Serum pepsinogen concentration as a marker of <Emphasis Type="Italic">Helicobacter pylori </Emphasis>infection and the histologic grade of gastritis; evaluation of gastric mucosa by serum pepsinogen levels

Background: Helicobacter pylori infection and associated gastritis are well-known significant factors in many gastrointestinal diseases, and evaluation of these conditions is important for health evaluation. We investigated the utility of serum pepsinogen (PG) concentrations for the diagnosis of H. pylori infection and evaluation of the grade of histologic gastritis. Methods: The subjects consisted of 283 individuals (147 men and 136 women; mean age, 44.0 years). Biopsy specimens were obtained from the gastric antrum and body to assess grade of inflammation and atrophy and histologic evidence of H. pylori infection. H. pylori infection was judged by Giemsa staining and serum IgG antibodies against H. pylori. PG concentrations were determined by radioimmunoassay. Results: In subjects with H. pylori infection, serum PGII concentrations were increased, and the PGI/PGII ratio (I/II ratio) was decreased. In patients with marked atrophy or intestinal metaplasia, both serum PGI and the I/II ratio were decreased. When PGII concentrations of 12 ng/ml or more, or a I/II ratio of 4.0 or less were used as the cutoff points for the diagnosis of H. pylori infection, the sensitivity and specificity of diagnosis were 90.0% and 93.5%, respectively. All subjects with serum PGI concentrations of 85 or more ng/ml, or serum PGII concentrations of 15 or more ng/ml were H. pylori-positive and all subjects with a I/II ratio of more than 6.5 were H. pylori-negative. Conclusions: These results suggest that H. pylori infection, gastritis, and glandular atrophy of the stomach can be evaluated via serum PG concentrations, allowing the evaluation of gastric mucosal integrity. Received: April 1, 2002 / Accepted: September 6, 2002 Acknowledgments. The authors thank Goro Kajiyama, M.D., Ph.D., and Koji Sumii, MD., PhD. (First Department of Internal Medicine, Hiroshima University School of Medicine) for helpful advice and supervision. This work was supported in part by a Grant-in-Aid for Cancer Research from the Ministry of Health, Labour and Welfare of Japan. Reprint requests to: M. Yoshihara     

Prevalence of Barrett's esophagus in Japan

Norman Barrett originally described two special conditions, namely, a congenital short esophagus with an intrathoracic gastric columnar lining and congenital gastric heterotropia in the esophagus with ulceration. Thereafter, these conditions began to be known as “Barrett's esophagus.” It is an acquired condition of esophageal columnar metaplasia following chronic gastroesophageal reflux, and the classical Barrett's esophagus has been defined as having a circumferential columnar metaplasia spreading minimally 3 cm or more upward from the esophagogastric junction, because the esophagogastric junction still tends to be difficult to recognize precisely. Recently, from the point of view of adenocarcinogenesis of the esophagus, the term and concept of short-segment Barrett's esophagus (SSBE) as a developing condition of the classical Barrett's esophagus and the confirmation of intestinal metaplasia has been required; however, the definition of Barrett's esophagus still remains controversial. In Japan, although the prevalence of short-segment Barrett's esophagus has been reported to vary considerably, from 1% to 52%, the prevalence of long-segment Barrett's esophagus (LSBE) tends to range from 0% to 2%, which is a quite lower rate than that observed in Western countries. The great difference in the prevalence of SSBE is caused by the differences in the criteria of the esophagogastric junction and the definition concerning the necessity of intestinal metaplasia. A universally accepted definition of Barrett's esophagus is thus needed to accurately determine its actual prevalence.     

Barrett's oesophagus and Helicobacter pylori

Abstract In order to demonstrate the presence of Helicobacter pylori in the metaplastic epithelium of Barrett's oesophagus and to evaluate its possible association with this entity, we examined 29 cases of Barrett's oesophagus where concomitant antral biopsies were also available. These cases were compared with an equal number of age and sex matched controls of uncomplicated reflux oesophagitis. H. pylori was present in 11 of 29 cases of Barrett's oesophagus (38%). No increase in the frequency of H. pylori antral gastritis was found in patients of Barrett's oesophagus compared to the control group of uncomplicated reflux oesophagitis. The positivity of Barrett's oesophagus for H. pylori correlated with the presence of H. pylori antral gastritis ( P < 0.05), although in two cases of H. pylori -positive Barrett's oesophagus antral biopsies were negative for H. pylori. No difference was found in the severity of inflammatory and dysplastic changes of H. pylori- positive and H. pylori -negative Barrett's oesophagus. Presence of H. pylori does not seem to alter the natural history of Barrett's oesophagus.     

Correlation between serum pepsinogen levels and gastric mucosal histological findings before and after Helicobacter pylori eradication therapy

Background: Helicobacter pylori causes chronic gastritis and is also associated with many other gastrointestinal diseases. The incidence of gastric cancer is thought to vary according to the degree and topography of chronic gastritis. Histological findings of specimens obtained at endoscopy are therefore important. In the present study, we investigated the correlation between these histological findings and serum pepsinogen (PG) levels. Methods: Helicobacter pylori eradication therapy was conducted in 100 H. pylori‐positive patients. Endoscopies were performed prior to, and 2 months after, eradication therapy; gastric mucosal biopsies were taken from the antrum and corpus. Helicobacter pylori infection was diagnosed using the rapid urease test, culture and histology. Using the Updated Sydney System, histological findings of inflammation, activity, atrophy and intestinal metaplasia were each graded. Blood was taken on the same two occasions for determination of serum levels of PG I and II. Results: Levels of PG I were highest in association with antrum‐predominant gastritis (APG), followed in order by pangastritis (PAN) and corpus‐predominant gastritis (CPG), with a significant difference between APG and CPG. No correlations were seen between PG II levels and gastritis topography. Examination of the relationship between PG levels and histological findings revealed significant correlations between PG I levels after eradication atrophy and intestinal metaplasia in the gastric corpus. No significant correlations were seen between PG II levels and before or after eradication histological findings. Conclusion: Our results indicate that serum PG levels may be a useful indicator of before‐eradication gastritis topography and after‐eradication gastric atrophy in the gastric corpus.     

不同检测方法探讨幽门螺杆菌感染与Barrett食管之间的关系

目的比较不同检测方法显示的幽门螺杆菌(Helicobacter pylori,H.pylori)感染状况与Barrett食管(Barrett’s esophagus,BE)之间的关系。方法随机收集确诊BE患者84例,同期收集无消化道症状的内镜检测阴性的正常体检者84例作为对照。采用快速尿素酶法、病理中性复红染色法及13C呼气法分别检测患者的幽门螺杆菌感染情况,并收集患者的临床病理资料进行统计学分析。结果快速尿素酶法或病理中性复红染色法检测H.pylori阳性的患者BE组食管下段黏膜阳性率为14.3%(12/84),胃窦部黏膜阳性率为45.2%(38/84),对照组食管下段黏膜及胃窦部黏膜H.pylori阳性率分别为16.7%(14/84)、61.9%(52/84);13C呼气试验检测H.pylori阳性的患者BE组为64.3%(54/84),对照组为66.7%(56/84)。快速尿素酶法或病理中性复红染色法检测食管下段黏膜H.pylori阳性率BE组与对照组比较无显著差异(P>0.05),胃窦黏膜H.pylori阳性率在两组间有显著差异(P<0.05);13C呼气法显示BE组与对照组H.pylori阳性率无显著差异(P>0.05)。结论快速尿素酶法及病理中性复红染色法显示胃窦部H.pylori感染对BE可能具有保护作用,而13C呼气试验显示H.pylori感染可能对BE不具有保护作用,两者的确切关系尚需要进行大样本、多因素的深入研究。     

洛阳地区Barrett''''s食管的发病情况、内镜和病理学特点

目的探讨洛阳地区一组Barrett’s食管(BE)的发病情况、内镜和病理学特点及其与幽门螺杆菌(H.pylori)感染的关系。方法采用普通胃镜检查结合病理检查结果,对洛阳地区有消化道症状的一组BE患者进行分析,同时采用尿素[14C]呼气试验药盒检查H.pylori感染对BE发病学的影响。结果2006年8月~2007年4月共有593例接受胃镜检查,有22例诊断为BE,BE发病率为3.71%;以短段、舌型发病率最高,分别占81.81%和77.27%;7例(31.8%)有典型反流症状;伴有低度异型性增生3例(13.64%),重度异型性增生1例(4.55%),并发腺癌1例(4.55%),其中伴有重度异型性增生的1例随访1年后并发腺癌;对其中的10例进行H.pylori检查,阳性率为90%。结论洛阳地区BE发病率较高,以短段、舌型为主,有典型反流症状者较少,伴有异型性增生、腺癌者及并发H.pylori感染者常见。     

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。     

蒙古族、汉族胃癌患者血清胃蛋白酶原水平及与幽门螺杆菌关系的研究

[目的]研究蒙古族、汉族胃癌患者血清胃蛋白酶原（PG）水平及幽门螺旋杆菌（Helicopter pylori,Hp）感染对血清PG的影响,探讨血清PG的地域和民族特征及规律,提供有价值的临床流行病学资料.[方法]选择2013年1月～2014年1月在赤峰医学院附属医院经内镜检查和病理学确诊的胃癌患者68例（连续3代均为同一民族,蒙古族30例,汉族38例）,选择42例健康体检者作为正常对照组,应用酶联免疫方法进行血清PG Ⅰ、PGⅡ的检测,并计算PG Ⅰ/PGⅡ比值;并应用War Thin-starry染色、快速尿素酶试验及C14-尿素呼气试验进行Hp检测.受检对象4周内均未服用过抑酸药、抗生素、铋剂等药物.[结果]①蒙古族、汉族胃癌组血清PG Ⅰ及PG Ⅰ/PGⅡ值明显低于正常对照组,差异有统计学意义（P＜0.05）,各组血清PGⅡ水平之间差异无统计学意义;②蒙古族胃癌组患者血清PG Ⅰ及PG Ⅰ/PGⅡ值低于汉族胃癌组,差异有统计学意义（P＜0.05）,2组血清PGⅡ水平之间差异无统计学意义;③蒙古族、汉族胃癌组Hp感染率分别是70.00％、68.42％,明显高于正常对照组的52.38％,差异有统计学意义（P＜0.05）,而蒙古族胃癌组和汉族胃癌组Hp感染率之间差异无统计学意义;④蒙古族、汉族胃癌组Hp阳性组血清PG Ⅰ及PG Ⅰ/PGⅡ值低于Hp阴性组,差异有统计学意义（P＜0.05）,2组血清PGⅡ水平的差异无统计学意义;⑤蒙古族、汉族胃癌组不同性别血清PGⅠ、PGⅡ及PG Ⅰ/PGⅡ值之间差异无统计学意义.[结论]①蒙古族、汉族胃癌患者血清PGⅠ及PG Ⅰ/PGⅡ值较正常对照组降低,提示血清PGⅠ及PG Ⅰ/PGⅡ值降低有助于胃癌的诊断,可以作为地区人群筛查和辅助诊断胃癌的一项血清学指标;②蒙古族胃癌患者血清PG Ⅰ及PG Ⅰ/PGⅡ值低于汉族胃癌患者,提示血清PG水平在不同种族人群中存在差异;③蒙古族、汉族胃癌患者血清PG Ⅰ及PGⅠ/PGⅡ值的改     

Serum pepsinogen II levels are doubled with Helicobacter pylori infection in an asymptomatic population of 40,383 Chinese subjects

Pepsinogen (PG) I and II are crucial in the gastric digestive processes. This study is to examine the relationship of serum PGI, PGII, and PGI/PGII ratio with Helicobacter pylori (Hp) infection, age, sex, and body mass index (BMI) in subjects in Beijing, China.A total of 40,383 asymptomatic subjects, who underwent medical examination in Beijing Rehabilitation Hospital, were included in this study. Serum PG levels were measured using chemoluminescence techniques. The age, sex, and BMI data were collected, and Hp infection was identified with ¹³C-urea breath test. Statistical analysis was conducted with Python, Pandas and Seaborn software.Asymptomatic subjects with Hp infection (Hp+) had a significantly higher level of PGI in the serum (111 ng/mL [median]) than those without Hp infection (Hp−) (94 ng/mL, P < .001). The asymptomatic Hp+ subjects had 2-fold higher PGII levels (7.2 ng/mL) than Hp− subjects (3.2 ng/mL, P < .001). These changes produced significantly lower PGI/II ratio in Hp+ patients than in Hp− subjects (16:30, P < .001). The serum PGI and PGII levels were higher in males than in females (PGI: 104 ng/mL vs 95 ng/mL, PGII: 4.3 ng/mL vs 3.7 ng/mL, both P < .001), PGI/II ratio of males is at 95% of that in females (P < .001). PGI and PGII levels gradually increased in older people (P < .001), whereas the PGI/II ratio decreased significantly with age (P < .001). The levels of the two serum PGs were decreased and the ratio increased when BMI were higher than 28 kg/cm² (P < .05).The levels of serum PGI, especial PGII, were increased by Hp infection, and also influenced by age, sex, and BMI. Therefore, these influencing factors should be considered during clinical practice.     

Prevalence of Barrett's esophagus and expression of mucin antigens detected by a panel of monoclonal antibodies in Barrett's esophagus and esophageal adenocarcinoma in Japan

Barrett's esophagus (BE) is an acquired disorder associated with a high incidence of adenocarcinoma of the lower esophagus. Moreover, it has been reported that short-segment BE may be associated with adenocarcinoma of the esophagogastric junction. The objective of this study was to define the prevalence of BE and the mucin profile in BE, including the short-segment type, and to compare the mucin profile in BE with the profiles of Barrett's adenocarcinoma and distal esophageal adenocarcinoma among Japanese. In total, 650 adult subjects underwent endoscopic examination for evaluation of BE. Although the prevalence of traditional (long segment) BE was 0.62%, the overall prevalence of BE including short-segment type was 15.7%. In Barrett's epithelium, the short-segment type predominantly had gastric type mucin, while the middle- and long-segment types possessed intestinal mucin, especially colonic type mucin (sulfo-Lewis^a), with high frequency. In Barrett's epithelium with adenocarcinoma, all Barrett's epithelium adjacent to carcinomas showed a predominance of immunoreactivity to sulfo-Lewis^a. In Barrett's adenocarcinomas, colonic type mucin was detected in 100% by monoclonal antibody (MoAb) 91.9H. Small-intestinal mucin and gastric mucin were stained in 50% and 12.5% of the subjects, respectively. Colonic type mucin was also detected with high frequency (80%) in distal esophageal adenocarcinomas without Barrett's epithelium. These data suggest that the epitope, not of small-intestinal type or gastric type mucin, but of colonic type mucin (sulfo-Lewis^a), may be associated with, at least in part, the malignant phenotype of BE. Received: July 28, 1999 / Accepted: February 25, 2000     

Racial differences in Helicobacter pylori, serum pepsinogen and gastric cancer incidence in an urban Asian population

BACKGROUND: In Singapore, the highest incidence of gastric cancer occurs in the Chinese (C), with lower rates among Malay (M) and Indian (I) subjects. The purpose of the present paper was to examine whether racial differences in the prevalence of Helicobacter pylori and serum pepsinogen (PG) could account for this difference. METHODS: A randomized community health survey involving 7000 asymptomatic healthy individuals was conducted. Among the Chinese, Malay and Indian respondents, subjects were matched for age, gender and race and a total of 595 sera were obtained. The H. pylori seropositivity and serum PG levels were determined by ELISA. The dependency of the cumulative gastric incidence rate on H. pylori seroprevalence was evaluated by linear regression. The racial difference in the seroprevalence of H. pylori and low serum PG was determined. RESULTS: The H. pylori seroprevalence was similar between Chinese and Indian subjects, but significantly lower among Malay subjects (C, 46.3%; M, 27.9%; I, 48.1%). The gastric cancer incidence rates correlated with H. pylori seropositivity for the Chinese and Malay subjects, but not for the Indian subjects. The prevalence of low PG was highest in Indian subjects (PG I low: C, 2.1%; M, 5.4%; I, 14.2%; P < 0.0001; PG I:II ratio low: C, 5.3%; M, 5.9%; I, 12.6%; P = 0.012), even when adjusted for gender and the presence of H. pylori. CONCLUSIONS: The difference in gastric cancer incidence correlated with H. pylori seroprevalence for Chinese and Malay subjects. The lower incidence of gastric cancer among Indian subjects cannot be explained by differences in H. pylori or serum PG. Other modifying factors such as host and environmental factors may be important.     

幽门螺杆菌感染对肝硬化患者血氨浓度的影响

探讨肝硬化患者幽门螺杆菌(Hp)感染与血氨的关系,及根除性治疗Hp对血氨的影响。84例肝硬化高血氨患者,分为Hp阳性组51例,阴性组33例。两组都给予支链氨基酸、乳果糖、基础护肝治疗两周,治疗前后分别测空腹静脉血氨。随后将Hp阳性组随机分两组,A组26例,应用三联疗法治疗一周;B组25例,奥美拉唑治疗一周,治疗结束一个月后复查血氨。发现阳性组的血氨与阴性组相比有显著差异(P＜0．01)。阳性组不同肝功能分级组血氨浓度之间有显著差异(P＜0．01);阴性组则否。Hp阴性组治疗前后血氨浓度变化差异有显著性(P＜0．01),阳性组则无显著差异。根除Hp治疗后血氨明显下降(P＜0．01),而用洛赛克治疗后血氨轻度升高,但无统计学意义。说明Hp感染与肝硬化患者血氨升高有密切相关性,根除Hp的治疗能有效降低血氨。     

Severe gastric mucosal damage induced by NSAIDs in healthy subjects is associated withHelicobacter pylori infection and high levels of serum pepsinogens

Helicobacter pylori infection and NSAIDs are considered the two most important exogenous factors in ulcer disease. The interrelation between the two factors is not, however, clear. Moreover, serum pepsinogen has been suggested as a risk marker for the development of NSAID-induced gastrointestinal lesions. Fifty-one healthy volunteers, enrolled in a prospective, double-blind study carried out to evaluate gastrointestinal side effects of meloxicam and piroxicam, were analyzed to determine whether: (1) the prevalence ofH. pylori correlates with the occurrence and severity of NSAID-induced gastrointestinal lesions, and (2) serum pepsinogen A and C levels could be used as markers of NSAID-induced mucosal damage. Upper endoscopy was performed by the same investigator before and after 28 days of treatment with placebo, meloxicam (7.5 mg/day and 15 mg/day), or piroxicam (20 mg/day). NSAID-induced damage was graded separately for hemorrhages and erosion ulcers according to Lanza's scale. There were no statistically significant differences in the prevalence ofH. pylori in subjects with and without NSAID-induced mucosal lesions. However, there was a positive association betweenH. pylori infection and the severity of mucosal damage: total mean endoscopic score was 2.9±0.3 inH. pylori-positive subjects versus 1.6±0.5 inH. pylori-negative subjects (P<0.05). Pepsinogen A and C levels increased from 55.3±3 to 149.4±15 and from 6.3±0.5 to 11.5±2.2, respectively (P<0.05) in subjects who developed severe endoscopic injury. It is concluded thatH. pylori increases the severity of NSAID-induced gastrotoxicity and that pepsinogen A and C levels are valid markers of severe NSAID-induced mucosal lesions.     

Analysis of factors associated with recovery of the serum pepsinogen ratio after Helicobacter pylori eradication: a long-term follow-up study in Korea

Abstract

Objective: Serum levels of pepsinogen (PG) are related to Helicobacter pylori-induced inflammation of the gastric mucosa. This study aimed to examine the influence of H. pylori eradication on serum PG, analyze its associated factors, and evaluate the long-term outcomes.

Methods: H. pylori-positive patients who underwent gastroscopy and serum PG measurement were enrolled in a single academic hospital. After H. pylori eradication, the measurement of serum PG level was performed. Recovery of serum PG I/II ratio was defined as a PG I/II ratio after eradication of >3.0 in patients with a PG I/II ratio ≤ 3.0 before eradication. Follow-up involved serum PG measurement and gastroscopy with a rapid urease test annually.

Results: In all, 327 patients were eligible for study inclusion. Compared to those before H. pylori eradication, serum PG I (74.9 vs. 44.3?ng/mL, p?<?.001) and PG II (25.4 vs. 9.1?ng/mL, p?<?.001) levels significantly decreased after successful eradication. In addition, there was a significant increase in serum PG I/II ratio after eradication (3.07 vs. 4.98, p?<?.001). In multivariate analyses, the following were independently associated with failed recovery of serum PG I/II ratio despite successful eradication: age ≥ 60?years (odds ratio [OR]?=?0.231, 95% confidence interval [CI]?=?0.084–0.629, p?=?.004) and severe gastric atrophy (OR = 0.156, 95% CI = 0.055–0.440, p?<?.001).

Conclusions: Recovery of serum PG I/II ratio after H. pylori eradication may be achieved in H. pylori-infected patients aged <60?years without severe gastric atrophy.     

幽门螺杆菌感染和吸烟对胃腺癌患者胃蛋白酶原水平的影响

目的　探讨幽门螺杆菌 (H·pylori,简称Hp)感染和吸烟对胃腺癌 (GAC)患者胃蛋白酶原 (PG)水平的影响。方法　PGⅠ、PGⅡ水平用放射免疫法检测 ,用14 C 尿素呼气试验及ELISA法测血清抗Hp IgG抗体确定Hp感染。结果　 (1)Hp阴性吸烟的GAC患者PGⅠ水平均数明显高于Hp阴性不吸烟和曾吸烟的GAC患者 (前者t =2 70 9,P <0 0 5 ;后者t =2 15 7,P <0 0 5 ) ;Hp阳性不吸烟及曾吸烟的GAC患者 ,PGⅠ水平均数明显低于Hp阳性吸烟的GAC患者 (前者 t =2 5 37,P <0 0 5 ;后者t =2 185 ,P <0 0 5 )。 (2 )Hp阴性不吸烟及曾吸烟的GAC患者 ,其PGⅡ水平均数明显低于其Hp阳性不吸烟及曾吸烟的GAC患者 (前者 t =2 94 4 ,P <0 0 1;后者t =2 4 2 7,P <0 0 5 )。结论　吸烟可使GAC患者PGⅠ水平升高 ,停止吸烟后PGⅠ水平均数下降 ;Hp感染可提高不吸烟和曾吸烟患者PGⅡ水平     

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.     

Frequencies of the expression of main protein antigens from Helicobacter pylori isolates and production of specific serum antibodies in infected patients

AIM: To investigate the frequencies of the expression of main protein antigens of Helicobacter pylori (H py/ori) isolates, such as UreB, VacA, CagA1, HpaA, NapA, FlaA and FlaB and the production of specific antibodies in sera from H pylori-infected patients, and to understand the correlations among the different clinical types of chronic gastritis and peptic ulcer and the infection and virulence of H pylori. METHODS: H pylori strains in biopsy specimens from 157 patients with chronic gastritis and peptic ulcer were isolated and serum samples from the patients were also collected. The target recombinant proteins rUreB, rVacA, rCagAl, rHpaA, rNapA, rFlaA and rFlaB expressed by the prokaryotic expression systems constructed in our previous studies were collected through Ni-NTA affinity chromatography. Rabbit antisera against rUreB, rVacA, rCagAl, rHpaA, rNapA, rFlaA and rFlaB were prepared by using routine subcutaneous immunization. By using ultrasonic lysates of the isolates as coated antigens, and the self-prepared rabbit antisera as the first antibodies and commercial HRP-labeling sheep anti-rabbit IgG as the second antibody, expression frequencies of the seven antigens in the isolates were detected by ELISA. Another ELISA was established to detect antibodies against the seven antigens in sera of the patients by using the corresponding recombinant proteins as coated antigens, and the sera as the first antibody and HRP-labeling sheep anti-human IgG as the second antibody respectively. Correlations among the different clinical types of chronic gastritis and peptic ulcer and the infection and virulence of H pylori were statistically analysed. RESULTS: In the 125 isolates of H pylori, the positive rates of UreB, VacA, CagAl, HpaA, NapA, FlaA and FlaB were 100%, 65.6%, 92.8%, 100%, 93.6%, 100% and 99.2% respectively. In the 125 serum samples from the H pylori infected patients, the positive rates of antibodies against recombinant UreB, VacA, CagA1, HpaA, NapA, FIaA and FlaB were 100%, 42.4%, 89.6%, 81.6%, 93.6%, 98.4% and 92.8% respectively. H pylori strains were isolated from 79.6% (125/157) of the biopsy specimens, but no close correlations among the H pylori infection frequencies and different types of chronic gastritis and peptic ulcer could be found (P>0.05, x2 = 0.01-0.87). The VacA positive rate (82.40%) in the strains isolated from the specimens of patients with peptic ulcer and the anti-VacA positive rate (54.3%) in the sera from the patients were significantly higher than those (51.5%, 32.3%) from the patients with chronic gastritis (P<0.01, x2= 13.19; P<0.05, x2= 6.13). When analysis was performed in the different types of chronic gastritis, the VacA in the strains isolated from the specimems of patients with active gastritis showed a higher expression frequency (90.0%) than those from superficial (47.9%) and atrophic gastritis (30.0%) (P<0.05, x2 = 5.93; P<0.01,x2 = 7.50). While analysis was carried out in the strains isolated from the specimens with superficial (93.8%) and active gastritis (100%), NapA showed a higher expression frequency compared to that from atrophic gastritis (60.0%) (P<0.01, x2 = 8.88; P<0.05, X2=5.00). CONCLUSION: The types of chronic gastritis and peptic ulcer and their severity are not associated with H pylori infection frequency but closely related to the infection frequency of different virulent H pylori strains. The optimal antigens for developing vaccine and diagnostic kit are UreB, FlaA, HpaA, FlaB, NapA and CagAl, but not VacA.