Examination of Tissue Distribution of Helicobacter pylori Within Columnar-Lined Esophagus

H. pylori may colonize columnar-lined esophagus,although an etiologic role in esophageal adenocarcinomais unproven. H. pylori can adhere to intestinalmetaplasia in the stomach. This study was designed to examine if H. pylori adheres to specializedintestinal metaplasia in columnar-lined esophagus.Esophageal biopsies from patients with columnar-linedesophagus were reviewed. Patients with only gastric metaplasia were excluded. Sections withspecialized intestinal metaplasia in at least one thirdof at least one gland were recut, stained using theGiemsa stain, and reexamined by two independentpathologists using strict criteria for adherence by H.pylori . The 209 esophageal biopsies with adequatespecialized intestinal metaplasia from 58 patients wereexamined: H. pylori was only seen on gastric metaplasia in three patients — and never onspecialized intestinal metaplasia. Within the esophagus,H. pylori adheres only to gastric metaplasia, which isnot considered premalignant for esophagealadenocarcinoma.     

Influence of H. pylori Infection on Gastric Motor and Sensory Function in Asymptomatic Volunteers

The effect of H. pylori infection on gastricmotility and sensation is unclear. Our hypothesis isthat H. pylori infection increases gastric sensation andreduces gastric accommodation and emptying. In eight H. pylori-positive and eight H.pylori-negative asymptomatic subjects, infection wasproven by antral histology or culture. We evaluated: (1)gastric emptying of solids, (2) proximal gastriccompliance, (3) fasting and postprandial proximal gastrictone and phasic contractions, (4) gastric sensationduring balloon inflations or ingestion of cold water,and (5) abdominal vagal function. H. pylori infection was associated with lower gastric accommodation(median 75% postprandial increase in barostat balloonvolume compared to fasting) when compared to theaccommodation in uninfected volunteers (median 211% change from fasting). One H. pylori-positivesubject had an abnormal abdominal vagal function testand her gastric accommodation response was reduced.Other motor and sensory functions in the two groups were similar. In asymptomatic volunteers, H.pylori infection and gastritis result in reducedaccommodation (diastolic dysfunction) but no change inoverall sensation or motor functions of thestomach.     

Pretreatment Gastric Histology Is Helpful to Predict the Symptomatic Response After H. pylori Eradication in Patients with Nonulcer Dyspepsia

This study aimed to test whether pretreatment gastric pathology in H. pylori-infected nonulcer dyspepsia (HpNUD) patients is relevant to and predictive of the symptomatic response after H. pylori eradication. Anti-H. pylori triple therapy was administered to 250 HpNUD patients, enrolled as the therapy group. In addition, 60 patients were enrolled as the control group, in which omeprazole was an alternatives to the triple therapy. Pretreatment gastric histology was evaluated thoroughly by the updated Sydney system. A [¹³C] urea breath test was also performed to evaluate the H. pylori eradication two months and 12 months later. For each patient, the baseline, month 2, and month 12 symptom scores were assessed for the month 2 or month 12 residual symptom ratio (RSR-2m or RSR-12m), calculated from: 100% × month 2 or month 12 score/baseline score. Based on either RSR-2m or RSR-12m, patients were categorized as good response (RSR < 50%), moderate response (50–70%), and poor response (>70%) subgroups in both therapy and control groups to define the short-term and long-term symptomatic responses. Patients with successful H. pylori eradication in the therapy group showed a higher incidence of good symptomatic response (RSR < 50%) than those from the control group (month 2: 30.3 vs 12%, P < 0.05; month 12: 34.7 vs 17.1%, P < 0.05). Univariate and multivariate analysis disclosed that patients with a higher acute inflammation score (AIS) and the lowest incidence of lymphoid follicles (LF) at pretreatment gastric histology are predisposed to having a good symptom response after H. pylori eradication (P < 0.05). For HpNUD patients who have an AIS of more than three and an absence of LF at gastric histology, more than 85% had good short-term (month 2) and long-term (month 12) symptomatic relief after H. pylori eradication. In conclusion, nearly 30% of HpNUD patients can obtain symptomatic relief following H. pylori eradication. The pretreatment gastric histology of HpNUD can be helpful to monitor the symptomatic response after H. pylori eradication.     

H. pylori Infection in HIV-Positive Patients (A Serohistological Study)

Sixty-seven consecutive patients infected withthe human immunodeficiency virus (HIV-1), 72% of whichwith overt AIDS, were examinated by upper endoscopy dueto various indications and evaluated for the prevalence of H. pylori infection. Theinfection was studied by performing both histologicalexamination of gastric biopsies and serological testingfor anti-H. pylori IgG antibodies. The H. pyloriprevalence rate was 55% in histology; no significantdifferences were observed in HIV-infected subjects andthose with overt AIDS (52% vs 63%, respectively; P =NS). Positive histological testing appeared to bedirectly related to the peripheral CD4⁺lymphocyte count (minimum rates of 43% were detected in6 patients with CD4⁺ < 100 ×10⁶/liter and maximum rates of 78% inpatients with CD4⁺ > 200 ×10⁶/liter, respectively; P < 0.05) and inversely related to the frequency ofantibiotic treatments performed over the six monthsprior to endoscopy. Low CD4⁺ counts were alsoapparently associated with low-grade H. pyloriinfection. Serological testing was positive for anti-H. pylori IgGantibodies in 39% of patients; compared to histology,serology displayed a sensitivity of 57% and aspecificity of 81%. The discrepancy between histologicaland serological positive results for H. pylori wasnoted to be higher in the more advanced phases of HIVinfection. Based upon our results, the serologicaltesting for anti-H. pylori IgG antibodies seems to require cautious interpretation in HIV-positivepatients.     

Gastric Dysrhythmias and Delayed Gastric Emptying in Patients with Functional Dyspepsia

An association between dyspepsia, gastricmotility disorders, and myoelectrical abnormalities hasbeen noted. The objective of the present study was toinvestigate both antral myoelectrical activity and gastric emptying in patients with functionaldyspepsia (FD). Electrogastrography (EGG) was performedin 25 adult patients with FD, which had been evaluatedby score. After an overnight fast, for 1 hr in the pre- and postprandial state (370 kcalliquid-solid test meal) the following EGG parameterswere determined: dominant frequency [DF (cpm)], DF (%)in the normal range (2-4 cpm), bradygastria (<2 cpm), tachygastria (4-10 cpm), dominant frequencyinstability coefficient (DFIC), and postprandial tofasting power ratio (PR). The data were correlated toresults obtained in 20 age- and gender-matched controls. In addition, in 17 consecutive patients the EGGdata were compared to the gastric retention ofradionuclides after 60 min (liquid-solid phase labeledwith ^99mTc colloid). Patients with FDrevealed a preprandial increase in tachygastria compared to controls(P < 0.001). Of 17 FD, seven patients exhibiteddelayed gastric emptying (t60 retention >68%). Thesepatients showed significantly more pre- and postprandial tachygastrias than patients with normal gastricemptying (P < 0.05). The dyspeptic symptology and H.pylori status did not correlate with EGG andradioscintigraphy. Patients with FD frequently revealimpaired gastric emptying and increased tachygastria,which may have pathophysiological significance in someof these patients.     

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.     

Pathological Changes in the Formation of Helicobacter pylori-Induced Gastric Lesions in Mongolian Gerbils

We examined pathological changes in theformation of Helicobacter pylori-induced gastric lesionsin Mongorian gerbils. H. pylori (NCTC11637) was orallyadministered once to the animals and was detected in the gastric mucosa of all gerbils given thebacteria. The number of viable H. pylori increasedduring the initial two weeks and thereafter reached aplateau level. The initial pathological changes were found at one week, ie, edema/congestion and awhite viscous substance only in the antrum. At twoweeks, superficial damage appeared in the antrum,although inflammatory cell infiltration had notoccurred. Gastritis with lymphoid follicles was observedin the antrum and fundus from three weeks. At fourweeks, mucosal lesions were detected as a fewhemorrhagic spots in the fundus adjacent to the antrum.In the control animals, however, no pathologicalchanges were observed even at four weeks. In the gastricmucosa infected with H. pylori , myeloperoxidaseactivity was negligible at two weeks, but was extremely elevated at four weeks. Similarly, neutrophilchemotactic activity was only slightly increased at twoweeks, but was markedly elevated at four weeks. Theseresults indicate that H. pylori infection induces initial pathological changes only in theantrum, but mucosal lesions occur in the fundus adjacentto the antrum. Furthermore, it is demonstrated that theinitial superficial damage is generated by factors other than chemokines and neutrophil-associatedfactors, although mucosal inflammation may contribute tothe subsequent formation of lesions andulcers.     

Selection of Lower Cutoff Point of [13C]Urea Breath Test Is Helpful to Monitor H. pylori Eradication After Proton Pump Inhibitor-Based Triple Therapy

Our objectives were to test the efficacy of [¹³C] urea breath test (UBT) for H. pylori infection in patients before and after proton pump inhibitor (PPI) based triple therapy, and thus to trace the optimal cutoff value of UBT to monitor H. pylori eradication; and to analyze the histologic bacterial density and distribution of H. pylori in patients with equivocal UBT. A total of 441 dyspeptic cases patients enrolled and completed the study design, including 120 noninfected and 321 H. pylori-infected patients. All 441 cases had received the same protocol of UBT, in which the baseline and 15-min gas samples after ingestion of 100 mg ¹³C-labeled urea were analyzed for excess ¹³CO₂/¹²CO₂ ratio (ECR). In addition, a first endoscopy was performed in each patient to evaluate the initial status of H. pylori by culture and histology. Of the 321 H. pylori-infected patients, 286 received a second endoscopy and a second UBT six weeks after completing any one of four regimens of the PPI-based triple therapy to document the success of H. pylori eradication. During both sessions of endoscopy, topographic gastric biopsies for histology were sampled to evaluate the distribution and density of H. pylori. Based on the diagnostic standard by culture and histology, the sensitivity and specificity of the first UBT achieved most optimally was 97.5% and 96.7%, respectively, by setting the cutoff point of ECR at 4.0. In contrast, using the same cutoff point of 4.0, the sensitivity and specificity of the second UBT in patients after therapy achieved just 80% and 97.6%, respectively. By applying cutoff points downward of 4.0, 3.5, 3, and 2.5 for the second UBT, the sensitivity was elevated to 80%, 82.8%, 88.6%, and 94.3%, respectively, while the specificity was preserved at more than 95.2%. The overall eradication rate of H. pylori was 87.8% (251/286). Seven of 35 patients with failure of therapy had equivocal ECR at the second UBT (range 2–5), and this accounted for the false negative result. All seven patients had low bacterial densities, and three patients had bacteria distributed only in high body near the cardia. In conclusion, selection of a lower cutoff value of ECR at 2.5 is helpful to maintain the diagnostic accuracy of UBT for monitoring the H. pylori eradication. The equivocal ECR of UBT after therapy would be related to the low bacterial load and its distribution.     

Proximal and Distal Gastric Distension in Normal Subjects and H. pylori-Positive and -Negative Dyspeptic Patients and Correlation with Symptoms

Aim of the study was to analyze gastricdistension with water in H. pylori-positive and-negative dyspeptic patients and normal subjects and thecorrelation with symptoms. Twenty dyspeptic patients and 19 normal subjects were studied. H. pylori wasdetermined in each dyspeptic patient with the rapid ureatest at endoscopy. Gastric distension was evaluated byreal-time ultrasonography with the ingestion of stepwise-increasing amounts of water up toa total of 600 ml. During distension, the symptom scorewas evaluated as well. The proximal stomach wassignificantly smaller in dyspeptic patients than in healthy controls, at 100-600 ml water (P <0.01). A larger distal stomach was observed at 500 and600 ml of water (P < 0.01). The score of bloating andfullness was greater in dyspeptics than in controls at 300 and 600 ml of water distension.The symptoms score was linearly correlated with proximaland distal gastric measurements in dyspeptic patientsand in controls. No significant difference was found in dyspeptic patients regarding theH. pylori status. In conclusion, dyspeptic patients showa defective adaptation of the whole stomach to waterdistension and an increased symptom perception score as compared to controls. H. pyloriinfection does not seem to be a determining factor inthese observed findings.     

根除幽门螺杆菌对胃溃疡粘膜局部氧化应激反应的影响

目的:研究幽门螺杆菌(H.pylori)阳性胃溃疡患者根除H.pylori前后冒粘膜局部氧化应激反应的改变。方法:对72例 H.pylori阳性胃溃疡患者三联杀菌治疗前后的溃疡边缘粘膜组织行活性氧(ROS)、白细胞介素8(IL-8)含量及炎症积分测定。结果:在H.pylori根除后,胃粘膜ROS、IL-8含量及炎症积分均较根除前明显下降(P<0.001及P<0.01)。结论:根除 H.pylori可抑制致炎因子IL-8表达及减少ROS生成,从而降低胃溃疡粘膜局部氧化应激反应,减轻粘膜炎症,利于溃疡愈合。     

Serologic Response to Lower-Molecular-Weight Proteins of H. pylori Is Related to Clinical Outcome of H. pylori Infection in Taiwan

The study aimed to examine the serum serological response among H. pylori-infected patients with various upper gastrointestinal diagnoses; to ascertain whether it could be predictive to the diagnostic outcome of dyspepsia. One hundred seventy H. pylori-infected patients with dyspeptic symptoms but without previous treatment were enrolled, including those with duodenal ulcer disease (N = 47), gastric ulcer (N = 23), nonulcer dyspepsia (N = 60), gastric cancer (N = 34), and MALToma (N = 6). Sera from dyspeptic patients without H. pylori infection (N = 33) were used as controls. During endoscopy, gastric biopsies were taken for CLO-test, histology, and culture for the detection of H. pylori infection, defined by a positive culture or positive results of both CLO-test and histology. Total H. pylori IgG antibody was tested by an ELISA method. Antibody responses to specific H. pylori proteins were tested by a western blotting system. Of patients with H. pylori-infected gastroduodenal diseases, 76.5%, 42.9%, 23.6%, 46.7%, 84.1%, 76.5%, 82.9%, and 32.4% on average, showed responses to the 116-kDa (CagA), 89-kDa (VacA), 60-kDa, 45-kDa, 35-kDa, 30-kDa, 26.5-kDa, and 19.5-kDa H. pylori-specific proteins, respectively. A significant association was found between the serological response to 19.5-kDa and 26.5-kDa proteins and malignant outcome of H. pylori infection (P < 0.02). Among patients without malignancy, the absence of a band at 19.5 kDa was statistically associated with the presence of an ulcer (P < 0.05). The presence of serum antibody against CagA is not different between patients with ulcer and with malignancy in clinical diagnosis. The serum test for detecting antibodies against lower-molecular-weight proteins of H. pylori, such as those of 19.5 and 26.5 kDa, could be useful to identify H. pylori-infected patients at risk of peptic ulcer or malignancy.     

Prevalence of Gastric Myoelectrical Abnormalities in Patients with Nonulcer Dyspepsia and H. pylori Infection

The aims of this study were to investigate the effects of H. pylori eradication on gastric myoelectrical activity and dyspeptic symptoms. Sixty-two subjects with H. pylori infection and no active peptic ulcer participated in this study, which involved three sessions. Anti-H. pylori therapy consisting of clarithromycin and omeprazole was given for two weeks. Gastric myoelectrical activity was measured using surface electrogastrography and dyspeptic symptoms were scored at each session. A [¹⁴C] urea breath test was performed at baseline and one month after treatment. In comparison with baseline, the percentage of normal slow waves was significantly increased and the mean total symptom score was significantly reduced one and three months after therapy (P < 0.05). Approximately 40% of patients with nonulcer dyspepsia symptoms and H. pylori infection have abnormal gastric myoelectrical activity, which may be normalized following the eradication of H. pylori infection. The normalization of gastric myoelectrical activity may be one explanation for the significant symptom improvement in this subset of the dyspepsia population after H. pylori eradication.     

Comparative Study of Nigella sativa and Triple Therapy in Eradication of Helicobacter pylori in Patients with Non-Ulcer Dyspepsia

Background/Aim:

A large number of diseases are ascribed to Helicobacter pylori (H. pylori), particularly chronic active gastritis, peptic ulcer disease and gastric cancer. Successful treatment of H. pylori infection with antimicrobial agents can lead to regression of H. pylori–associated disorders. Antibiotic resistance against H. pylori is increasing, and it is necessary to find new effective agents. Nigella sativa seed (NS), a commonly used herb, possesses in vitro anti-helicobacter activity. The present study was undertaken to evaluate the efficacy of NS in eradication of H. pylori infection in non-ulcer dyspeptic patients.

Materials and Methods:

The study was conducted on 88 adult patients attending King Fahd Hospital of the University, Al-Khobar, Saudi Arabia, from 2007 to 2008, with dyspeptic symptoms and found positive for H. pylori infection by histopathology and urease test. Patients were randomly assigned to four groups, receiving i) triple therapy (TT) comprising of clarithromycin, amoxicillin, omeprazole [n= 23], ii) 1 g NS + 40 mg omeprazole (OM) [n= 21], iii) 2 g NS + OM [n= 21] or iv) 3 g NS + OM [n= 23]. Negative H. pylori stool antigen test four weeks after end of treatment was considered as eradication.

Results:

H. pylori eradication was 82.6, 47.6, 66.7 and 47.8% with TT, 1 g NS, 2 g NS and 3 g NS, respectively. Eradication rates with 2 g NS and TT were statistically not different from each other, whereas H. pylori eradication with other doses was significantly less than that with TT (P < 0.05). Dyspepsia symptoms improved in all groups to a similar extent.

Conclusions:

N. sativa seeds possess clinically useful anti-H. pylori activity, comparable to triple therapy. Further clinical studies combining N. sativa with antibiotics are suggested.     

重视幽门螺杆菌相关性胃癌的线粒体机制研究

日益增多的资料提示，幽门螺杆菌（H．pylori）感染与胃癌的发生有密切关系，世界卫生织织（WHO）已把其列为胃癌的首要致病因子。长期大规模的随访研究证明，胃癌只发生于有H．pylori感染的胃黏膜，而不发生于无H．pylori感染胃黏膜，动物实验研究亦发现，H．pylori不仅可以增强甲基硝基亚硝基胍的诱癌作用，长期H．pylori感染本身即可诱发出胃窦腺癌。尽管众多研究证明H．pylori感染与胃癌有关，但H．pylori感染引起胃癌的分子机制仍不清楚。线粒体是迄今发现的人类细胞核外唯一具有自己基因组，且能不依赖nDNA进行复制、转录和翻译的细胞器，被称为“人类第25号染色体”。过去认为线粒体只是人体的“能量供应站”，但线粒体的功能远比人们了解的更为复杂。近年，我们对H．pylori致胃黏膜细胞损伤的线粒体途径进行了深入的研究，结合国内外文献，综合叙述如下。     

Attributable Risk of H. pylori in Peptic Ulcer Disease

Recent reports in the United States have found that fewer peptic ulcers are due to Helicobacter pylori than previously believed. The aim of this study is to determine if the declining prevalence of H. pylori infection in the general population can account for the apparent increase in the frequency of non-H. pylori ulcers. A total of 396 patients with peptic ulcer or ulcer scar were enrolled in this study. The pre-1950 population consisted of 149 patients with gastric ulcers and with 44 duodenal ulcers. The post-1950 population consisted of 96 patients with gastric ulcers and 107 with duodenal ulcers. The frequency of H. pylori-negative gastric ulcers was 5.4% in patients born before 1950 and 4.2% in patients born after 1950, and the frequency of H. pylori-negative duodenal ulcers was 0% and 1.9%, respectively. There are no statistical differences between the two populations in gastric and duodenal ulcers. H. pylori seropositivity was 74.9% in asymptomatic volunteers born before 1950 and 20.7% in those born after 1950 (P < 0.01) in the general population. The attributable risk of H. pylori infection in peptic ulcer diseases was not affected by the prevalence of H. pylori infection in the general population in Japan. This suggests that the apparent increase in frequency of non-H. pylori ulcers in the United States is not simply due to the declining prevalence of infection. Other explanations for non-H. pylori ulcers should be sought.     

Inhibitory Potency of Twice-a-Day Omeprazole on Gastric Acidity Is Enhanced by Eradication of H. pylori in Duodenal Ulcer Patients

The gastric pH-elevating effect of proton pump inhibitors such as omeprazole has been reported to be greater in the presence than in the absence of an H. pylori infection. It is unknown if this effect persists when a higher dose of omeprazole is taken. We undertook both 24-hr pH-metry and 24-hr aspiration studies in 12 H. pylori-positive patients with a history of duodenal ulcer (DU); (1) when not on omeprazole; (2) when on omeprazole 20 mg twice a day for 8 days; (3) two months after eradication of H. pylori and when not on omeprazole; and (4) after eradication of H. pylori and when on omeprazole twice a day. Eradication of H. pylori in DU results in lower mean and median pH; decreased percent pH q 3/ 4, and greater median H⁺ after breakfast, after lunch, and overnight; and omeprazole appears to have less of a pH-elevating effect in the absence than in the presence of an H. pylori infection. The fall in gastric juice NH₃ concentration as a result of eradicating H. pylori partially explained the lower pH-elevating effect of omeprazole. The variation in acid inhibitory effect of omeprazole after as compared with before eradication of H. pylori could not be explained by differences; (1) in gastric juice concentrations of IL-1, IL-8, IL-13, or epidermal growth factor; (2) in the fasting or fed total concentration of gastric juice bile acids; (3) in the fasting concentrations or area under-the-curve (AUC) of the gastric H⁺ concentrations in response to food; or (4) in the pharmacokinetics of omeprazole. The difference in H⁺ AUC without omeprazole minus with omeprazole was actually greater when compared after versus before eradication of H. pylori. Thus, in DU the pH-elevating potency of omeprazole taken twice a day is greater in the presence than in the absence of an H. pylori infection.     

Rabeprazole in Treatment of Acid Peptic Diseases (Results of Three Placebo-Controlled Dose-Response Clinical Trials in Duodenal Ulcer, Gastric Ulcer, and Gastroesophageal Reflux Disease (GERD))

Rabeprazole, a new proton pump inhibitor, wasstudied in patients with acid-pepticrelated diseases(duodenal ulcer, gastric ulcer, GERD) in threeplacebo-controlled, double-blind, randomized clinicaltrials. Men and women over the age of 18 were enrolledif the presence of an active duodenal or gastric ulceror erosive or ulcerative esophagitis was confirmed onupper gastrointestinal endoscopy. Patients were randomly allocated to either placebo orrabeprazole 20 mg or 40 mg in the duodenal and gastriculcer protocols or to placebo or rabeprazole 10 mg, 20mg, or 40 mg in the GERD protocol. All doses ofrabeprazole in all three studies were statisticallysignificantly superior to placebo in healingacid-related lesions. There were no treatmentdifferences between the rabeprazole doses in healingactive peptic lesions. The incidence of positive [¹³C]ureabreath test for H. pylori was 53% in patients withduodenal or gastric ulcers. H. pylori status was noteffected by treatment with rabeprazole.     

幽门螺杆菌感染对Fas/FasL表达的影响在胃癌发生中的作用

目的：观察幽门螺杆菌（Hp）及其不同毒力株（cagA阳性与cagA阴性株）感染对胃黏膜上皮细胞Fas/FasL表达的影响，进而探讨胃癌的发生机制。方法：胃镜下取胃窦黏膜标本，将研究对象按病理结果分为黏膜萎缩组，黏膜萎缩伴轻度不典型增生组，黏膜萎缩伴中度不典型增生组，胃腺癌组，黏膜大致正常组为对照组，再根据Hp感染情况为分Hp阳性组与阴性组，并将Hp阳性组进一步成cagA阳性组及阴性组，共9组80例。以快速尿素酶试验，PCR及组织学第三种方法检测Hp，用PCR方法对Hp进行分型。用免疫组化法检测Fas、FasL等表达情况。结果Hp感染率为60．0％，cagA阳性率为90．47％，非腺癌病人Hp阳性组Fas/FasL表达明显高于Hp阴性组（P＜0．05），腺癌组Fas/FasL表达明显高于大致正常组及黏膜萎缩，黏膜萎缩伴轻度不典型增生，黏萎缩伴中度不典型增生组（P＜0．01）。cagA阳性组Fas/FasL表达与cagA阴性组差异无显著性（P＞0．05）。结论：幽门螺杆菌感染后早期即黏 萎缩阶段已出现Fas、FasL等的表达增加，随细胞凋亡的增加，黏膜上皮细胞萎缩加重，细胞DNA不稳定性增加，并出现不典型增生加重， Fas、FasL的表达随之增强，一旦肿瘤细胞形成，Fas/FasL表达进一步增加，形成局部免疫豁免区，导致肿瘤的浸润生长。cagA阳性的菌株在促成肿瘤的发生过程中无明显作用。     

Identification of H. pylori in Saliva by a Nested PCR Assay Derived from a Newly Cloned DNA Probe

A novel probe was developed from genomic DNA ofHelicobacter pylori ATCC type strain 43629. Ithybridized with all 73 H. pylori clinical isolatestested but not with any of 183 non-H. pylori DNAs in dot blot hybridization. Typing tests revealed 41different HaeIII-digestion patterns from 57 H. pyloristrains tested. Based on the sequence of the probe, anested PCR was developed that detected as little as 2 fg of H. pylori DNA or approximatelyequivalent to one cell. No PCR products were amplifiedfrom any of 21 non-H. pylori strains tested. Using thisnested PCR, H. pylori DNA was detected in 33 of 45 (73%) saliva samples collected from patientswith gastric H. pylori infection. These data suggestthat the probe is useful for typing H. pylori and thatthe nested PCR is a valuable tool for detecting H. pylori DNA in saliva.