慢性胃炎中医证侯与胃窦十二指肠运动及胃炎程度的相 …

研究慢性胃炎中医辩证分型与幽门螺杆菌（Ｈｐ）感染、胃粘膜炎症程度以及胃窦十二指肠消化间期移行性运动复合波之间的关系。将慢性胃炎１１７例,按中医辩证分为实证和虚证,实施包括脾胃湿热型３７例和肝胃不和型３４例,虚证包括脾胃虚型２６例和胃阴不足型２０例。均进行内镜、Ｈｐ及病理检查,分型统计并进行显著性检验。其中３８例用腔内测压法分别测定其消化间期移行性运动复合波（ＭＭＣ）。实证组Ｈｐ阳性率高于虚证组,依     

柴芩平胃胶囊对反流性胃炎胃粘膜细胞凋亡及调控基因的影响

[目的]观察柴芩平胃胶囊（CQPC）对反流性胃炎模型大鼠胃粘膜细胞凋亡及调控基因的影响.[方法]Wistar大鼠随机分为假手术组,模型组,CQPC高、中、低剂量组（剂量分别为16.66、8.33、4.17g/kg）,小柴胡冲剂组（10g/kg）;除假手术组外,均采用B-Ⅱ式胃部分切除（胃空肠吻合）术复制大鼠反流性残胃炎模型,各组按设计剂量灌胃给药,连续4周;分别采用ELISA、原位杂交、免疫组化方法观察CQPC对胃粘膜细胞凋亡及调控基因p53 mRNA、Bax和Bcl-2表达的影响.[结果]模型组结果显示胆汁反流可引起模型大鼠胃粘膜细胞凋亡增加,野生型p53 mRNA、Bax蛋白表达上调,Bcl-2蛋白表达下调,与假手术组比较具有显著性差异（均P＜0.05或P＜0.01）;高、中、低剂量CQPC均可减少胆汁反流引起的细胞凋亡,减少野生型P53 mRNA、Bax蛋白表达,增加Bcl-2蛋白表达（均P＜0.05或P＜0.01）.[结论]柴芩平胃胶囊治疗反流性胃炎的作用机制,可能与减少胃粘膜细胞凋亡,调节各种凋亡调控基因的表达有关.     

Asymptomatic Helicobacter pylori Gastritis Is Associated with Increased Sucrose Permeability

Our aim was to investigate whether there arechanges in permeability to sucrose in asymptomaticHelicobacter pylori gastritis. Nineteen asymptomaticsubjects with Helicobacter pylori associated gastritis with no or mild mucosal atrophy and 19 age- andsex-matched normal controls were studied by peroral loadof sucrose (100 g). The fraction of the given oral doseof sucrose excreted in urine was increased in subjects with Helicobacter pylori gastritis(median 0.08% versus 0.04% in controls). Sucroseexcretion was not related to atrophy, intestinalmetaplasia, or inflammation in the gastric mucosa.However, sucrose permeability was related to the degreeof inflammatory (neutrophil) activity, since moderateactivity was associated with higher sucrose excretionthan mild activity (median 0.13% vs 0.07% ).Asymptomatic Helicobacter pylori gastritis was associatedwith an increased sucrose permeability, which could bea sign of gastric mucosal leakage. This could haveimplications for the diseases and complicationsassociated with Helicobacter pylori infection.     

Regional Differences on Production of Chemokines in Gastric Mucosa Between Helicobacter pylori-Positive Duodenal Ulcer and Gastric Ulcer

It is well known that antrum-predominantgastritis and pan-gastritis occurs in the patients withHelicobacter pylori-positive duodenal ulcer (DU) andgastric ulcer (GU), respectively. However, the role of chemokines in the pathogenesis of thesepathologies is unclear. We examined the regionaldifferences in mucosal chemokine production in patientswith DU and GU. The production of interleukin-8 (IL-8), growth-related gene (GRO) , andmacrophage inflammatory protein (MIP)-1 wasgreater in the antrum than in the corpus in DU patients.In the patients with GU, monocyte chemoattractantprotein (MCP)-1 levels in the mucosa adjacent to ulcer weregreater than those away for the ulcer in the corpus. Thereduction in chemokine production occurring inassociation with the eradication of H. pylori differed between DU and GU patients in the antrum (IL-8,P = 0.0394; GRO, P = 0.0149; MIP-1, P =0.0246; MCP-1, P = 0.0087). The data imply a differentpathogenesis may exist for the gastritis present in patients with DU and GU occurring in H.pylori-positive individuals.     

穴注黄芪、当归注射液对实验性慢性萎缩性胃炎胃粘膜屏障的影响

[目的]探讨穴注黄芪、当归注射液对大鼠慢性萎缩性胃炎胃粘膜屏障的影响。[方法]采用N－甲基－N－硝基亚硝基胍（MNNG）诱发大鼠慢性萎缩性胃炎模型。随机将70只大鼠分为正常组、模型1组（40μg/mL MNNG造模）、模型2组（60μg/mL MNNG造模）、穴位1组（40μg/mL MNNG造模＋穴注)与穴位2组（60μg/mL MNNG造模＋穴注）。穴注组均于造模10周开始以黄芪、当归注射液等份混合注入足三里穴。造模31周时观察各组大鼠胃粘膜病理及胃粘膜屏障的改变。[结果]随造模浓度的增加，胃粘膜损伤，粘膜上皮细胞连接减少、间隙增宽，其变化与胃粘膜萎缩、肠上皮化生、异型增生发生数呈正相关（均P＜0.05)。穴注组均细胞间隙明显缩小，胃粘膜损伤减轻（均P＜0.05)。[结论]黄芪、当归注射液注射足三里穴，可以抑制实验性萎缩性胃炎胃粘膜屏障的损伤。     

The Influence of Helicobacter pylori Infection and Corpus Gastritis on the Postoperative Outcomes of Laparoscopic Vertical Banded Gastroplasty

Background: Helicobacter pylori (HP) infection is linked to weight control through gastric inflammation-induced deregulation of satiety-related hormone, and eradication of HP before a weight reduction operation has been advocated. We aimed to examine the impact of HP infection and corpus gastritis on preoperative patient characteristics, postoperative complications and weight loss following laparoscopic vertical banded gastroplasty (LVBG). Methods: A prospective cohort of 152 patients undergoing LVBG was enrolled. Gastric specimens at the corpus were obtained during LVBG operation and scored histologically according to the Sydney classification of gastritis. Excess weight loss, and early and late complications following LVBG, were recorded and correlated. Results: 63 and 89 patients were identified as HP positive and negative groups respectively. The prevalence of individual components of the metabolic syndrome was comparable in both groups except hypertension. The occurrence of early and late complications, either minor or major, in both groups was similar. The severity of gastritis was correlated positively with age and negatively with preoperative BMI and excess weight. Patients with higher neutrophil activity, chronic inflammation, and HP density experienced less excess weight loss at 24 to 48 months follow-up. The impact of gastritis on weight loss became less recognizable after 48 months follow-up. Conclusions: HP infection and gastric inflammation play a significant role in the amount of weight loss after LVBG. Further prospective studies should examine possible mechanisms and long-term effects on weight loss to determine the utility of preventive eradication of HP in different types of bariatric surgery.     

Gastric Ghrelin Expression Associated with Helicobacter pylori Infection and Chronic Gastritis in Obese Patients

Background: Helicobacter pylori is a major pathogen of stomach. Ghrelin is secreted from the stomach, and it plays a role in the coordination of eating behavior, and facilitates fat storage and weight regulation. The effects of H. pylori infection on gastric ghrelin production are still not well known. Recent exciting studies linked H. pylori infection to ghrelin, then to obesity. The aim of the present study is to investigate gastric ghrelin immunoreactivity associated with H. pylori infection, chronic gastritis and the clinical correlation in obese patients. Methods: The histologic findings of stomach were examined in 156 patients who were undergoing laparoscopic vertical-banded gastroplasty for obesity. Ghrelin immunoreactivity was evaluated immunohistochemically with an anti-ghrelin antibody, and the density of ghrelin-positive cells determined per total glands of the gastric mucosa. Relationship between density of ghrelin-positive cells, histopathology of chronic gastritis scored by the Sydney system and clinical correlation was analyzed. Results: H. pylori was present in 62 (39.7%) out of 156 patients. The density of ghrelin-positive cells was significantly lower for H. pylori-infected patients. There was a significant stepwise decrease in density of ghrelin-positive cells, with progression of histological severity of chronic inflammation, neutrophil activity and glandular atrophy in the corpus. Obese patients positive for H. pylori were associated with older age and abnormal plasma triglyceride level, but not with sex, body mass index, liver function tests or glucose level. There was no relationship between density of gastric ghrelin-positive cells and body mass index. Conclusion: H. pylori infection has a negative impact on density of gastric ghrelin-positive cells in obese patients. Impaired density of gastric ghrelinpositive cells is associated with neutrophil activity, chronic inflammation and glandular atrophy induced by H. pylori infection. The potential role of H. pylori infection and density of gastric ghrelin-positive cells on the development of obesity and their biological significance warrants further investigation.     

Comparison of Two Rapid Urease Tests for Detection of Helicobacter pylori Infection

Rapid urease tests are widely used at endoscopyto determine the presence of Helicobacter pyloriinfection. In this prospective study, we compared theaccuracy of two rapid urease tests, CLOtest andPyloriTek, using histology as the gold standard.Histologic staining was performed using both H&E andGiemsa, and all slides were reviewed by a singlepathologist who was blinded to the results of the rapidurease tests and endoscopic findings. One hundred twopatients were enrolled; their mean age was 59 years(range 16 to 95 years), and there were 45 males and 57females. Histology confirmed the presence of H. pylori infection in 39% of patients. Theproportions of false positives for CLOtest (8.0%) andPyloriTek measured at 1 hr (29.0%) were significantlydifferent (Z = 2.90, P = 0.0038). No significantdifference was seen between the proportions of falsenegatives. We conclude that the clinical usefulness ofPyloriTek urease test is limited by its lack ofspecificity.     

Helicobacter pylori Infection and Gastric Cancer (A Nested Case-Control Study in a Rural Area of Japan)

We conducted a seroepidemiological nested case-control study to determine the association of gastriccancer with Helicobacter pylori infection and atrophicgastritis. A cohort of 2858 participants in an annual multiphasic health check-up werefollowed for eight years. Data for 45 gastric cancercases and 225 sex-, age-, and address-matched controlsubjects were analyzed. Helicobacter pylori infectionwas determined by IgG antibodies, and atrophicgastritis was diagnosed by both serum pepsinogen I level(70 ng/ml) and the pepsinogen I/II ratio (3.0).Univariate analysis showed that Helicobacter pylori and atrophic gastritis were significantlyassociated with gastric cancer. In a multivariateanalysis, atrophic gastritis was associated withsignificantly increased risk of cancer (odds ratio,3.38; 95% confidence interval, 1.54-7.42); however,Helicobacter pylori was not associated with cancer (oddsratio, 1.84; 95% confidence interval, 0.59-5.72). Theseresults suggest that Helicobacter pylori infection alone is not directly associated with gastriccarcinogenesis but has an indirect relation to gastriccancer through the development of atrophicgastritis.     

Expression of bcl-2 in Autoimmune and Helicobacter pylori-Associated Atrophic Gastritis

Chronic atrophic gastritis can be induced eitherby H. pylori or by an autoimmune process. The proteinproduct of bcl-2, which is a protooncogene, blocksapoptosis. Aberrant bcl-2 expression has been found in 68% of atrophic gastritis patients. The aimof this study was to compare bcl-2 expression in 20autoimmune atrophic gastritis patients to that in 20 H.pylori-associated atrophic gastritis patients. Twenty patients with H. pylori antral gastritisbut without atrophy served as controls. The bcl-2expression was assessed by immunohistochemical stainingof gastric biopsies, using mouse anti-human bcl-2 monoclonal antibodies. Autoimmune atrophicgastritis patients were younger, mainly females, with asignificantly higher serum gastrin level than the H.pylori-associated atrophic gastritis group (P < 0.001). The bcl-2 was expressed in 10/20 (50%)of autoimmune atrophic gastritis patients, in 9/20 (45%)of H. pylori-associated atrophic gastritis patients (P= 0.73), and in 2/20 (10%) of controls. There was no correlation between bcl-2expression and the presence of intestinal metaplasia (P= 0.35). Our findings confirm that H. pylori-associatedatrophic gastritis and autoimmune atrophic gastritis are two different conditions, but with equalexpression of bcl-2. Excessive expression of bcl-2 isfound only in atrophic gastritis, but not in H. pyloriantral gastritis without atrophy.