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

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

Helicobacter pylori: the primary cause of duodenal ulceration or a secondary infection?

INTRODUCTIONIt is generally accepted that Helicobacter pylori ( H.pylori) infection has a role in duodenal ulceration .Eradicaton of H .pylori accelerates healing compared with placebo in the absence of control of gastric secretion and reduces ulcer recurrence .There is increasing evidence ,however ,that is may not be the primary cause of duodenal ulceration ,but that is may be a secondary factor in a nnmber of cases .This possibility is supported by four sets of observations : 1 Geographical distribution:

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

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

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

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

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

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

Effect of Xiaokuiling Prescription on the Expression of HSP_(72) , HSP B in Gastric Mucosa of Patients with Helicobacter Pylori associated Duodenal Ulcer

In order to investigate the mechanism of Xiaokuiling prescription (XKL) in the treatment of Helicobacter pylori (HP) associated duodenal ulcer (DU) and the pathophysiologic role of heat shock proteins (HSPs) in the healing of ulcer, the expression of HSP 72 and HSP B in gastric mucosa was detected by using SABC immunohistochemistry method and processed by micro image analysis system. The method of Western blotting was used to measure the contents of HSP 72 and HSP B in the tissue emulsion of gastric mucosa. The results were as follows: (1) HSP 72 expression of the gastric mucosa in the treated group was obviously increased as compared with that in the control group ( P <0.05); (2) HSP B expression of the gastric mucosa in the treated group was significantly decreased as compared with that in the control group ( P <0.01). It was suggested that the increased expression of HSP 72 and the elimination of HP might be related to the mechanism of action of XKL. HSPs might play an pathological and physiological role in the process of healing of gastric ulcer.

Patients with Helicobacter pylori positive and negative duodenal ulcers have distinct clinical characteristics

AIM: To assess the clinical characteristics of Helicobacterpylori(H pylori) negative duodenal ulcer.METHODS: Patients with an endoscopic diagnosis of duodenal ulcer between 1996 and 2002 were included in the present study. Patients were considered to be negative for Hpylori, if both histological examination and rapid urease test of biopsy specimens were negative. A comparison was made between patients with H pyloripositive and negative duodenal ulcers.RESULTS: A total of 1 343 patients were studied. Their mean age was 54.7±0.5 years. There was a male preponderance (M:F = 2.5:1). Three hundred and ninetyeight patients (29.6%) did not have H pylori infection. The annual proportion of patients with H pylori negative duodenal ulcers increased progressively from 1996 to2002. On multivariate analysis, patients with H pylorinegative duodenal ulcer were more likely to be older, have concomitant medical problem, pre-existing malignancy, recent surgery, underlying sepsis, or taken non-steroidal anti-inflammatory drugs. In terms of clinical presentations, patients with H pylori negative duodenal ulcer were more likely to present with bleeding, multiple ulcers and larger ulcers.CONCLUSION: The proportion of patients with H pylori negative duodenal ulcers is on the rise because of a continued drop in incidence of H pylori positive duodenalulcers in recent years. Such patients have distinct clinical characteristics and it is important to ascertain the H pylori status before starting eradication therapy.

Helicobacterpylori virulence factors in duodenal ulceration:A primary cause or a secondary infection causing chronicity

Reports from countries with a high prevalence of Helicobacter pylori （H pylori） infection do not show a proportionately high prevalence of duodenal ulceration, suggesting the possibility that H pylori cannot be a primary cause of duodenal ulceration. It has been mooted that this discrepancy might be explained by variations in the prevalence of virulence factors in different populations. The aim of this paper is to determine whether the published literature gives support to this possibility. The relevant literature was reviewed and analyzed separately for countries with a high and low prevalence of Hpylori infection and virulence factors. Although virulent strains of Hpylori were significantly more often present in patients with duodenal ulcer than without the disease in countries with a low prevalence of H pylori infection in the population, there was no difference in the prevalence of virulence factors between duodenal ulcer, nonulcer dyspepsia or normal subjects in many countries, where the prevalence of both Hpylori infection and of virulence factors was high. In these countries, the presence of virulence factors was not predictive the clinical outcome. To explain the association between virulence factors and duodenal ulcer in countries where H pylori prevalence is low, only two papers were found that give little support to the usual model proposed, namely that organisms with the virulence factors are more likely than those without them to initiate a duodenal ulcer. We offer an alternative hypothesis that suggests virulence factors are more likely to interfere with the healing of a previously produced ulcer. The presence of virulence factors only correlates with the prevalence of duodenal ulcer in countries where the prevalence of H pylori is low. There is very little evidence that virulence factors initiate duodenal ulceration, but they may be related to failure of the ulcer to heal.

Response of blood endothelin-1 and nitric oxide activity in duodenal ulcer patients undergoing Helicobacter pylori eradication

AIM: To investigate the effect of Helicobacter pylori eradication on endothelin-1 (ET-1) and nitric oxide (NO) in duodenal ulcer (DU) patients. METHODS: Sixty-six Hpylori-infected active DU patients were consecutively enrolled to receive one-week triple therapy (rabeprazole, amoxicillin and metronidazole) and then one-month rabeprazole therapy. They were asked back to determine ulcer and Hpylori status using endoscopy one month later. Thirty-seven healthy controls (H pylori +/-:17/20) were enrolled for comparison. Blood samples were collected in each visit to measure plasma ET-1 and nitrate/nitrite levels using an enzyme immunoassay kit. RESULTS: Sixty DU patients finished trial per protocol. The ulcer healing and Hpylori-eradication rates were 86.7% and 83.3%, respectively. Plasma ET-1 level in DU patients was higher than that of Hpylori-negative and positive controls (3.59±0.96 vs0.89±0.54 vs0.3±0.2 pg/mL,P<0.01), while nitrate/nitrite levels among them were also significantly different (8.55±0.71 vs5.27±0.68 vs 6.39±0.92 μmol/L, P<0.05). H pylori eradication diminished ET-1 levels (3.64±0.55 vs2.64±0.55 pg/mL, P<0.01) but elevated nitrate/ nitrite level (8.16±0.84 vs11.41±1.42 umol/L,P<0.05). CONCLUSION: Both plasma ET-1 and nitrate/nitrite levels increase in active DU patients. After an effective H pylori eradication, DU healing is associated with diminished blood ET-1 level and elevated nitrate/nitrite level.

Helicobacter pylori infection in bleeding peptic ulcer patients after non-steroidal antiinflammatory drug consumption

AIM： TO establish the prevalence of He/icobacterpy/on （H. pylori） infection in patients with a bleeding peptic ulcer after consumption of non-steroidal antiinflammatory drugs （NSAIDs）.METHODS： A very early upper endoscopy was performed to find the source of upper gastrointestinal bleeding and to take biopsy specimens for analysis of H. pylori infection by the rapid urease （CLO） test, his- tological examination, and bacterial culture. TgG anti- CagA were also sought. The gold standard for identifying H. pylori infection was positive culture of biopsy specimens or contemporary positivity of the CLO test and the presence of H. pylori on tissue sections.RESULTS： Eighty patients, 61 males （76.3%）, mean age 61.2 ~ 15.9 years, were consecutively enrolled. Forty-seven （58.8%） patients occasionally consumed NSAIDs, while 33 （41.3%） were on chronic treatment with low-dose aspirin （LD ASA）. Forty-four （55.0%） patients were considered infected by H. pylori. The infection rate was not different between patients who occasionally or chronically consumed NSAIDs. The culture of biopsy specimens had a sensitivity of 86.4% and a specificity of 100%; corresponding figures for histological analysis were 65.9% and 77.8%, for the CLO test were 68.2% and 75%, for the combined use of histology and the CLO test were 56.8% and 100%, and for IgG anti-CagA were 90% and 98%. The high- est accuracy （92.5%） was obtained with the culture of biopsy specimens.CONCLUSION： Patients with a bleeding peptic ulcer after NSAID/LD ASA consumption frequently have H. pylori infection. Biopsy specimen culture after an early upper gastrointestinal tract endoscopy seems the most efficient test to detect this infection.

Detection of anti-Helicobacter pyloriantibodies in serum and duodenal fluid in peptic gastroduodenal disease

AIM:To study the diagnosis of Helicobacter pylori(H pylori) infection through the determination of serum levels of anti- H pylori IgG and IgA antibodies,and the levels of anti-H pylori IgA antibodies in duodenal fluid. METHODS:Data were collected from 93 patients submitted to upper digestive endoscopy due to dyspeptic symptoms. The patients were either negative(group A)or positive (group B)to H pylori by means of both histological detection and urease tests.Before endoscopy,peripheral blood was collected for the investigation of anti-H pylori IgG and IgA antibodies.To perform the urease test,biopsies were obtained from the gastric antrum.For the histological evaluation,biopsies were collected from the gastric antrum (greater and lesser curvatures)and the gastric body. Following this,duodenal fluid was collected from the first and second portions of the duodenum.For the serological assaying of anti-Hpylori IgG and IgA,and anti-Hpylori IgA in duodenal fluids,the ELISA method was utilized. RESULTS:The concentration of serum IgG showed sensitivity of 64.0%,specificity of 83.7%,positive predictive value of 82.0%,negative predictive value of 66.6% and accuracy of 73.1% for the diagnosis of H pylori infection.For the same purpose,serum IgA showed sensitivity of 72.0%, specificity of 65.9%,positive predictive value of 72.0%, negative predictive value of 67.4% and accuracy of 69.8%. If the serological tests were considered together,i.e.when both were positive or negative,the accuracy was 80.0%, sensitivity was 86.6%,specificity was 74.2%,positive predictive value was 74.2% and negative predictive value was 86.6%.When values obtained in the test for detecting IgA in the duodenal fluid were analyzed,no significant difference(P=0.43)was observed between the values obtained from patients with or without H pylori infection. CONCLUSION:The results of serum IgG and IgA tests for H pylori detection when used simultaneously,are more efficient in accuracy,sensitivity and negative predictive value, than those when used alone.The concentration of IgA antibodies in duodenal fluid is not useful in identifying patients with or without H pylori.

Helicobacter Pylori Infection: Epidemiological, Clinical and Endoscopic Aspects in Brazzaville

Introduction: Helicobacter pylori infection is a real health problem worldwide. It is the most common chronic bacterial infection in the world, and is particularly prevalent in developing countries. Objective: To determine the frequency of Helicobacter pylori infection and to study the epidemiological, clinical and endoscopic characteristics associated with this infection in Brazzaville. Patients and Methods: This was a descriptive cross-sectional study conducted from January to November 2020, i.e. 11 months. This work focused on 100 symptomatic patients over 18 years old referred for upper GI endoscopy. Gastric biopsies for biological study by urease test and molecular study by real time PCR technique were taken. Results: With a mean age of 46.32 ± 15.20 years, the frequency of Hp infection was 91%, with a female predominance of 53%. The sex ratio was 0.92. The average age was 46.32 ± 15.20 years. Carriage of the infection was more important in households with more than 3 persons, in patients consuming public tap water and in those using both types of sanitary facilities. Endoscopy was indicated for epigastralgia in 93.1% of cases. About 56.14% of the infected patients had normal mucosa versus 12.28% with ulcerated lesions and 22.81% with gastritis. Conclusion: The prevalence of Helicobacter pylori infection is significant in Congo, justifying early detection in order to improve management.

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.

To be or not to be:The host genetic factor and beyond in Helicobacter pylori mediated gastro-duodenal diseases

Helicobacter pylori(H.pylori)have long been associated with a spectrum of disease outcomes in the gastroduodenal system.Heterogeneity in bacterial virulence factors or strains is not enough to explain the divergent disease phenotypes manifested by the infection.This review focuses on host genetic factors that are involved during infection and eventually are thought to influence the disease phenotype.We have summarizedthe different host genes that have been investigated for association studies in H.pylori mediated duodenal ulcer or gastric cancer.We discuss that as the bacteria co-evolved with the host;these host gene also show much variation across different ethnic population.We illustrate the allelic distribution of interleukin-1B,across different population which is one of the most popular candidate gene studied with respect to H.pylori infections.Further,we highlight that several polymorphisms in the pathway gene can by itself or collectively affect the acid secretion pathway axis(gastrin:somatostatin)thereby resulting in a spectrum of disease

Clinical characteristics of Helicobacter pylori-negative drugnegative peptic ulcer bleeding

AIM:To investigate the clinical characteristics and outcomes of idiopathic Helicobacter pylori(H.pylori)-negative and drug-negative]peptic ulcer bleeding(PUB).METHODS:A consecutive series of patients who experienced PUB between 2006 and 2012 was retrospectively analyzed.A total of 232 patients were enrolled in this study.The patients were divided into four groups according to the etiologies of PUB:idiopathic,H.pylori-associated,drug-induced and combined(H.pylori-associated and drug-induced)types.We compared the clinical characteristics and outcomes between the groups.When the silver stain or rapid urease tests were H.pylori-negative,we obtained an additional biopsy specimen by endoscopic re-examination and performed an H.pylori antibody test 6-8 wk after the initial endoscopic examination.For a diagnosis of idiopathic PUB,a negative result of an H.pylori antibody test was confirmed.In all cases,re-bleeding was confirmed by endoscopic examination.For the risk assessment,the Blatchford and the Rockall scores were calculated for all patients.RESULTS:For PUB,the frequency of H.pylori infection was 59.5%(138/232),whereas the frequency of idiopathic cases was 8.6%(20/232).When idiopathic PUB was compared to H.pylori-associated PUB,the idiopathic PUB group showed a higher rate of rebleeding after initial hemostasis during the hospital stay(30%vs 7.4%,P = 0.02).When idiopathic PUB was compared to drug-induced PUB,the patients in the idiopathic PUB group showed a higher rate of rebleeding after initial hemostasis upon admission(30%vs 2.7%,P < 0.01).When drug-induced PUB was compared to H.pylori-associated PUB,the patients in the drug-induced PUB were older(68.49 ± 14.76 years vs 47.83 ± 15.15 years,P< 0.01) and showed a higher proportion of gastric ulcer(77%vs 49%,P < 0.01).However,the Blatchford and the Rockall scores were not significantly different between the two groups.Among the patients who experienced drug-induced PUB,no significant differences were found with respect to clinical characteristics,irrespective of H.pylori infection.CONCLUSION:Idiopathic PUB has unique clinical characteristics such as re-bleeding after initial hemostasis upon admission.Therefore,these patients need to undergo close surveillance upon admission.

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.

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.

Does Helicobacter pylori eradication therapy for peptic ulcer prevent gastric cancer?

AIM:To investigate the effects of Helicobacter pylori (H pylori)eradication therapy for treatment of peptic ulcer on the incidence of gastric cancer. METHODS:A multicenter prospective cohort study was conducted between November 2000 and December 2007 in Yamagata Prefecture,Japan.The study included patients with H pylori-positive peptic ulcer who decided themselves whether to receive H pylori eradication(eradication group)or conventional antacid therapy(non-eradication group).Incidence of gastric cancer in the two groups was determined based on the results of annual endoscopy and questionnaire surveys,as well as Yamagata Prefectural Cancer Registry data,and was compared between the two groups and by results of H pylori therapy.RESULTS:A total of 4133 patients aged between 13 and 91 years(mean 52.9 years)were registered,and 56 cases of gastric cancer were identified over a mean follow-up of 5.6 years.The sex-and age-adjusted incidence ratio of gastric cancer in the eradication group, as compared with the non-eradication group,was 0.58 (95%CI:0.28-1.19)and ratios by follow-up period(<1 year,1-3 years,>3 years)were 1.16(0.27-5.00),0.50 (0.17-1.49),and 0.34(0.09-1.28),respectively.Longer follow-up tended to be associated with better prevention of gastric cancer,although not to a significant extent.No significant difference in incidence of gastric cancer was observed between patients with successful eradication therapy(32/2451 patients,1.31%)and those with treatment failure(11/639 patients,1.72%).Among patients with duodenal ulcer,which is known to be more prevalent in younger individuals,the incidence of gastric cancer was significantly less in those with successful eradication therapy(2/845 patients,0.24%)than in those with treatment failure(3/216 patients,1.39%). CONCLUSION:H pylori eradication therapy for peptic ulcer patients with a mean age of 52.9 years at registration did not significantly decrease the incidence of gastric cancer.

High rate of Helicobacter pylori reinfection in Lithuanianpeptic 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.

Helicobacter pylori may be an initiating factor in newly diagnosed ulcerative colitis patients: A pilot study

AIM To directly visualize Helicobacter pylori(H. pylori) by the highly sensitive and specific technique of immunohistochemical staining in colonic tissue from patients newly diagnosed with ulcerative colitis(UC).METHODS Colonoscopic biopsies from thirty patients with newly diagnosed UC and thirty controls were stained with Giemsa stain and immunohistochemical stain for detection of H. pylori in the colonic tissue. Results were confirmed by testing H. pylori Ag in the stool then infected patients were randomized to receive either anti H. pylori treatment or placebo.RESULTS Twelve/30(40%) of the UC patients were positive for H. pylori by Giemsa, and 17/30(56.6%) by immunohistochemistry stain. Among the control group 4/30(13.3%) and 6/30(20 %) were positive for H. pylori by Giemsa and immunohistochemistry staining respectively. H. pylori was significantly higher in UC than in controls(P = 0.04 and 0.007). All Giemsa positive patients and controls were positive by immunohistochemical stain. Four cases of the control group positive for H. pylori also showed microscopic features consistent with early UC.CONCLUSION H. pylori can be detected in colonic mucosa of patients with UC and patients with histological superficial ulcerations and mild infiltration consistent with early UC. There seems to be an association between UC and presence of H. pylori in the colonic tissue. Whether this is a causal relationship or not remains to be discovered.