Pylori IgG Antibodies Research Articles

Non-invasive diagnosis of H pylori infection: Evaluation of serological tests with and without current infection marker CIM

To evaluate the performance of commercially available immunochromatographic (ICT) and immunoblot tests covering the current infection marker CIM and conventional ELISA for the diagnosis of H pylori infection in adult dyspeptic patients. Consecutive non-treated dyspeptic patients undergoing diagnostic endoscopy were tested for H pylori infection by culture, rapid urease test, and histology of gastric biopsy specimens. Serum from 61 H pylori infected and 21 non-infected patients were tested for anti-H pylori IgG antibodies by commercial ELISA (AccuBind ELISA, Monobind, USA), ICT (Assure H pylori Rapid Test, Genelabs Diagnostics, Singapore), and immunoblot (Helico Blot 2.1, Genelabs Diagnostics, Singapore) assays. ICT and immunoblot kits cover CIM among other parameters and their performance with and without CIM was evaluated separately. Sensitivity, specificity, positive predictive value (PPV), negative predictive value (NPV), and accuracy of ELISA were 96.7%, 42.8%, 83.1%, 81.8%, and 82.9%, of ICT were 90.1%, 80.9%, 93.2%, 73.9%, and 87.8%, of ICT with CIM were 88.5%, 90.4%, 96.4%, 73.0%, and 89.0%, of immunoblot were 98.3%, 80.9%, 93.7%, 94.4%, and 93.9%, and of immunoblot with CIM were 98.3%, 90.4%, 96.7%, 95.0%, and 96.3%, respectively. Immunoblot with CIM had the best performance. ICT with CIM was found to be more specific and accurate than the conventional ELISA and may be useful for non-invasive diagnosis of H pylori infection.

Prevalence of cagA in relation to clinical presentation of Helicobacter pylori infection in Egypt

Helicobacter pylori infection, peptic ulcer and gastric cancer are common problems in Egypt. We investigated the prevalence of cagA-positive Helicobacter pylori infections among Egyptian adults in relation to presentation (e.g. dyspepsia vs asymptomatic controls) in Minofyia, Egypt. Patients included men or women seeking care for at least 3 months of upper gastrointestinal symptoms. Helicobacter pylori status was determined by rapid urease test and gastric histopathology in patients and by anti-Helicobacter pylori IgG antibodies in controls. CagA status was determined using an anti-cag A ELISA. 99 Helicobacter pylori infected patients were entered including 90 dyspeptic patients (30 each with gastric cancer, peptic ulcer, and non-ulcer dyspepsia) and 9 non-dyspeptic healthy controls. Age ranged from 27 to 78 y (mean 49.5 y); 50% were men. Anti-cagA antibodies were present in 62.2% of dyspeptic patients compared with 11% of asymptomatic controls (p = 0.004). Anti-cagA antibodies were more prevalent among dyspeptic patients with gastric cancer or peptic ulcer (73.3%) compared to those with non-ulcer dyspepsia (40%) (p = 0.004). The prevalence of cagA in Egypt was related to the clinical presentation of Helicobacter pylori infection being lowest in asymptomatic controls (11.1%) and increasingly prevalent in non-ulcer dyspepsia (40%), peptic ulcer (66.7%), and gastric cancer (89%).

Prevalence of mild serum vitamin B12 deficiency in rural and urban Costa Rican young adults

Recent studies have shown an increase of mild serum cobalamin (vitamin B(12)) deficiency in some Latin American countries; however, no data are available from Costa Rica. The purpose of this work was to establish the prevalence of serum vitamin B(12) deficiency among Costa Rican young adults and to study some factors that may help explain the serum cobalamin concentrations. A cross-sectional survey was conducted among 400 adults aged 20 to 40 years old from urban and rural areas of the central valley of Costa Rica to determine serum vitamin B(12) levels. Additionally, cobalamin dietary intake and the detection of Helicobacter pylori IgG antibodies were studied as possible determinants of the serum vitamin B(12) concentrations. The mean serum concentration of vitamin B(12) was 268 +/- 125 pmol/L, and no significant differences were found by gender or area. Study data indicate an overall prevalence of inadequate serum cobalamin levels of 42.4% (11.2% deficient and 31.2% marginal); more than 50% but less than 75% of individuals had an intake of vitamin B(12) below the U.S. Estimated Average Requirement (EAR) and 61.2% had IgG antibodies to H. pylori. The prevalence of mild serum vitamin B(12) deficiency in young Costa Rican subjects is as high as in other Latin American countries. More investigation should be done to elucidate the etiological factors that are generating deficient and marginal serum cobalamin levels in Costa Rican adults in order to define appropriate public health actions.

Resolving the Riddle of Obscure Iron Deficiency Anemia.

Conventional endoscopic and radiographic methods fail to identify a source of gastrointestinal blood loss in about one third of males and post-menopausal females and in most women of reproductive age with iron deficiency anemia (IDA). Such patients are often referred for hematologic evaluation. In recent years there is increasing awareness of non-bleeding conditions with abnormal iron absorption as possible causes of unexplained IDA. Both H pylori gastritis and autoimmune atrophic gastritis are associated with impaired gastric acidity interfering with iron absorption. In a prospective study performed in a community hematology clinic, 300 consecutive IDA patients were screened for non-bleeding GI conditions including celiac disease (antiendomysial antibodies), autoimmune atrophic gastritis (hypergastrinemia with strongly positive antiparietal cell antibodies) and H pylori gastritis (IgG antibodies confirmed by urease breath test). Their mean age was 39±18 y, and 251 of 300 (84%) were women. A likely cause of IDA was identified in 93% of patients. As expected in a population of females of reproductive age, only 10% had a source of gastrointestinal bleeding identified. There were 13 new cases of adult celiac disease (4%). A history suggestive of menorrhagia was present in 32%. Autoimmune atrophic gastritis was documented in 77 IDA patients (26%) of whom 39 had coexistent H pylori infection. H pylori infection was the only positive finding in 57 patients (19%). To exclude the compounding effect of menstrual blood loss in evaluating the role of H pylori in the pathogenesis of IDA, we have focused on the 29 male IDA patients with negative gastrointestinal workup, poor initial response to oral iron treatment, and a high prevalence of H pylori infection (25 of 29). Following H pylori eradication, all patients achieved normal hemoglobin levels with follow-up periods ranging from 4 to 69 months (38±15 months mean± 1SD). This was accompanied by a significant decrease in H pylori IgG antibodies and serum gastrin. Sixteen patients discontinued iron treatment, maintaining normal hemoglobin and ferritin and may be considered cured. Remarkably, 4 of the 16 achieved normal hemoglobin without ever having received oral iron after H pylori eradication. To define the relation between IDA-associated autoimmune gastritis, and pernicious anemia, we studied 160 patients with autoimmune gastritis including 83 subjects presenting with IDA, 48 presenting with normocytic indices, and 29 with macrocytic anemia. Stratification by age cohorts of autoimmune gastritis from <20 to >60 y showed coexistent H pylori infection in 87.5% at age <20 y, 47% at 20–40 y, 37.5% at 41–60 y, but only 12.5% at age > 60y. With increasing age cohorts, there was a regular and progressive increase in MCV from 68±9 to 95±16 fl, serum gastrin from 349±247 to 800±627 u/mL, and a decrease in cobalamin from 392±179 to 108±65 pg/mL. Conclusions: The favorable long-term clinical results of H pylori eradication offer strong evidence for a cause-and-effect relation between H pylori and IDA. A proportion of H pylori patients will develop autoimmune gastritis. Our findings in autoimmune gastritis imply a disease presenting as IDA many years before the establishment of clinical cobalamin deficiency. It is likely caused by an autoimmune process triggered by antigenic mimicry between H pylori epitopes and major autoantigens of the gastric mucosa. Recognition of H pylori and autoimmune gastritis as common causes of obscure iron deficiency anemia should have a strong impact on the efficacy of diagnostic workup and management of unexplained, or refractory iron deficiency anemia.

Prevalence of Celiac Disease, Helicobacter pylori and Gastroesophageal Reflux in Patients with Refractory Iron Deficiency Anemia

The aim of this article is to determine the prevalence of celiac disease (CD), Helicobacter pylori (H. pylori) and gastroesophageal reflux (GER) in patients with resistant iron deficiency anemia (IDA). The study included 25 patients <18 years of age with refractory IDA (not responding to iron therapy for 3 months in a dose of 6 mg elemental iron/kg/day). All patients included in the study were subjected to careful history taking and thorough clinical examination. Blood sample was taken for analysis of antibodies for CD including: antigliadin antibody (AGA), antiendomysial antibody (EMA), antireticulin antibody (ARA) and antitissue Transglutaminase (tTg) IgG antibody. Anti-H. pylori IgG antibodies and a (13)C-urea breath test (UBT) was done to all patients to diagnose H. pylori. Upper gastrointestinal tract endoscopy was done for all patients to evaluate for the presence of some etiologies of intractable anemia as chronic blood loss. These included: CD, H. pylori infection and GER. The upper gastrointestinal tract endoscopy was also done to evaluate the presence of bleeding spots, ulcers or angiomatous malformations. In addition, gastric antral biopsies were taken for diagnosis of H. pylori infection by the following tests: rapid urease test, histopathological examination and culture. CD was positive in 11 out of 25 patients (44%), H. pylori infection in 12 out of 25 patients (48%), while GER was diagnosed in 11 out of 25 patients (44%). Patients with CD had age of presentation < or =2 years in two patients (18.2%) while the remaining nine patients (81.8%) had age of presentation >2 years and it was statistically significant (p = 0.05*). Also patients with H. pylori had age of presentation < or =4 years in five patients (41.7%) and the remaining seven patients (81.8%) had age of presentation >4 years and it was statistically significant (p = 0.03*). Logistic regression analysis demonstrated that the risk factors for severity of anemia were age of patients and duration of anemia. On the other hand, other parameters have no significant influence on the severity of anemia. Also risk factors of short stature were age of presentation of anemia, degree of anemia and H. pylori infection. AGA had the highest sensitivity (100%) followed by antiendomysium antibody (81.8%) while the tTG antibody had the highest specificity (85.7%) for diagnosis of CD. UBT and histopathology had the highest sensitivity (100%) for diagnosis of H. pylori while rapid urease test, culture, H. pylori stool antigen and anti-H. pylori IgG antibody had the highest specificity (100%). In conclusion, refractory IDA may be due to clinically unapparent H. pylori gastritis and CD. CD is one of the most common causes of intestinal malabsorption during childhood which leads to impairment of iron absorption. Apart from offering them gluten-free diet rich in iron, early detection and treatment of IDA and prophylactic iron and folic acid supplementation will go a long way to optimize their mental and psychological functions. Eradication of H. pylori infection with concomitant iron therapy should correct the anemia.

The relationship between Helicobacter pylori IgG titre and coronary

Objectives — The role of Helicobacter pylori (HP) in the progression of atherosclerosis is con-troversial.We investigated the relation between HP IgG antibody titres and severity and intensity of coronary atherosclerosis and also clinical presentation of coronary artery disease (CAD).Methods — The patient group consisted of 353 patients with angiographically proven CAD, which contains 3 different subgroups: 163 patients with myocardial infarction (MI), 106 patients with unstable angina (USAP) and 84 patients with stable angina (SAP). Control group included 163 subjects with angiographically proven normal coronary arteries. Helicobacter pylori IgG antibody titres were measured by an enzyme immunoassay method in all patients. Gensini and Extent scores were used to evaluate the angiographic severity and extent of atherosclerosis. C-reactive protein levels were measured by Behring nephelometry system kits.Results — Seropositivity rates for HP were similar between groups (82.7% in the patient group and 86.6% in the control group (P > 0.05)). Also HP-IgG levels were similar among the MI, USAP and SAP groups. No significant correlation was observed between CRP levels and HP-IgG level titres. There was no significant correlation between HP-IgG level (r = 0.086, P = 0.2) and Gensini score but a significant poor correlation was observed between HP-IgG level and Extent score (r = + 0.156, P = 0.03).Conclusions — Helicobacter pylori IgG titres do not play an important role in the presentation of CAD and do not increase systemic inflammatory response. However, Helicobacter pylori IgG antibody titres may be correlated with the extent of CAD.

Seroprevalence of Helicobacter pylori in South Korea

Helicobacter pylori-associated gastrointestinal diseases have been widely recognized. The aims of this study were to investigate the interval change of seropositivity of H. pylori between 1998 and 2005 in Korean adult population and to find the factors related to H. pylori infection. Between January and December of 2005, a total of 15,916 health check-up subjects (aged > or = 16 years) from all parts of South Korea responded to the questionnaire, and the prevalence of H. pylori was investigated by measuring anti-H pylori IgG antibodies. The seropositivity in asymptomatic subjects (aged > or = 16 years) was compared with that of 1998, which was surveyed by the Korean H. pylori Study Group. The overall seropositivity rate (aged > or = 16 years) was 56.0%, and 13.9% of seropositive subjects were found to have a history of H. pylori eradication therapy. With the exclusion of subjects who had a history of H. pylori eradication and current gastrointestinal symptoms, the seropositivity rate of H. pylori became 59.6% in 8020 subjects. Seroprevalence of H. pylori was significantly higher in subjects aged 50-59 years, males, low income group, and subjects from provinces. The seroprevalence in 2005 (59.6%) significantly decreased compared with that of 1998 (66.9%), and the decrease was significant in subjects aged < 70 years, Seoul and Gyeonggi province (which is close to Seoul). The seroprevalence of H. pylori in asymptomatic health check-up adult subjects in 2005 decreased to 59.6% from 66.9% in 1998, probably as a result of the improvement of socioeconomic status and hygiene.

Host and environmental factors for gastric cancer in Babol, the Caspian Sea Coast, Iran

To clarify host and environmental factors for gastric carcinogenesis, we obtained information about gastric cancer mortality in Babol, in the North of Iran, and recruited 130 participants aged 30-80 years from the general population of Babol in 2004. A urea breath test, assessment of IgG antibodies to Helicobacter pylori, a pepsinogen test, a marker of chronic atrophic gastritis, and determination of urinary excretions of sodium and potassium were performed. Diet and lifestyle information was also obtained using a questionnaire. The stomach cancer mortality rate for men in Babol (38.2/10(5)) was found to be somewhat lower than that for Japanese men (45.1/10(5)), while the mortality for women (26.9/10(5)) was higher than for Japanese women (20.9/10(5)). Positive rates for the urea breath test were 77.5 and 81.8% for Iranian men and women, respectively. Helicobacter pylori IgG antibodies were present in 68.7 and 73.7% of Iranian men and women, respectively, both values being marginally higher than for Japanese. We also found 51.0 and 52.8% to be positive for a pepsinogen test, significantly higher than the Japanese values. Urinary excretions of salt and potassium in this population appeared approximately the same as the consumption in Japanese. The elevated gastric cancer mortality in both men and women in Babol seems, by and large, to be related to higher H. pylori infection rates and prevalence of chronic atrophic gastritis. Certain factors, including H. pylori DNA diversity, host factors and their interactions, together with the level of medical practice, prevalence of and access to secondary prevention of stomach cancer, may also be associated with the relatively high mortality.

Factors affecting the serum gastrin 17 level: an evidence‐based analysis of 3906 serum samples among Chinese

To investigate the influence of gender, age, site of lesion, disease type and Helicobacter pylori (H. pylori) infection on the human serum gastrin-17 level and to study the diagnostic value of serum gastrin-17 in gastric precancerous lesions and gastric cancer. Serum gastrin-17 and serum H. pylori IgG antibody were detected by the ELISA method. The different gastric disease groups were confirmed by endoscopy and histopathology. Among the 3906 serum samples according to the gender, age, site of lesion and the data of different gastric disease groups, the serum gastrin-17 level was markedly higher in people>or=60 years old than that in younger age groups. The serum gastrin-17 level increased progressively in the following order: healthy control group, nonatrophic gastritis group, gastric ulcer group, and the serum gastrin-17 level was higher in the atrophic gastritis with dysplasia group than that without it, the lowest level being in the gastric cancer group. Among the 2946 serum samples matched with the site of the lesion, the serum gastrin-17 level was higher in those with antral diseases than in those with gastric corpus diseases. Among the 3805 serum samples matched with the H. pylori infection data, the serum gastrin-17 level was higher in the H. pylori-positive group than in the H. pylori-negative group. In people over 60 years of age, the serum gastrin-17 level tends to increase. In subjects with precancerous gastric lesions, it may increase significantly with the progression of gastric disease, and ultimately decrease in gastric cancer. Serum gastrin-17 is a good biomarker to differentiate benign from malignant gastric diseases. The site of the gastric lesions is an important factor affecting the serum gastrin-17 level, whereas H. pylori infection is usually associated with its increment.

Gastric Status and Vitamin B12 Levels in Cardiovascular Patients

Proper absorption of vitamin B12 requires gastric corpus mucosa that functions appropriately and secretes intrinsic factor needed as an essential cofactor for the absorption of dietary vitamin B12 in the small bowel. Here we describe the prevalence of vitamin B12 deficiency and atrophic corpus gastritis (ACG) in patients with coronary heart disease. Fasting serum was obtained from patients who were admitted for cardiovascular diseases at the Coronary Care Unit in Nijmegen, the Netherlands. The status of gastric mucosa was assessed by using the serum levels of pepsinogens I and II, gastrin-17, and Helicobacter pylori IgG antibodies and analyzed over vitamin B12 level subgroups. The study population consisted of 376 patients (mean age, 65 years [SD, 13 years], 227 [60%] males). Low vitamin B12 levels (<150 pM) were detected in 28 patients (7%). Of these 28 patients, 5 (18%) had ACG according to the biomarker assays. Altogether, another 140 patients (37%) had vitamin B12 levels between 150 and 250 pM, of whom 10 (7%) had ACG. Of the remaining patients, five (2%) had ACG. Deficiency of vitamin B12 is common among subjects with coronary heart disease. Up to 20% of these deficiencies are related to ACG.

Gastric Cancer is Related to Early Helicobacter pylori Infection in a High-Prevalence Country

Chile ranks fifth in the world among countries with the highest incidence of gastric cancer. The aim was to quantify the association between Helicobacter pylori infection and gastric cancer mortality at the county of residence. A cross-sectional household survey, a probability sample of the Chilean adult population, provided 2,615 participants in whom serum H. pylori IgG antibodies were measured (ELISA). The spatial pattern of 48,367 deaths due to gastric cancer which occurred from 1985 to 2002 was analyzed using a hierarchical Poisson regression model; 333 counties were categorized as low, medium, and high gastric cancer mortality with median gastric cancer death rates of 11.4, 19.1, and 26.0 per 100,000 inhabitants, respectively. The association between H. pylori positivity and gastric cancer mortality in the county of residence was assessed by multivariate Poisson regression for complex samples. H. pylori prevalence was 73.0% [95% confidence intervals (CI), 70.0-76.0], higher in men [prevalence rate ratio (PRR), 1.1 (95% CI, 1.01-1.20)], peaked at ages 45 to 64, and dropped after age 65. It was higher among residents in counties with high gastric cancer mortality (79.7%; 95% CI, 76.4-82.6) compared to counties with low gastric cancer mortality (62.3%; 95% CI, 53.8-70.2; corresponding PRR, 1.3; 95% CI, 1.1-1.5); under age 24, H. pylori infection was 79.7% (95% CI, 72.2-85.6) versus 39.8% (95% CI, 19.6-64.2) among residents in counties with high and low gastric cancer mortalities, respectively (PRR, 2.0; 95% CI, 1.1-3.7). The high prevalence of H. pylori at younger ages was associated with high gastric cancer mortality in the base population.

Helicobacter pylori infection in combination with the serum pepsinogen I/II ratio and interleukin-1β-511 polymorphisms are independent risk factors for gastric cancer in Thais

Thailand has the lowest incidence of gastric cancer in the world. Helicobacter pylori infection, a low serum pepsinogen I/II ratio, and interleukin (IL)-1beta-511 polymorphisms are suspected to be risk factors for gastric cancer. A total of 167 Thais, comprising 56 cancer patients and 111 volunteers without cancer, underwent an esophagogastroduodenoscopic examination and three fixed-point biopsies; a cancer tissue biopsy was also done, and blood samples were collected. The subjects without cancer were divided into normal subjects and chronic gastritis patients. IL-1beta-511 polymorphisms were analyzed by polymerase chain reaction-restriction fragment length polymorphism, and the serum levels of pepsinogen I and II were determined by a radioimmunoassay. Helicobacter pylori IgG antibody and tissue pathology were tested in all groups. The pepsinogen I/II ratio was significantly lower in the gastric cancer group than in the normal and chronic gastritis groups [odds ratio (OR), 2.3; 95% confidence interval (CI), 1.10-4.80; P = 0.025]. Gastric cancer patients were positive for the H. pylori IgG antibody more frequently than negative (OR, 2.946; 95% CI, 1.4-6.39; P = 0.005). However, only 15 (27%) cancer patients were both positive for H. pylori IgG antibody and had low serum pepsinogen I/II. The C/C genotype was found more frequently in the gastric cancer group than in the group with a normal gastric mucosa (OR, 0.64; 95% CI, 0.50-0.81; P = 0.014). A low serum pepsinogen I/II ratio combined with positivity for H. pylori IgG, and a IL-1beta-511 C/C genotype may be independent risk factors for gastric cancer in Thais.

Implications of Oral Helicobacter pylori for the Outcome of its Gastric Eradication Therapy

Helicobacter pylori (H. pylori) is an important pathogen in gastritis, peptic ulcer and possibly gastric cancer, but several questions remain unanswered. Particularly how the organism is transmitted and what is the relationship between oral presence of H. pylori and the gastric infection. Accordingly, we aimed to characterize the H. pylori in oral cavity and to evaluate its relationship to gastric H. pylori infection. Out of total 100 screened for H. pylori infection female subjects (40 to 85 y), 49 patients (pts), who had positive C-urea breath test (UBT) and dyspeptic symptoms, agreed for 1 week regimen of triple anti-H. pylori therapy. The presence of H. pylori in oral cavity was assessed using bacterial culture from saliva and gingival pockets. Gastric H. pylori infection was estimated using capsulated C-urea breath test and plasma anti-H. pylori IgG and saliva IgA antibodies. In addition, plasma gastrin, ghrelin, and pepsinogen I were measured by radioimmunoassay. In selected patients, gastroscopy was additionally performed and gastric biopsy samples were taken for H. pylori random amplification of polymorphic DNA genetic profiling. The triple therapy resulted in gastric H. pylori eradication in 79% pts, along with significant decrease of plasma gastrin combined with an increase in plasma ghrelin and pepsinogen I (PgI) levels and a marked alleviation of dyspeptic symptoms. In contrast to gastric effects, the eradication therapy failed to cause any changes in the presence of H. pylori in oral cavity. Moreover no relationship was observed between the presence of H. pylori in oral cavity and the gastric H. pylori eradication. In line with these findings, no relationship between gastric and oral H. pylori was found using genetic profiling by random amplification of polymorphic DNA. H. pylori was detected both in the oral cavity and the stomach but oral H. pylori had no relation to gastric H. pylori and remained unaffected by eradication of gastric H. pylori.

Screening of atrophic gastritis and gastric cancer by serum pepsinogen, gastrin‐17 and Helicobacter pylori immunoglobulin G antibodies

Currently the screening and diagnosis of gastric cancer and atrophic gastritis are mainly made by endoscopy and biopsy. The aim of this study was to evaluate the use of serum tests: serum pepsinogen I (PGI pepsinogen I/II ratio (PGR), gastrin-17 (G-17) and H. pylori-immunoglobulin G (IgG) antibodies to screen atrophic gastritis and gastric cancer. A total of 458 patients were recruited, and each underwent endoscopy with biopsies before the serum tests were performed. These patients were divided into five groups based on the endoscopic and histological findings: 92 patients in the atrophic gastritis group, 58 in the gastric ulcer group, 90 in the duodenal ulcer group, 141 in the gastric cancer group (40 early gastric cancer and 101 advanced gastric cancer) and 77 (including mild non-atrophic gastritis) served as a control group. Serum samples for PGI and II, G-17, and H. pylori-IgG antibodies estimation were analyzed by ELISA. PGI and PGR values decreased significantly both in atrophic gastritis and gastric cancer groups (P<0.01). For the best discrimination of atrophic gastritis, the cut-off values of PGI and PGR were 82.3 microg/L and 6.05, respectively. The PGI, PGR and G-17 values were related significantly with the grades and/or sites of atrophic gastritis (P<0.01). Patients with atrophic corpus gastritis had low PGI and PGR values and high G-17 level, and patients with atrophic antral gastritis had low G-17 level. G-17 increased significantly in the gastric cancer group (P<0.01). PGI and PGR values were significantly lower in patients with advanced gastric cancer than in patients with early gastric cancer, while there was no difference in G-17 level between them. The positivity rate of H. pylori-IgG antibodies was 54.55% in the control group. The PGI level was higher in H. pylori positive patients than in H. pylori negative ones (P<0.001), while there was no difference in G-17 level between them. The positivity rates of H. pylori-IgG antibodies were over 85% in all other four groups. Low serum PGI, PGR and G-17 values are biomarkers of atrophic antral gastritis. Atrophic be screened by serum PGI and PGR values. Gastric cancer can be screened on the basis of increased serum G-17 and remarkedly low serum PGI and PGR values. The H. pylori infection is related to the change of PG level.

Helicobacter pylori, chronic atrophic gastritis, inactive aldehyde dehydrogenase‐2, macrocytosis and multiple upper aerodigestive tract cancers and the risk for gastric cancer in alcoholic Japanese men

Gastric carcinoma occurs at a high rate in alcoholic Japanese men. Inactive heterozygous aldehyde dehydrogenase-2 (ALDH2*1/2*2) and macrocytosis (mean corpuscular volume [MCV] > or = 106 fl) enhance the risk for esophageal carcinoma, which frequently occurs with gastric carcinoma in this population. Whether alcoholism affects Helicobacter pylori-induced chronic atrophic gastritis (CAG) is unknown. This study of Japanese alcoholic men with (n = 45) and without (n = 281) gastric carcinoma included assessment of H. pylori IgG antibody, serum pepsinogen-confirmed CAG, MCV, and ALDH2 genotype. The gastric carcinoma cases had a significantly higher age-adjusted prevalence of H. pylori-positivity (78%vs 57%), CAG (78%vs 42%), ALDH2*1/2*2 (36%vs 14%), MCV > or =106 fl (38%vs 20%), and concurrent esophageal/oropharyngolaryngeal carcinoma (18%vs 5%) than controls. Among gastric cancer-free controls, the prevalence of CAG was higher than generally reported in Japan, regardless of H. pylori status (H. pylori-positive, 56%vs 35-36% for Japanese general population; H. pylori-negative, 8%vs 1-3%). Alcoholism may accelerate the progression of CAG. Each of these factors increased the risk of gastric carcinoma (OR(s) = 3.7 for H. pylori-positive, 2.7 for non-severe CAG, 8.7 for severe CAG, 3.5 for ALDH2*1/2*2, 2.5 for MCV > or =106 fl, and 3.7 for concurrent carcinoma). A multivariate analysis showed that CAG and ALDH2*1/2*2 were independently related to the risk of gastric carcinoma. Combinations of CAG and ALDH2*1/2*2 showed greater risks of gastric carcinoma (OR(s) = 4.0 for non-severe CAG alone, 17.6 for severe CAG alone, 9.7 for ALDH2*1/2*2 alone, 17.1 for non-severe CAG plus ALDH2*1/2*2, and 39.2 for severe CAG plus ALDH2*1/2*2). Combining blood tests for H. pylori, CAG, MCV and ALDH2 genotype could offer a new means of predicting risk of gastric carcinoma in Japanese alcoholic men.

Analysis of immune responses againstH pyloriin rabbits

To investigate the immunogenicity of H pylori proteins, to evaluate the production rate of anti H pylori IgG antibodies in relation to time and to demonstrate the fidelity of newly optimized in-house enzyme-linked immunosorbent assay (ELISA) technique as an alternative for H pylori infection assay. In the present study, 100 microg of formalin-fixed H pylori whole cell antigens was injected into an experimental animal (New Zealand white female rabbit) intramuscularly on d 0, 16, 27 and 36. The first two doses were injected with adjuvants. On d 0, a serum sample was collected from the rabbit before immunization and this pre-immunized serum was used as a negative control for the whole study. To evaluate the immunogenic responses of the injected antigen, serum samples were collected from the rabbit at regular intervals up to d 42. The sera were analyzed using in-house ELISA and Western blot techniques. The production of anti H pylori IgG antibodies in the rabbit in response to the injected antigen increased almost exponentially up to d 14 and after that it was maintained at the same level until the last day (d 42). By analyzing the immune profiles of immunized sera, 11 proteins were identified to be immunogenic, among them 2 (approximately 100 kDa and 85 kDa) were most prominent. Analysis of the immune responses against pathogenic microorganisms like H pylori is necessary for the development of various diagnostic and preventive approaches. The results of this experiment reveal that the formalin-fixed H pylori whole cell antigens injected into the rabbit are highly immunogenic. These prominent proteins (approximately 100 kDa and 85 kDa) might have higher immunogenic effects among humans infected with H pylori and some of these immunogenic proteins can be included in diagnostic approaches based on serology and also for vaccine formulation. The in-house ELISA is a promising alternative compared to invasive techniques.

Serum anti-Helicobacter pylori IgA and IgG antibodies in asymptomatic children in Serbia

The aim of this study was to determine the seroprevalence of Helicobacter pylori and the distribution of anti-H.pylori IgA and IgG antibodies in asymptomatic children aged between 7 and 18 y. We studied the serum samples of 283 children using the commercial ELISA test for the detection of anti-H. pylori IgA and IgG antibodies. The overall prevalence of anti-H. pylori antibodies was 36.4%. The seroprevalence was 35%, 28.3%, 37.5%, and 42.2% for the ages of 7, 10, 14 and 18 y, respectively. Serum IgG antibodies alone were detected in 88.3%, IgA alone in 4.9%, and both IgA and IgG antibodies were detected in 6.8% of samples. The mean levels of IgG antibodies to H. pylori increased with age. We concluded that the prevalence of H. pylori antibodies in Serbian children was high (36.4%), ranging from 35% to 42.2%. The detection of IgG antibodies is useful for the determination of seroprevalence in asymptomatic children.

Size of the peptic ulcer in Helicobacter pylori-positive patients: association with the clinical and histological characteristics

Objective. Based on a large trial of Helicobacter pylori-positive peptic ulcer patients, we studied whether the size of the ulcer, along with other clinical and histological characteristics, has any effect on healing. We also studied the clinical and endoscopic characteristics associated with size of the peptic ulcer. Material and methods. A total of 333 consecutive patients with H. pylori infection and peptic ulcer were enrolled (mean age 54.8±12.7 years). Location of the ulcer was recorded by gastroscopy and the presence of H. pylori was assured by rapid urease test, histology and by serum H. pylori IgG and IgA antibody measurement. The diameter of the ulcer was measured by placing the opened biopsy forceps (7 mm) beside it. Biopsy specimens were examined in accordance with the Sydney system. Results. Mean size of the peptic ulcer was 13.2±8.3 in corpus, 11.3±5.3 in antrum, 13.8±7.8 in angulus, 9.5±5.3 in prepylorus and 9.2±4.7 mm in duodenum (duodenal versus gastric type; p<0.05). Average size of the ulcers was 9.4±5.3 mm in patients with Forrest III type and 11.5±6.8 in other types (p<0.05). Patients who were ≥50 years of age, currently smoking, or who had corpus-predominant chronic gastritis or atrophic gastritis, had larger ulcers than others. Size of index ulcers, successful eradication of H. pylori and the presence of atrophic gastritis were independent factors for healing. The odds ratio was 11.5 (95% CI 3.3–40.5; p<0.01) for eradication of H. pylori, 3.5 (95% CI 1.1–11.2; p<0.05) for size of the index ulcer (≤10 mm versus >10 mm) and 3.4 (95% CI 1.2–9.8; p<0.05) for atrophic gastritis versus no atrophy. Conclusions. Size of the peptic ulcer, successful H. pylori eradication and atrophic gastritis were independent factors for the healing of peptic ulcers. A number of clinical and endoscopic variables (age, current smoking, corpus-predominant gastritis, Forrest classification) were associated with size of the peptic ulcer in H. pylori-positive patients.

Impact of Helicobacter pylori Infection on the Humoral Immune Response to MUC1 Peptide in Patients with Chronic Gastric Diseases and Gastric Cancer

Many investigators have demonstrated alteration of gastric mucins in H. pylori infected individuals. The inflammatory environment induced by H. pylori leading to aberrant glycosylation of MUC1 and demasking of core peptide MUC1 epitope could enhance immune responses to MUC1. IgG and IgM immune response to MUC1 in patients with gastric cancer (n = 214) chronic gastroduodenal diseases (n = 160) and healthy blood donors (n = 91) was studied with ELISA using bovine serum albumin-MUC1 60-mer peptide as antigen. H. pylori serologic status was evaluated with ELISA and CagA status by immunoblotting. Gastric mucosa histology was scored according to the Sydney system. Compared to H. pylori seronegative individuals, higher levels of IgG antibody to MUC1 were found in H. pylori seropositive patients with benign gastric diseases (p < 0.01) and blood donors (p < 0.03). Higher MUC1 IgG antibody levels were associated with a higher degree of gastric corpus mucosa inflammation in patients with chronic gastroduodenal diseases (p < 0.0025). There was a positive correlation between the levels of anti-H. pylori IgG and MUC1 IgG antibody levels in blood donors (p = 0.03), and in patients with benign diseases (p < 0.0001). In patients with gastric cancer (n = 214) a significantly higher level of anti-MUC1 IgG than in blood donors was observed (p < 0.001) irrespective of H. pylori status or stage of cancer. MUC1 IgM antibody levels were not related to the H. pylori serology. IgG immune response to tumor-associated MUC1 is up regulated in H. pylori infected individuals. This increase is associated with a higher IgG immune response to H. pylori and with a higher degree of gastric mucosa inflammation. High levels of MUC1 IgG antibody irrespective of H. pylori serologic status characterized patients with gastric cancer. The findings suggest that, in some individuals, the H. pylori infection may stimulate immune response to tumor-associated MUC1 peptide antigen thus modulating tumor immunity.

CAN DENTAL TREATMENT BE THE INFECTION ROUTE OFH. PYLORITRANSMISSION IN ADULTS? THREE CASES OF ACUTE GASTRIC MUCOSAL LESIONS AFTER DENTAL TREATMENT

Acute gastric mucosal lesions (AGML) comprise a typical clinical entity in patients with acute gastritis, which is characterized by severe erosion, hemorrhage, and ulceration. It is thought that most Helicobacter pylori (H. pylori) infections are established during childhood through human-to-human contact. Initial H. pylori infection in an adult is rare, and the transmission route is unknown. The first patient was a 27-year-old woman whose chief complaint was epigastric pain. She underwent dental treatment for 30 min and developed sudden epigastric pain 6 h after the treatment. Endoscopic examination revealed multiple hemorrhagic erosions in the antrum. Rapid urease test and histology for H. pylori were positive, but serum anti-H. pylori IgG antibody was negative at the onset. Serology and urea breath test were positive for H. pylori 2 months after the dental treatment. The second and third patients were diagnosed as having AGML 2 and 4 days after dental treatment, respectively. Culture for H. pylori was positive and serology was negative at the onset, but serology showed seroconversion 2 months after the dental treatment in both patients. These findings indicate that dental treatment is a possible route for H. pylori infection in patients with AGML.