Seroprevalence ofHelicobacter pylori and association with atrophic gastritis in patients with Sjögren’s syndrome

To investigate the association betweenHelicobacter pylori (HP) infection and atrophic gastritis in Sjögren’s syndrome (SS), we conducted an age-matched case-control study examining serum HP-IgG antibodies and pepsinogen (PG) I and II levels using ELISA. The sera of 82 primary SS (1-SS), and 57 secondary SS (2-SS) were studied, as well as 198 controls having a diagnosis of connective tissue disease (CTD), except for SS which were obtained according to age. The titers of HP-IgG in 1-SS were significantly much higher than those in either 2-SS or control. The HP-IgG level revealed an exclusively positive correlation with the serum PG II level and a negative correlation with the PG I/II ratio. Serum PG II levels and PG I/II ratios were associated with the positivity of HP-IgG antibodies. The age-specific seroprevalence rates of HP infection in SS patients compared with controls showed a high positivity in patients less than 49 years old, but no difference among the higher age groups because of increasing positive rates with advancing age in the control. The matched odds ratio with HP infection in all SS (1-SS and 2-SS) and in 1-SS were 2.33 (95% CI: 1.43–3.81) and 2.75 (95% CI: 1.50–5.05), respectively. However, the positive PG I/II ratio did not show a statistically significant odds ratio for SS. We conclude that SS patients have a highly positive association with HP infection and that atrophic gastritis with SS may occur as a result of HP infection.     

Seroprevalence of Helicobacter pylori and association with atrophic gastritis in patients with Sjögren’s syndrome

Abstract

To investigate the association between Helicobacter pylori (HP) infection and atrophic gastritis in Sjögren’s syndrome (SS), we conducted an age-matched case-control study examining serum HP-IgG antibodies and pepsinogen (PG) I and II levels using ELISA. The sera of 82 primary SS (1-SS), and 57 secondary SS (2-SS) were studied, as well as 198 controls having a diagnosis of connective tissue disease (CTD), except for SS which were obtained according to age. The titers of HP-IgG in 1-SS were significantly much higher than those in either 2-SS or control. The HP-IgG level revealed an exclusively positive correlation with the serum PG II level and a negative correlation with the PG I/II ratio. Serum PG II levels and PG I/II ratios were associated with the positivity of HP-IgG antibodies. The age-specific seroprevalence rates of HP infection in SS patients compared with controls showed a high positivity in patients less than 49 years old, but no difference among the higher age groups because of increasing positive rates with advancing age in the control. The matched odds ratio with HP infection in all SS (1-SS and 2-SS) and in 1-SS were 2.33 (95% CI: 1.43–3.81) and 2.75 (95% CI: 1.50–5.05), respectively. However, the positive PG I/II ratio did not show a statistically significant odds ratio for SS. We conclude that SS patients have a highly positive association with HP infection and that atrophic gastritis with SS may occur as a result of HP infection.     

Study of Association Between Atrophic Gastritis and Body Mass Index: A Cross-Sectional Study in 10,197 Japanese Subjects

Objectives The aim of this study was to elucidate the association between body mass index (BMI) and both Helicobacter pylori and atrophic gastritis. Methods The study involved 10,197 subjects participating in a Japanese mass endoscopic gastric cancer screening program. Atrophic gastritis was assessed by pepsinogen I to II ratio. Results In logistic regression models, BMI had an inverse association with atrophic gastritis, with the odds ratios (OR) decreasing progressively to 0.67 (95% confidence interval [CI] 0.57–0.79, P < 0.0001) in the highest BMI quintiles (BMI ≥25.66) group compared with the lowest BMI quintiles (BMI <20.97) group. In linear regression models, atrophic gastritis predicted BMI (regression coefficient −0.326, 95% CI −0.469, −0.184, P < 0.0001), whereas H. pylori antibody was not a predictor (regression coefficient 0.072, 95% CI −0.053, 0.198, P = 0.3). Conclusions A small, inverse association between BMI and atrophic gastritis was found in the general population. In contrast, no association was observed between H. pylori seropositivity and BMI. Electronic supplementary material  The online version of this article (doi:) contains supplementary material, which is available to authorized users.     

Severity of atrophic gastritis related to antiparietal cell antibody and gastric carcinogenesis, including p53 mutations

BACKGROUND AND AIMS: Infection with Helicobacter pylori (Hp) has been linked to atrophic gastritis, an inflammatory precursor of non-cardia gastric carcinoma. Mutations in the p53 gene are one of the most frequent genetic alterations in gastric carcinoma. In a subgroup of atrophic gastritis, antiparietal cell antibody (APCA) has been detected. This study was aimed to clarify the role of APCA in the progression of atrophic gastritis and gastric carcinogenesis, and to determine the relationship of the severity of atrophic gastritis to gastric carcinoma and to p53 mutations. METHODS: In 494 control subjects and 284 gastric carcinoma patients, serum APCA was evaluated and all subjects and patients were classified into four groups using serologic markers (anti-Hp IgG antibody and pepsinogen (PG) test: positive; PG I < 70 microg/L and PG I/II ratio < 3.0) as follows: A, HP- PG-; B, HP+ PG-; C, HP+ PG+ and D, HP- PG+. p53 mutations were analyzed in 174 of 284 patients. RESULTS: Antiparietal cell antibody seropositivity increased from group B to D, however, no difference in its positivity was found between controls and patients. The incidence of gastric carcinoma increased from A to D, especially the intestinal subtype. The frequency of p53 gene mutations was higher in PG+ than in PG- gastric carcinoma. CONCLUSIONS: Antiparietal cell antibody seropositivity is involved in the progression of a subgroup of atrophic gastritis, but not associated with gastric carcinogenesis. Severe atrophic gastritis is associated with susceptibility to gastric carcinoma, especially the intestinal subtype, and p53 mutations.     

Cigarette Smoking Promotes Atrophic Gastritis in Helicobacter pylori-Positive Subjects

Aging and smoking are known to promote atrophic gastritis (AG) and intestinal metaplasia (IM). This study investigated the relationship between Helicobacter pylori (Hp) infection, aging, smoking, and AG/IM. Ninety-six Hp-negative and 231 Hp-positive subjects were divided according to age; (39 years, 40–59 years, and 60 years) and smoking history (never smoked, or currently smoking). Histologic grading was performed according to the updated Sydney system. Fasting pH, total bile acid (TBA) concentration, and ammonia (NH₃) concentration in gastric juice were measured. Comparisons were made based on Hp status, age, and smoking. Independent relative risks for severe AG and IM were calculated. Grades of atrophy and IM were significantly higher in Hp-positive subjects, and these increased with age. Within Hp-positive subjects, grades of atrophy and IM were higher in smokers and in the middle and upper age groups. Within Hp-positive subjects, gastric pH and TBA were similarly higher in smokers and older subjects. An increased risk of severe AG/IM was statistically associated with smoking (OR 9.31, 3.85–22.50/OR 4.91, 1.90–12.68) and high TBA concentrations (OR 2.92, 1.19–7.17/OR 3.28, 1.25–8.62). Both Hp infection and aging are closely related to the development of AG and IM. Cigarette use and high TBA concentrations may play a role in the progression of AG and IM in Hp-positive subjects.     

Relationship between pepsinogen I/II ratio and age or upper gastrointestinal diseases in Helicobacter pylori-positive and -negative subjects]

BACKGROUND/AIMS: Although previous reports suggested that pepsinogen (PG) I/II ratio was the index of gastric atrophy, PG I/II ratio was also related to other factors such as Helicobacter pylori (H. pylori) infection, various gastrointestinal diseases, and aging. The aim of this study was to evaluate the relationship between serum PG I/II ratio and age or upper gastro-intestinal diseases according to H. pylori infection status. METHODS: A total of 529 individuals (307 male; mean age, 57.2 years) were divided into 4 groups (94 gastric ulcers, 35 duodenal ulcers, 105 reflux esophagitis, and 295 atrophic gastritis) according to endoscopic diagnosis. H. pylori infection was determined by H. pylori IgG antibody (ELISA) and PG was measured by latex immunoassay. RESULTS: H. pylori infected patients showed markedly increased serum PG II levels (24.0+/-14.7 ng/mL vs. 13.8+/-16.6 ng/mL, p0.001) and low PG I/II ratio (3.9+/-2.0 vs. 6.0+/-2.5, p0.001) than non-infected subjects. In H. pylori infected patients, mean PG I/II ratios in the gastric ulcer and atrophic gastritis group were significantly lower than those of the duodenal ulcer and reflux esophagitis group (p0.001, ANOVA, Turkey's multiples comparison test). The mean ratio of open type atrophic gastritis was lower than that of close type atrophic gastritis (3.0+/-1.4 vs. 3.8+/-1.7, p0.005). PG I/II ratio gradually decreased with age in H. pylori-infected patients with atrophic gastritis (R(2)=0.9, p=0.005, linear regression analysis). CONCLUSION: Serum PG I/II ratio reflects H. pylori infection and gastric atrophy. In the presence of H. pylori infection, gastric atrophy progresses with age.     

Circulating Ghrelin Levels in Patients with Various Upper Gastrointestinal Diseases

The stomach is the main source of circulating ghrelin. Plasma concentrations of this hormone in patients with various upper gastrointestinal diseases remain undetermined. Thus we measured plasma ghrelin levels by radioimmunoassay in 225 subjects, including 134 Helicobacter pylori-infected and 91 uninfected subjects. They included 67 patients with chronic gastritis (CG), 26 with benign gastric polyp (BGP), 24 with gastric ulcer (GU), 24 with reflux esophagitis (RE), 18 with duodenal ulcer (DU), 28 with acute gastritis (AG), 23 with gastric cancer (GC), and 39 who had normal mucosa on upper endoscopy (N). Plasma pepsinogen I and II levels were also measured. The extent of gastritis was assessed endoscopically. Ghrelin levels differed significantly among the different disease groups. Plasma ghrelin concentrations were lowest in the CG group, followed by the GU group, and highest in the AG patients. There was a significant difference in the levels between differentiated and undifferentiated GC. Ghrelin concentrations in BGP, RE, and DU patients were comparable to those in the N group. Ghrelin circulating levels were lower in H. pylori-positive than –negative individuals, but the significant differences among disease groups were still observed in H. pylori-infected and uninfected populations. Ghrelin concentrations correlated positively with plasma pepsinogen I levels and I/II ratios and inversely with the extent of H. pylori-related gastritis. Plasma ghrelin levels varied widely in diverse conditions of the upper digestive tract, reflecting the inflammatory and atrophic events of the background gastric mucosa. Further investigation is warranted to unravel the mechanisms of the high circulating ghrelin levels in certain upper gastrointestinal diseases.     

Chronic atrophic antral gastritis and risk of metaplasia and dysplasia in an area with low prevalence of Helicobacter pylori

Introduction  The Northeastern region of Peninsular Malaysia is an area with exceptionally low prevalence for Helicobacter pylori infection. The risk of intestinal metaplasia and dysplasia in patients with chronic atrophic gastritis (CAG) and its association with Helicobacter pylori is unknown in this region. Methods  This was a cross-sectional study on gastric biopsies from 234 consecutive patients (mean age 53.5 [14.8] years) who underwent upper gastrointestinal endoscopy between January 2006 and December 2006. Results  There were 137 (59%) men and 185 (79%) Malay patients. Among 234 biopsies, CAG was found in 99 and non-atrophic gastritis in 135. Intestinal metaplasia and dysplasia were detected in 8 and 6 atrophic gastritis biopsies, respectively, and in 10 and 3 of non-atrophic gastritis biopsies, respectively. H. pylori were detected in 16 (9 Malays, 7 non- Malays) biopsies (p=0.024); intestinal metaplasia was detected in 4 biopsies (p=0.3) and dysplasia in 5 biopsies (p=0.3). Of the 218 biopsies negative for H. pylori, intestinal metaplasia was found in 14 and dysplasia in 4. The risk of intestinal metaplasia as well as dysplasia was associated with presence of H. pylori infection (p=0.029 and p<0.001 respectively). Conclusion  Even in a setting of low prevalence of H. pylori, intestinal metaplasia and dysplasia were significantly associated with H. pylori infection. The frequency of intestinal metaplasia and dysplasia was similar different between biopsies with atrophic gastritis and non-atrophic gastritis.     

胃蛋白酶原和胃泌素筛查胃癌及萎缩性胃炎

目的探讨血清胃蛋白酶原(PG)和胃泌素-17(G-17)与胃癌及萎缩性胃炎的关系,并分析幽门螺杆菌感染、服用抑酸药、年龄及性别等多种因素对血清PG和G-17的影响,建立本地区胃癌及萎缩性胃炎的血清学筛查方法。方法选择2013年2月至2013年8月在我院消化内镜中心行胃镜检查符合入选研究标准的100例患者,根据组织病理学诊断将结果分为3组:对照组28例,萎缩性胃炎组52例,胃癌组20例,以免疫放射测定法和放射免疫法检测血清PGⅠ、PGⅡ和G-17水平。结果与正常对照组比较,萎缩性胃炎组、胃癌组的PGⅠ和PGⅠ/PGⅡ比值(PGR)水平均降低(P0.05),萎缩性胃炎组的G-17水平显著降低(P0.01),胃癌组的G-17水平显著增高(P0.01)。采用Bayes判别法分析多种因素、PG和G-17并建立Bayes判别函数作为筛查胃癌及萎缩性胃炎的血清学方法。结论检测血清PG和G-17可以作为一种无创性的筛查胃癌及萎缩性胃炎的方法,适合大规模人群普查。     

The relationship of gastrin, pepsinogen, and Helicobacter pylori in erosive reflux esophagitis]

BACKGROUND/AIMS: Helicobacter pylori (H. pylori) infection is known as a major cause of atrophic gastritis and is associated with serum gastrin, pepsinogen, and gastric acid secretion. There is still a controversial association between gastroesophageal reflux disease and H. pylori infection. This study was designed to investigate the relationship among serum gastrin, pepsinogen, and H. pylori infection in the erosive reflux esophagitis (ERD) patients. METHODS: Patients who were diagnosed as ERD by one gastroenterologist at the Kangnam St. Mary's hospital were prospectively enrolled. The persons without ERD in the control group were matched for age and sex. We examined the gastrin, pepsinogen I (PG I), PG II, PG I/II ratio, and H. pylori infection. RESULTS: Forty five patients were enrolled in ERD group and 66 persons in control group. The H. pylori infection rate in ERD group was lower than that in the control group (11.1% vs. 43.9%, p<0.001). PG I/II ratio in ERD group was higher than that in the control group (7.0+/-3.1 vs. 5.3+/-2.6, p=0.003). The PG II (p=0.016) and gastrin (p=0.029) in ERD group were lower than those in the control group. BMI in ERD group was higher than that in the control group (24.5 vs. 23.1 kg/m2, p=0.013). CONCLUSIONS: The H. pylori infection rate in ERD group was lower and PG I/II ratio was higher than that in the control group. Reflux esophagitis is thought to be reversely associated with the atrophy of gastric mucosa.     

Novel risk markers for gastric cancer screening: Present status and future prospects

Initial identification of populations at high risk of gastric cancer (GC) is important for endoscopic screening of GC. As serum pepsinogen (PG) test-positive subjects with progression of chronic atrophic gastritis (CAG) show a high likelihood of future cancer development, this population warrants careful follow-up observation as a high-risk GC group. By combining the PG test with Helicobacter pylori (HP) antibody titers, the HP-related chronic gastritis stage can be classified, thus identifying not only a GC high-risk group but also a low-risk group. Among PG test-negative patients without CAG, those with high serum PG II levels and HP antibody titers are thought to have severe gastric mucosal inflammation and the risk of diffuse-type GC is also high. Meanwhile, in gastric mucosae obtained by endoscopic biopsy, HP infection induces aberrant DNA methylation in CpG islands in multiple gene regions and the extent of methylation clearly correlates with GC risk. By quantifying aberrant DNA methylation in suitable gene markers, we can determine the extent of the epigenetic field for cancerization. These novel concepts and risk markers will have many clinical applications in gastrointestinal endoscopy, including more efficient endoscopic GC screening and a strategic approach to metachronous multiple GCs after endoscopic treatment.     

Impact of pepsinogen C polymorphism on individual susceptibility to gastric cancer and its precancerous conditions in a Northeast Chinese population

Purpose  Human pepsinogen C (PGC) is an aspartic protease produced specifically by the gastric mucosa, and is considered as a mature marker of gastric epithelium. This study examined the contributions of PGC polymorphisms and the Helicobacter pylori (H. pylori) infection to the risk of gastric cancer (GC), and its precancerous conditions in a Northeast Chinese population. Methods  The PGC insertion/deletion polymorphism was evaluated by polymerase chain reaction analysis, followed by direct DNA sequencing in 564 cases of GC, atrophic gastritis (AG), gastric ulcer (GU) and superficial gastritis (as control). All cases were frequency-matched 1:1 by gender and age (±5). H. pylori infection was identified by serum anti-H. pylori IgG measurement through enzyme-linked immunosorbent assay. Results  Patients with a homozygous PGC allele 1 genotype had a significant risk of AG [adjusted odds ratio (OR) 3.11; 95% confidence interval (CI) 1.44–6.71] or of GC (OR 3.00; 95% CI 1.38–6.51), and a significantly elevated risk of intestinal metaplasia (OR 1.90, 95% CI 1.11–3.27). PGC polymorphism with H. pylori infection increased risk of GU (OR 8.69; 95% CI 1.01–74.69), and AG (OR 11.12; 95% CI 1.37–90.84) or GC (OR 10.61; 95% CI 1.28–87.79) in a super-multiplicative manner. The S value was 5.40, 6.48 and 4.34; and the AP value was 72.09, 7.00 and 69.69%, respectively. Conclusions  The PGC gene polymorphism increases an individual’s susceptibility to GC and its precancerous conditions. Moreover, the PGC gene polymorphism shows a positive link to H. pylori infection in the development of GC.     

Helicobacter antibodies in Finnish centenarians.

BACKGROUND: The prevalence of helicobacter antibodies increases with age and, in many developed countries, is highest in people born before 1940. Data on very old subjects are, however, limited. In this study we wanted to determine whether the age-related increase in the seroprevalence of H. pylori infection continues even in the oldest age group alive in Finland, the centenarians. METHODS: Sera from 173 subjects (93% of all centenarians alive in Finland in 1991) were available for the present study. IgG and IgA antibodies against H. pylori were determined by an in-house enzyme immunoassay. To estimate the influence of atrophic gastritis on the prevalence of helicobacter antibodies, serum pepsinogen I (PG I) concentrations and parietal cell antibodies (PCAs) were measured by an enzyme immunoassay and indirect immunofluorescence, respectively. RESULTS: The prevalence of helicobacter antibodies in Finnish centenarians was 66%. Low PG I values (<28 microg/l) were found in 36% and positive PCAs in 16% of the subjects studied. The prevalence of PCAs was especially high (50%) in H. pylori-negative subjects with low PG I values, suggesting severe gastric atrophy. CONCLUSIONS: The age-related increase in H. pylori seroprevalence did not continue in the oldest age group alive in Finland. This may be explained partly by a relatively high frequency of atrophic gastritis (as suggested by low PG I values) in H. pylori-negative centenarians, but other factors--such as selective H. pylori-related mortality--may also have contributed to the fairly low seroprevalence (66%) observed.     

血清胃蛋白酶原和胃泌素检测对幽门螺杆菌相关十二指肠溃疡的意义

目的测定十二指肠溃疡(DU)患者血清胃蛋白酶原PGⅠ、PGⅡ、PGⅠ/PGⅡ、血清胃泌素-17(G-17),分析胃肠肽类激素与幽门螺杆菌(Hp)引起的DU的相关性。方法选取胃镜检查确诊的患者306例,分成Hp阳性、Hp阴性DU组,Hp阳性、Hp阴性浅表性胃炎组,Hp阳性、Hp阴性萎缩性胃炎组,以ELISA检测血清PG和G-17含量。结果 Hp阳性DU组血清PGⅠ较慢性萎缩性胃炎和慢性浅表性胃炎Hp阳性组显著升高,差异有统计学意义(P均<0.05);Hp阴性DU组血清PGⅠ较萎缩性胃炎和慢性浅表性胃炎Hp阴性组明显升高,差异有统计学意义(P均<0.05)。DU各组PGⅠ/PGⅡ比值与慢性浅表性胃炎各组比较,差异有统计学意义(P均<0.05)。结论 Hp阳性DU患者血清PGⅠ和G-17升高;血清PGⅠ和G-17含量对分析胃肠肽类激素与Hp引起的DU以及症状程度和疗效评价有较好的参考价值。     

Chemoprevention of gastric cancer by Helicobacter pylori eradication and its underlying mechanism

The cascade of gastric cancer, a leading cause of cancer incidence and mortality, is multifactorial. Helicobacter pylori (HP) infection plays a major role in gastric cancer (GC), and there has been an accumulation of data regarding the chemopreventive effect of HP eradication. However, it remains unclear how HP infection causes GC and how HP eradication prevents GC. To clarify this issue, the following approaches were performed in this review article. First, how HP‐induced atrophic gastritis (AG) and intestinal metaplasia (IM) provoke the development of GC is shown, followed by how long HP eradication takes to induce a reversible change in AG and IM. Second, epigenetic studies of PTPN6, MOS, DCC, CRK, and VAV1 were performed in noncancerous gastric specimens in terms of HP status. Among these genes, MOS was found to be a possible surrogate marker for GC development. HP eradication decreased aberrant DNA methylation in a gene‐specific manner, and MOS played a role in metachronous gastric neoplasms. Third, transforming growth factor‐β1 (TGF‐β1) and TGF‐β1‐induced epithelial‐mesenchymal transition (EMT) markers were investigated in gastric mucosa. HP infection triggered the TGF‐β1‐induced EMT pathway and caused the emergence of GC stem cells, such as CD44v8‐10. When HP was eradicated, these two pathways were inhibited. Finally, a 2222 cohort study showed that HP eradication significantly decreased the risk of noncardiac GC. Taken together, HP eradication is effective as a primary GC prevention method, and its underlying mechanism includes reversibility of AG and IM, methylation, EMT, and stem cells.     

Interleukin 1beta polymorphisms increase risk of hypochlorhydria and atrophic gastritis and reduce risk of duodenal ulcer recurrence in Japan

BACKGROUND & AIMS: Interleukin-1 beta (IL-1beta) polymorphisms are associated with increased risk of gastric cancer in whites. This study aimed to examine effects of these polymorphisms on gastric acid secretion, atrophic gastritis, and risk of peptic ulcer in Japan. METHODS: We determined IL-1B-511/-31 and IL-1RN genotypes and measured gastric juice pH, serum pepsinogen (PG) I and II levels, and gastritis and atrophy scores in Helicobacter pylori-positive patients with gastritis only, gastric ulcers, or duodenal ulcers (DUs), and H. pylori-negative controls. RESULTS: In the H. pylori-positive group, subjects with the proinflammatory IL-1B-511 T/T genotype had the highest atrophy and gastritis scores, the highest median gastric juice pH, and the lowest median serum PG I/PG II ratios. Although gastric juice pH significantly increased and serum PG I and PG I/PG II ratios significantly decreased in the IL-1B-511 T/T genotype group with age, no such age-dependent changes were observed in the C/C genotype group. Changes in the C/T genotype group were intermediate. In the H. pylori-negative group, the IL-1 loci had no effect on any of the physiologic or morphologic parameters. Carriage of IL-1RN allele 2 significantly protected against DU disease while the IL-1B-511 T/T genotype significantly protected against DU recurrence in patients older than 60 years. CONCLUSIONS: Proinflammatory IL-1beta polymorphisms are associated with hypochlorhydria and atrophic gastritis in Japan. The effects are dependent on H. pylori infection and become more significant with advancing age. This may explain the high incidence of gastric cancer in Japan and also the age-dependent decrease in DU recurrence in infected subjects.     

Helicobacter pylori infection and gastritis: the Systematic Investigation of gastrointestinaL diseases in China (SILC)

Background and Aim: Helicobacter pylori infection remains common in East Asia, though its prevalence is decreasing in Western countries. H. pylori‐related atrophic gastritis (AG) may reduce the likelihood of gastroesophageal reflux disease (GERD). We investigated the prevalence of H. pylori infection and AG and their association with endoscopic findings and symptom‐defined GERD in Shanghai. Methods: A representative random sample of 3600 Shanghai residents aged 18–80 years was invited to complete a general information questionnaire and a Chinese version of the Reflux Disease Questionnaire, to provide blood samples for H. pylori serology and pepsinogen (PG) I/II assay (to detect AG, defined as PGI < 70 µg/L and/or PGI/PGII < 7), and to undergo endoscopy. Odds ratios (ORs) and 95% confidence intervals (CIs) were calculated by multivariate logistic regression. Results: A total of 1022 Shanghai residents underwent endoscopy and were valid for inclusion in the study. Of these, 71.7% tested positive for H. pylori, 63.8% had AG and 30.5% had moderate/severe AG (PGI < 50 µg/L and/or PGI/PGII < 5). Helicobacter pylori infection was equally common in all age groups. Severity of AG increased with age in women. Reflux esophagitis was inversely associated with AG (OR, 0.23 [CI, 0.09–0.55] for moderate/severe AG compared with no H. pylori or gastritis). However, symptom‐defined GERD showed no clear association with AG. Conclusions: Helicobacter pylori infection and AG are very common in Shanghai, and the infection is acquired early in life. Atrophic gastritis is inversely associated with reflux esophagitis but is not significantly associated with symptom‐defined GERD.     

血清胃蛋白酶原检测在慢性萎缩性胃炎筛查中的价值

目的探讨血清胃蛋白酶原Ⅰ(PGⅠ)、胃蛋白酶原Ⅰ/胃蛋白酶原Ⅱ(PGⅠ/PGⅡ)比值(PGR)与慢性萎缩性胃炎的关系,确定其在萎缩性胃炎中的变化规律。方法选择在我院消化科行胃镜检查符合入选研究标准的200例患者,根据组织病理学诊断结果分为慢性非萎缩性胃炎组(135例)和慢性萎缩性胃炎组(65例)。采用化学发光方法定量测定空腹血清PGⅠ、PGⅡ,并计算PGⅠ/PGⅡ比值(PGR)。结果慢性萎缩性胃炎组与非萎缩性胃炎组血清PGⅠ分别为(78.55±15.42)μg/L和(130.51±55.23)μg/L,有显著差异(P<0.05)。PGR分别为4.09±2.15和8.95±5.18,显著差异(P<0.05);以PGⅠ≤70μg/L且PGR≤3.0为界值来计算诊断慢性萎缩性胃炎的敏感性和特异性分别为72.3%和93.3%。结论检测血清PG及PGR可用于慢性萎缩性胃炎的筛查,如有异常,应进一步行胃镜检查以确诊并指导治疗。     

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

OBJECTIVE: 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. METHODS: 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. RESULTS: 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 µg/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. CONCLUSIONS: Low serum PGI, PGR and G‐17 values are biomarkers of atrophic antral gastritis. Atrophic corpus gastritis can be screened by lower serum PGI, PGR and high G‐17 values. [Correction added after online publication on 2 February 2007: the preceding sentence has replaced one that read ‘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.     

血清胃蛋白酶原与胃泌素检测对慢性萎缩性胃炎的诊断价值

目的探讨血清胃蛋白酶原Ⅰ（PGⅠ）、胃蛋白酶原Ⅰ/胃蛋白酶原Ⅱ（PGⅠ/PGⅡ）比值（PGR）和胃泌素-17（G-17）与慢性萎缩性胃炎的关系,确定其在萎缩性胃炎中的变化规律。方法 选择在我院消化科行胃镜检查符合入选研究标准的300例患者,根据组织病理学诊断结果分为慢性非萎缩性胃炎组（202例）和慢性萎缩性胃炎组（98例）。采用酶联免疫吸附试验（ELISA）方法定量测定空腹血清PGⅠ、PGⅡ和G-17水平,并计算PGⅠ/PGⅡ比值（PGR）。采用14C-或13C-呼气试验和快速尿素酶试验两种方法联合判定幽门螺杆菌（Hp）感染情况。结果 慢性萎缩性胃炎组与非萎缩性胃炎组相比,血清PGⅠ分别为128.55±61.42μg/L和150.61±75.33μg/L,比较有显著差异（P〈0.05）。PGR分别为10.09±5.15和10.95±7.18,比较无显著差异（P〉0.05）;G-17分别为9.68±15.51pmol/L和18.93±18.92pmol/L,比较有显著差异（P〈0.05）。Hp阳性组PGR（8.96±7.72）与阴性组（11.63±5.56）比较有显著差异（P〈0.05）;Hp阳性组PGⅠ（125.39±65.90μg/L）与阴性组（154.19±65.13μg/L）比较有显著差异（P〈0.05）;Hp阳性组G-17（10.91±15.50pmol/L）与阴性组（10.68±19.12pmol/L）比较无显著差异（P〉0.05）。结论 联合检测血清PG和G-17水平可用于慢性萎缩性胃炎的筛查,如有异常,应进一步行胃镜检查以确诊并指导治疗。Hp感染与PG水平的变化有关。