anti-Helicobacter Pylori Antibody Research Articles

Identification of Helicobacterpylori-related gastric cancer risk using serological gastritis markers and endoscopic findings: a large-scale retrospective cohort study

BackgroundGastric cancer remains a severe public health problem worldwide, particularly in Japan. Recent studies have demonstrated that serum markers are beneficial for risk stratification in gastric cancer development. We aimed to evaluate the usefulness of serum markers either alone or in combination (serum markers plus endoscopy) for effective risk stratification of gastric cancer development.MethodsWe enrolled 22,736 patients aged 20–95 years who underwent blood sampling and endoscopic examination at Hiroshima University Hospital in Japan between 1990 and 2014. The serum pepsinogen (PG) levels and anti-Helicobacter pylori antibody (Hp-Ab) titers were evaluated in each patient. The enrolled patients were matched with the database of the Hiroshima Prefecture Regional Cancer Registry. We processed the medical records and excluded patients with possible confounding factors for PG levels, such as proton pump inhibitor use, prior successful eradication therapy, post-gastrectomy, severe hepatorenal dysfunction, Zollinger–Ellison syndrome, and autoimmune gastritis. Among the remaining 5131 patients, we reviewed records of endoscopic examinations and selected 1507 patients (mean age, 62.5 years; 985 men and 522 women) who underwent endoscopic examination more than three months after blood sampling.First, based on the ABC method, patients were classified as follows: High PG levels and negative Hp-Ab, group A, high PG levels and positive Hp-Ab, group B, low PG levels and positive Hp-Ab, group C, and low PG levels and negative Hp-Ab, group D. Group A was further classified into two subgroups using endoscopic findings: true A without atrophic gastritis and pseudo A with atrophic gastritis. All patients underwent annual endoscopy follow-up.ResultsAmong the 1,507 patients (mean age, 62.5 years; 985 men), 24 were diagnosed with newly developed gastric cancer. No significant difference in cancer development was found between group A (PG negative and Hp-Ab negative) and the other groups. Remarkably, no true A group subjects developed gastric cancer.ConclusionsThe combination of serum markers and endoscopic findings is essential for the risk evaluation of gastric cancer.

Polyacrylamide Gel Electrophoresis of Proteins Method versus Enzyme-Linked Immunosorbent Assay and Immunochromatography with Monoclonal Antibodies in Pediatric Infection with Helicobacter Pylori

The current methods for the diagnosis of Helicobacter pylori infection in children include invasive (direct) methods, that enable the detection of the bacteria or the bacterial urease in gastric biopsies, or noninvasive (indirect) methods, which consist of researching specific antibodies, antigens and urease in other different samples (serum, saliva, urine, stool, exhaled air). The urease functions in H. pylori infection is to neutralize gastric acid by producing NH3 through the hydrolysis of urea. Monochloramine, a NH3-derived compounds has cytotoxic effects on host cells. The Western Blot method refers to the extraction of a a sodium dodecyl sulphate from a Helicobacter pylori strain followed by a separation of the solubilised protein using discontinous polyacrylamide gel electrophoresis according to molecular mass and transfer of the separated proteins to nitrocellulose. The ELISA (enzyme-linked immunosorbent assay) technique refers to the detection of Anti-Helicobacter pylori antibodies type Ig G. We also used an immunochromatographic system with the lateral leakage test strip based on the principle of the sandwich technique with monoclonal antibodies. As a result, more than two types of reactions can be detected on a single assay device by the combination of colloidal gold �labelled antibodies and complementary oligonucleotide-labelled immobilized at different places on a nitrocellulose membrane. Our study aims to assess the performances of the Western Blot method for determining anti-Helicobacter pylori Ig A and Ig G antibodies in correlation with clinical data and other available diagnosis methods. For validation purposes, the results were compared to those obtained using the enzyme-linked immunosorbent assay technique, gastric biopsy and immunochromatography.

Correlation between Helicobacter pylori Infection and Gastric Atrophy Examined in the Sera of Mongolian People

Serum specimens obtained from 680 individuals were examined to measure the amounts of pepsinogens 1 and 2, anti-CagA antibodies, and anti-Helicobacter pylori antibodies. We examined sera obtained from 610 Mongolian individuals living in the capital city, Ulaanbaatar. Seventy serum specimens were collected from Japanese people who were health-screened: These were stored at the gastroenterology laboratory of Jichi Medical University. The sera of the Japanese people were used as a control specimen. Two enzyme-linked immunosorbent assay (ELISA) kits, an E-plate ELISA kit from Eiken Chemical Co., Ltd. (Tokyo, Japan), and a Biohit ELISA kit from Biohit Oyj (Helsinki, Finland), were used for the detection of anti-H. pylori IgG antibodies in the sera of the 610 Mongolian people. An ELISA kit EIA-4138 from DRG Instruments GmbH (Germany) was used for the detection of anti-CagA IgG antibodies in the serum specimens. Serum pepsinogens were detected by an ELISA kit from Biohit Oyj. Of the 610 serum specimens, 385 specimens tested positive for the detection of anti-H. pylori antibodies using the two ELISA kits, and 47 tested negative. For the detection of anti-H. pylori antibodies by the Biohit ELISA kit, 560 and 50 specimens were positive and negative, respectively. The ratio of serum pepsinogen 1/2 was statistically lower (p < 0.0001) in the H. pylori-positive (560 specimens) than in the H. pylori-negative (50 specimens) specimens. However, the levels of serum pepsinogen 1 had no statistical significance (p = 0.465) between the specimens of the H. pylori-positive and -negative specimens. The ratio of serum pepsinogen 1/2 was 6.74 ± 0.12 in the H. pylori-positive specimens, whereas the ratio of serum pepsinogen 1/2 was 12.69 ± 1.02 in the H. pylori-negative specimens. This study demonstrated the high prevalence of H. pylori infection in Mongolian people, including young generations, and the people infected with H. pylori possessed low pepsinogen 1/2 ratios, indicating atrophic gastritis. The serological examinations by the two ELISA kits did not consistently reflect the prevalence of H. pylori infection in Mongolian people.

Serological Evaluation of Gastric Cancer Risk Based on Pepsinogen and Helicobacter pylori Antibody: Relationship to Endoscopic Findings

Backgrounds and Aims: The serological risk-prediction system combined the pepsinogen (PG) test, and anti-Helicobacter pylori antibody is available for evaluation of gastric cancer risk. In this system, chronic atrophic gastritis (CAG) or H. pylori infection is diagnosed. Subjects with H. pylori negative and PG test negative (group A) are supposed to be those who have never been infected with H. pylori and are at extremely low risk for gastric cancer. However, a certain proportion of patients with CAG has been identified as the extremely low-risk group (group A). Here we examined endoscopic atrophy and investigated its relationship with the ABC classification system. Methods: We examined 540 patients. All patients underwent an endoscopic examination for evaluating corpus atrophy. Fasting sera were collected and serum PGs and anti-H. pylori antibody (Hp-Ab) titer (E-plate Eiken) were evaluated. Results: Of the 540 patients, 306 were classified into group A. However, 136 of them showed signs of endoscopic atrophy (group A with CAG). Group A with CAG frequently comprised the elderly. A new titer cut-off (<3 U/mL) of the Hp-Ab improved the discrimination of group A with CAG by 8%. Conclusion: The prevalence of group A with CAG patients is a critical problem, especially in elderly subjects.

Association between Helicobacter pylori infection and the presence of anti-sperm antibodies

ABSTRACTThe aim of this study was to investigate the possible association between serum anti-Helicobacter pylori antibodies and anti-sperm antibodies (ASA) in patients with gastroduodenal diseases caused by H. pylori, infertile patients positive for ASA and healthy fertile blood donors as controls. Serum ASA were studied by sperm agglutination tests, sperm immobilization test and ELISA against sperm antigens (ELISAsp). Serum IgG anti-H. pylori antibodies were detected by ELISA (ELISAHp). The tests revealed significantly higher incidence of ASA in patients with gastroduodenal diseases compared to the controls (P < 0.0001). The median levels of both types of antibodies were significantly higher in infertile patients than in patients with upper gastroduodenal diseases in all tests applied (sperm agglutination and immobilization tests P < 0.0001; ELISAsp P = 0.006; ELISAHp, P = 0.0008). Significant linear correlation was found between anti-H. pylori antibodies and ASA detected by sperm immobilization test (r = 0.613, P = 0.05) in the group of patients with gastroduodenal disease, as well as a weak linear correlation was established between anti-H. pylori antibodies and ASA in ELISAsp (r = 0.275, P = 0.0051) in the same group. These results suggest that H. pylori infection may play a role in the induction of ASA.

Helicobacter pylori Infection, Gastric Cancer and Gastropanel.

Gastric cancer (GC) is one of the most widespread types of cancer worldwide. Helicobacter pylori infection has been clearly correlated with gastric carcinogenesis. At present and in the near future, the most important challenge is and will be the significant reduction of mortality due to GC. That goal can be achieved through the identification of higher-risk patients, such as those with atrophic gastritis, intestinal metaplasia and dysplasia. In this review we intend to discuss the importance of diagnosing H. pylori infection and chronic atrophic gastritis in preventing gastric cancer, using a new non-invasive test called GastroPanel. This test is a classification algorithm including four biochemical parameters pepsinogen I and II (PGI and PGII), gastrin-17 (G17), and anti-Helicobacter pylori antibodies (Ig G anti-Hp) measured in fasting sera, which allows to classify patients as having atrophic or non-atrophic gastritis and to find whether gastritis is associated or not with H. pylori infection. GastroPanel is not a "cancer test", but it can and should be used in the screening and diagnosis of subjects with a high cancer risk; still, a careful diagnostic made by superior digestive endoscopy is compulsory to find possible precancerous or cancerous lesions at an early and curable stage.

Association of 4p14 TLR locus with antibodies to Helicobacter pylori.

A genome-wide association study among Europeans related polymorphisms of the TLR locus at 4p14 and the FCGR2A locus at 1q23.3 to Helicobacter pylori serologic status. We replicated associations of 4p14 but not 1q23.3 with anti-H. pylori antibodies in 1,402 Finnish males. Importantly, our analysis clarified that the phenotype affected by 4p14 is quantitative level of these antibodies rather than association with seropositivity per se. Additionally, we annotated variants at 4p14 as expression quantitative trait loci associated with TLR6/10 and FAM114A1. Our findings suggest that 4p14 polymorphisms are linked to host immune response to H. pylori infection but not to its acquisition.

Serologically Determined Gastric Mucosal Condition Is a Predictive Factor for Osteoporosis in Japanese Men.

There are few reports about the influence of Helicobacter pylori infection and/or atrophic gastritis on bone conditions in Japan. To assess whether the combination of serologically determined Helicobacter pylori infection and atrophic gastritis is available as a biomarker for bone conditions. We studied 230 men in their 50s and 60s. Helicobacter pylori infection was determined using serum antibody to this bacterium. Atrophic gastritis was diagnosed on the basis of the serum pepsinogen I and II criteria. The characteristics of the participants' bone were measured at the radius using an ultrasonic bone densitometry system. The risks of low trabecular bone density, low elastic modulus of trabecular bone, and low cortical thickness among subjects who were positive for Helicobacter pylori infection and/or atrophic gastritis relative to those who were not were calculated. Helicobacter pylori infection significantly increased the risk of low trabecular bone density (odds ratio 1.83, 95 % confidence interval 1.04-3.21, P = 0.03). Atrophic gastritis significantly increased the risk of low trabecular bone density (2.22, 1.17-4.22, 0.01). Compared with anti-Helicobacter pylori antibody (-) and atrophic gastritis (-) subjects, anti-Helicobacter pylori antibody (+) and atrophic gastritis (+) subjects were a significant high-risk group for low trabecular bone density (2.65, 1.27-5.55, 0.01). A serological diagnosis of Helicobacter pylori infection and atrophic gastritis, which is utilized for risk assessment of gastric cancer, was suggested to be useful for risk assessment of osteoporosis.

Complete Histopathological Disappearance of Rectal Malt Lymphoma after Eradication of Helicobacter pylori Confirmed by ESD

In a 77-year-old Japanese housewife who was undergoing regular colonoscopy for follow-up of a colon polyp, a total colonoscopy showed an elevated lesion in the rectum. Histological findings of a conventional biopsy from the lesion showed a mucosa-associated lymphoid tissue (MALT) lymphoma, and the patient was diagnosed as having clinical stage 1 disease. We elected to administer antibiotic therapy as the serological test for anti-Helicobacter pylori antibody was positive and Helicobacter pylori was detected in a culture of the biopsy specimens. The antibiotic therapy was successful, however, colonoscopy after the eradication therapy showed a residual lesion. Histologic examination can’t deny the possibility of the presence of a residual MALT lymphoma. Endoscopic ultrasonography revealed that the lesion was confined to the mucosa. We performed endoscopic submucosal dissection (ESD) and histological examination of the ESD specimen showed complete disappearance of the tumor. The patient remains in complete remission now, 1 year after the treatment.

Evaluation of clinico-pathological features and Helicobacter pylori infection in gastric inflammatory fibroid polyps.

Inflammatory fibroid polyps are rare mesenchymal lesions. The frequency of Helicobacter pylori infection in the gastric mucosa overlying inflammatory fibroid polyps and its relation with the histologic features of the polyps are undetermined. The clinico-pathological features of inflammatory fibroid polyps, the frequency of Helicobacter pylori infection in the overlying gastric mucosa, and its putative impact on the phenotype of the polyps were evaluated. Gastric inflammatory fibroid polyps diagnosed in our Hospital from 1998 to 2012 were reviewed and the histological. The histological sections were stained with hematoxylin and eosin and modified Giemsa for the evaluation of Helicobacter pylori infection. Inconclusive cases were further analyzed by immunohistochemistry with anti-Helicobacter pylori antibody. Diagnosis was confirmed in 54 polyps, 85 % developed in females, mean age 63 ± 11 years. Most polyps were sessile (74 %), with a mean size of 15 ± 12 mm, 96 % were located in the antrum and 85 % were removed by snare polypectomy. Helicobacter pylori infection was identified in 48 % of the polyps. Most inflammatory fibroid polyps developed in the submucosa, and mucosal extension was observed in 96 % of the cases. Chronic gastritis was observed in all cases (63 % with activity, 31 % with intestinal metaplasia, and 61 % with foveolar hyperplasia). Erosion and ulceration of the overlying gastric mucosa was observed in 48 % and 11 % of the polyps, respectively. Onion skin features were present in 52 % of the polyps and were more frequently observed in cases without evidence of Helicobacter pylori infection. Background changes in gastric mucosa were not distinctive according to Helicobacter pylori infection. Chronic atrophic gastritis with intestinal metaplasia was associated with the presence of perivascular onion skin lesions. To our knowledge, this is the second largest series of gastric inflammatory fibroid polyps. Helicobacter pylori infection was identified in about half of the cases and was associated with a lower frequency of onion skin features in the polyps.

Effect of sera from chronic urticaria patients with anti-Helicobacter pylori antibodies on the release of histamine by human mast cells

Objective To investigate the relationship between anti-Helicobacter pylori (Hp) antibodies and development of chronic urticaria (CU).Methods Fifty CU patients with positive 13C-urea breath test and anti-Hp antibodies,as well as 50 healthy human controls were recruited in this study.Serum samples were collected from all the subjects.The samples from the patients were subjected to tests for anti-high affinity IgE receptor (anti-FceRI) and-IgE antibodies.Human mast cells (HMCs) were classified into several parts to be incubated with the sera of patients with CU,the sera of healthy controls with anti-IgE and-FceRI antibodies respectively for 20 minutes.Those incubated with the sera of healthy controls without these antibodies served as the control.Subsequently,the levels of histamine released by HMCs were measured by enzyme-linked immunosorbent assay (ELISA).Results The sera of CU patients showed a stronger ability to activate HMCs to release histamine than those of healthy controls ((3.13 ± 0.93) μg/L vs (2.92 ± 0.75) μg/L,t =2.39,P ＜ 0.05).Anti-FceRI antibodies were detected in 4 patients,and antiIgE antibodies in 3 patients.A significant increase was observed in the levels of histamine released by HMCs incubated with anti-FceRI antibody-positive and anti-IgE antibody-positive patient-derived sera (t =4.82,6.34,respectively,both P ＜ 0.01),but not in those incubated with patient-derived sera only positive for anti-Hp antibodies (t =1.74,P ＞ 0.05) compared with those incubated with healthy control-derived sera.In comparison with the antibody-free healthy control-derived sera,those with anti-Hp IgG antibodies showed no significant effect on the release of histamines by HMCs (t =1.95,P ＞ 0.05),whereas those with anti-FceRI antibodies and anti-IgE antibodies exhibited an obvious promoting effect (t =3.72,3.02,respectively,both P ＜ 0.01).Conclusions The anti-Hp antibodies appears to have no role in the pathogenesis of CU,but the presence of anti-FceRI and anti-IgE antibodies may contribute to the initiation of CU in patients with Hp infection. Key words: Urticaria; Helicobacter pylori; Antibody; Mast cells

No evidence for Helicobacter pylori in oral lichen planus.

Oral lichen planus is a T-cell-mediated mucosal disease of unknown etiology. Numerous predisposing factors have been put forward in the etiology of this disease. This includes stress, drugs, genetic susceptibility, certain viruses, and bacterial infections. Recently, there have been studies published on possible role of Helicobacter pylori infection in pathogenesis of mucocutaneous diseases including oral lichen planus (OLP). The aim of this study was to detect immunohistochemically the presence of Helicobacter pylori in oral lichen planus. Paraffin-embedded tissue blocks of 50 cases of OLP and 10 cases of normal buccal mucosal biopsies and 6 endoscopic biopsies of patients with peptic ulcer (control group) were sectioned and stained by hematoxylin and eosin. Serial sections of same were stained immunohistochemically using Anti-Helicobacter pylori antibody and observed under microscope for presence or absence of Helicobacter pylori. Except for the control group, none of the cases of OLP and normal buccal mucosal biopsies showed positivity for Helicobacter pylori. As we did not detect the presence of Helicobacter pylori in any of the OLP cases, we question the role of these organisms in the pathogenesis of OLP planus if any.

Seroprevalence of anti-Helicobacter pylori antibodies in population of Sulaimani governorate/Kurdistan Region/Iraq

Helicobacter pylori (H. pylori) infection is one of the most common chronic bacterial infection in the world. Objective: This study was done to assess the extent of H. pylori infection in Suleimani governorate by noninvasive ELISA technique for quantitative detection of anti-H. pylori IgM, IgG and IgA antibodies in serum. Methods: The study included 335 adult and children volunteers from Chamchamal and Sulaimani cities in Kurdistan region / Iraq. The participants answered a structured questionnaire and a blood sample was taken for serological analysis from each participant. The level of serum antibodies for IgM, IgG and IgA were detected using ELISA technique. Results: In the total sample 20.4% had positive IgM, 32.3% positive IgG and 58.2% positive IgA. Two hundred thirty four (74%) subjects had one or more of the antibodies, 138 subjects (41.1%) had at least one antibody positive (IgM 11 (3.2%), IgG 35 (10.4%), IgA 92 (27.4%). In this study 20% had at least two antibodies positive {IgM 25 (7.4%): IgG 45 (13.4%): IgA 64 (19.1%)}. Conclusions: H. pylori infection is common in population of Sulaimani governorate. IgA anti-H. pylori is the most prevalent antibody of population in Sulaimani governorate. The age group of 20-30 years old has the most seroprevalence of antibodies specific to H. pylori.

Prevalence and risk factors of Helicobacter pylori infection in Chinese maritime workers

Background: Helicobacter pylori infection is very common worldwide.Aim: To evaluate the prevalence and identify the risk factors for Helicobacter pylori infection in Chinese maritime workers.Subjects and methods: Between March 2010 and October 2010, 3995 subjects were selected in the Hospital of Dalian Port. The presence of Helicobacter pylori infection was confirmed using laboratory tests (serum IgG anti-Helicobacter pylori antibodies) and background information, family history, lifestyle and eating habits were collected using questionnaires.Results: The prevalence of Helicobacter pylori infection was 44.9% in these Chinese maritime workers. Prevalence of Helicobacter pylori infection was associated with family income, living space, family history of gastrointestinal diseases, smoking, drinking tea, raw vegetables consumption, spicy food, pickle food, dining outside, no regular meal and dish sharing. Further analysis with multivariate logistic regression analysis indicated that raw vegetables consumption, pickle food consumption, family income and family history of gastrointestinal diseases were independent predictors for Helicobacter pylori infection. No association was found between infection and gender, marital status, education, alcohol consumption and tap water consumption.Conclusion: Helicobacter pylori infection is associated with raw vegetables consumption, pickle food consumption, family income and family history of gastrointestinal disease among Chinese maritime workers.

Sa1977 A Preliminary Longitudinal Assessment of Mutational Load in Patients With Barrett's Esophagus

INTRODUCTION: Chronic Atrophic Gastritis (CAG) is the most important independent risk condition for gastric cancer, histology being considered the gold standard for both diagnosis and follow up. The Operative Link for Gastritis Assessment (OLGA) is an innovative histological system proposed for staging atrophic gastritis in a prognostic view. GastroPanel (Biohit, Helsinki, Finland) is a serological kit for a non-invasive diagnosis of chronic atrophic gastritis (CAG), including serum pepsinogen I (PGI), pepsinogen II (PGII), gastrin-17 (G17) and IgG anti-Helicobacter pylori antibodies (IgG-Hp). Clinical practice is lacking of a non invasive instrument useful to predict and to follow the stage of atrophic gastritis. AIMS& METHODS: To evaluate correlation between GastroPanel and OLGA stage, in a cohort of dyspeptic patients referred from a primary care setting to our G.I. Unit Histological evaluation of gastric biopsies was performed in 125 pts (83 females, mean age 53 yrs). Atrophy was assessed according to the OLGA staging system. OLGA stages III and IV are considered at high risk for gastric cancer development. From each subject, a blood sample was taken for GastroPanel analysis. RESULTS: GastroPanel analysis showed that 79 pts (63,2%) have no gastritis, 22 pts (17,6%) a Hp-related chronic gastritis and 24 (19,2%) atrophic gastritis picture. Comparing GastroPanel results to the histological findings, 48 pts of the first group were confirmed normal at histology, 27 pts have an OLGA stage 0-II, 4 pts have an OLGA stage III, none stage IV. Among the patients with Hp-related gastritis, 1 pt results normal at the histological evaluation, 20 pts have an OLGA stage 0-II, 1 pt has an OLGA stage III; 6 out of the 24 pts with evidence of CAG at GastroPanel have an OLGA stage 0-II, 18 pts have an OLGA stage III-IV. The negative predictive value (NPV) of GastroPanel for CAG is 95,0%, being the positive predictive value (PPV) 75,0%. CONCLUSION: GastroPanel shows an high NPV to predict absence of atrophic gastritis. The relationship beetween GastroPanel and OLGA system seems to confirm the clinical performances of the test

Stage IV intramucosal gastric marginal zone B cell lymphoma of mucosa-associated lymphoid tissue type.

A 45-year-old woman with no symptoms underwent upper gastrointestinal endoscopy. A discolored area was noted at the greater curvature of the gastric upper body. Endoscopic ultrasonography demonstrated thickening of the second sonographic layer indicating that the depth of invasion was confined to the mucosa. A urea breath test and anti-Helicobacter pylori antibody test were negative. A computed tomography scan showed a consolidation at the right lung. Gastric biopsy and transbronchial lung biopsy (TBLB) demonstrated a monotonous proliferation of atypical small lymphocytes. A diagnosis of gastric marginal zone B cell lymphoma of mucosa-associated lymphoid tissue type (MALT lymphoma) was made. The clinical stage was stage IV. A genetic analysis showed rearrangement of the joining region of the immunoglobulin heavy chain gene and identical clones in both lesions. An API2-MALT1 fusion gene was detected in the gastric lesion. After H. pylori eradication treatment, combination treatment with rituximab plus CHOP (R-CHOP) was performed; 6months later an endoscopy revealed complete disappearance of the lesion. Multiple gastric biopsies showed no infiltrating atypical lymphocytes. Similarly, the lesion in the lung showed complete remission (CR) on CT and TBLB. This report shows that a gastric MALT lymphoma located in the mucosa and disseminated to the lung maintained CR by R-CHOP.

Authors’ Response: Anti-Helicobacter pylori antibodies, autoimmunity, aldosterone and infertility: causal or casual association with polycystic ovary syndrome?

Authors’ Response: Anti-Helicobacter pylori antibodies, autoimmunity, aldosterone and infertility: causal or casual association with polycystic ovary syndrome?

Anti-Helicobacter pylori antibodies and polycystic ovary syndrome

Anti-Helicobacter pylori antibodies and polycystic ovary syndrome

Gastric injury caused by low-dose aspirin therapy in consecutive Japanese patients: a prospective study

Low-dose aspirin (<325 mg/day), administered to those with several conditions involving ischemic disorders, can cause upper gastrointestinal (GI) complications. In this prospective study, we aimed to clarify the incidence of aspirin-induced gastric ulcers in consecutive Japanese patients and identify suitable preventive measures. We recruited 125 consecutive adult outpatients who received low-dose aspirin (enteric-coated tablets 100 mg) for >8 weeks. Endoscopy and blood tests were used to evaluate their gastric injury (which was scored using a modified Lanza scale) and anti-Helicobacter pylori antibody titer, respectively. We found that 39.8% of patients received either no upper GI drug or only mucoprotective drugs, 39.8% received medium-dose histamine H2 blockers, and 20.4% received proton-pump inhibitors (PPIs). Anti-H. pylori antibody titers were positive in 43.7% of patients. The incidence of definitive gastric ulcers in this population was 0.97%. Ordered logistic regression analysis revealed that the odds ratio for the increase in the modified Lanza score was 0.20 for medium-dose histamine H2 blockers and 0.09 for PPIs. The incidence of postoperative definitive gastric ulcers in Japanese patients receiving ≤100 mg enteric-coated aspirin was 0.97%. The use of PPIs and histamine H(2) blockers may prevent aspirin-induced gastric injury in such patients.

Impact of Helicobacter pylori infection on liver fibrosis in Egyptian patients with chronic hepatitis C

Both Helicobacter pylori (HP) and hepatitis C virus (HCV) infections are endemic in Egypt. This work aimed to investigate the presence of HP in the liver of patients with chronic hepatitis C (CHC) and explore the relation between HP infection, liver histopathology and HCV viral load. The study included 60 patients with CHC. Virological, biochemical, liver biopsy and testing for anti-Hp and anti-schistosomal antibodies in serum were done. Liver tissues were examined for histopathological and presence of Hp by detection of HP 16S rRNA gene by PCR and sequence analysis. Anti-schistosomal and anti HP antibody was found in 45% and 61.7%, respectively. Low stages of fibrosis (F0–F3) were found in 73.3% and advanced fibrosis (F4–F6) in 26.7%. HP DNA was found in 10% of the liver specimens. Although the frequency HP antibodies was equally high in patients with advanced and low fibrosis (68.8% and 59.1%, P>0.05), the HP DNA in liver tissue was significantly more frequent in patients with advanced fibrosis (31.25% vs. 2.7%, P=0.004). Meanwhile, the median viral load of HCV was higher in patients with HP DNA in liver tissue compared to patients with no HP DNA in liver tissue (337.000 vs. 165.000, P=0.3491). HCV RNA titer, fibrosis score and history of blood transfusion, are independent factors associated with HP DNA in liver tissue. In conclusion, the presence of HP in liver tissue of patients with advanced fibrosis suggests a potential relation between HP infection and progression of liver fibrosis due to HCV.