The expression profiling of circulating miR-204, miR-182, and lncRNA H19 as novel potential biomarkers for the progression of peptic ulcer to gastric cancer.

Deregulation of noncoding RNAs, microRNAs (miRNAs) and long noncoding RNA (lncRNA), are implicated in the initiation and progression of gastric cancer (GC). This study is a pilot case-control study carried out on 75 subjects, 40 of them were Helicobacter pylori-gastric ulcer patients and 35 were GC patients recruited from the Gastrointestinal Endoscopy Unit in Al-Kasr Al-Aini Hospital, Cairo University in Egypt. Real-time PCR was performed to evaluate the expression level of serum miR-204, miR-182, and lncRNA H19 in patients with peptic ulcer-progressed GC vs nonprogressed peptic ulcer patients. Fibroblast growth factor 18 (FGF-18)/FGF receptor 2 (FGFR2) expression and their downstream immunological and inflammatory signaling markers were assessed and their association with the addressed noncoding RNAs investigated. As regards miR-204 and miR-182, they were significantly increased (12.5 and 2.6 folds, respectively) in GU samples, compared with those of healthy control levels. The elevated levels of these miRNAs were significantly de-escalated in GC samples compared with GU and the fold decrease valued 2.2 fold for miR-204 and 1.8 folds for miR-182. On the other hand, the significant escalation in the level of lnRNA H19 in GU recorded a 16.6 fold increase and further elevation in its levels was evident in GC samples. The herein assessed miRNAs are correlated with disease duration and FGFR2 with miR-182 being significantly correlated with all inflammatory markers, TAC, INF-γ, matrix metallopeptidase 9, and FGF-18. In terms of diagnostic accuracy of assessed miRNAs (stages III to IV), the receiver operating characteristic analysis indicated that serum lncRNA H19 showed the highest diagnostic accuracy (95.5%), specificity (100%), and sensitivity (90.9%), compared with miR-204 and miR-182, which showed the same specificity (60%), sensitivity (72.7%), and diagnostic accuracy (68.8%). Our findings conclude that lnRNA H19, miR-204, and miR-182 may function as novel prospective plasma biomarkers to detect GC and its progression from H. pylori-peptic ulcer, which would be helpful to improve the theranostics of GC.

Correlations of Acute Cerebral Hemorrhage Complicated with Stress Ulcer Bleeding with Acute Physiology and Chronic Health Evaluation (APACHE) II Score, Endothelin (ET), Tumor Necrosis Factor-alpha (TNF-α), and Blood Lipids.

BACKGROUND This study investigated the correlations between acute cerebral hemorrhage complicated with stress ulcer bleeding and corresponding indexes, including the Acute Physiology and Chronic Health Evaluation (APACHE) II score, vascular endothelin-1 (ET-1), tumor necrosis factor-alpha (TNF-α), and blood lipid factors. MATERIAL AND METHODS A total of 53 patients with acute cerebral hemorrhage complicated with stress ulcer bleeding were selected as the observation group and 50 patients with simple acute cerebral hemorrhage were selected as the control group. The APACHE II score and the levels of ET-1, TNF-α, and blood lipid factors, including total cholesterol (TC), triglyceride (TG), high-density lipoprotein-cholesterol (HDL-C), low-density lipoprotein-cholesterol (LDL-C), and malondialdehyde (MDA), were detected and the correlations of were analyzed between the 2 groups of patients. RESULTS The blood lipid index TG, APACHE II score, ET-1, TNF-a, renal function indexes [blood urea nitrogen (BUN) and creatinine (Cr)], mortality rate, hemoglobin, and MDA in the observation group were significantly higher than those in the control group, while HDL-C in the observation group was obviously lower than in the control group (p<0.05). The APACHEII score had positive correlations with TG and TNF-α (r=0.8960, r=0.8563, respectively), while it was negatively correlated with TC, HDL-C, LDL-C, and ET-1 (r=-0.909, r=-0.9292, r=-0.8543, and r=-0.8899, respectively) (p<0.001 in all comparisons). APACHEII score, BUN, and Cr were all risk factors. CONCLUSIONS Stress ulcer in patients with acute cerebral hemorrhage is associated with blood lipid changes and inflammation, which provides clues for the diagnosis and treatment of acute cerebral hemorrhage.

Catching the Zebra: Clinical Pearls and Pitfalls for the Successful Diagnosis of Zollinger-Ellison Syndrome.

Zollinger-Ellison syndrome (ZES) results from an ectopic gastrin-secreting tumor leading to peptic ulcer disease, reflux, and chronic diarrhea. While early recognition portends an excellent prognosis with >80% survival at 15 years, symptoms are often nonspecific making the diagnosis difficult to establish. Diagnosis involves a series of tests, including fasting gastrin, gastric pH, chromogranin A, and secretin stimulation. Performing these tests in the correct sequence and at the proper time is essential to avoid inaccurate results. Tumor localization is equally nuanced. Although providers have classically used 111indium-radiolabeled octreotide with somatostatin receptor scintigraphy to evaluate tumor size and metastases, recent studies have shown superior results with newer imaging modalities. In particular, 68gallium (68Ga)-labeled somatostatin radiotracers (i.e., 68Ga-DOTATOC, 68Ga-DOTANOC and 68Ga-DOTATATE) used with positron emission tomography/computed tomography can provide excellent results. Endoscopic ultrasound is another useful modality, particularly in patients with ZES in the setting of multiple endocrine neoplasia type 1. This review aims to provide clinicians with an overview of ZES with a focus on both clinical presentation and the proper utilization of the various biochemical and imaging tests available.

Changes in plasma ghrelin and leptin levels in patients with peptic ulcer and gastritis following eradication of Helicobacter pylori infection.

BACKGROUND: Helicobacter pylori (H. pylori) infection and eradication therapy have been known to influence gastric ghrelin and leptin secretion, which may lead to weight gain. However, the exact relationship between plasma ghrelin/leptin levels and H. pylori infection has remained controversial. The aim of this study was to investigate plasma ghrelin and leptin levels in H. pylori-positive and -negative patients, to compare the two levels of the hormones before and after H. pylori eradication, and to examine the correlation between body mass index (BMI) and active ghrelin or leptin levels, as well as that between atrophic pattern and active ghrelin or leptin levels. METHODS: Seventy-two H. pylori-positive patients who underwent upper gastrointestinal endoscopy, 46 diagnosed as having peptic ulcer and 26 as atrophic gastritis, were enrolled. Control samples were obtained from 15 healthy H. pylori-negative volunteers. The extent of atrophic change of the gastric mucosa was assessed endoscopically. Body weight was measured and blood was collected before and 12 weeks after H. pylori eradication therapy. Blood samples were taken between 8 and 10 AM after an overnight fast. RESULTS: Plasma ghrelin levels were significantly lower in H. pylori-positive patients than in H. pylori-negative patients. In particular, plasma active ghrelin levels were significantly lower in patients with gastritis compared with patients with peptic ulcer. Plasma ghrelin levels decreased after H. pylori eradication in both peptic ulcer and gastritis patients, while plasma leptin levels increased only in peptic ulcer patients. Plasma leptin levels and BMI were positively correlated, and active ghrelin levels and atrophic pattern were weakly negatively correlated in peptic ulcer patients. CONCLUSION: H. pylori infection and eradication therapy may affect circulating ghrelin/leptin levels. This finding suggests a relationship between gastric mucosal injury induced by H. pylori infection and changes in plasma ghrelin and leptin levels.

CXC chemokine CXCL12 tissue expression and circulating levels in peptic ulcer patients with Helicobacter pylori infection.

Helicobacter pylori (H. pylori) infection is among the most prevalent human infections. CXCL12 is a well-known CXC chemokine involved in inflammation and play major roles in angiogenesis. There is currently very limited data on the role of CXCL12 in peptic ulcer disease. Hence, we aimed to explore whether CXCL12 is involved in the pathogenesis of peptic ulcer induced by H. pylori. In this study, we enrolled 102 H. pylori-infected patients, including 51 with active ulcer (GA) and 51 with healing ulcer (GH). We also recruited 50 healthy subjects as control, which did not show any sign or symptoms of chronic inflammatory diseases, infection, or immune-related disorders. Endoscopy was performed to determine the stage of the disease. ELISA was used for detection of H. pylori infection and CXCL12 measurement. We also employed western blotting to detect CXCL12 in ulcerative lesions of H. pylori. Demographic data were also collected by questionnaire. Our results demonstrated that CXCL12 serum levels in GA group (151.8±18.31pg/mL) were significantly higher than those in GH (36.89±6.78pg/mL) and control groups (33.77±9.12pg/mL) (P<0.0001). However, we did not observe a significant difference between GH and control groups. Moreover, overexpression of CXCL12 in gastric lesions of patients in GA group was confirmed by Western blot analysis. According to the result of the present study, it could be concluded that CXCL12 is involved in the pathogenesis and healing of H. pylori-induced peptic ulcer. CXCL12 serum levels may also be used to distinguish between GA and GH phases of the disease.

Toll-Like Receptor 4 Wild Type Homozygozity of Polymorphisms +896 and +1196 Is Associated with High Gastrin Serum Levels and Peptic Ulcer Risk.

Toll-like receptor 4 is a part of the innate immune system and recognizes Helicobacter pylori lipopolysaccharide. The goal of this study was to analyze the role of Toll-like receptor 4 polymorphisms +896 (rs4986790) and +1196 (rs4986791) in the pathogenesis of Helicobacter pylori related gastroduodenal diseases in relation to gastric secretion and inflammation. Toll-like receptor 4 polymorphisms, serum gastrin-17 and pepsinogen I and II concentrations were determined, and gastroscopies with histopathological analyses were performed to 216 dyspeptic patients. As genotype controls, 179 controls and 61 gastric cancer patients were studied. In our study, the Toll-like receptor 4 +896 and +1196 polymorphisms were in total linkage disequilibrium. The homozygous wild types displayed higher gastrin-17 serum concentrations than the mutants (p = 0.001) and this effect was independent of Helicobacter pylori. The homozygous wild types also displayed an increased risk for peptic ulcers (OR: 4.390). Toll-like receptor 4 genotypes did not show any association with Helicobacter pylori positivity or the features of gastric inflammation. Toll-like receptor 4 expression was seen in gastrin and somatostatin expressing cells of antral mucosa by immunohistochemistry. Our results suggest a role for Toll-like receptor 4 in gastric acid regulation and that the Toll-like receptor 4 +896 and +1196 wild type homozygozity increases peptic ulcer risk via gastrin secretion.

Serum 8 Hydroxydeoxyguanosine and Cytotoxin Associated Gene A as Markers for Helicobacter pylori Infection.

BACKGROUND: Helicobacter pylori (H.pylori) is associated with chronic gastritis, peptic ulcers, gastric adenocarcinomas and mucosa associated tissue lymphomas. Cytotoxin associated gene A (CagA) is one of the virulence factors of H.pylori. It is hypothesized that reactive oxygen species (ROS) play roles in H.pylori associated disease especially in development of gastric adenocarcinoma. Individuals infected with H.pylori bearing CagA produce more ROS than others. 8-hydroxydeoxyguanosine (8OHdG) is an in vitro marker of DNA damage and oxidative stress. The aim of this study was to investigate the relationship between 8OHdG level, H.pylori infection and CagA and alterations of serum 8OHdG level after H.pylori eradication. MATERIALS AND METHODS: Patients admitted with dyspeptic complaints and upper gastrointestinal endoscopy were assessed. H.pylori was determined from histopathology of specimens. Serum 8OHdG levels of three groups (H.pylori negative, H. pylori positive CagA negative and H.pylori positive CagA positive) were compared. Patients with H.pylori infection received eradication therapy. Serum 8OHdG levels pretreatment and posttreatment were also compared. RESULTS: In total, 129 patients (M/F, 57/72) were enrolled in the study. Serum 8OHdG level of H.pylori negative, H. pylori positive CagA negative and H.pylori positive CagA positive groups were significantly different (5.77±1.35 ng/ml, 5.43±1.14 ng/ml and 7.57±1.25 ng/ml respectively, p=0.05). Furthermore, eradication therapy reduced serum 8OHdG level (6.10±1.54 ng/ml vs 5.55±1.23 ng/ml, p=0.05). CONCLUSIONS: Individuals infected with H.pylori bearing CagA strains have the highest serum 8OHdG level and eradication therapy decreases the serum 8OHdG level. To the best of our knowledge this is the first study that evaluated the effect of CagA virulence factor on serum 8OHdG level and the effect of eradication therapy on serum 8OHdG levels together. Eradication of CagA bearing H.pylori may prevent gastric adenocarcinoma by decreasing ROS. 8OHdG level may thus be a good marker for prevention from gastric adenocarcinoma.

[Mucosal changes in the periulcer zone and endocrine system in patients with gastroduodenal ulcer, complicated by hemorrhage].

Examination of patients, suffering gastroduodenal ulcer, complicated by hemorrhage, was conducted, using clinical, microbiological, immunohistochemical methods and chromatomassspectrography. Enhanced activity of inducible NO-synthase, contamination of periulcer zone with microorganisms Klebsiella pneumoniae, Streptococcus beta-haemoliticus, enhancement of contents of catecholamines and serotonin in the blood serum were revealed. These changes are most expressed in severe blood loss, unstable local endoscopic hemostasis, high risk of a recurrent hemorrhage occurrence. The data obtained permit to prognosticate severity of a pathologic process course and to improve the treatment programe.

[Dynamics of catecholamines in serum of patients with gastroduodenal ulcers complicated by hemorrhage].

The dynamics of the catecholamines content in the blood serum of the patients, suffering gastroduodenal ulcer, complicated by hemorrhage, was analyzed. The biggest raising of the investigated index level was observed in patients while presence of gastric cancer, complicated by hemorrhage. These changes correlate with the blood loss severity enhancement, the state of unstable endoscopic hemostasis, high activity of the inducible NO-synthase of the peri-ulceral zone mucosa. The data obtained permit to prognosticate the pathological process and to improve the treatment program.

[Experience of using reamberin for detoxification therapy at the stage of deworming in children with chronic opisthorchiasis].

The study presents data on the reversible aggregation of erythrocytes in 50 children with chronic opisthorchiasis and 45 children with inflammatory diseases of the upper digestive tract without opisthorchiasis (chronic gastroduodenitis, duodenal ulcers), all patients aged from 7 to 17 years. The results of using reamberin for detoxification therapy at the stage of deworming in children with chronic opisthorchiasis are assessed.

Serum zinc status and Helicobacter pylori infection in gastric disease patients.

The role of Helicobacter pylori status and serum zinc value in gastric disease patients and healthy controls were investigated. Cases used in this work were 45 gastric cancer patients, 44 with peptic ulcers, 52 suffering gastritis and 64 healthy controls, all diagnosed histologically with the controls undergoing medical checkups. Helicobacter pylori status and serum levels of Zn were determined by 13C-urea breath test and flame atomic absorption spectrophotometer, respectively. Our study showed that Helicobacter pylori infection has no change in gastritis, peptic ulcer and gastric cancer group, on the contrast, serum levels of Zn were significantly reduced in gastritis, peptic ulcer and gastric cancer group, compared with healthy controls, and the higher the Zn levels are, the more increased risk of gastric cancer. Helicobacter pylori infection is a cause of gastritis, peptic ulcers and even gastric cancer, while serum zinc level is an indicator of protection of gastric membranes against damage.

ABO research in the modern era of genomics.

Research on ABO has advanced significantly in recent years. A database was established to manage the sequence information of an increasing number of novel alleles. Genome sequencings have identified ABO orthologues and paralogues in various organisms and enhanced the knowledge on the evolution of the ABO and related genes. The most prominent advancements include clarification of the association between ABO and different disease processes. For instance, ABO status affects the infectivity of certain strains of Helicobacter pylori and Noroviruses as well as the sequestration and rosetting of red blood cells infected with Plasmodium falciparum. Genome-wide association studies have conclusively linked the ABO locus to pancreatic cancer, venous thromboembolism, and myocardial infarction in the presence of coronary atherosclerosis. These findings suggest ABO's important role in determining an individual's susceptibility to such diseases. Furthermore, our understanding of the structures of A and B transferases and their enzymology has been dramatically improved. ABO has also become a research subject in neurobiology and the preparation of artificial/universal blood and became a topic in the pseudoscience of "blood type diets." With such new progress, it has become evident that ABO is a critical player in the modern era of genomic medicine. This article provides the most up-to-date information regarding ABO genomics.

Serum sTREM-1 as a surrogate marker of treatment outcome in patients with peptic ulcer disease.

OBJECTIVE: Soluble triggering receptor expressed on myeloid cells-1 (sTREM-1) is elevated in the gastric juice and in cultures of gastric mucosa of patients with peptic ulcer disease (PUD). Its application as a surrogate marker for the treatment of PUD was assessed. METHODS: From 138 eligible patients, 96 were enrolled; 50 with duodenal ulcer, 29 with gastric ulcer and 17 with chronic gastritis. Patients were endoscoped twice; once before treatment and once after treatment. Biopsy specimens were collected for histopathologic estimation of gastritis. Blood was sampled prior to each endoscopy. Serum was collected and sTREM-1 was measured by an enzyme immunoabsorbent assay ( http://www.clinicaltrials.gov identifier NCT00534443). RESULTS: At the end of treatment sTREM-1 was either: (a) below the limit of detection (this occurred in 62 patients and it was accompanied by lacks signs of residual disease in 58 patients, 93.5%); or (b) above the limit of detection (this occurred in 17 patients and it was accompanied by residual disease in 14 patients, 82.3%) (p < 0.0001). Odds ratio for complete healing of peptic ulcer with sTREM-1 below detection limit was 5.30 (95% CI: 1.89-14.83, p < 0.001) compared to serum sTREM-1 above the limit of detection. CONCLUSIONS: Serum sTREM-1 below detection limit may effectively distinguish patients who successfully completed therapy for PUD from those with residual disease and apply as a surrogate marker.

Risk of gastric cancer and peptic ulcers in relation to ABO blood type: a cohort study.

Blood group A was found to be associated with gastric cancer in the 1950s. Strikingly, for peptic ulcers an increased risk has been shown for blood group O. However, previous investigations have generally been poorly conducted and have failed to take a unifying approach to these observations. Using the Scandinavian Donations and Transfusions (referred to as "SCANDAT") database, the authors established a cohort of Swedish and Danish blood donors with known blood type and followed these for the occurrence of gastric cancer and peptic ulcers through December 31, 2002. Cases were ascertained by using nationwide cancer and hospital registers. Altogether, 1,089,022 donors were followed for up to 35 years, during which 688 gastric cancer cases and 5,667 peptic ulcer cases accrued. Poisson regression analyses confirmed an increased risk of gastric cancer among individuals with blood group A (incidence rate ratio = 1.20, 95% confidence interval: 1.02, 1.42) and conversely that peptic ulcer risk was instead highest among those with blood group O. In this large, population-based cohort study, the authors have confirmed the association between blood group A and gastric cancer. In addition, they give further support to the notion that individuals with blood group O have a higher risk of peptic ulcers than those with other blood groups.

Antisecretory, antioxidative and antiapoptotic effects of montelukast on pyloric ligation and water immersion stress induced peptic ulcer in rat.

In the present study, we tried to explore the mechanism of montelukast as an antiulcerogenic agent in pyloric ligation (PL) and water immersion stress (WIS) induced peptic ulcer. The ameliorative effects of montelukast (5, 10, and 20 mg/kg, p.o.) on gastric volume and total acidity were studied in PL model. We have investigated the alteration in the ulcerative index, thiobarbituric acid reactive substances, reduced glutathione, activity of myeloperoxidase, and total calcium level in both models. Estimation of DNA fragmentation by gel electrophoresis was also performed. Medium and higher doses of montelukast showed significant (p<0.05) ameliorative potential on all the above parameters as compared with omeprazole treated group. DNA fragmentation pattern clearly indicated the antiapoptotic effect of montelukast in preventing mucosal erosion in both models. Hence, the gastroprotective effect of montelukast may be attributed to its antisecretory, antioxidative along with its antiapoptotic effect.

ABO blood groups and Helicobacter pylori cagA infection: evidence of an association

Diseases resulting from Helicobacter pylori infection appear to be dependent on a host of genetic traits and virulence factors possessed by this microorganism. This paper aimed to investigate the association between the ABO histo-blood groups and H. pylori cagA infections. Genomic DNA samples (n = 110) of gastric biopsies obtained from patients with endoscopic diagnosis of peptic ulcers (n = 25) and chronic active gastritis (n = 85) were analyzed by PCR using specific primers for the cagA gene. Of the samples, 66.4 percent (n = 73) tested positive and 33.6 percent (n = 37) negative for the gene. The cagA strain was predominant in peptic ulcers (n = 21; 84.0 percent) compared with chronic active gastritis (n = 52; 61.2 percent) (p = 0.05; OR 3.332; 95 percent CI: 1.050-10.576). Additionally, the cagA strain was prevalent in the type O blood (48/63; 76.2 percent) compared with other ABO phenotypes (25/47; 53.2 percent) (p = 0.01; OR 2.816; 95 percent CI: 1.246-6.364). These results suggest that H. pylori cagA infection is associated with the O blood group in Brazilian patients suffering from chronic active gastritis and peptic ulcers.

The influence of Helicobacter pylori eradication on leptin, soluble CD40 ligand, oxidative stress and body composition in patients with peptic ulcer disease.

OBJECTIVE: To determine the effect of Helicobacter pylori (H. pylori) eradication on blood levels of soluble CD40 ligand, leptin, oxidative stress and body composition in patients with dyspepsia infected with H. pylori. METHODS: The infection of H. pylori was based on the presence of both (14)C urea breath test (UBT) and histology. Patients were given triple eradication therapy for 14 days and at 3 months after the treatment, (14)C UBT was reinstituted. Fasting glucose, leptin, body composition, soluble CD40 ligand, total oxidant status (TOS) were studied before and at 3 months after the treatment. RESULTS: In 33 subjects, H. pylori infection was successfully eradicated. sCD40L, and TOS levels were significantly decreased after H. pylori eradication. The percentage of body fat and body fat mass significantly decreased whereas the fat free mass (FFM) increased after eradication. However, eradication of the organism yielded no differences in leptin levels. CONCLUSION: These findings suggest that H. pylori eradication reduces the sCD40L and oxidative stress, fat mass with a significant increase in fat free mass. Thus, eradication of H. pylori infection not only improves ulcer healing, but may also reduce the presumed atherosclerosis risk.

Blood concentration of pantoprazole sodium is significantly high in hepatogenic peptic ulcer patients, especially those with a poor CYP2C19 metabolism.

OBJECTIVE: To determine the plasma concentration of pantoprazole sodium by high performance liquid chromatography and its distribution in patients with different CYP2C19 genotypes in an attempt to provide experimental data for the clinical dosage adjustment of the drug. METHODS: Patients with liver disease and associated peptic ulcer were genotyped according to their CYP2C19 wild-type sequences and mutations in CYP2C19m1 and CYP2C19m2 by the principles of the American Surgical Association using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). The plasma concentration of pantoprazole sodium was detected after oral administration of the enteric-coated capsules in all patients. Included in the present study were 21 patients with primary liver cancer complicated by pathogenic peptic ulcers (confirmed by endoscopy), 22 patients with fatty liver and 25 healthy volunteers between January 2006 and October 2007. The subjects were administered orally with pantoprazole sodium at 40 mg/day for 1 week consecutively. The drug concentration was detected at 24 h and 1 week after drug administration by drawing 3.0 mL blood from the cubital vein. RESULTS: The plasma concentration of pantoprazole sodium was related to the CYP2C19 enzyme type. The plasma concentration of extensive metabolizers (EM) was lower than that of poor metabolizers (PM) in the healthy control group at day 7 of drug administration. Regardless of PM or EM, the plasma concentration of pantoprazole sodium in primary liver cancer patients was higher than that in fatty liver patients, and even higher than that in healthy controls (P < 0.05). CONCLUSION: These results suggest that CYP2C19 activity is inversely correlated with the severity of liver disease, especially in PM patients.

[The erythrocyte and plasma glutathione system under peptic ulcer].

In erythrocytes and blood plasma of patients with the complicated peptic ulcer and postresectional syndromes there was the increase of conjugated dienes (and in the second group the increase in antioxidant activity). Under these conditions the main change was the sharp and identical decrease in glutathione activity. In patients with uncomplicated peptic ulcer there was sharp increase in erythrocyte and plasma glutathione activity and plasma GSH. In operated but basically healthy patients plasma glutathione peroxidase remained decreased but plasma GSH sharply increased. Evidently complicated peptic ulcer is characterized by decreased functioning of the glutathione system. Activation of this system and the decrease or disappearance of manifestations of oxidative stress are associated with a favorable course of this disease, especially at uncomplicated peptic ulcer. The revealed changes significantly differ from those observed in viral hepatitis, bile excretory treat diseases and strokes.

cagA gene and protein status among Iranian Helicobacter pylori strains.

The wide geographic genetic diversity of Helicobacter pylori (Hp) and, in particular, the varying prevalence of cagA in different countries has been documented repeatedly. This study was designed to determine the frequency of cagA in Iranian Hp strains by means of genotyping and assessment of host antibodies. Helicobacter pylori strains from 235 patients, including 174 non-ulcer dyspepsia, 25 peptic ulcer and 36 gastric cancer patients, were studied. The frequencies of the 5', middle and 3' terminal regions of the cagA gene were 90.6, 57.6, 89%, respectively, with no correlation to the clinical outcomes. Antibodies against the CagA protein were present in 90.7% of patients. Multiple biopsy sampling in 97 cases revealed multiple infection in 16.5% of the patients. Sequencing of the seven variants of the 3' end of the cagA gene revealed no clustering and the distribution of the Iranian strains among those of other countries. Our results from the genotyping and serology analyses confirm that the majority of Iranian Hp strains are cagA-positive.