associated with a significant difference (p < 0.001) in prostaglandin E2 (PGE2) synthesis between those colonised with Helicobacter pylori (37.5(22.0-77.3) pg/mg) compared with patients not infected (12.6(7.0-19.3) pg/mg). Values in patients taking NSAIDs who were colonised were not different from control subjects. Synthesis of PGE2 was strongly associated with type B (chronic active), but not type C (chemical) gastritis. Dyspeptic symptoms were more common in subject colonised with Helicobacter pylori (p < 0.002) and were associated with higher PGE2 synthesis. In patients taking NSAIDs Helicobacter pylori colonisation removes rather then enhances depression of PGE2 synthesis associated with NSAIDs and may promote dyspepsia associated with ulcers and prevent superficial mucosal injury.     

Distribution of cagG gene in Helicobacter pylori isolates from Chinese patients with different gastroduodenal diseases and its clinical and pathological significance

AIM: To determine the distribution of cagG gene of Helicobacter pylori(Hpylori) isolates cultured from patients with various digestive diseases and its relationship with gastroduodenal diseases.METHODS: cagG was amplified by polymerase chain reaction in 145 H pylori isolates cultured from patients with chronic gastritis (n=72), duodenal ulcer (n=48), gastric ulcer (n=17), or gastric and duodenal ulcer (n=8), and the relationship between cagGstatus and the grade of gastric mucosal inflammation was determined.RESULTS: cagG was present in 91.7% of the 145 H pylori isolates, with the rates were 90.3%, 93.8%, 88.2% and 100.0%, respectively, in those from patients with chronic gastritis, duodenal ulcer, gastric ulcer, and gastric and duodenal ulcer. There was no significant difference among the four groups (P＞0.05). The average grade of gastric mucosal inflammation in the antrum and corpus was 1.819±0.325and 1.768±0.312, respectively in cagG positive patients,whereas the average inflammation grade was 1.649±0.297,1.598±0.278 respectively in cagG negative cases (P＞0.05).CONCLUSION: cagG gene of H pylori was quite conservative,and most H pylori strains in Chinese patients were cagG positive.cagG status was not related to clinical outcome or the degree of gastric mucosal inflammation. Therefore, cagG can notbe used as a single marker for discrimination of H pylori strains with respect to a specific digestive disease.     

Effect on gastric and duodenal mucosal prostaglandins of repeated intake of therapeutic doses of naproxen and etodolac in rheumatoid arthritis.

The synthesis of gastric and duodenal mucosal prostaglandin E2, prostaglandin I2, and thromboxane B2 during a 60 minute incubation of biopsy specimens, the degree of endoscopic and histological damage, and the anti-inflammatory response were all studied after a four week, double blind study of therapeutic doses of two non-steroidal anti-inflammatory drugs, naproxen and etodolac, received by 27 patients with active rheumatoid arthritis (13 receiving naproxen, 14 etodolac). Prostaglandin values after treatment did not differ from the baseline levels when all the patients were analysed as one group. Subgroup analysis showed that naproxen suppressed gastric prostaglandin E2 from a median of 29 to 9 ng/mg protein, duodenal prostaglandin E2 from 34 to 11 ng/mg, and duodenal prostaglandin I2 from 62 to 15 ng/mg protein. No overall suppression occurred with etodolac. Also, on the second assessment patients receiving naproxen had lower gastric and duodenal prostaglandin E2 and prostaglandin I2, but higher values of duodenal thromboxane B2, than patients receiving etodolac. Both drugs had comparable anti-arthritic activity and caused microscopic gastritis in similar proportions of patients. No correlation was detected between prostaglandin values and the mucosal damage which developed in seven patients receiving naproxen (54%) and three receiving etodolac (21%). These findings indicate that, unlike naproxen, etodolac does not seem to affect gastric or duodenal prostaglandin synthesis; other mechanisms of injury need to be considered.     

Effect of Helicobacter pylori eradication on anti-thrombotic dose aspirin-induced gastroduodenal mucosal injury

BACKGROUND: Helicobacter pylori infection and non-steroidal anti-inflammatory drugs are two major causes of gastric injury but the effect of H. pylori eradication on the development of aspirin-induced gastric mucosal injury is unclear. The aim of the present study was to investigate the effect of Helicobacter pylori eradication on gastroduodenal mucosal injury induced by antithrombotic doses of aspirin. METHODS: Patients who had been planned to start on medium-dose aspirin (300 mg) for any kind of indication were included in the study. All subjects underwent upper gastrointestinal endoscopy for determination of H. pylori status and Lanza score. The H. pylori-positive patients were randomized to receive either aspirin + eradication (omeprazole 20 mg b.i.d. and amoxicillin 500 mg q.i.d. for 2 weeks) or aspirin + placebo eradication. Endoscopic reassessment was done 4 months after the onset of aspirin or when symptoms developed. RESULTS: Thirty-two patients (placebo group n = 16, H. pylori-eradicated group n = 16) completed the study and Lanza scores of both groups were similar before treatment. Lanza scores significantly increased in the placebo group (0.69 +/- 0.87 vs 2.25 +/- 1.3, P < 0.0001) and did not change in the H. pylori-eradicated group after aspirin treatment (0.43 +/- 0.72 vs 0.75 +/- 0.93, P > 0.05). CONCLUSION: Helicobacter pylori eradication may prevent medium-dose aspirin-induced gastroduodenal mucosal injury.     

Enhanced gastric mucosal leukotriene B4 synthesis in patients taking non-steroidal anti-inflammatory drugs.

The effects of longstanding non-steroidal anti-inflammatory drug (NSAID) treatment on gastric mucosal synthesis of leukotriene B4 (LTB4), leukotriene C4 (LTC4), and prostaglandin E2 (PGE2) was studied. Gastric antral biopsies in 65 patients with arthritis taking NSAIDs and 23 control patients were taken and eicosanoid concentrations, stimulated by vortex mixing or calcium ionophore, were measured by radioimmunoassay. Median gastric mucosal synthesis of LTB4 was increased in patients taking NSAIDs compared with non-users: (0.9(0.2-2.5) pg/mg v 0 (0-0.6) pg/mg (p < 0.001)). These differences persisted when subgroups of patients were analysed according to Helicobacter pylori colonisation or degree of mucosal injury. Synthesis of LTB4 was strongly associated with the presence of type C (chemical) gastritis. Increased synthesis of LTC4 was associated with Helicobacter pylori colonisation but not NSAID use. Synthesis of PGE2 was decreased in patients taking NSAIDs compared with control patients (p < 0.001). Enhanced gastric mucosal synthesis of LTB4 in patients taking NSAIDs may represent a primary effect of these drugs and could be implicated in the pathogenesis of gastritis and ulceration associated with NSAIDs.     

Upper gastrointestinal disorders induced by non-steroidal anti-inflammatory drugs

BACKGROUND/AIMS: We examined the characteristics of upper gastrointestinal (GI) disorders induced by non-steroidal anti-inflammatory drugs (NSAIDs). METHODOLOGY: The questionnaire investigation was performed over a five-year period. RESULTS: A study was performed on 354 patients (161 men and 193 women with mean ages of 66.0 and 70.7 years, respectively) who developed NSAID associated upper GI disorders: 21 patients had acute gastric mucosal lesion (AGML), 212 had gastric ulcer, 63 had duodenal ulcer, 17 had gastroduodenal ulcers and 41 other cases. About 75% of patients received NSAIDs for orthopedic conditions. Sixty percent of gastric disorders induced by NSAIDs affected the antrum or angulus of the stomach. The incidence of disorders of the gastric antrum was significantly higher in women than in men whilst the incidence of disorders on the gastric angulus was significantly higher in men than in women (p<0.05). The proportion of patients with GI symptoms was significantly lower in patients over 65 years old than in those under 65 years old (p<0.05). The time taken to achieve the healing stage was significantly longer in patients with greater than 3 months NSAID ingestion compared to patients that had received NSAIDs for less than 3 months (p<0.05). CONCLUSIONS: We should examine the association between upper GI disorders induced by NSAIDs and H. pylori as well as the rate of GI disorders induced by new Cox-2 inhibitors.     

Gastroduodenal mucosal prostaglandin generation in patients withHelicobacter pylori before and after treatment with bismuth subsalicylate

To determine whether Helicobacter pylori has an effect on gastroduodenal mucosal prostaglandin generation, mucosal biopsies were obtained from the gastric body, antrum, and duodenal bulb of 30 patients who were undergoing upper gastrointestinal endoscopy for clinical indications. One biopsy from the gastric body and one from the antrum were tested for urease activity (urea broth) and one biopsy from each area including the duodenum was processed for histology. Two other biopsies form each area were incubated and the accumulation of prostaglandin E2 and 6-keto prostaglandin F1 alpha in the incubation medium was measured by radioimmunoassay. Twelve of the 17 H. pylori-positive patients and seven of the 13 H. pylori-negative patients agreed to take bismuth subsalicylate (Pepto-Bismol) two tablets four times a day for four weeks. One week after treatment, these patients again underwent endoscopy and the above studies. This study indicates that: (1) mucosal PGE2 generation may be increased in the duodenum, gastric body, and antrum in H. pylori-positive patients compared to H. pylori-negative patients, and (2) treatment with bismuth subsalicylate for four weeks results in reduction of mucosal PGE2 in the duodenum, gastric body, and antrum of H. pylori-positive patients and fails to eradicate H. pylori or reduce gastric inflammation.     

Is Helicobacter pylori the primary cause of duodenal ulceration?

Helicobacter pylori infection may not be the primary cause of duodenal ulceration in cases not associated with non-steroidal anti-inflammatory drugs, but may be a secondary complication. In developing countries with a uniformly high prevalence of H. pylori infection there are marked regional differences in the prevalence of duodenal ulcer (DU). In some countries, especially those with a low prevalence of H. pylori, 30-40% or more patients with DU may be H. pylori negative. The absence of H. pylori infection in early cases of DU is also reported. In DU patients with antral H. pylori infection, duodenal colonization by H. pylori may often be absent. After complete H. pylori eradication, recurrence of DU within 6 months in some reports is as high as 20%. The evidence suggests that high acidity and reduced duodenal mucosal resistance remain the primary causes of DU and that H. pylori infection, when present, results in chronicity. Reduced mucosal resistance results in duodenal gastric metaplasia which permits colonization of the duodenum with H. pylori from the antrum. Therefore, whatever causes reduced mucosal resistance may be the primary factor and evidence suggests that this cause may be diet related. This would explain the enigma of regional variations in DU prevalence unrelated to H. pylori prevalence.     

Oxidative stress in gastric mucosa in Helicobacter pylori infection.

BACKGROUND: Infection with Helicobacter pylori is believed to be associated with generation of reactive oxygen molecules which leads to oxidative stress in the gastric mucosa; but the relation between oxidative stress and gastrointestinal mucosal damage has not been documented. AIM: To look for evidence of oxidative stress and lipid peroxidation in the gastric mucosa in H. pylori-associated peptic ulcer. METHODS: 34 duodenal ulcer (DU) patients with H. pylori infection, 14 DU patients without H. pylori infection and 10 healthy subjects without H. pylori infection were studied. H. pylori infection was diagnosed by histology and rapid urease test on endoscopic biopsies from the gastric body and antrum. Reduced glutathione (GSH) and malondialdehyde (MDA) content were measured in biopsies taken from the gastric antrum. Statistical analysis was done using Student's t test. RESULTS: Tissue levels of GSH were significantly lower (91.7 [35.4] nmole/100 mg versus 147.3 [41.2] nmole/100 mg; p < 0.001) and MDA higher (163.0 [83.4] nmole/100 mg versus 109.2 [51.3] nmole/100 mg; p < 0.01) in patients with DU associated with H. pylori infection as compared to those without H. pylori infection. GSH levels were significantly lower and MDA levels higher in DU patients with or without H. pylori infection as compared to control subjects. Serum MDA levels in DU patients with H. pylori infection were also significantly higher than in patients without H. pylori infection. CONCLUSION: Depletion of gastric mucosal glutathione in H. pylori-infected DU patients may be due to failure of the antioxidant defense system. Failure of the glutathione-dependent defense system results in accumulation of free radicals which can initiate membrane damage by lipid peroxidation.     

Gastric and Duodenal Mucosal Prostaglandin Concentrations in Gastric or Duodenal Ulcer Disease: Relationships with Demographics, Environmental, and Histological Factors, including Helicobacter pylori

We measured gastric and duodenal mucosal prostaglandin concentrations in 69 patients with active or inactive duodenal or gastric ulcer disease and 26 non-ulcer controls. Each underwent endoscopy enabling us to obtain multiple biopsies from the gastric body and antrum and from the duodenal bulb and postbulbar duodenum for measurement of mucosal prostaglandin concentrations, as well as a single biopsy from each region for mucosal histology. Using a multivariate linear regression model, we found that neither gastric nor duodenal ulcer disease significantly affected gastric or duodenal mucosal prostaglandin concentrations. Mucosal prostaglandin concentrations were similar at the edge of the ulcer and in the adjacent non-ulcerated mucosa. Neither gender symptoms, smoking, use of H2-receptor antagonists, disease activity, nor Helicobacter pylori infection had an independent effect on mucosal prostaglandins in any region. Gastritis in the body of the stomach was associated with significantly higher prostaglandins, while older age was associated with significantly lower gastric and duodenal prostaglandins. Gastroduodenal mucosal prostaglandins are thus not altered in patients with active or inactive peptic ulcer disease, even when multiple demographic and histologic variables are taken into consideration.     

Healing of Helicobacter pylori gastric ulcers: only eradication matters.

INTRODUCTION: some authors suggest that Helicobacter pylori eradication favors gastric ulcer healing. OBJECTIVE: to study which factors influence ulcer healing in patients suffering from gastric ulcer with H. pylori infection. SUBJECTS AND METHODS: a prospective study of 230 patients with gastric ulcer associated to H. pylori infection. Chronic ingestion of non-steroidal anti-inflammatory drugs was considered as an exclusion. In an initial endoscopy, malignancy was histologically excluded and two biopsies each of antrum and body were obtained. Also, ELISA IgG serology and a 13C-urea breath test were performed. Eradication therapy with omeprazole (20 mg twice a day), clarithromycin (500 mg twice a day) and amoxicillin (1 g twice a day) was administered for seven days, followed by omeprazole 20 mg once a day for five more weeks. Endoscopy was repeated after 6 weeks of treatment and breath test was repeated 2 month after completing therapy. RESULTS: overall gastric ulcer healing was achieved in 80.8% (95% CI: 75-85%) of cases by intention-to-treat, and in 82.6% (77-87%) per protocol. Ulcer healing was achieved in 94.3% (90-97%) of patients with eradication success, but only in 40.8% (28-54%) of patients with eradication failure (p<0.0001). In the multivariate analysis, H. pylori eradication was the only variable that correlated with ulcer healing (odds ratio 24; 95% CI: 10-56; p<0.0001) (x2 model: 64.4; p<0.0001). Additional variables (age, sex, sporadic ingestion of NSAIDs, smoking, previous ulcer disease, ulcer size and location) were not related to healing. CONCLUSION: H. pylori eradication favors ulcer healing in patients with gastric ulcer, which is an argument in favor of the etiological role of the microorganism in this disease. Other factors did not influence ulcer healing.     

Hypersecretory duodenal ulcer and Helicobacter pylori infection: a four-year follow-up study.

BACKGROUND: About 10% of duodenal ulcer patients are characterized by gastric acid hypersecretion with normal gastrin values. Relapsing duodenal ulcer after Helicobacter pylori cure has been related to high acid output and maintenance antisecretory therapy has been suggested in hypersecretory duodenal ulcer patients. The role of Helicobacter pylori infection and the effects of Helicobacter pylori cure in hypersecretory duodenal ulcer patients still remain to be fully studied. AIM: To study: a) whether gastric acid hypersecretion "per se" is a risk factor for duodenal ulcer recurrence; b) whether maintenance antisecretory therapy is necessary after eradication in hypersecretory duodenal ulcer patients. PATIENTS: The study population comprised 8 hypersecretory duodenal ulcer patients, selected from a population of 79 Helicobacter pylori-positive duodenal ulcer patients. METHODS: Hypersecretory duodenal ulcer patients were followed-up for at least 4 years after eradication. Gastric acid secretion was measured again 12 months after Helicobacter pylori eradication. Gastroscopy with histology was performed 3, 6, 12 and 36 months after treatment, 13C-urea breath test after 42 months; clinical questionnaires were completed every 6 months. RESULTS: After eradication, despite a not significantly reduced high acid output (median value of basal acid output and pentagastrin-stimulated acid output, respectively, 23.1 mEq/h and 64.1 mEq/h before treatment vs 16 mEq/h and 49.7 mEq/h 12 months after treatment), all patients were free from symptoms, none of them had duodenal ulcer relapse or complications (7/8 before treatment), or needed antisecretory maintenance therapy, except for one patient taking non-steroidal anti-inflammatory drugs. CONCLUSIONS: These findings, obtained in a selected population of hypersecretory duodenal ulcer patients with long-term follow-up, suggest that after successful Helicobacter pylori eradication gastric acid hypersecretion "per se" is not able to determine the recurrence of duodenal ulcer.     

Helicobacter pylori eradication reduces platelet count in patients without idiopathic thrombocytopenic purpura

Discrepant outcomes of Helicobacter pylori eradication in patients with idiopathic thrombocytopenic purpura have been reported. Here patients with dyspepsia and no other complications underwent gastroendoscopic examination and evaluation for Helicobacter pylori infection. Helicobacter pylori-infected patients with gastritis and gastric ulcer received eradication therapy: lansoprazole (60 mg/day), clarithromycin (400 mg/day), and amoxicillin (1500 mg/day) for 1 week. Lansoprazole 30 mg/day was administrated additional 7 weeks. Peripheral platelets were counted before treatment, 8 weeks after initiation of therapy, and at follow-up periods. Platelet counts in patients with both gastritis and gastric ulcer were evaluated with reference to the presence of Helicobacter pylori infection. Eighty-seven patients with gastritis and 35 of those with gastric ulcer underwent successful eradication therapy. Peripheral platelet counts in patients with gastritis decreased from 235+/-55 to 228+/-58 (10(3)/microL) (p=0.0337), and those with gastric ulcer decreased from 248+/-60 to 232+/-48 (10(3)/microL) (p=0.020) 8 weeks after initiation of therapy. Non-eradicated patients did not show such a tendency. Helicobacter pylori eradication reduced peripheral platelet counts in patients with gastritis and gastric ulcer. Amelioration of thrombocytopenia by eradicating Helicobacter pylori appears to involve mechanisms specific to idiopathic thrombocytopenic purpura.     

Regression of duodenal gastric metaplasia in Helicobacter pylori positive patients with duodenal ulcer disease.

BACKGROUND: It is unclear whether the extent of duodenal gastric metaplasia is due to Helicobacter pylori and/or acid. AIMS: To investigate the role of Helicobacter pylori eradication in the regression of duodenal gastric metaplasia in patients with duodenal ulcer maintained in acid suppression conditions. METHODS:. Duodenal (anterior, superior inferior walls of first part of duodenum) and gastric antrum biopsies were obtained from 44 Helicobacter pylori positive duodenal ulcer patients. Helicobacter pylori infection was diagnosed by rapid urease test, histology and 13C-Urea Breath Test. Patients were treated with 20 mg omeprazole tid associated with 250 mg clarithromycin and 500 mg amoxycillin four times daily for 10 days and maintained with 20 mg omeprazole daily for 18 weeks. Control endoscopies were performed at 6 and 18 weeks after beginning treatment. RESULTS: Duodenal gastric metaplasia regression was observed in all (32/32) patients in whom Helicobacter pylori was eradicated, but in only 3 out of 6 patients in whom eradication was not achieved (p<0. 001). CONCLUSIONS:. The present results suggest that Helicobacter pylori eradication associated with prolonged acid suppression may represent a good therapeutic strategy to achieve duodenal gastric metaplasia regression and highlight the combined role of acid and Helicobacter pylori in the pathogenesis of duodenal gastric metaplasia.     

Eradication of Helicobacter pylori significantly reduced gastric damage in nonsteroidal anti-inflammatory drug-treated Mongolian gerbils

AIM: To examine the effect of eradication of Hellcobacter pylori prior to usage of NSAIDs, by investigating gastric inflammatory activity, myeloperoxidase (MPO) activity, prostaglandin (PG) E_2 synthesis in H Pylori-infected, and H pylori-eradicated gerbils followed by administration of indomethacin and rofecoxib. METHODS: Six-week-old male gerbils were orally inoculated with H pylori. Seven weeks later, anti-H pylori triple therapy and vehicle were given to gerbils respectively and followed by oral indomethacin (2 mg/kg·d) or rofecoxib (10 mg/kg·d) for 2 wk. We examined the area of lesions, gastric inflammatory activity, PGE_2 synthesis and MPO activity in the stomach. RESULTS: In indomethacin and rofecoxib-treated gerbils, the following results were obtained in H pylori-infected group vs H pylori-eradicated group respectively: hyperplasia area of the stomach (mm~2): 82.4±9.2 vs 13.9±3.5 (P＜0.05), 30.5±5.1 vs 1.3±0.6 (P＜0.05); erosion and ulcer area (mm~2): 14.4±4.9 vs 0.86±0.5 (P＜0.05), 1.3±0.6 vs0.4±0.3 (P＜0.05); score of gastritis: 7.0±0.0 vs3.6±0.5 (P＜0.05), 7.0±0.0 vs 2.7±0.5 (P＜0.05); MPO activity (μmol H_2O_2/min/g tissue): 104.7±9.2 vs9.0±2.3(P＜0.05), 133.5±15.0 vs2.9±0.7 (P＜0.05); PGE_2 synthesis (pg/mg wet weight/min): 299.2±81.5 vs102.8±26.2 (P＜0.05), 321.4±30.3 vs 11.9±4.8(P＜0.05). CONCLUSION: Eradication of H pylori reduced gastric damage of NSAID-treated Mongolian gerbils. Rofecoxib caused less severe gastric damage than indomethacin in H pylori-eradicated gerbils.     

Effect of Helicobacter pylori eradication on bulbitis and duodenal gastric metaplasia

BACKGROUND/AIMS: Duodenal gastric metaplasia seems to be linked to infection by Helicobacter pylori, to the extent of acid secretion and to bulbitis. An investigation was made of the relationship between bulbitis and duodenal gastric metaplasia, or whether bulbitis can arise along with duodenal gastric metaplasia after Helicobacter pylori eradication in an average of six years. METHODOLOGY: We compared 22 patients with duodenal ulcers [male/female 16/6; (mean age+/-SD) 55+/-12 years] Helicobacter pylori-negative after eradication, with 23 Helicobacter pylori-positive patients free from active duodenal ulcers [male/female 17/6; (mean age+/-SD) 59+/-12 years]. RESULTS: The bulbitis score was found to be lower in the Helicobacter pylori-negative than in the Helicobacter pylori-positive group (p=0.02). The duodenal gastric metaplasia score in the Helicobacter pylori-negative was higher than in the Helicobacter pylori-positive group (p=0.001). We failed to find any relationship between the presence of bulbitis and duodenal gastric metaplasia. We found a non-significant inverse correlation between the presence of duodenal gastric metaplasia and chronic body gastritis (p=0.07). CONCLUSIONS: Bulbitis and duodenal gastric metaplasia may depend on different causal factors not related to Helicobacter pylori infection. The extension of duodenal gastric metaplasia with time following recovery from peptic ulcer disease may represent a mucosal protection factor against acid.     

The effectiveness of (IgG-ELISA) serology as an alternative diagnostic method for detecting Helicobacter pylori infection in patients with gastro-intestinal bleeding due to gastro-duodenal ulcer.

OBJECTIVES: To establish the sensitivity, specificity, positive predictive value and negative predictive value of serology (IgG ELISA) as an alternative diagnostic method for Helicobacter pylori infection in patients with gastro-duodenal peptic ulcer and digestive hemorrhage. The diagnosis of Helicobacter pylori infection in these patients is difficult due to the low sensitivity of invasive tests and the need to discontinue treatment with proton pump inhibitors to perform a breath test with urea 13C or the detection of Helicobacter pylori antigens in feces. PATIENTS AND METHODS: We included 214 patients (164 men and 50 women) with an average age of 58 +/- 15 years, who were admitted to hospital due to upper gastro-intestinal bleeding caused by a gastro-duodenal peptic ulcer. The presence of Helicobacter pylori was established by means of gastric biopsy (fast urease test histology and/or culture) and a breath test with 13C-labeled urea. Serology was performed with the ELISA method (Pyloriset EIA-G by Orion Diagnostica). Positive Helicobacter pylori infection was accepted with any positive invasive method or breath test, and no infection was established if all invasive tests performed and the breath test with 13C-labeled urea were negative. We calculated the sensitivity, specificity, positive predictive value and negative predictive value of serology in the global series and in different subgroups of patients according to age (> 60 and < 40 years), recent exposure to non-steroidal anti-inflammatory drugs, type of endoscopic wound and history of gastro-duodenal peptic ulcer. RESULTS: 192 patients (89.7%) showed infection due to Helicobacter pylori. In the global series (n = 214) we obtained a sensitivity, specificity, positive predictive value and negative predictive value of 87.5, 54.5, 94.3 and 33.3%, respectively. Specificity was greater in the group not exposed to non-steroidal anti-inflammatory drugs (n = 110) as compared to the exposed group (n = 104), in the < 40 year old group (n = 28) with respect to the > 60 years group (n = 105), in the duodenal ulcer group (n = 141) with respect to the gastric ulcer group (n = 59), and in the group with a history of gastro-duodenal peptic ulcers (n = 92) as compared to the group without any of these past events (n = 122); nevertheless, no significant statistics were reached. CONCLUSIONS: IgG (ELISA) serology shows low specificity and a low negative predictive value in the diagnosis of Helicobacter pylori infection in patients with gastro-intestinal bleeding due to gastro-duodenal peptic ulcer. The diagnostic value of serology did not improve significantly when age, recent exposure to non-steroidal anti-inflammatory drugs, type of endoscopic wound or history of gastro-duodenal peptic ulcer was taken into consideration. We may consider that serology is not a good diagnostic method for the detection of Helicobacter pylori in patients with digestive hemorrhage caused by gastro-duodenal ulcer.     

胃、十二指肠溃疡幽门螺杆菌感染及相关病因回顾性分析204例

目的:研究福建省立医院胃、十二指肠溃疡患者幽门螺杆菌(H.pylori)感染及其他致病因素对疾病发生的作用.方法:选取2003-2008年福建省立医院胃镜中心进行检查并确诊为消化性溃疡的患者204例,所有患者在胃镜检查前记录详细情况,包括H.pylori感染,胃黏膜活检尿素酶法(14C-UBT),吸烟史(每日>10支)...     

Reactive oxygen species activity, mucosal lipoperoxidation and glutathione in Helicobacter pylori-infected gastric mucosa

BACKGROUND AND AIM: Helicobacter pylori is considered as the major pathogen in Helicobacter pylori-associated gastroduodenal disease, but the mechanism of its action has not been fully explained. This study was performed to assess the reactive oxygen species activity and the damage in Helicobacter pylori-infected gastric mucosa. METHODS: Gastric biopsy specimens were obtained from 308 patients undergoing endoscopy. Gastric mucosal damage was assessed by using luminol enhanced chemiluminescence, thiobarbituric acid-reactive substance, and mucosal glutathione. RESULTS: The chemiluminescence and thiobarbituric acid-reactive substance-equivalent levels in the mucosa of patients with Helicobacter pylori-positive gastric mucosa (43.8 +/- 134.9 c.p.m./microg tissue, 157.0 +/- 96.2 nmol/g tissue, respectively) were significantly higher than in those with Helicobacter pylori-negative mucosa (6.8 +/- 20.3 c.p.m./microg tissue, 110.0 +/- 51.6 nmol/g tissue, respectively; P=0.000, P=0.016, respectively). The glutathione levels in the mucosa of patients with Helicobacter pylori-positive gastric mucosa (159.3 +/- 76.6 nmol/microg tissue) were significantly lower than in those with Helicobacter pylori-negative gastric mucosa (212.3 +/- 134.3 nmol/microg tissue; P=0.008). After the data were divided according to the presence of Helicobacter pylori, there were no significant differences in chemiluminescence, thiobarbituric acid-reactive substance, and glutathione among the different macroscopic findings within Helicobacter pylori-positive and -negative gastric mucosa. CONCLUSIONS: Helicobacter pylori infection plays a pathological role in many gastrointestinal diseases through excessive mucosal-reactive oxygen species production, pronounced membrane damage, and the depletion of gastric anti-oxidants.