A confirmatory report for the close interaction of Helicobacter pylori with gastric epithelial MUC5AC expression

BACKGROUND: Helicobacter pylori (H. pylori) infection is associated with the development of gastritis and peptic ulcer and is presumed to be a risk factor for low-grade B-cell lymphoma and gastric cancer. H. pylori also causes critical alterations in gastric mucin structure. Our aim was to determine the effect of H. pylori on MUC1, MUC2, and MUC5AC expression. METHODS: Thirty H. pylori-positive and 15 H. pylori-negative antral gastric endoscopic biopsy specimens were evaluated for MUC1, MUC2, and MUC5AC expression with immunohistochemical staining. From the same specimens, we scrutinized the presence of H. pylori infection by hematoxylin and eosin and immunohistochemical staining. RESULTS: In H. pylori infected patients, the expression of MUC5AC was found to be localized to the cells in the superficial epithelium and upper parts of the gastric glands. The number of MUC5AC-expressing cells and the staining intensity of MUC5AC were shown to decrease in patients with H. pylori infection. Histopathology and immunostaining patterns of gastric mucins implied that H. pylori was physically associated with extracellular MUC5AC and MUC5AC-producing cells. H. pylori infection does not significantly affect staining intensity and patterns of MUC1 and MUC2 expressions. MUC1 was not found in dysplastic tissues or intestinal metaplasia areas. MUC5AC was expressed in dysplastic areas, but not in intestinal metaplasia. MUC2 was expressed in both dysplastic and intestinal metaplasia areas. CONCLUSION: H. pylori decreases the amount of MUC5AC expression. With reducing MUC5AC-producing cells and MUC5AC mucin, H. pylori may potentially cause significant alterations of the structure and function of gastric mucins. H. pylori-dependent inhibition of mucin synthesis deserves more investigations to clarify the role of H. pylori and gastric MUC5AC interaction.     

Effects of Helicobacter pylori infection on mucin expression in gastric carcinoma and pericancerous tissues

BACKGROUND: Helicobacter pylori infection is one of the major causes of human gastric carcinoma and can disturb the gastric mucosa barrier. Mucins have not only lubricating and protecting functions, but are also related to signal transduction, turnover of gastric epithelium and carcinogenesis of gastric mucosa. The aim of this study was to investigate the relationship between H. pylori infection and aberrant mucin expression in patients with gastric carcinoma. METHODS: H. pylori infection was diagnosed by the Warthin-Starry staining method. Different kinds of mucins were detected using an immunohistochemical method. RESULTS: Of 46 patients with gastric carcinoma, there were 26 patients who had H. pylori infection (56.5%). Of 21 pericancerous mucosas from the H. pylori-positive patients, 14 had MUC2 expression (66.7%), seven had strong MUC1 expression (+ + +) (33.7%), seven had strong MUC6 expression (+ + +) (33.3%), and five had strong MUC5AC expression (+ + +) (23.8%). In contrast, only six of 18 H. pylori-negative pericancerous mucosas had MUC2 expression (33.3%) (P < 0.05 compared with H. pylori-positive pericancerous mucosas), 12 had strong MUC1 expression (+ + +) in 16 H. pylori-negative pericancerous mucosas (75%) (P < 0.05), 11 had strong MUC6 expression (+ + +) in 16 H. pylori-negative pericancerous mucosas (68.8%) (P < 0.05), and 10 had strong MUC5AC expression (+ + +) in 14 H. pylori-negative pericancerous mucosas (71.4%) (P < 0.01). Of the H. pylori-positive cancerous tissues, 50% (13/26) had MUC1 expression and 38.5% (10/26) had MUC6 expression. In comparison, of the H. pylori-negative cancerous tissues, 80% (16/20) had MUC1 expression (P < 0.05) and 80% (16/20) had MUC6 expression (P < 0.01). CONCLUSIONS: The results indicate that H. pylori infection can alter the expression of some mucin genes in pericancerous mucosa and cancerous tissues of gastric carcinoma, then destroy the gastric mucosa barrier.     

Does Helicobacter pylori affect gastric mucin expression? Relationship between gastric antral mucin expression and H. pylori colonization

BACKGROUND/OBJECTIVE: Helicobacter pylori colonizes the gastric mucous gel layer, the surface epithelium and glands. It has been shown that H. pylori infection causes aberrant expression of gastric mucins MUC 5 and MUC 6. This study aimed to determine the distribution of MUC 5 and MUC 6 in the gastric antrum of dyspeptic patients, and to investigate changes in this pattern in the presence of H. pylori and after successful eradication. MATERIALS AND METHODS: Gastric antrum biopsy specimens were examined by immunohistochemistry for mucin gene (MUC 5 and MUC 6) expression. Polyclonal antibodies were used to detect amino acid tandem repeats of each protein. A scoring system (0-3) was used to assess staining intensity at three sites: foveola, mucous neck cells and glands. H. pylori status was determined by histology and rapid urease test, and considered positive or negative when both tests were positive or negative, respectively. The study included 49 patients positive for H. pylori, in 36 of whom successful eradication was performed, and 11 H. pylori-negative patients. RESULTS: There was a gradient of MUC 5 expression, higher to lower, from the surface to the glands, which was more pronounced before eradication. Increased MUC 5 synthesis in the mucous neck cells and in the glands was found after H. pylori eradication (P = 0.016). MUC 6 was synthesized in the glands more than in the mucous neck cells or foveola. MUC 6 was also secreted into the lumen and probably comprised the superficial part of the unstirred mucous layer. CONCLUSION: The change in MUC 5 synthesis may reflect H. pylori colonization.     

Effect of Helicobacter pylori eradication on bulbitis and duodenal gastric metaplasia

BACKGROUND/AIMS: Duodenal gastric metaplasia seems to be linked to infection by Helicobacter pylori, to the extent of acid secretion and to bulbitis. An investigation was made of the relationship between bulbitis and duodenal gastric metaplasia, or whether bulbitis can arise along with duodenal gastric metaplasia after Helicobacter pylori eradication in an average of six years. METHODOLOGY: We compared 22 patients with duodenal ulcers [male/female 16/6; (mean age+/-SD) 55+/-12 years] Helicobacter pylori-negative after eradication, with 23 Helicobacter pylori-positive patients free from active duodenal ulcers [male/female 17/6; (mean age+/-SD) 59+/-12 years]. RESULTS: The bulbitis score was found to be lower in the Helicobacter pylori-negative than in the Helicobacter pylori-positive group (p=0.02). The duodenal gastric metaplasia score in the Helicobacter pylori-negative was higher than in the Helicobacter pylori-positive group (p=0.001). We failed to find any relationship between the presence of bulbitis and duodenal gastric metaplasia. We found a non-significant inverse correlation between the presence of duodenal gastric metaplasia and chronic body gastritis (p=0.07). CONCLUSIONS: Bulbitis and duodenal gastric metaplasia may depend on different causal factors not related to Helicobacter pylori infection. The extension of duodenal gastric metaplasia with time following recovery from peptic ulcer disease may represent a mucosal protection factor against acid.     

Expression of mutant type-p53 products in H pylori-associated chronic gastritis

AIM:To investigate the mutation of p 53 immuno-histochemically in non-tumorous gastric mucosa with H pylori infection before and after H pylori eradication therapy.METHODS:53 subjects(36 male,17 female,mean age ± SEM,57.1 ± 12.1)undergoing endoscopic examination were included in this study.42 of 53 patients were H pylori-positive,and 11 were H pylori-negative.All H pylori-positive patients had successful eradication therapy.Biopsy specimens were taken from five points of the stomach,as recommended by the updated Sydney system.Immunohistochemical studies were performed by using primary antibodies against p53(DO-7 and PAb240).RESULTS:p53(DO-7 and PAb240)immunoreactivity was shown in the neck region of the gastric pits,however,quite a few cells were found to be immunopositive for p 53(PAb240)in the H pylori-infected gastric mucosa.The proportion of patients immunopositive for p 53(PAb240)was significantly reduced 6 mo after eradication [28/42(66.7%)to 6/42(14.3%)](P < 0.05),while the biopsies taken from H pylori-negative patients showed no immunoreactivity for p53(PAb240).p53(PAb240)-positive patients were divided into two groups by the number of positive cells detected:one with more than six positive cells per 10 gastric pits(group A,n = 12),and the other with less than five positive cells per 10 gastric pits(group B,n = 30).Atrophy scores in group A were significant higher than those in group B at the greater curvature of the antrum(group A:2.00 ± 0.14 vs group B:1.40 ± 0.15,P = 0.012),the lesser curvature of the corpus(group A:2.00 ± 0.21 vs group B:1.07 ± 0.23,P = 0.017),and the greater curvature of the corpus(group A:1.20 ± 0.30vs group B:0.47 ± 0.21,P = 0.031).Group A showed significant higher intestinal metaplasia scores than group B only at the lesser curvature of the antrum(group A:2.10 ± 0.41 vs group B:1.12 ± 0.29,P = 0.035).CONCLUSION:H pylori-associated chronic gastritis expressed the mutant-type p53,which was significantly associated with more severe atrophic and metaplastic changes.H pylori eradication led to a significant reduction in the expression of the mutant-type p53.It is considered that H pylori-infected chronic gastritis is associated with a genetic instability that leads to gastric carcinogenesis,and H pylori eradication may prevent gastric cancer.     

Endoscopic duodenitis, gastric metaplasia and Helicobacter pylori

BACKGROUND AND AIMS: The purpose of this study was to investigate the relationship between gastric metaplasia and Helicobacter pylori in patients with endoscopic duodenitis. METHODS: The subjects were 57 patients with endoscopic duodentitis with or without H. pylori-associated gastritis. Biopsy specimens were obtained from the stomach and duodenal bulb to assess the histological findings and H. pylori infection. Gastric metaplasia was divided into three types: complete, intermediate and incomplete, according to the amount of mucus in the metaplastic cells. In 10 H. pylori-positive patients, endoscopic and histological findings of duodenitis were compared before and after eradication of the bacteria. RESULTS: There was no significant difference in the extent of gastric metaplasia or the appearance and severity of endoscopic duodenitis between H. pylori-positive and -negative groups. The complete type of gastric metaplasia was frequently detected in the H. pylori-negative group, whereas the incomplete type was frequently observed in the H. pylori-positive group. After eradication of H. pylori, the incomplete type changed to the complete type with a decrease of histological inflammation. CONCLUSIONS: The complete type of gastric metaplasia occurred frequently without H. pylori infection, whereas the incomplete type was frequently associated with H. pylori infection.     

Apoptosis, proliferation and p53 gene expression of H. pylori associated gastric epithelial lesions

AIM:To study the relationship between Helicobacter pylori(H.pylori)and gaatric carcinoma and its possiblepathogenesis by H.pylori.METHODS:DNEL technique and immunohistochemicaltechnique were used to study the state of apoptosis,proliferation and p53 gone expression.A total of 100 gastricmucosal biopsy specimens,including 20 normal mucosa,30H.pylori-negative and 30 H.pylori-positive gastricprecancerous lesions along with 20 gastric carcinomas werestudied.RESULTS:There were several apoptotic cells in thesuperficial epithelium and a few proliferative cells within theneck of gestric glands,and no p53 protein expression innormal mucosa.In gestric carcinoma,there ware fewapoptotic cells,while there were a large number ofproliferative cells,and expression of p53 proteinsignificantly was increased.In the phase of metaplasia,theapoptotic index(Al,4.36%±1.95%),proliferative index(Pl,19.11%±6.79%)and positivity of p53 expression(46.7%)in H.pylori-positive group ware higher than thosein normal mucosa(P<0.01).Al in H.pylori-positive groupwas higher than that in H.pylori-negative group(3.81%±1.76%),Pl in H.pylori-positive group was higher than thatin H.pylori-negative group(12.23%±5.63%,P<0.01).Inthe phase of dysplasia,Al(2.31%±1.10%) in H.pylori-positive group was lower(3.05%±1.29%)than that in H.pylori-negative group,but Pl(33.89%±11.65%)wassignificantly higher(22.09±8018%,P<0.01).In phases ofmetaplasia,dysplasia and gastric cancer in the H.pylori-positive group,Als had an evidently greduall decreasingtrend(P<0.01),while Pls had an evidently gradualincreasing trend(P<0.05 or P<0.01),and there was alsoa trend of gradual increase in the expression of p53 gone.CONCLUSION:In the course of the formation of gastriccarcinoma,proliferation of gastric mucosa can be greatlyIncreased by H.pylori,and H.pylori can induce apoptosisin the phase of metaplasia,but in the phase of dysplesia H.pylorl can inhibit cellular apptosis.And H.pylori infectioncan strengthen the expression of mutated p53 gene.     

Histological changes in the gastric mucosa after Helicobacter pylori eradication

BACKGROUND AND AIM: Correa described a stepwise model of changes in the gastric mucosa after Helicobacter pylori infection, from the normal gastric epithelium to chronic gastritis, atrophy, intestinal metaplasia, dysplasia and adenocarcinoma. The aim of this study is to assess the reversibility of these mucosal changes after H. pylori eradication. METHODS: The study sample consisted of 89 patients who underwent at least two gastric biopsies from 1990 to 2000, with a positive finding for H. pylori in the first and a negative finding in the second. Specimens were evaluated for acute and chronic inflammation, lymphoid aggregates, proliferation, mucosal atrophy, intestinal metaplasia, dysplasia, and MUC5AC and MUC6 expression using histochemical and immunohistochemical methods. RESULTS: The average time between biopsies was 23.15 +/- 26.30 months. There was a significant decrease in acute and chronic inflammation scores, from 1.48 +/- 1.10 to 0.23 +/- 0.63 and from 2.67 +/- 0.68 to 1.44 +/- 1.04, respectively (P < 0.001), and in a number of lymphoid follicles, from 42.68% to 21.95% of cases (P < 0.008). The number of glands increased from 39.08 +/- 16.67/mm to 48.86 +/- 17.93/mm after eradication (P = 0.062). Intestinal metaplasia was found in 17.07% of the cases, with no change over time. Dysplasia appeared in one case 2 years after eradication. In 27 patients, the Ki67 labeling index decreased significantly after eradication, while MUC5AC and MUC6 expression increased. CONCLUSION: Our findings, although not conclusive for arrest of the malignant potential, support the importance of H. pylori eradication in the prevention of gastric cancer.     

Helicobacter pylori infection influences tumor growth of human gastric carcinomas

BACKGROUND: Helicobacter pylori infection is considered a risk factor for gastric carcinoma. However, the effect of eradication therapy in gastric carcinoma patients is not well known. The aim of this study was to investigate the relationship between H. pylori infection and tumor growth of gastric carcinoma. METHODS: Fifty-one patients with gastric carcinoma participated in the study. Thirty-three were H. pylori-positive, 6 were H. pylori-negative, and 12 were diagnosed with gastric carcinoma after eradication of H. pylori. To investigate tumor growth of gastric carcinoma, cell proliferation and angiogenesis of the tumors were evaluated by immunohistochemical techniques using Ki-67 and CD34. RESULTS: The Ki-67 labeling index was 47.9 +/- 2.6 (mean +/- s) in the H. pylori-positive group, 38.1 +/- 3.6 in the H. pylori-eradicated group, and 22.2 +/- 5.5 in the H. pylori-negative group. It was significantly lower in the H. pylori-eradicated and H. pylori-negative groups than in the H. pylori-positive one, and a significant difference was also found between the H. pylori-positive and H. pylori-eradicated groups. The microvessel counts were 62.5 +/- 3.0, 50.2 +/- 4.0, and 66.0 +/- 9.8 in the positive, eradicated, and negative groups, respectively. A significant difference was found between the H. pylori-positive and H. pylori-eradicated groups. CONCLUSION: Our results suggest that H. pylori infection is associated with cell proliferation, and its eradication may influence tumor vascularity of gastric carcinoma. Therefore, H. pylori eradication therapy may contribute to the suppression of tumor growth.     

Endoscopic therapy after laparoscopic cholecystectomy

Twelve different genes for mucin have been described. MUC5AC and MUC6 encode the secreted apomucins of the stomach. A gradient from the surface epithelium (foveola) to the glands is typical for MUC5AC synthesis, whereas a gradient in the opposite direction was found for MUC6. Our goal was to determine the distribution of MUC5AC and MUC6 in the postoperative stomach, with relation to the H. pylori status. Gastric corpus biopsy specimens from patients who underwent partial gastrectomy were examined by immunohistochemistry for mucin gene (MUC5AC and MUC6) apoproteins. We used polyclonal antibodies for amino acid tandem repeats of both proteins. A scoring system (0-3) was used to assess staining intensity at four sites: the lumen, the foveola, the mucous neck cells, and the glands. Helicobacter pylori status was determined by histology and rapid urease test and was considered positive or negative when both tests were positive or negative, respectively. We studied 19 H. pylori-positive and 32 H. pylori-negative patients. No significant change in MUC5AC or MUC6 synthesis and secretion was demonstrated between H. pylori-positive or -negative patients. A gradient similar to that shown for the intact stomach (from the surface epithelium to the glands) for MUC5AC protein and an increase of MUC6 protein presentation from the mucous neck cell to the glands were demonstrated. The pattern of MUC5AC protein synthesis was not different between H. pylori-positive and -negative patients in the postoperative stomach. MUC6 expression was higher in the foveola in H. pylori-positive patients, whereas there was no difference in the other cell layers.     

Cell kinetic balance in gastric mucosa with intestinal metaplasia after Helicobacter pylori eradication: 2-year follow-up study

BACKGROUND: Proliferation and apoptosis events are altered in Helicobacter pylori infection. However, whether H. pylori eradication has an effect on the disturbed kinetics in metaplastic mucosa has not been well elucidated. AIM: To investigate the effect of eradication on the gastric cell kinetics. SUBJECTS AND METHODS: Initially, biopsies were obtained from 74 H. pylori-infected subjects and repeated 12 and 24 months after eradication. Biopsies were immunohistochemically stained for apoptosis by single-stranded DNA, for proliferation by Ki-67 antibodies and for intestinal metaplasia MUC2, MUC5AC, MUC6 and CD10. RESULTS: While antral apoptosis in intestinal metaplasia was significantly lower than in non-intestinal metaplasia, proliferation was significantly higher (greater and lesser curvatures, P < 0.05, respectively). This resulted in a significantly lower apoptosis/proliferation ratio in intestinal metaplasia than in non-intestinal metaplasia (antrum greater and lesser curvatures and corpus greater curvature, P < 0.05). After successful eradication, apoptosis and proliferation decreased in both intestinal metaplasia and non-intestinal metaplasia. The pattern of reduction of apoptosis and proliferation differed in these two groups. However, in the corpus, the reduction resulted in a significant increase in the apoptosis/proliferation ratio in both. CONCLUSION: Proliferation and apoptosis are unevenly and disproportionately altered in H. pylori infection leading to an imbalance in cell kinetics. Eradication of the organism improves the balance and may possibly play a role in the prevention of malignancy transformation in the metaplastic mucosa.     

根除幽门螺杆菌对胃窦黏膜萎缩和肠上皮化生逆转影响的前瞻性研究

目的 探讨根除幽门螺杆菌(Hp)对逆转胃窦黏膜萎缩和肠上皮化生(肠化生)病理改变的作用.方法 对行胃镜检查的门诊患者,于胃窦处取黏膜活检行病理学检查,并确定Hp感染状态.将Hp感染的慢性胃炎伴胃窦黏膜萎缩或(和)肠化生患者作为入选对象并分为两组,一组行Hp根除治疗,为Hp根除组(48例);另一组未行抗Hp治疗,为对照组(38例).分别在1年和5年后对两组患者进行胃镜随访,并在同一部位取材,根据2次病理结果的不同分为逆转和未逆转两种情况.结果 胃窦黏膜萎缩逆转率在Hp根除组显著高于对照组(37.1%比12.0%).5年后Hp根除组的胃窦黏膜萎缩逆转率显著高于1年后,45岁以下者显著高于45岁以上者.而在对照组中,胃窦黏膜萎缩逆转和随访的时间及年龄无明显关系.在2次随访中,肠化生逆转率在Hp根除组和对照组间差异均无统计学意义(P>0.05).结论 根除Hp尚不能逆转胃窦黏膜肠化生,但对逆转胃窦黏膜萎缩有作用,这种作用与随访观察时间及患者的年龄有关.因此,对有Hp感染的胃窦黏膜萎缩者应及早行根除Hp治疗.     

Evaluation of the effects of Helicobacter pylori eradication therapy on gastric antral epithelial hyperproliferation: a prospective six-month follow-up study

BACKGROUND/AIMS: H. pylori-induced hyperproliferation of the gastric epithelium may have a critical role in gastric carcinogenesis. H. pylori-related hyperproliferation and reversibility of hyperproliferation after eradication therapy is still controversial. Therefore, we have evaluated the effects of H. pylori and its eradication on gastric antral epithelial proliferation. METHODOLOGY: A total of 32 H. pylori-positive and 22 H. pylori-negative subjects were enrolled into the study. Triple eradication therapy was given to the H. pylori-positive group. Upper endoscopy was repeated one month after the therapy and six months later, antral biopsy specimens were taken in each endoscopy. Biopsy specimens from H. pylori-negative subject were taken at the beginning of the study and sixth months later also. RESULTS: Proliferative index was 40.2% in H. pylori-positive state; it regressed to 27.6% after eradication and six months later the proliferative index was 30.7%. H. pylori-negative group's proliferative index was 25.5% initially and six months later it was 25.6%. The difference between the H. pylori-positive and -negative group was statistically significant (p<0.0001). The difference between H. pylori-positive group's values at the beginning of the study and one month after the eradication was significant (p<0.0001). In addition, the difference between H. pylori-positive group's initial values and those six months after eradication was also significant (p<0.0001). CONCLUSIONS: H. pylori increased the gastric epithelial proliferation and after the eradication therapy proliferative index decreased to control values. H. pylori and the related factors inducing gastric antral hyperproliferation may have an important role in H. pylori-related gastric malignancies.     

幽门螺杆菌感染诱导胃黏膜上皮细胞凋亡及端粒酶逆转录酶表达

目的研究幽门螺杆菌（Hp）根除前后胃黏膜上皮细胞凋亡和端粒酶逆转录酶（hTERT）表达及其与bcl-2、c-myc蛋白表达的关系。方法采用脱氧核糖核酸末端转移酶介导的缺口末端标记（TUNEL）技术及免疫组化染色方法检测39例却Hp性患者根除治疗及21例却阴性患者对症治疗前后胃黏膜上皮细胞凋亡、hTERT、bcl-2、c—myc蛋白表达的变化。结果治疗前却阳性者胃黏膜上皮细胞凋亡指数为16．2％，显著高于却阴性者（P〈0．05）；却阳性者hTERT、c—myc蛋白表达显著高于却阴性者（53．8％比23．8％；53．8％比28．6％，P〈0．05）。邯根除者治疗后胃黏膜上皮细胞凋亡、hTERT及bcl-2、c—myc蛋白表达与根除前相比均显著下降（16．9％比9．0％；59．3％比22．2％；59．3％比25．9％；59．3％比14．8％，P〈0．01），且与却阴性对照组相比差异无统计学意义（P〈0．05）；而邯未根治组及对照组上述指标均无显著变化。治疗前bcl-2、c—myc蛋白与hTERT呈显著正相关，秩相关系数r分别为0．269、0．474（P〈0．05）。结论却感染诱导细胞凋亡及hTERT过度表达，使胃黏膜不稳定性增加。根除却可纠正细胞凋亡失调，使hTERT表达下降或消失，从而降低胃癌发生的可能性。bcl-2及c—myc蛋白对hTERT表达可能具有调控作用。     

Effect of Helicobacter pylori eradication on gastric mucosal phospholipid content and its fatty acid composition

BACKGROUND AND AIMS: Whether Helicobacter pylori eradication alters gastric mucosal phospholipid contents and their fatty acid composition remains unclear. The aim of the present study was to clarify the effect of H. pylori eradication on gastric mucosal phosphatidylcholine (PC) content and its fatty acid composition. METHODS: Endoscopic biopsy specimens were taken from the antrum and body of each of 19 asymtomatic male volunteers for detection of H. pylori, histopathological assessment of gastritis, phospholipid determination and fatty acid analysis. All the subjects with H. pylori infection were treated with eradication therapy. Endoscopy and tissue sampling were repeated again 1 and 6 months after all treatment. RESULTS: In eight subjects, H. pylori infection was evident and was successfully eradicated. Pretreatment degrees of lymphocytes and plasma cells (inflammation) and polymorphonuclear neutrophils (activity) were greater in H. pylori-positive subjects compared with H. pylori-negative subjects (P<0.001), whereas the degree of inflammation decreased (P<0.001), and neutrophils had completely disappeared at 6 months after eradication. Moreover, the gastric mucosal PC contents at the antrum and body were unchanged within 1 month after cessation of treatment, but increased at 6 months after eradication (P<0.05). At 6 months after cessation of treatment, H. pylori-eradicated subjects had an increase (+30% at antrum, +18% at body) in linoleic acid composition and a decrease (-37%, -43%) in arachidonic acid composition of PC at the antrum and body, respectively. CONCLUSIONS: These findings suggest that H. pylori eradication reduces the production of various eicosanoids, resulting in the normalization of gastric mucosal PC content and its fatty acid composition, which may consequently cause the gastric mucosal hydrophobicity to be normalized.     

幽门螺杆菌感染患者胃癌及癌旁组织中p53,p16和bc1—2基因的表达

研究幽门螺杆菌（Ｈ．ｐｙｌｏｒｉ）感染胃癌得胃粘膜病变中抑癌基因ｐ５３、ｐ１６和关键性凋亡调节基因ｂｃ１－２蛋白的表达,进一步探讨Ｈ．ｐｙｌｏｒｉ在胃癌发生、发展过程中作用的分子机制。方法：胃镜检查及外科手术中取４０例胃癌患者的癌组织和癌旁２ ｃｍ处组织各２块,石蜡包埋,切片ＨＥ染色作病理诊断及免疫组化检查ｐ５３、ｐ１６及ｂｃ１－２蛋白的表达。Ｈ．ｐｙｌｏｒｉ阳性由快速尿素酶试验结合病理染色／＾１     

Comparison of He/icobacter py/ori infection and gastric mucosal histological features of gastric ulcer patients with chronic gastritis patients

AIM: To compare Helicobacter pylori infection and gastric mucosal histological features of gastric ulcer patients with chronic gastritis patients in different age groups and from different biopsy sites. METHODS: The biopsy specimens were taken from the antrum, corpus and upper angulus of gastric ulcer and chronic gastritis patients. Giemsa staining, improved Toluidine-blue staining and H pylori-specific antibody immune staining were performed as appropriate for the histological diagnosis of H pylori infection. Hematoxylineosin staining was used for the histological diagnosis of activity of H pylori infection, mucosal inflammation, glandular atrophy and intestinal metaplasia and scored into four grades according to the Updated Sydney System. RESULTS: Total rate of H pylori infection, mucosal inflammation, activity of H pylori infection, glandular atrophy and intestinal metaplasia in 3 839 gastric ulcer patients (78.5%, 97.4%, 82.1%, 61.1% and 64.2%, respectively) were significantly higher than those in 4 102 chronic gastritis patients (55.0%, 90.3%, 56.2%, 36.8%, and 37.0%, respectively, P<0.05). The rate of H pylori colonization of chronic gastritis in <30 years, 31-40 years, 41-50 years, 51-60 years, 61-70 years and >70 years age groups in antrum was 33.3%, 41.7%, 53.6%, 57.3%, 50.7%, 43.5%, respectively; in corpus, it was 32.6%, 41.9%, 53.8%, 60.2%, 58.0%, 54.8%, respectively; in angulus, it was 32.4%, 42.1%, 51.6%, 54.5%, 49.7%, 43.5%, respectively. The rate of H pylori colonization of gastric ulcer in <30 years, 31-40 years, 41-50 years, 51-60 years, 61-70 years and >70 years age groups in antrum was 60.5%, 79.9%, 80.9%, 66.8%, 59.6%, 45.6%, respectively; in corpus, it was 59.7%, 79.6%, 83.6%, 80.1%, 70.6%, 59.1%, respectively; in angulus, it was 61.3%, 77.8%, 75.3%, 68.8%, 59.7%, 45.8%, respectively. The rate of H pylori colonization at antrum was similar to corpus and angulus in patients, below 50 years, with chronic gastritis and in patients, below 40 years, with gastric ulcer. In the other age- groups, the rate of H pylori colonization was highest in corpus, lower in antrum and lowest in angulus (all P<0.05). The rates of glandular atrophy and intestinal metaplasia were higher and earlier in H pylori-positive patients than those without H pylori infection (both P<0.01). In comparison of gastric ulcer patients with chronic gastritis patients, the rate of glandular atrophy and intestinal metaplasia was higher in H pylori-positive patients with gastric ulcer than in H pylori-positive patients with chronic gastritis (both P<0.01); the rate of glandular atrophy and intestinal metaplasia were also higher in H pylori-negative patients with gastric ulcer than in H pylori-negative patients with chronic gastritis (both P<0.01). Both glandular atrophy and intestinal metaplasia were much more commonly identified in the angulus than in the antrum, lowest in corpus (all P<0.01). CONCLUSION: Rate of H pylori infection, glandular atrophy and intestinal metaplasia in gastric ulcer were higher than in chronic gastritis in all-different age -groups. Distribution of H pylori colonization is pangastric in the younger patients. It is highest in corpus, lower in antrum and lowest in angulus in the older age groups. Progression of glandular atrophy and intestinal metaplasia seem to have a key role in the distribution of H pylori colonization. H pylori appears to be the most important risk factor for the development of glandular atrophy and intestinal metaplasia, but it is not the only risk.     

Helicobacter pylori infection upregulates endothelial nitric oxide synthase expression and induces angiogenesis in gastric mucosa of dyspeptic patients

BACKGROUND: Helicobacter pylori (H. pylori) infection induces nitric acid (NO) overproduction through inducible NO synthase (NOS) expression, subsequent DNA damage and enhanced antiapoptosis signal transduction sequence in the human gastric mucosa, whereas its possible effect on endothelial nitric oxide synthase (eNOS) expression has not as yet been investigated. The aim of this study was to evaluate the effect of H. pylori infection in the expression of eNOS in gastric mucosa. PATIENTS AND METHODS: We prospectively studied 30 nonsmoking dyspeptic patients (12 men, 18 women, mean age 54.26+/-12.89 years). The diagnosis of H. pylori infection was based mainly on histology. The histological grading of H. pylori infection was evaluated according to the modified Sydney classification. Histological grading of eNOS expression and microvessel density as estimated by CD34 expression were determined by immunohistochemistry (degree 0-3) and correlated with H. pylori infection and histological degree of gastritis. RESULTS: Twelve patients were H. pylori-positive and 18 patients were H. pylori-negative. The two groups were matched for age (P=0.139), sex (P=0.342) and similar degree of gastritis. Intensity of eNOS and CD34 expression in the corpus and antrum were significantly correlated (P<0.001). eNOS expression was correlated with H. pylori infection in the mucosa of the body and antrum (P=0.013 and 0.037, respectively) but not with gastric inflammation and activity (P=0.848 and 0.871, respectively, for the corpus and P=0.565 and 0.793, respectively, for the antrum). H. pylori-positive patients showed higher expression of CD34-positive blood vessels in the mucosa of the antrum (P=0.048). CD34 expression was correlated with gastric inflammation and activity (P=0.03 and 0.044, respectively) in the mucosa of the antrum of H. pylori-positive patients. CONCLUSION: H. pylori infection upregulates eNOS, and induces angiogenesis, contributing to H. pylori-associated pathophysiology in gastric mucosa.     

Comparison of Helicobacter pylori infection and gastric mucosal histological features of gastric ulcer patients with chronic gastritis patients

AIM: To compare Helicobacter pylori infection and gastric mucosal histological features of gastric ulcer patients with chronic gastritis patients in different age groups and from different biopsy sites. METHODS: The biopsy specimens were taken from the antrum, corpus and upper angulus of gastric ulcer and chronic gastritis patients. Giemsa staining, improved Toluidine-blue staining and H pylori-specific antibody immune staining were performed as appropriate for the histological diagnosis of H pylori infection. Hematoxylin-eosin staining was used for the histological diagnosis of activity of H pylori infection, mucosal inflammation, glandular atrophy and intestinal metaplasia and scored into four grades according to the Updated Sydney System. RESULTS: Total rate of H pylori infection, mucosal inflammation, activity of H pylori infection, glandular atrophy and intestinal metaplasia in 3 839 gastric ulcer patients (78.5%, 97.4%, 82.1%, 61.1% and 64.2%, respectively) were significantly higher than those in 4 102 chronic gastritis patients (55.0%, 90.3%, 56.2%, 36.8%, and 37.0%, respectively, P<0.05). The rate of H pylori colonization of chronic gastritis in <30 years, 31-40 years, 41-50 years, 51-60 years, 61-70 years and >70 years age groups in antrum was 33.3%, 41.7%, 53.6%, 57.3%, 50.7%, 43.5%, respectively; in corpus, it was 32.6%, 41.9%, 53.8%, 60.2%, 58.0%, 54.8%, respectively; in angulus, it was 32.4%, 42.1%, 51.6%, 54.5%, 49.7%, 43.5%, respectively. The rate of H pylori colonization of gastric ulcer in <30 years, 31-40 years, 41-50 years, 51-60 years, 61-70 years and >70 years age groups in antrum was 60.5%, 79.9%, 80.9%, 66.8%, 59.6%, 45.6%, respectively; in corpus, it was 59.7%, 79.6%, 83.6%, 80.1%, 70.6%, 59.1%, respectively; in angulus, it was 61.3%, 77.8%, 75.3%, 68.8%, 59.7%, 45.8%, respectively. The rate of H pylori colonization at antrum was similar to corpus and angulus in patients, below 50 years, with chronic gastritis and in patients, below 40 years, with gastric ulcer. In the other age- groups, the rate of H pylori colonization was highest in corpus, lower in antrum and lowest in angulus (all P<0.05). The rates of glandular atrophy and intestinal metaplasia were higher and earlier in H pylori-positive patients than those without H pylori infection (both P<0.01). In comparison of gastric ulcer patients with chronic gastritis patients, the rate of glandular atrophy and intestinal metaplasia was higher in H pylori-positive patients with gastric ulcer than in H pylori-positive patients with chronic gastritis (both P<0.01); the rate of glandular atrophy and intestinal metaplasia were also higher in H pylori-negative patients with gastric ulcer than in H pylori-negative patients with chronic gastritis (both P<0.01). Both glandular atrophy and intestinal metaplasia were much more commonly identified in the angulus than in the antrum, lowest in corpus (all P<0.01). CONCLUSION: Rate of H pylori infection, glandular atrophy and intestinal metaplasia in gastric ulcer were higher than in chronic gastritis in all-different age -groups. Distribution of H pylori colonization is pangastric in the younger patients. It is highest in corpus, lower in antrum and lowest in angulus in the older age groups. Progression of glandular atrophy and intestinal metaplasia seem to have a key role in the distribution of H pylori colonization. H pylori appears to be the most important risk factor for the development of glandular atrophy and intestinal metaplasia, but it is not the only risk.