Serum Helicobacter Pylori IgG Research Articles

Determining Gastric Cancer-Related Risk Factors in Mongolian Population Using ABC(D) Method: A Matched Case-Control Study

Objective:We aimed to identify gastric cancer-related risk factors and evaluate the efficacy of screening ABC(D) method in determining high risk gastric cancer individuals in Mongolian population. Methods: A total of 240 participants (120 gastric cancer patients and 120 healthy individuals) were included in this study. Data were collecting using a structured questionnaire consisting of 56 questions covering 5 categories. Serum Helicobacter pylori IgG (H. pylori IgG), pepsinogen I (PGI), and pepsinogen II (PGII) were tested in one third of all the participants (40 gastric cancer patients and 40 controls). PGI, PGII, and H. pylori IgG levels were measured using GastroPanel enzyme-linked immunosorbent assay kit (Biohit, Helsinki, Finland). Results:Habits of having leftover meals (OR 2.22, 95%CI 1.27-3.86, p<0.01), daily consumption of tea with salt (OR 1.97, 95%CI 1.18-3.30, p<0.01), smoking on an empty stomach (OR 2.44, 95%CI 1.11-5.37, p<0.05), daily consumption of vegetables (OR 0.45, 95%CI 0.27-0.76, p<0.01), and daily consumption of fruit juice (OR 0.36, 95%CI 0.15-0.85, p<0.05), family history of gastric cancer (parents OR 2.88, 95%CI 1.07-7.78, p<0.05, siblings (OR 3.09, 95%CI 1.09-8.81, p<0.05), and history of gastric diseases (OR 3.65, 95%CI 2.10-6.35, p<0.0001) were identified as protective factors. A low PGI level (<35.25ng/ml) and low PGI/II ratio (<4) were associated with gastric cancer risk. According to ABC(D) method, groups C and D had higher proportion of gastric cancer cases than group A and B (group C, OR 7.50, 95%CI 1.20-47.05, p<0.05; group D, OR 8.3, 95%CI 1.33-51.26, p<0.05). Conclusion: Our findings suggested that gastric cancer risk was more closely related to eating habits, smoking, family history, and precancerous lesions. ABC(D) method seems to be a plausible alternative or supplementary method for stratifying patients at high risk of gastric cancer in this country.

Hypergastrinemia in Long-Term Use of Proton Pump Inhibitors

Background/Aim: The use of proton pump inhibitors (PPIs) is known to lead to hypergastrinemia; however, the data in patients with atrophic gastritis is still lacking. The aim of this study was to investigate the effects of long-term PPIs use on the gastrin levels in patients with atrophic gastritis and to determine factors affecting hypergastrinemia in long-term users of PPIs. Methods: Serum Helicobacter pylori IgG, gastrin and pepsinogen levels were measured. Atrophic gastritis was assessed by upper gastrointestinal endoscopies based on the Kimura-Takemoto classification and pepsinogen levels. CYP2C19 polymorphisms were assessed using DNA extracted from peripheral blood. Results: A total number of 382 patients (275 men and 107 women) were enrolled. Median serum gastrin levels were higher in PPI users than in non- users (234 vs. 113 pg/mL, p < 0.001) and in women than in men (252 vs. 155 pg/mL, p = 0.006). Gastrin levels were significantly associated with corpus atrophy only in the subgroup of non-users of PPIs. Multivariate analysis revealed that hypergastrinemia (over 150 pg/mL) was significantly associated with PPI use (OR 5.30; 95% CI 3.32–8.47), women (OR 2.22; 95% CI 1.33–3.72) and corpus atrophy (OR 1.82; 95% CI 1.14–2.90). Conclusion: PPI use, women and corpus atrophy were risk factors for hypergastrinemia. Gender, but not corpus atrophy, affected the gastrin levels in long-term users of PPIs.

Detection and analysis on serum antibodies for five common pathogenic microbes in patients with Posner-Schlossmarm syndrome

Background Posner-Schlossman syndrome (PSS) is often recurrent and is a cause of blindness.The etiology of PSS remains to be elucidated.It is reported that there is a certain association between pathogenic microorganisms and PSS in rather small samples. Objective This study was to analyze the related serum antibody levels of cytomegalovirus (CMV), herpes simplex virus (HSV), rubella virus (RV), helicobacter pylori (HP) and anti-streptolysin O (ASO) and provide a clue for the study on pathogenesis and therapy of PSS. Methods A prospective cases-controlled study was carried out in Shenzhen Eye Hospital from December, 2014 to December, 2016 under the approval of Ethic Committee of this hospital and informed consent of each subject prior to initial of any medical examination.Peripheral blood samples were collected from 82 PSS patients as the PSS group and 100 age-and gender-matched healthy blood donors as the normal control group.The positive rates of serum CMV IgG, CMV IgM, HSV IgG, HSV IgM, RV IgG, RV IgM, HP IgG and HP IgM in the subjects were detected by indirect ELISA, and the positive rate of serum ASO antibody was determined by immuno-scatter turbidmetry. Results The positive rates of serum CMV-IgG, CMV-IgM, HP-IgG, HP-IgM and ASO antibody were 22.0%, 17.1%, 22.0%, 17.1% and 17.1% in the PSS group, which were significantly higher than 5.0%, 0.0%, 10.0%, 2.0% and 7.0% in the normal control group (χ2=11.726, 18.496, 4.943, 12.766, 4.479, all at P 0.05). Conclusions CMV, HP and hemolytic streptococcal infection may participate in the occurrence and development of PSS. Key words: Posner-Schlossman syndrome; Etiology; Cytomegalovirus; Herpes simplex virus; Rubella virus; Helicobacter pylori; Anti-streptolysin O; Antibody

Associated factors of atrophic gastritis diagnosed by double-contrast upper gastrointestinal barium X-ray radiography: a cross-sectional study analyzing 6,901 healthy subjects in Japan.

BackgroundDouble-contrast upper gastrointestinal barium X-ray radiography (UGI-XR) is one of the most widely conducted gastric cancer screening methods. It has been executed to find gastric cancer, but has not been usually executed to detect premalignant atrophic mucosa of stomach. To understand the meaning of UGI-XR-based atrophic gastritis, we analyzed its association with several causative factors including Helicobacter pylori (HP) infection.MethodsWe evaluated 6,901 healthy adults in Japan. UGI-XR-based atrophic gastritis was diagnosed based on the irregular shape of areae gastricae and its expansion in the stomach.ResultsOf the 6,433 subjects with no history of HP eradication and free from gastric acid suppressants, 1,936 were diagnosed as UGI-XR-based atrophic gastritis (mild: 234, moderate: 822, severe: 880). These were univariately associated with serum HP IgG and serum pepsinogen I/II ratio with statistical significance. The multiple logistic analysis calculating standardized coefficients (β) and odds ratio (OR) demonstrated that serum HP IgG (β = 1.499, OR = 4.48), current smoking (β = 0.526, OR = 1.69), age (β = 0.401, OR = 1.49), low serum pepsinogen I/II ratio (β = 0.339, OR = 1.40), and male gender (β = 0.306, OR = 1.36) showed significant positive association with UGI-XR-based atrophic gastritis whereas drinking and body mass index did not. Among the age/sex/smoking/drinking-matched 227 pairs derived from chronically HP-infected and successfully HP-eradicated subjects, UGI-XR-based atrophic gastritis was detected in 99.1% of the former but in only 59.5% of the latter subjects (p<0.0001). Contrastively, UGI-XR-based atrophic gastritis was detected in 13 of 14 HP-positive proton pump inhibitor users (92.9%) and 33 of 34 HP-positive histamine H2-receptor antagonist users (97.1%), which are not significantly different from gastric acid suppressant-free subjects.ConclusionsThe presence of UGI-XR-based atrophic gastritis is positively associated with Helicobacter pylori infection, current smoking, age, decreased serum pepsinogen I/II ratio, and male gender. Eradication of Helicobacter pylori seems to superficially improve UGI-XR-based atrophic gastritis whereas intake of gastric acid suppressants does not.

Helicobacter pylori seropositivity in fibromyalgia syndrome

Although there are some studies suggesting relation between different types of infection and fibromyalgia syndrome (FM), there is presently no proof that FM is caused by an infection. Helicobacter pylori (HP) infection may cause extragastric manifestations. Inflammation is an important mediator of increased sympathetic nervous system activity and may lead to pain in fibromyalgia patients. In this study, we aimed to investigate the HP seropositivity in fibromyalgia patients compared with controls for possible role of HP infection in FM. Sixty-seven patients with fibromyalgia were evaluated. Two of them were excluded from the study because of high level of acute phase reactants. Sixty-five female patients with fibromyalgia and 41 randomly selected age-matched female healthy controls were enrolled to study. Serum HP IgA and IgG antibodies were measured by enzyme-linked immunosorbent assay technique. Fibromyalgia Impact Questionnaire was assessed in patients and controls. Seropositivity of HP IgG antibody in the fibromyalgia patients was significantly higher than in the control group. No statistically significant differences were found regarding the clinical features between fibromyalgia patients with HP IgG antibody and patients without IgG antibody. Our study suggests that former HP infection may have a role in the etiopathogenesis of fibromyalgia syndrome or may act as a triggering factor. However, high seroprevalence of HP in general population and prevalent asymptomatic infection make it difficult to interpret these results for the definite role of HP in FM. Highlighting the pathophysiologic mechanisms of FM will result in more effective treatment regimens.

Helicobacter pylori seropositivity in fibromyalgia syndrome

Although there are some studies suggesting relation between different types of infection and fibromyalgia syndrome (FM), there is presently no proof that FM is caused by an infection. Helicobacter pylori (HP) infection may cause extragastric manifestations. Inflammation is an important mediator of increased sympathetic nervous system activity and may lead to pain in fibromyalgia patients. In this study, we aimed to investigate the HP seropositivity in fibromyalgia patients compared with controls for possible role of HP infection in FM. Sixty-seven patients with fibromyalgia were evaluated. Two of them were excluded from the study because of high level of acute phase reactants. Sixty-five female patients with fibromyalgia and 41 randomly selected age-matched female healthy controls were enrolled to study. Serum HP IgA and IgG antibodies were measured by enzyme-linked immunosorbent assay technique. Fibromyalgia Impact Questionnaire was assessed in patients and controls. Seropositivity of HP IgG antibody in the fibromyalgia patients was significantly higher than in the control group. No statistically significant differences were found regarding the clinical features between fibromyalgia patients with HP IgG antibody and patients without IgG antibody. Our study suggests that former HP infection may have a role in the etiopathogenesis of fibromyalgia syndrome or may act as a triggering factor. However, high seroprevalence of HP in general population and prevalent asymptomatic infection make it difficult to interpret these results for the definite role of HP in FM. Highlighting the pathophysiologic mechanisms of FM will result in more effective treatment regimens.

The Influence of Chronic Helicobacter Pylori Infection on some Serum Lipid Profile Parameters, Apolipoproteins A-I and B and Lp(a) Lipoprotein

The Influence of Chronic Helicobacter Pylori Infection on some Serum Lipid Profile Parameters, Apolipoproteins A-I and B and Lp(a) Lipoprotein Data on proatherogenic lipid profile alterations due to chronic Helicobacter pylori (HP) infection are contradictory. Aim of this study was to examine the differences in some lipid parameters between 55 subjects of both gender with a chronic HP infection (IgG&gt;50 U/mL and IgA &lt;20 U/mL) and 55 gender matched HP seronegative subjects (IgG and IgA &lt;20 U/mL). Total cholesterol (TC) (p&lt;0.001), triglycerides (TG) (p&lt;0.05), LDL-cholesterol (LDL-C) (p&lt;0.02), non-HDL-cholesterol (non-HDL-C), apolipoprotein (apo) B (p&lt;0.001), Lp(a) and HDL-cholesterol (HDL-C) serum levels were higher in HP seropositive than in seronegative subjects, while there were almost no differences in apo A-I. In HP seropositive subjects, the frequency of pathological TC (p&lt;0.001), TG (p&lt;0.05), LDL-C (p&lt;0.01), non-HDL-C (p&lt;0.01), apo B (p&lt;0.02) and Lp(a) serum levels was higher compared to seronegative. Serum HP IgG titers correlated negatively with TC, LDL-C (p&lt;0.05), non-HDL-C, apo B and Lp(a) levels, and positively with TG, HDL-C and apo A-I levels. Results are similar for both genders. Our results confirm the hypothesis that a chronic HP infection could modify the lipid profile in a proatherogenic way.