High rate of Helicobacter pylori reinfection in Lithuanian peptic ulcer patients

AIM: To evaluate the frequency of Helicobacter pylori(H. pylori) reinfection in peptic ulcer patients during 9 years after H. pylori eradication.METHODS: We invited 117 peptic ulcer patients in whom eradication of H. pylori was confirmed 1 year after eradication treatment both by histology and by rapid urease test. In total, 57 patients were available for the study procedures: 34(59.6%) male, 23(40.4%) female; mean age 52.3 ± 13.0 years. There were 45(78.9%) patients with duodenal ulcer and 12(21.1%) with gastric ulcer. H. pylori was diagnosed by a rapid urease test and histology if endoscopy was performed. If endoscopy was refused, H. pylori was diagnosed by the C14-urea breath test and serology. H. pylori was established if at least one of the tests was positive.RESULTS: The mean follow-up was 8.9 ± 1.0 years(range, 6-12). H. pylori was established in 15 patients. In 2 H. pylori-negative patients, H. pylori was established during the follow-up period and eradicated. Therefore, we consider that reinfection occurred in 17 patients. In the per protocol analysis, reinfection was established in 17 of 57(29.8%; 95%CI: 19.2-42.2) patients during the follow-up period. The annual rate of infection was 3.36%. If all non-responders were considered H. pylori-negative, reinfection would be 14.5%(17/117), the annual ratebeing 1.63%. The mean age of patients with reinfection was 51.8 ± 14.0 years, and without reinfection was 52.5 ± 13.0 years, P 0.05; the mean body mass index of patients with reinfection was 27.2 ± 4.1 kg/m2, and without reinfection was 25.7 ± 4.2 kg/m2, P 0.05. There were no differences in the reinfection rates according the location of the peptic ulcer, the eradication regimen used, and smoking status.CONCLUSION: The reinfection rate of H. pylori is relatively high in Lithuania and probably related to the high prevalence of H. pylori, what may reflect differences in the socioeconomic status between Western and Eastern European countries.     

Dramatic decline in prevalence of Helicobacter pylori and peptic ulcer disease in an endoscopy-referral population

Purpose

To determine if endoscopic Helicobacter pylori and peptic ulcer disease prevalence has changed over an 11-year period in a rural region.

Methods

Current endoscopic records were reviewed and compared with similar data obtained over a time period 11 years earlier at the same institution with regard to H. pylori status, endoscopic findings, microscopic pathologic findings, and medication use.

Results

There were 251 records reviewed in the current study group (mean age 52.8 years, 59.0% female) and 263 in the previous group (mean age 60.1 years, 56.7% female). H. pylori was positive in 17 (6.8%) in the current study and 173 (65.8%) in the earlier study (P <.0001). Peptic ulcer disease (PUD) was present in 14 (5.6%) in the current study and in 102 (38.8%) in the earlier study (P <.0001). H. pylori was positive in 1 of the 14 PUD patients (7.1%) in the current study and in 78 of 102 (76.5%) in the previous study (P <.0001).

Conclusions

Endoscopic H. pylori prevalence in our rural locality has decreased substantially over the past decade and may reflect local overall prevalence trends, although underestimation is likely due to widespread prior noninvasive H. pylori diagnosis and treatment. Endoscopic PUD also has decreased precipitously, possibly related to changes in regional H. pylori characteristics and prolific use of antisecretory agents. Changing geographic trends regarding acid-peptic disease may prompt modification of diagnostic approach and treatment.     

Role of Helicobacter pylori infection and nonsteroidal anti-inflammatory drug use in bleeding peptic ulcers in Japan

Background Helicobacter pylori infection and nonsteroidal anti-inflammatory drugs (NSAIDs) are well-known major causes of peptic ulcers. This study aimed to characterize the features of bleeding peptic ulcers in Japan. Methods This prospective study evaluated 116 patients revealed to have bleeding peptic ulcers from January 2000 to December 2002. Results Eighty-eight of the 116 patients (75.9%) had H. pylori infection. Seventy (60.3%) patients were positive for H. pylori with no history of NSAID use (group A), and 18 (15.5%) were positive for H. pylori with a history of NSAID use (group B). Among the H. pylori-negative patients, 15 (12.9%) were associated with NSAID use (group C). Thirteen (11.2%) patients had no H. pylori infection or history of NSAID use (group D). Among the 33 patients with a history of NSAID use, 11 were on-demand NSAID users and 14 took daily low-dose aspirin. The patients in groups B and C were significantly older that those in groups A and D, and they more frequently had coexisting diseases compared with group A. In group D, 11 patients had atrophic changes revealed by endoscopic examination, suggesting a past H. pylori infection, and these atrophic changes remained at the time of bleeding. Many of the patients in group D had serious comorbidity. Compared with healthy control subjects, the concentrations of both phosphatidylcholine and phosphatidylethanolamine were significantly decreased in the antral gastric mucosa in all patient groups. Conclusions NSAID use contributed to bleeding ulcers in 28.4% of patients; thus, low-dose aspirin or on-demand NSAID use may cause bleeding ulcers. There were only two (1.7%) confirmed cases of H. pylori-negative, non-NSAID ulcers.     

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.     

Membrane-bound mucins and mucin terminal glycans expression in idiopathic or Helicobacter pylori,NSAID associated peptic ulcers

AIM: To determine the expression of membrane-bound mucins and glycan side chain sialic acids in Helicobacter pylori (H. pylori)-associated, non-steroidal inflammatory drug (NSAID)-associated and idiopathic-gastric ulcers.METHODS: We studied a cohort of randomly selected patients with H. pylori (group 1, n = 30), NSAID (group 2, n = 18), combined H. pylori and NSAID associated gastric ulcers (group 3, n = 24), and patients with idiopathic gastric ulcers (group 4, n = 20). Immunohistochemistry for MUC1, MUC4, MUC17, and staining for Erythrina cristagalli agglutinin and Sambucus nigra agglutinin (SNA) lectins was performed on sections from the ulcer margins.RESULTS: Staining intensity of MUC17 was higher in H. pylori ulcers (group 1) than in idiopathic ulcers (group 4), 11.05 ± 3.67 vs 6.93 ± 4.00 for foveola cells, and 10.29 ± 4.67 vs 8.00 ± 3.48 for gland cells, respectively (P < 0.0001). In contrast, MUC1 expression was higher in group 4 compared group 1, 9.89 ± 4.17 vs 2.93 ± 5.13 in foveola cells and 7.63 ± 4.60 vs 2.57± 4.50 for glands, respectively (P < 0.0001). SNA lectin staining was increased in group 4, in parallel to elevated MUC1 expression, indicating more abundant α2-6 sialylation in that group.CONCLUSION: Cytoplasmic MUC17 staining was significantly decreased in the cases with idiopathic ulcer. The opposite was observed for both MUC1 and SNA lectin. This observation may reflect important pathogenic mechanisms, since different mucins with altered sialylation patterns may differ in their protection efficiency against acid and pepsin.     

Optimal initiation of Helicobacter pylori eradication in patients with peptic ulcer bleeding

AIM:To evaluate when Helicobacter pylori(H.pylori)eradication therapy(ET)should be started in patients with peptic ulcer bleeding(PUB).METHODS:Clinical data concerning adults hospitalizedwith PUB were retrospectively collected and analyzed.Age,sex,type and stage of peptic ulcer,whether endoscopic therapy was performed or not,methods of H.pylori detection,duration of hospitalization,and specialty of the attending physician were investigated.Factors influencing the confirmation of H.pylori infection prior to discharge were determined using multiple logistic regression analysis.The H.pylori eradication rates of patients who received ET during hospitalization and those who commenced ET as outpatients were compared.RESULTS:A total of 232 patients with PUB were evaluated for H.pylori infection by histology and/or rapid urease testing.Of these patients,53.7%(127/232)had confirmed results of H.pylori infection prior to discharge.In multivariate analysis,duration of hospitalization and ulcer stage were factors independently influencing whether H.pylori infection was confirmed before or after discharge.Among the patients discharged before confirmation of H.pylori infection,13.3%(14/105)were lost to follow-up.Among the patients found to be H.pylori-positive after discharge,41.4%(12/29)did not receive ET.There was no significant difference in the H.pylori eradication rate between patients who received ET during hospitalization a n d t h o s e w h o c o m m e n c e d E T a s o u t p a t i e n t s[intention-to-treat:68.8%(53/77)vs 60%(12/20),P=0.594;per-protocol:82.8%(53/64)vs 80%(12/15),P=0.723].CONCLUSION:Because many patients with PUB who were discharged before H.pylori infection status was confirmed lost an opportunity to receive ET,we should confirm H.pylori infection and start ET prior to discharge.     

Antigastric autoantibodies in Helicobacter pylori infection: implications of histological and clinical parameters of gastritis

Background—It has recently been shown thathumoral antigastric autoreactivities occur in a substantial number ofHelicobacter pylori infected patients.
Aims—To analyse the relevance of such antigastricautoantibodies for histological and serological parameters of theinfection as well as for the clinical course.
Methods—Gastric biopsy samples and sera from 126 patients with upper abdominal complaints were investigated for evidenceof H pylori infection using histology and serology.Autoantibodies against epitopes in human gastric mucosa were detectedby immunohistochemical techniques. Histological and clinical findingsof all patients were then correlated with the detection of antigastric autoantibodies.
Results—H pylori infection wassignificantly associated with antigastric autoantibodies reactive withthe luminal membrane of the foveolar epithelium and with canalicularstructures within parietal cells. The presence of the latterautoantibodies was significantly correlated with the severity of bodygastritis, gastric mucosa atrophy, elevated fasting gastrinconcentrations, and a decreased ratio of serum pepsinogen I:II.Furthermore the presence of anticanalicular autoantibodies wasassociated with a greater than twofold reduced prevalence for duodenal ulcer.
Conclusion—The data indicate that antigastricautoantibodies play a role in the pathogenesis and outcome of Hpylori gastritis, in particular in the development of gastricmucosal atrophy.

Keywords:gastritis; Helicobacter pylori; autoimmunity; gastric atrophy

     

Helicobacter pylori eradication in the management of patients with idiopathic thrombocytopenic purpura

PURPOSE: To investigate the relation between Helicobacter pylori infection and the clinical features of idiopathic thrombocytopenic purpura (ITP), and to examine the effects of H. pylori eradication on platelet counts. METHODS: A(13)C urea breath test for H. pylori infection was performed in a cohort of 137 consecutive patients with ITP. Patients who tested positive received standard eradication therapy if their platelet count was <50 x 10(9)/L or if they had symptoms of dyspepsia. RESULTS: H. pylori infection was detected in 64 patients (47%), and was not associated with dyspepsia or other clinical or laboratory features. Eradication therapy was successfully administered to 52 patients. Platelet responses were observed in 17 (33%) of these patients, which lasted for more than 1 year in 11 patients. Duration of ITP was shorter among responders than nonresponders. Only one response was observed among patients with severe thrombocytopenia (platelet count <30 x 10(9)/L). CONCLUSION: The prevalence of H. pylori infection in patients with ITP is similar to that found in the general population. Infection is not associated with distinctive features of the disease. H. pylori eradication may improve the platelet counts in adults in whom the ITP is of recent onset and in those with less severe degrees of thrombocytopenia, but was not effective in patients with chronic severe ITP.     

Low prevalence of idiopathic peptic ulcer disease: An Italian endoscopic survey

Background

Peptic ulcer disease (PUD) represents a common condition, although its incidence is decreasing. Previous studies reported a high rate of idiopathic PUD prevalence.

Aim

To investigate prevalence, relative distribution of etiologic factors and prevalence of complication of PUD in an Italian endoscopic series.

Materials and methods

All gastroscopies performed in adult patients during 3 years were considered. Patients with PUD, with antral and corporal histology, were included in the study. Helicobacter pylori infection was assessed by histology. Idiopathic PUD was defined as an ulcer without evidence H. pylori infection or prior exposure to NSAIDs.

Results

300 patients with PUD out of 11,148 gastroscopies were included in our study accounting for a prevalence of 2.7%. H. pylori-associated PUD was diagnosed in 62.3%, NSAID/aspirin-associated PUD in 22%, H. pylori/NSAID/aspirin-associated PUD in 11.6%, and idiopathic PUD in the remaining 4% of cases. Regarding ulcer complications the logistic regression analysis identified the following significant risk factors for GI bleeding: NSAIDs and/or aspirin use, age >65 years and coexistent gastric and duodenal ulcers.

Conclusion

Our data found a low endoscopic prevalence of peptic ulcer. Both H. pylori infection and NSAIDs and/or aspirin use remain the main determinants and idiopathic ulcer prevalence is very low.     

Association of Helicobacter pylori babA2 with peptic ulcer disease and gastric cancer

AIM: To investigate the association between babA2 gene and peptic ulcer disease (PUD) and gastric cancer (GC) in Helicobacter pylori -infected populations. METHODS: We evaluated the relationship between babA2 and clinical outcomes (PUD and GC) using a meta-analysis. A literature search was performed using the PubMed and Web of Science databases for relevant case-control studies that met the defined inclusion criteria. The ORs and 95%CIs were calculated to estimate the association between babA2 genotype and clinical outcomes. A fixed-effect or random-effect model was performed depending on the absence or presence of significant heterogeneity. RESULTS: A total of 25 articles with 38 studies met the inclusion criteria and were finally included in this metaanalysis. The results showed that the babA2 genotype was significantly associated with an increased risk of PUD (OR = 2.069, 95%CI: 1.530-2.794, P < 0.001) and especially in the subgroup of duodenal ulcer (OR = 1.588, 95%CI: 1.141-2.209, P = 0.006). Moreover, a significant association between babA2 gene and PUD and duodenal ulcer (OR = 2.739, 95%CI: 1.860-4.032, P < 0.001; OR = 2.239, 95%CI: 1.468-3.415, P < 0.001, respectively) was observed in western countries but not in Asian countries. CONCLUSION: We demonstrated that the presence of babA2 may be associated with increased risks for PUD, especially duodenal ulcer, in western countries.     

Role ofHelicobacter pylori in cirrhotic patients with peptic ulcer

Helicobacter pylori was found to be a promoter factor of peptic ulcer that has an incidence higher in patients with hepatic cirrhosis. To clarify the role betweenH. pylori and peptic ulcer in patients with hepatic cirrhosis, a serological test (ELISA test, HEL-p, AMRAD, Australia), was used to measure the presence ofH. pylori of patients with hepatic cirrhosis. Within two years, 108 cirrhotic patients who had received a panendoscopic examination were enrolled in this study. There were 79 males and 27 females with a mean age of 53.2 years. Sixty-four cases had positive serum HBsAg and 44 had negative serum. The results showed that the prevalence ofHelicobacter pylori in cirrhosis was 43.5% (47/108). There was no difference of HEL-p-positive rate between peptic ulcer and normal gastroduodenal mucosa (45.2% vs 46.1%,P>0.05). According to this study, there appears to be no relation between peptic ulcer andH. pylori in patients with hepatic cirrhosis. The etiology of peptic ulcer in cirrhotic patients need further study.     

The prevalence of <Emphasis Type="Italic">Helicobacter pylori</Emphasis> in Japanese children with gastritis or peptic ulcer disease

Background Although Helicobacter pylori infection is typically acquired in childhood, the role of H. pylori infection in gastroduodenal diseases in childhood remains to be defined. The purpose of this study was to evaluate the prevalence of H. pylori infection in children with gastritis, duodenal ulcer, and gastric ulcer.Methods This was a retrospective analysis of 283 Japanese children (mean age, 11.5 years) with non-nodular gastritis (n = 73), nodular gastritis (n = 67), duodenal ulcer (n = 100), and gastric ulcer (n = 43). H. pylori status was based on biopsy tests. Clinical symptoms at the time of endoscopy were analyzed with regard to a possible association with the infection.Results The prevalence of H. pylori in non-nodular gastritis, nodular gastritis, duodenal ulcer, and gastric ulcer was 28.8%, 98.5%, 83.0%, and 44.2%, respectively. H. pylori was significantly linked to duodenal ulcer and gastric ulcers in the age group of 10–16 years, but not in the age group of 9 years and under. In children with H. pylori infection, nodular gastritis was observed in 26.3% of gastric ulcer patients and in 74.7% of duodenal ulcer patients (P < 0.001). H. pylori infection was significantly associated with the prevalence of anemia (P < 0.05).Conclusions H. pylori is the most important causal factor for the development of duodenal ulcer in childhood. While H. pylori infection appears to be a risk factor in gastric ulcer, other causes are responsible for most cases. Nodular gastritis is the most common type of H. pylori gastritis in childhood. Chronic infection with H. pylori is associated with anemia.     

广州胃病患者幽门螺杆菌多株感染的研究

目的了解我国Ｈｐ感染人群中的多株感染状况．方法取因上腹不适行内镜检查的２０例Ｈｐ阳性患者（胃溃疡６例,十二指肠溃疡８例,慢性胃炎６例）的胃窦和胃体粘膜组织,进行Ｈｐ培养．初代培养后,分别取胃窦和胃体各１０个菌落进行传代,抽提各菌落ＤＮＡ,应用聚合酶链反应随机引物扩增的ＤＮＡ多态指模技术［ＲＡＰＤＰＣＲ］进行菌株鉴定．结果ＰＣＲ扩增产物电泳分析显示有１８例患者胃窦和胃体的ＨｐＤＮＡ指模一致,提示这１８例患者均是单株感染;另有２例胃体菌株表现为两种指模形态,提示为２株Ｈｐ感染．结论广州地区存在Ｈｐ多株感染,但不普遍．     

Atrophic gastritis and Helicobacter pylori infection in outpatients referred for gastroscopy

BACKGROUND: Atrophic gastritis has been shown to be one of the long term sequelae of Helicobacter pylori infection. AIMS: To determine the prevalence of atrophic gastritis in outpatients, to study the accuracy of serological methods for revealing atrophy, and to define the association of H pylori infection with atrophic gastritis in these patients. PATIENTS/METHODS: A total of 207 consecutive outpatients referred for gastroscopy were included. Biopsy specimens from the antrum and corpus were assessed histologically according to the Sydney system. Serum samples were studied for H pylori IgG and IgA antibodies by enzyme immunoassay, CagA antibodies by immunoblot, pepsinogen I by an immunoenzymometric assay, gastrin by radioimmunoassay, and parietal cell antibodies by indirect immunofluorescence. RESULTS: Histological examination revealed atrophic gastritis in 52 (25%) of 207 patients. H pylori and CagA antibodies were strongly associated with atrophic antral gastritis but poorly associated with atrophic corpus gastritis. Low serum pepsinogen I was the most sensitive and specific indicator of moderate and severe atrophic corpus gastritis. All six patients with moderate atrophic corpus gastritis had H pylori infection but eight of 10 patients with severe atrophic corpus had increased parietal cell antibodies and nine had no signs of H pylori infection. CONCLUSIONS: Atrophic antral gastritis was strongly associated with CagA positive H pylori infection. Severe atrophic corpus gastritis was not determined by H pylori tests but low serum pepsinogen I, high gastrin, and parietal cell antibodies may be valuable in detecting these changes.     

Ethnicity association of Helicobacter pylori virulence genotype and metronidazole susceptibility

AIM:To characterise the cag pathogenicity island in Helicobacter pylori(H.pylori) isolates by analysing the strains’ vacA alleles and metronidazole susceptibilities in light of patient ethnicity and clinical outcome.METHODS:Ninety-five H.pylori clinical isolates obtained from patients with dyspepsia living in Malaysia were analysed in this study.Six genes in the cagPAI region(cagE,cagM,cagT,cag13,cag10 and cag67) andvacA alleles of theH.pylori isolates were identified by polymerase chain reaction.The isolates’ metronidazole susceptibility was also determined using the E-test method,and the resistant gene was characterised by sequencing.RESULTS:More than 90% of the tested isolates had at least one gene in the cagPAI region,and cag67 was predominantly detected in the strains isolated from the Chinese patients,compared with the Malay and Indian patients(P < 0.0001).The majority of the isolates(88%) exhibited partial deletion(rearrangement) in the cagPAI region,with nineteen different patterns observed.Strains with intact or deleted cagPAI regions were detected in 3.2% and 8.4% of isolates,respectively.The prevalence of vacA s1m1 was significantly higher in the Malay and Indian isolates,whereas the isolates from the Chinese patients were predominantly genotyped as vacA s1m2(P = 0.018).Additionally,the isolates from the Chinese patients were more sensitive to metronidazole than the isolates from the Malay and Indian patients(P = 0.047).Although we attempted to relate the cagPAI genotypes,vacA alleles and metronidazole susceptibilities to disease outcome,no association was observed.The vacA alleles were distributed evenly among the strains with intact,partially deleted or deleted cagPAI regions.Interestingly,the strains exhibiting an intact cagPAI region were sensitive to metronidazole,whereas the strains with a deleted cagPAI were more resistant.CONCLUSION:Successful colonisation by different H.pylori genotypes is dependent on the host’s genetic makeup and may play an important role in the clinical outcome.     

Smoking increases the treatment failure for Helicobacter pylori eradication

Purpose

Treatment failure for Helicobacter pylori (H. pylori) eradication is encountered in approximately 10-20% of patients, and many studies have pointed to a link with smoking. To investigate the effects of smoking on eradication outcome, we performed a meta-analysis.

Methods

A PubMed search was performed to retrieve articles published up to August 2005. Pooled odds ratio (OR) and differences rate for H. pylori eradication failure in smokers compared with nonsmokers were used as summary statistics. Meta-regression was used for examining the source of heterogeneity.

Results

Twenty-two published studies (5538 patients), which provided information on eradication failure according to smoking status, were included in the analysis. The summary OR for eradication failure among smokers relative to nonsmokers was 1.95 (95% confidence interval [CI]: 1.55-2.45; P <.01). It corresponds with the differences in eradication rates between smokers and nonsmokers (8.4% [95% CI: 3.3-13.5%, P <.01]). Meta-regression analysis demonstrated that a high proportion of nonulcer dyspepsia patients in studies revealed a higher failure rate among smokers, compared with a low proportion of nonulcer dyspepsia.

Conclusions

Our meta-analysis demonstrated that smoking increases the treatment failure rate for H. pylori eradication.     

Helicobacter pylori is killed by nitrite under acidic conditions

Background—Due to the expression of urease,Helicobacter pylori is able to establish itself in the humanstomach under acidic conditions. A novel host defence mechanism wasrecently proposed, suggesting that the formation of salivary nitrite insymbiosis with facultative anaerobic bacteria in the oropharynx, isaimed at enhancing the antimicrobial activity of gastric juice.
Aims—To investigate whether the addition ofnitrite in physiological concentrations influences the resistance ofH pylori to acid.
Methods—H pylori cultured from freshgastric biopsy specimens was exposed for 30 minutes to normal salineand to HCl/KCl buffer (0.2M) at pH 2 with urea (5 mM) added. Theinfluence of potassium nitrite (50-1000 µmol/l) on bacterialsurvival was determined.
Results—Addition of nitrite (1 mM) to acidicsolutions (pH 2) resulted in complete kill of H pyloriwithin 30 minutes exposure time whereas acid alone allowed the organismto survive (p<0.001). The antimicrobial effect of nitrite at pH 2 against H pylori was dose dependent and complete kill oforganisms occurred at concentrations 500 µmol/l.
Conclusion—Acidified nitrite has antibacterialactivity against H pylori. This should prompt furtherresearch into the effect of salivary nitrite on the survival of Hpylori in the human stomach.

Keywords:nitrite; Helicobacter pylori; acidicconditions

     

Ultrastructural observation of Helicobacter pylori to the gastric epithelia in chronic gastritis and peptic ulcers

AIM: The relationship between Helicobacter pylori (Hp) and gastric epithelia in chronic gastritis and in peptic ulcers was studied by transmission electron microscopy (TEM). METHODS: Seventy-five patients were screened for Hp. Gastric antral biopsy specimens were fixed in glutaraldehyde and treated with tannic acid before OsO₄ staining. Samples were routinely processed for TEM studies (at least four semi-thin sections oriented for ultrathin sections in each sample). RESULTS: The bacilli were detected by TEM within the gastric mucosa in 53 of 55 patients infected with Hp. Ultrathin sections revealed clear glycocalyx by which the bacillus was connected to the epithelium. As the bacilli colonized, the adjacent mucous cells degenerated. They were characterized by erosion of the juxtaluminal cytoplasm, vacuolation or blebbing, and desquamation of the cell membrane. The bacilli located in the lumen attracted neutrophils, which migrated into intercellular space of the epithelia or into the lumen to begin phagocytosis of Hp. CONCLUSION: The sensitivity and specificity of TEM diagnosis is 96% and 95%, respectively. Tannic acid is suitable for the preservation of the glycocalyx of a cell. The colonized bacilli, usually with the wide periplasm, contributed to the degeneration of epithelia, including mucous neck cells. If Hp infection persists, the degeneration and regeneration of mucous neck cells occurs alternatively. Ultimately the generative stem cells were damaged, and as a result chronic atrophic gastritis could occur.     

Analysis of Helicobacter pylori vacA Gene and Serum Antibodies to VacA in Japan

Vacuolating cytotoxin, VacA, is one of the most important pathogenetic factors produced by Helicobacter pylori. However, it is not clear whether the diversity in disease outcome may be ascribed to variations in strain and/or to the host responses to virulence factors. In this study, we analyzed the vacA middle region sequence among 65 Japanese isolates to clarify the variation in strain and assayed antibody titer to VacA by ELISA using purified VacA to evaluate the host response to cytotoxin. The nucleotide sequence identities compared among Japanese isolates were 92.8 ± 3.56%, and compared to 88.3 ± 2.89% in tox⁺ strains reported in GenBank. Positive correlation was found between the antibody titers and the severity of atrophic change of the stomach. In Japan the nucleotide sequences of the vacA middle region were highly homologous and genetically closer to tox⁺ strains. Antibody titers and host response to cytotoxin may be associated with atrophy of the stomach.