Prevalence of atrophic gastritis in different populations in Siberia on medical evidence of the serological survey

Prevalence of atrophic gastritis in various population of Siberia with serological tests was studied. Representative samples of Novosibirsk adult population and also urban and rural population of Yakutia were examined. 348 persons at the age more than 45 years (180 males and 168 females) were studied. Concentration of pepsinogen I, gastrin 17 and antibodies to Helicobacter pilori in blood serum was estimated with immune-enzyme analysis ("Biohit GastroPanel", "Biohit", Finland). In addition, domestic test-systems were used for detection cytotoxic (expressing CagA-protein) strains H. pylori. Level of markers (pepsinogen, gastrin, antibodies to Helicobacter pilori and antibodies to CagA H. pilori) in observing populations had no difference between males and females, and also did not depend on age. Occurrence of atrophy in body of stomach in Novosibirsk population, urban and rural population of Yakutia was 10.1, 16.7 and 25.6% respectively, and in antral part--10.7, 25.6 and 8.9% respectively. Total atrophy was registered in 1% in all groups. Helicobacter infection was detected in 78-88% of population. Domestic immune-enzyme test-systems were comparable with data of histological examination and demonstrated greater sensitivity at H. pylori detection vs. foreign. High prevalence of atrophic gastritis in various groups of Siberia population was noticed, which must be was bounded with great level of H. pylori infection in population.     

Association of CagA-positive infection with Helicobacter pylori antibodies of IgA class

cagA gene, the best known virulence factor of Helicobacter pylori, codes for an immunodominant CagA protein. In this study, CagA antibodies of the IgG class were measured by immunoblot or enzyme immunoassay in subjects with positive H. pylori serology, and the presence of CagA antibodies was compared with that of H. pylori antibodies of IgA and IgG classes. Serum samples were available for a total of 1,481 subjects, including gastroscopied patients with biopsy-verified H. pylori infection, smoking men with a normal or low serum pepsinogen I level indicating atrophic corpus gastritis, and subjects who later developed gastric cancer and their matched controls. CagA antibodies were significantly more prevalent among individuals with elevated H. pylori antibody titres of the IgA class than in those with IgG antibodies only, with the exception of a small subgroup of individuals who later developed gastric cancer. CagA-positive H. pylori strains seem to induce an immune response with a markedly higher frequency of IgA than what is found in inflammation caused by CagA-negative strains. The presence of serum IgA antibodies to H. pylori seems to indicate a higher risk for CagA-positive H. pylori infection and possibly more severe late sequelae of the disease.     

消化性溃疡患者CagA-Hp感染与血清IL-8、IL-10的相关性研究

目的：探讨消化性溃疡（PU）患者伴有CagA-Hp感染与其血清IL-8、IL-10之间的关系。方法：取H.pylori阳性PU患者100例，其中CagA-Hp抗体阳性患者50例，CagA-Hp抗体阴性患者50例，采用ELISA法分别测定其血清IL-8和IL-10水平。结果：消化性溃疡患者中CagA-Hp抗体阳性组血清IL-8和IL-10显著高于CagA-Hp抗体阴性组。CagA-HpIgG抗体阳性患者中，胃溃疡与十二指肠球溃疡患者血清中IL-8和IL-10水平与溃疡发生的部位无关。     

Is GastroPanel serum assay useful in the diagnosis of Helicobacter pylori infection and associated gastritis in children?

GastroPanel (Biohit, Helsinki, Finland) is a serum test kit that measures Helicobacter pylori antibodies (HPABs) and pepsinogens I and II and gastrin 17, which reflect the degree of atrophic gastritis. We assessed whether GastroPanel can replace endoscopic biopsies in the diagnostics of H. pylori in children and whether the H. pylori-infected children show markers for atrophic gastritis. Eighty children (median age, 6.8 years; range, 0.6-18.7 years) underwent gastroscopy for H. pylori-related abdominal complaints (n = 40), surveillance after surgery for gastrointestinal tract malformations (n = 20), gastroesophageal reflux (GER) (n = 10), and miscellaneous diseases (n = 10). Gastric biopsies and a serum sample were obtained from all 80 children. HPAB levels of 38 and 15 IU were tested as cutoff values for H. pylori gastritis. The biopsies showed H. pylori-positive gastritis in 30 children, 9 had gastritis not associated with H. pylori, and 41 had normal biopsies. Atrophic gastritis was not found. The sensitivity and specificity of HPAB for H. pylori were 47% and 98% (cutoff, 38 IU), and 73% and 85% (cutoff, 15 IU), respectively. The assays of pepsinogens and gastrin did not improve sensitivity. None of the markers of pepsinogen (PG) I, PGII, and gastrin 17 (G17) indicated atrophic gastritis. GastroPanel is too insensitive for H. pylori screening and does not replace endoscopy. Markers indicative of atrophic gastritis were negative in all children with H. pylori gastritis.     

幽门螺杆菌感染及其毒力因子和胃十二指肠疾病关系的研究

目的 探讨幽门螺杆菌（Hp)感染病人中Hp细胞毒相关蛋白（CagA)、细胞空泡毒素（VacA)抗体在胃十二指肠疾病的比例，并评估不同类型幽门螺杆菌感染对胃窦粘膜炎症程度的影响。方法 应用免疫印迹法测定Hp感染者病人体内的CagA、VacA抗体。结果 73％的Hp感染者病人中出现CagA抗体，61％Hp感染者病人中出现VacA抗体。CagA抗体和VacA抗体在各疾病之间差异无显著性（P＞0．05）。在胃溃疡、十二指肠溃疡和复合性溃疡三类病人中，具CagA和VacA双阳性的比例较CagA和VacA双阴性的比例差异有显著性（P＜0．05）。胃窦萎缩病变在CagA和VacA双阳性的病人中比CagA和VacA双阴性的病人严重（P＜0．05）。结论 具有高毒力因子（CagA和VacA)的Hp是胃肠疾病病人感染的常见菌株，具有CagA和VacA的Hp可能在诱导胃粘膜发展到萎缩病变过程中起重要作用。但不能作为特异性指标来判断胃十二指肠疾病。     

Investigation about usefulness of serum antibody of Helicobacter pylori and serum pepsinogen I/II ratio as a marker of the judgment after eradication therapy

To clarify that serum antibody of Helicobacter pylori (H. pylori) and serum pepsinogen I/II ratio are useful or not as a marker of the judgment after eradication therapy, we followed up 84 cases who received eradication therapy comparing with culture and histology (Carnoy's fixation and immunostaining using anti-H. pylori antibody, MIA method). Successful eradication was recognized in 45 of 84 cases (successful group), and remaining 39 cases were unsuccessful (unsuccessful group). Titers of serum H. pylori antibody went down gradually in the successful group, on the other hand, they did not go down constantly and often re-went up in the unsuccessful group. The difference of the various rate of titers in the both groups became clear statistically since 6 months after eradication therapy (p < 0.05). Supposing that cut-off rate of titer was 60% of pre-eradicated titer, sensitivity, specificity, and accuracy were 86.2%, 77.7%, and 84.2%, respectively, at 6 months after eradication therapy. Serum pepsinogen I/II ratio increased regardless of successful or unsuccessful eradication, but the various rate of serum pepsinogen I/II ratio was different in both groups at 1 month and 3 months after eradication therapy (p < 0.05). Serum antibody of H. pylori and serum pepsinogen I/II ratio could be a marker of the judgment after eradication therapy, especially the various rate of serum antibody of H. pylori is useful for the monitor of H. pylori infection in the long term.     

消化性溃疡幽门螺杆菌(Hp)清除前后血Hp抗体、PG、GAS 变化的研究

幽门螺杆菌(Helicobacter pylori,Hp)阳性消化性溃疡患者在Hp清除前后血清抗Hp-IgG,抗Hp-IgM,胃蛋白酶原(Pep-sinogen,PG)和胃泌素(Gastrin,GAS)水平如何?奥美拉唑,硫糖铝,罗红霉素治疗Hp感染的消化性溃疡的效果如何?本课题对上述问题进行了研究。1材料与方法1.1一般资料病例选     

Serum IL-8 as a possible marker for determining the status of<Emphasis Type="Italic">Helicobacter pylori</Emphasis> infection in patients with untreated and treated peptic ulcer

Failure to eradicateHelicobacter pylori can lead to peptic ulcer recurrence and gastric malignancy. Therefore, the objective of this study was to develop a noninvasive method for determining whetherH pylori infection was eradicated with antibiotic-based triple therapy. A total of 17 patients with duodenal ulcer (DU) and 17 with gastric ulcer (GU) were evaluated both before and after treatment. Outcomes included serum levels of interleukin-8 (IL-8), pepsinogen I, and gastrin, and the Wilcoxon signed rank test was used to test significance. Changes in these parameters were also correlated with disease status. In those patients where both GU and DU healing occurred as a result of treatment, most showed an increase in serum IL-8 and a decrease in serum pepsinogen. Serum gastrin levels were not significantly changed in either group. Posttreatment increases in serum IL-8 were seen in 15 of 17 (88%) recovered DU patients and 14 of 17 (82%) recovered GU patients (P < .05 for each). Posttreatment decreases in pepsinogen I were found in 15 of 17 DU and 15 of 17 GU patients (P < .05 for each). These preliminary findings suggest that an increase in serum IL-8 and possibly a decrease in pepsinogen I may be useful in identifying the successful eradication ofH pylori infection in patients with peptic ulcer treated with antibiotics. A more systematic analysis of these putative diagnostic markers is now warranted.     

Relationship of Helicobacter pylori CagA(+) status to gastric juice vitamin C levels

BACKGROUND: To date it is not known whether gastric juice vitamin C levels are influenced by Helicobacter pylori CagA(+) strains. The aim of the present study, therefore, was to study the impact of H. pylori CagA status on gastric juice vitamin C levels. MATERIALS AND METHODS: We studied 30 H. pylori(+) patients, and the results were compared with 10 endoscopically and histologically normal H. pylori(-) subjects (control group) who were similar to the H. pylori(+) group in terms of age and sex. In all patients, gastric juice vitamin C levels were determined and the severity of gastritis was graded on a scale of 0 (absent) to 3 (severe). CagA was determined by immunoblotting the sera from patients against H. pylori antigens. RESULTS: Among 30 H. pylori(+) patients, 20 were CagA(+) and 10 CagA(-). In the entire group of H. pylori(+) patients, the median gastric juice vitamin C levels (mg L-1) were 16.35 (range 3.5-33.6) and were significantly lower (P < 0.001) than in the control group of H. pylori(-) patients [35.5 (23.1-50.2)]. In addition, in the entire group of H. pylori(+) patients there was a highly significant (P < 0.0001) inverse correlation between the gastritis activity score and the gastric juice vitamin C levels. In the group of H. pylori CagA(+) patients, the median levels of gastric juice vitamin C were 13.8 (3.5-31.2) and were significantly lower than the corresponding levels in both the H. pylori CagA(-) group [24.8 (22-33.6), P < 0.01] and the H. pylori(-) control group [35.5 (23.1-50.2), P < 0.001], the last groups being similar. Furthermore, the gastritis activity median score in the H. pylori CagA(+) group [2 (1-3)] was significantly higher (P < 0.05) than in the H. pylori CagA(-) group [1 (1-2)]. CONCLUSION: These data indicate that infection with CagA(+) H. pylori strains significantly lowers the gastric juice vitamin C levels in comparison with CagA(-) H. pylori strains, which might have a significant impact on gastric carcinogenesis.     

Helicobacter pylori is associated with modified lipid profile: impact on Lipoprotein(a)

OBJECTIVES: Helicobacter pylori is a controversial risk factor for atherosclerosis. We investigated whether the bacterium persistent inflammation or the expression of the cytotoxin-associated gene A (CagA) may affect serum lipids as well as Lipoprotein(a). DESIGN AND METHODS: Two hundred-eleven healthy volunteers were evaluated for lipids and Lipoprotein(a). Helicobacter pylori was characterized by Urea Breath Test and IgG-anti-CagA. apo(a) Kringle-IV polymorphism was genotyped. RESULTS: Prevalence of the infection was 72%; 43% of subjects expressed CagA reactivity. Infected subjects showed increased levels of cholesterol, LDL-cholesterol, and cholesterol/HDL-cholesterol atherogenic index. Association with the Helicobacter pylori CagA(-) strains persisted after the adjustment for covariates. Significant difference between infected and uninfected subjects was found in Lipoprotein(a) levels. This difference did not arise from the Kringle-IV genotype. CONCLUSIONS: The infection per se significantly modified serum lipid and Lipoprotein(a) concentrations. CagA does not seem to be a reliable marker of pathogenicity for the atherogenic complications of H. pylori infection.     

Ratio between serum IL-8 and pepsinogen A/C: a marker for atrophic body gastritis

BACKGROUND AND AIMS: Elevated serum gastrin and a low pepsinogen A/C ratio are well-recognized markers for atrophic body gastritis (ABG). We have shown that the presence of body atrophy is also associated with elevated serum pro-inflammatory cytokines. This study tested the hypothesis that serum cytokines provide additional information to gastrin and pepsinogens in screening for ABG. METHODS: Two hundred and twenty-six consecutive patients were investigated on referral for upper gastrointestinal endoscopy: 150 were patients with gastro-oesophageal reflux disease, receiving acid inhibitory medication either with proton pump inhibitors (n = 113) or with histamine2-receptor antagonists (n = 37), and 76 were nontreated controls, who had normal endoscopic findings. Gastric mucosal biopsies were sampled for histological examination (Sydney classification). Serum samples were analyzed for gastrin, chromogranin A (CgA), and pepsinogens A and C by RIA, and for the interleukins (IL)-1beta, IL-6, and IL-8 by ELISA. RESULTS: Subjects with ABG had significantly higher serum gastrin (P < 0.01) and serum CgA (P < 0.01) levels and significantly lower pepsinogen A/C ratios (P < 0.001) than those without ABG. Additionally, serum IL-1beta, IL-6 and, especially, IL-8 levels were significantly higher in the subjects with than in those without ABG (P < 0.0001, for all cytokines). To optimize the detection of body atrophy we defined the ABG index: the ratio between the simultaneously measured IL-8 and pepsinogen A/C. The area under the ROC curve for the ABG index was significantly greater than that for serum gastrin and for serum pepsinogen A/C alone (0.91 +/- 0.029 vs. 0.72 +/- 0.042, and vs. 0.83 +/- 0.031, P = 0.018 and P = 0.049). Using the ABG index at a cut-off value of 1.8 pg mL-1, 91% of the cases were classified correctly. CONCLUSIONS: The ratio between serum IL-8 and pepsinogen A/C accurately predicts the presence of ABG. We therefore propose the ABG index as a noninvasive screening test for ABG in population-based studies.     

The rise in circulating gastrin with age is due to increases in gastric autoimmunity and Helicobacter pylori infection

To assess the effect of increasing age on circulating gastrin, we surveyed serum gastrin, Helicobactor pylori seroantibody status and gastric autoimmunity in 366 hospitalized patients aged 15-90 years. Data were subjected to multivariate analysis, using logarithmic transformation to normalize the distribution of gastrin concentrations (presented as geometric means and 95% CIs). The frequency of H. pylori-positive antibody status increased with age from 28% in the second decade to > 70% beyond the fourth decade. Fasting gastrin concentrations rose significantly from 44 ng/l (41-48) in the second decade to 95 ng/l (67-131) by the eighth decade (p = 0.001) in the total group. Twenty-seven patients (6.8% of the total) tested positive for gastric auto-antibodies: 2% of patients in the second decade, rising to 15.9% in the eighth decade. These patients formed a distinct group with respect to circulating gastrin concentrations. Excluding these 27, fasting gastrin concentrations still rose significantly, from 44 ng/l (41-48) in the second decade, to 67 ng/l (50-89) in the eighth decade (p = 0.003) in the remaining 341 patients. Fasting gastrin concentrations were significantly higher in patients who were H. pylori-seropositive (59 ng/l, 54-64 vs. sero-negative 41 ng/l, 37-46) (p = 0.002), and there was no increase in circulating gastrin concentrations with increasing age in either the H. pylori-positive or the H. pylori-negative group. The increase in circulating fasting gastrin observed with increasing age is due to an increased incidence of gastric antibodies associated with auto-immune atrophic gastritis, and an increased incidence of H. pylori infection.     

Adherence of Helicobacter pylori to gastric epithelial cells and mucosal inflammation

Adherence of Helicobacter pylori to the gastric epithelium is believed to be an important step in the induction of active inflammation of the mucosal layer. However, structural evidence showing a quantitative relationship between the adherence of H. pylori and severity of gastric mucosal inflammation is lacking. We therefore investigated the correlations between severity of gastritis and adherence of morphologically different forms of H. pylori. Fifty-seven biopsy specimens from the gastric bodies of patients with H. pylori-induced gastritis were examined. The severity of gastritis and the adherence and structure of H. pylori were determined with the use of light and scanning electron microscopy. We also investigated the ability of H. pylori organisms with different structural features to induce interleukin-8 secretion by human gastric adenocarcinoma (AGS) cells in vitro because production of interleukin-8 is related to H. pylori-associated gastritis. Furthermore, serum pepsinogen concentrations and cytotoxin-associated protein status in relation to adherence of H. pylori to the epithelial surface were examined. The results indicated that H. pylori organisms, which adhered firmly to the epithelial surface, were consistently long, tightly coiled bacilli. Histologically, those gastric mucosa samples with H. pylori firmly attached showed severe gastritis. H. pylori bacilli of greater length induced higher levels of interleukin-8 secretion. The serum pepsinogen I/II ratio showed a significant negative correlation with the grade of H. pylori adhesion (r = -0.401, P <.01). We also noted a significant correlation between cytotoxin-associated protein status and the adherence of H. pylori (r = 0.344, P <.05). A quantitative correlation was found between adherence of H. pylori and gastric inflammation. Both adherence and the induction of inflammation were found to be related to the structure of H. pylori.     

High prevalence of VacA, CagA protein expression and presence of cag pathogenicity island in Japanese Helicobacter pylori isolates

VacA, CagA proteins and cag pathogenicity island (PAI) were reported to be major virulence factors of Helicobacter pylori. By using specific antibodies, the expression of VacA and CagA was evaluated in Japanese isolates, together with vacuolating assay. To characterize the status of not only cagA, but entire cag PAI, H. pylori isolates were evaluated for cagA and 13 other cagPAI genes by Southern blot. VacA and CagA proteins were expressed in 87% and in 90%, respectively. Vacuolating assay was positive in 84% isolates. Most strains had all cag PAI genes and the only 6% were cag PAI deleted despite of retaining cagA gene. The majority of Japanese isolates were positive for VacA, CagA proteins and cag PAI, and the high prevalence of infection with virulence strains may contribute to the characteristics of H. pylori infection in Japan.     

Enzyme-linked immunosorbent assay of serum pepsinogen I

A hybridoma monoclonal antibody against human pepsinogen I was used to develop an enzyme-linked immunosorbent assay for pepsinogen I in serum. In the two-step competitive procedure using antimouse immunoglobulin F(ab')2 fragment coupled to alkaline phosphatase, the measurable assay range was 8-256 micrograms/l. No cross-reactivity with rat pepsinogen 1, human pepsinogen II, gastrin I, bombesin, somatostatin and peptide YY was shown. However, there was slight cross-reactivity (0.09%) with porcine pepsinogen. The coefficients of variation within and between series were 7.6% and 13.0%. This enzyme-linked immunosorbent assay for serum pepsinogen I correlated positively with radioimmunoassay (r = 0.87, n = 92). The concentration range of serum pepsinogen I in 354 healthy controls was 15-100 micrograms/l with a lognormal distribution. Serum pepsinogen I levels were significantly higher in the subjects who developed active duodenal ulcer or active gastric ulcer, but significantly lower in those who had gastric cancer, than in control subjects.     

Circulating gastrin and ghrelin levels in patients with colorectal cancer: correlation with tumour stage, Helicobacter pylori infection and BMI.

Many studies have pointed out a possible role of gut peptides, including gastrin and ghrelin, in the pathogenesis and natural history of gastrointestinal malignancies, one of the most common death cause in the Western world. The objective of this work is to check gastrin and ghrelin serum levels in patients with colorectal cancer according to tumour's location, stage, Helicobacter pylori infection and BMI, in order to understand the two peptides' behaviour through the tumour's natural history and evaluate their assay's use in research and clinical practice. Twenty-nine subjects affected by colorectal cancer and 50 healthy controls were studied. Circulating gastrin and ghrelin levels and H. pylori serum antibodies were assessed by radioimmunologic assay and ELISA method. Gastrin and ghrelin serum levels were respectively slightly higher and significantly lower in colon cancer patients than in controls. Gastrin levels were higher in patients carrying left colon cancer and H. pylori infection while ghrelin levels were lower in both these groups. Both hormones' serum levels decreased from tumour earlier to later stages. Significant differences persisted in the correlation between BMI and ghrelin levels in controls but not in patients. Additional studies are necessary to ascertain the significance of gastrin and ghrelin opposite behaviour in colon cancer probably linked with interferences in endocrine pathways involving other gut peptides in this compromised condition.     

Time course changes in morphological and functional characteristics of gastric mucosa after eradication of Helicobacter pylori in duodenal ulcers

AIM: To study trends in morphological changes of gastric mucosa (GM) and its functional characteristics (serum gastrin-17, pepsinogens I and II) in eradication of Helicobacter pylori (HP) in patients with duodenal ulcer (DU). MATERIAL AND METHODS: HP infection was detected with a rapid urease test, morphological study of gastrobiopsies and polymerase chain reaction in 59 patients with DU. The results of HP eradication were assessed two months after the treatment. Morphological study of gastrobiopsies, assays for gastrin-17, pepsinogens I and II in blood serum were made before the treatment and one year after HP eradication. RESULTS: By the results of eradication two groups were formed: with effective eradication and uneffective eradication of H. pylori. Examination of GM one year after successful H. pylori eradication in DU patients GM inflammation relieved: reduction in polymorphonuclear (by 42.6%), mononuclear (by 29.3%) infiltration and number of lymphocytic follicules (16.8-fold). GM atrophy decreased by 47.8%. In patients with uneffective eradication the above positive changes were not registered. After H. pylori eradication, serum gastrin-17 lowered by 46. 7%, pepsinogen I--by 30.5%, pepsinogen II--by 36.9%. In uneffective eradication this decrease did not occur. CONCLUSION: H. pylori eradication leads to positive changes in morphological and functional indices reflecting GM condition.     

不同毒力亚株幽门螺杆菌感染在特发性血小板减少性紫癜发病中的意义

目的分析幽门螺杆菌（H.pylori）不同毒力亚株感染与特发性血小板减少性紫癜（ITP）发病的相关性。方法应用免疫印记法检测64例ITP患者和59例对照者的血清H.pylori抗体：细胞毒素相关基因A（CagA）、空泡毒素蛋白A（VacA）、尿素酶A（UreA）、尿素酶B（UreB）,并对CagA＋和/或VacA＋阳性患者随机分组,一组抗H.pylori治疗,另一组、CagA-和VacA-以及H.pylori阴性患者组未作抗H.pylori治疗作为对照组,比较治疗前后血小板计数。结果ITP组患者H.pylori阳性率高于对照组,差异有统计学意义（P〈0.05）;ITP组H.pylori阳性患者CagA＋和/或VacA＋型者所占比例高于对照组,差异有统计学意义（P〈0.001）。CagA＋和/或VacA＋阳性患者经H.pylori根治后血小板计数较CagA＋和/或VacA＋阳性未根治组升高明显,P〉0.05有统计学意义。结论ITP患者幽门螺杆菌的感染率高,而且不同毒力亚株感染与其发病相关。     

High seroprevalence of Helicobacter pylori in chronic bronchitis among Chinese population

An increased seroprevalence of Helicobacter pylori (H. pylori), especially high virulent cytotoxin-associated gene-A (CagA) positive strains, has been found in many extragastrointestinal disorders. Moreover, it has been reported that the risk of chronic bronchitis may be increased in H. pylori infected patients. However, until now there are no data regarding the relationship between H. pylori infection and chronic bronchitis among Chinese population. Therefore the aim of the present study was to assess the seroprevalence of H. pylori and in particular of CagA positive virulent strains in patients with chronic bronchitis among Chinese population. We evaluated 46 patients with chronic bronchitis, 48 age- and sex-matched patients with peptic ulcer and 48 healthy control subjects. All enrolled subjects underwent a serologic test for H. pylori IgG and CagA by enzyme linked-immunosorbent assay (ELISA). There was no significant difference in the seropositivity for these parameters between chronic bronchitis and peptic ulcer groups (86.9% vs 89.6% for anti-H. pylori IgG and 67.4% vs 72.9% for anti-H. pylori-CagA IgG). However, these serological parameters were significantly higher in the patients with chronic bronchitis or peptic ulcer than those in control group, who showed 60.4% for anti-H. pylori IgG seropositivity and 20.8% for anti-H. pylori-CagA IgG seropositivity. Among the patients with chronic bronchitis, no significant difference was found in these serological parameters between the current cigarette smokers and never smokers. This is the first report of a high seroprevalence of H. pylori infection in chronic bronchitis among Chinese population.     

血清抗幽门螺杆菌IgG抗体、胃蛋白酶原水平与胃癌发病的相关性分析

目的研究长春地区人群血清抗幽门螺杆菌(Helicobacter pylori,Hp)IgG抗体、胃蛋白酶原水平和胃癌发病的相关性,为胃癌的防治研究提供依据和流行病学资料。方法选择2008年10月至2011年2月吉林大学第一医院明确诊断的450例原发性胃癌患者作为病例组,选择同时期体检中心1072例健康体检者作为对照组。采用酶联免疫吸附(ELISA)法检测血清中Hp IgG抗体、胃蛋白酶原Ⅰ(PGI)和Ⅱ(PGII)的水平,确定Hp菌感染和萎缩性胃炎的发生状况。以PGI≤82.3μg/L,同时PGI/PGII≤6.05作为萎缩性胃炎的诊断标准。结果胃癌组与对照组相比,Hp感染阳性率明显增高(69.1%vs.52.4%,χ2=36.1,P<0.001)。胃癌组中血清PGI水平与对照组比较无显著差异(93.2vs.88.9μg/L,P<0.001),而PGII浓度显著升高(15.9vs.11.3μg/L,P<0.001),同时PGI/PGII比值明显降低(5.4vs.7.8,P<0.001)。胃癌组中患萎缩性胃炎的比例明显高于对照组(31.4%vs.10.4%,P<0.001)。多因素回归分析显示:在调整年龄和性别因素后,Hp感染和萎缩性胃炎均为胃癌发病的独立危险因素。结论本研究对象人群中Hp感染率,尤其是青年胃癌患者中Hp感染率仍然较高,Hp感染和萎缩性胃炎是胃癌发病的危险因素。与PGI相比,血清PGII浓度和PGI/PGII比值可能成为胃癌筛选的潜在血清学标志物。