One year follow-up of patients after successful helicobacter pylori eradication therapy.

The aim of this study was to investigate the Helicobacter pylori (Hp) status of patients who underwent successful eradication therapy 1 year prior to the study and to evaluate their current symptoms. METHODS: all of the patients were initially evaluated by oesophago-gastro-bulboscopy and the Hp status was determined by at least two different methods [rapid urease test, histology or urea breath test (UBT)]. The Hp infection was treated with a 1-week triple therapy protocol, and the UBT was repeated 4-6 weeks later. We invited back 110 patients who had negative post-eradication UBT results 12+/-3 months prior to the study period. UBT was repeated and a questionnaire was completed about the previous and present complaints and medication. RESULTS: 80 of the 110 patients (73%) came back for the follow-up. Twenty five patients had peptic ulcer disease, 36 patients had gastritis or duodenitis without erosive lesions, and 19 patients had erosive form of gastritis or duodenitis initially. All of the patients except one in the erosive gastritis group had negative control UBT 1 year after the eradication, which means 1.25% recurrence rate within 1 year. The eradication therapy completely revealed the symptoms of 16 patients in the ulcer group (64%), 13 patients in the gastroduodenitis group (36%, P=0.03 vs. ulcer patients), 10 patients with erosive gastroduodenitis (52%), but this was only temporary. One year after the eradication therapy seven of the ulcer patients (28%), 11 patients with gastroduodenitis (31%) and seven patients with erosive gastroduodenitis (37%) were symptom-free. Most of the patients had epigastric pain (44%), heartburn (43%) and/or abdominal distension (33%). Nine ulcer patients (36%), 10 patients with gastroduodenitis (28%) and five patients with erosive gastroduodenitis (26%) were taking H(2)-blockers regularly. CONCLUSION: the 1-month post-eradication UBT was probable true negative in all of the evaluated cases, since 79 patients (98.75%) were also negative after 1 year. The Hp recurrence rate is very low (1.25%) in a 1-year period. The symptoms were relieved shortly after eradication therapy in the majority of patients with ulcer disease or erosive lesions. However, significantly smaller portion of the patients with gastroduodenitis became symptom-free. Only about one third of the treated patients remained symptom-free 1 year after the eradication.     

Effect of Helicobacter pylori infection and eradication on gastric epithelial cell proliferation and apoptosis.

OBJECTIVES: the effect of Helicobacter pylori infection on gastric epithelial cell proliferation and apoptosis is still controversial. Our aim was to evaluate the effect of H. pylori infection on cell kinetic parameters in normal gastric epithelium, gastritis with/without intestinal metaplasia and gastric cancer. PATIENTS AND METHODS: antral biopsies were taken from 121 patients (61 women, 60 men, mean age 58.5+/-14.3 years of age) who underwent routine gastroscopy for upper gastrointestinal symptoms. Sections were scored for normal epithelia (n=15), gastritis without intestinal metaplasia (n=74), gastritis with intestinal metaplasia (n=24), and gastric adenocarcinoma (n=8). Fifty-two patients had H. pylori positive gastritis, and success of H. pylori eradication therapy was controlled in 12 cases, all with intestinal metaplasia. To characterize cell proliferation and assess apoptosis, immunohistochemistry [Proliferating Cell Nuclear Antigen (PCNA)], histochemistry [Argyrophil Nucleolar Organizer Regions (AgNOR)], and terminal deoxynucleotidyl transferase (TdT)-mediated deoxyuridinetriphosphate (dUTP) nick end-labeling (TUNEL) were used, respectively. RESULTS: both cell proliferation and apoptosis is was higher in chronic gastritis when compared with normal epithelia, but neither PCNA LI (54.79+/-19.1 vs. 53.20+/-20.7) nor AgNOR counts (291.43+/-44.3 vs. 277.8+/-57.54) were different in H. pylori positive versus negative chronic gastritis. A significant positive correlation (P<0.05) was found in this group between PCNA and AgNOR techniques. Apoptosis was significantly higher (P<0.05) in H. pylori positive cases only when intestinal metaplasia was not present. Cell proliferation in intestinal metaplasia decreased to the activity of normal epithelium after successful eradication of H. pylori but remained high if eradication therapy failed. CONCLUSIONS: epithelial cell proliferation does not depend on H. pylori status in chronic gastritis. H. pylori increases apoptosis only in the absence of intestinal metaplasia.     

Resolution of gastrointestinal protein loss after Helicobacter pylori eradication in a patient with hypertrophic lymphocytic gastritis

BACKGROUND: Lymphocytic gastritis is a rare condition found in approximately 1% of dyspeptic patients. An association with Helicobacter pylori infection has been described. Hypertrophic lymphocytic gastritis is a rare cause of gastrointestinal protein loss. Here, we describe a patient with hypertrophic lymphocytic gastritis, in whom gastrointestinal protein loss resolved completely following H. pylori eradication. CASE REPORT: A 38-year old obese man without gastrointestinal symptoms showed a markedly decreased serum protein (53 g/l, normal 66-85 g/l), a decreased serum albumin (33 g/l, normal 35-52 g/l) and decreased serum immunoglobulin G and immunoglobulin M levels. A renal cause for protein loss was excluded, liver function was normal. Endoscopy of the upper gastrointestinal tract revealed enlarged rigid gastric folds, and an H. pylori-associated lymphocytic gastritis. 99mTc-labelled albumin scintigraphy showed an increased activity in the upper left abdomen compatible with protein secretion in the stomach, and tracer pooling in the upper small bowel. Push enteroscopy with histology demonstrated a normal upper small bowel. Two months after eradication therapy, cure of H. pylori infection was documented and serum protein (71 g/l) and albumin (41 g/l) had returned to normal, while lymphocytic gastritis was still present. One year after eradication therapy endoscopy of the upper gastrointestinal tract and histology and laboratory values were normal. CONCLUSION: Protein-losing gastropathy caused by H. pylori-associated hypertrophic lymphocytic gastritis can be cured solely by H. pylori eradication therapy.     

E-cadherin gene promoter hypermethylation in H. pylori-induced enlarged fold gastritis

BACKGROUND: Promoter hypermethylation of E-cadherin plays an important role on gastric carcinogenesis. We have previously reported that the odds ratio for gastric carcinoma and the prevalence of diffuse-type early gastric carcinoma in Helicobacter pylori-induced enlarged fold gastritis increased with increasing fold width. Thus, we examined E-cadherin methylation in gastric mucosa from H. pylori-induced enlarged fold gastritis before and after H. pylori eradication. Moreover, we analyzed the mechanism of H. pylori infection-induced E-cadherin hypermethylation. MATERIALS AND METHODS: Twenty-three H. pylori-positive patients with enlarged folds, 18 H. pylori-positive and seven H. pylori-negative patients without enlarged folds, were involved in the study. E-cadherin promoter methylation was studied using quantitative methylation-specific polymerase chain reaction. We investigated methylation percentage and DNA methyltransferase activity in gastric cancer cell lines treated with EGF, TNFalpha, and MG132. RESULTS: E-cadherin methylation percentage of the gastric antral and body mucosa in H. pylori-positive patients with enlarged folds was much greater than that in both H. pylori-positive and -negative patients without enlarged folds. After H. pylori eradication, the methylation percentage in six patients with enlarged fold gastritis decreased significantly from 15.6 +/- 3.9 to 8.8 +/- 2.2 (p < .05). Moreover, the methylation was induced by TNFalpha, MG132, and EGF treatment, and DNA methyltransferase activity was induced by EGF treatment in MKN-1 cells. CONCLUSIONS: Our findings suggest that the hypermethylation of E-cadherin promoter might be involved in the process of gastric carcinoma through the specialized factors in H. pylori-induced enlarged fold gastritis.     

四联疗法和序贯疗法治疗服用非甾体类消炎药人群幽门螺杆菌感染的临 床对照研究

目的:对比四联疗法和序贯疗法对根除服用非甾体类消炎药(NSAID)人群幽门螺杆菌(Hp),改善其消化道不良症状及促进消化性溃疡愈合的临床效果。方法:对有消化不良症状的服用非甾体类消炎药物患者行胃镜检查、快速尿激酶及13C呼气试验检查,将155例幽门螺杆菌阳性合并有慢性胃炎或消化性溃疡患者作为研究对象,随机分为两组,A组采用四联疗法,B组采用序贯疗法。A组予雷贝拉唑+克拉霉素+阿莫西林+枸橼酸铋钾治疗10天;B组前5天予雷贝拉唑+阿莫西林,后5天予雷贝拉唑+克拉霉素+甲硝唑。治疗结束后,予雷贝拉唑和胃黏膜保护剂治疗8周。停药4周后,复查胃镜、13C呼气试验,观察和比较两组Hp根除率、消化不良症状缓解率及溃疡愈合率。结果:A、B两组Hp根除率分别为(ITT分析:86.7%和81.9%;PP分析:87.8%和84.3%);症状缓解率为(81.9%对79.2%);胃溃疡愈合率为(68.8%对66.7%),十二指肠球部溃疡的愈合率为(68.2%对70.0%),两组患者间Hp根除率、症状缓解率及溃疡愈合率比较均未见明显统计学差异(P>0.05)。四联疗法组和序贯疗法组不良反应的发生率分别为4.9%和4.3%。两组比较无明显差异(P>0.05)。结论:四联疗法和序贯疗法对长期服用非甾体类消炎药物人群的Hp根除疗效、消化不良症状的缓解及促进溃疡愈合的治疗作用均无明显差异。     

One year follow-up of patients after successful helicobacter pylori eradication therapy

The aim of this study was to investigate the Helicobacter pylori (Hp) status of patients who underwent successful eradication therapy 1 year prior to the study and to evaluate their current symptoms. Methods: all of the patients were initially evaluated by oesophago-gastro-bulboscopy and the Hp status was determined by at least two different methods [rapid urease test, histology or urea breath test (UBT)]. The Hp infection was treated with a 1-week triple therapy protocol, and the UBT was repeated 4–6 weeks later. We invited back 110 patients who had negative post-eradication UBT results 12±3 months prior to the study period. UBT was repeated and a questionnaire was completed about the previous and present complaints and medication. Results: 80 of the 110 patients (73%) came back for the follow-up. Twenty five patients had peptic ulcer disease, 36 patients had gastritis or duodenitis without erosive lesions, and 19 patients had erosive form of gastritis or duodenitis initially. All of the patients except one in the erosive gastritis group had negative control UBT 1 year after the eradication, which means 1.25% recurrence rate within 1 year. The eradication therapy completely revealed the symptoms of 16 patients in the ulcer group (64%), 13 patients in the gastroduodenitis group (36%, P=0.03 vs. ulcer patients), 10 patients with erosive gastroduodenitis (52%), but this was only temporary. One year after the eradication therapy seven of the ulcer patients (28%), 11 patients with gastroduodenitis (31%) and seven patients with erosive gastroduodenitis (37%) were symptom-free. Most of the patients had epigastric pain (44%), heartburn (43%) and/or abdominal distension (33%). Nine ulcer patients (36%), 10 patients with gastroduodenitis (28%) and five patients with erosive gastroduodenitis (26%) were taking H₂-blockers regularly. Conclusion: the 1-month post-eradication UBT was probable true negative in all of the evaluated cases, since 79 patients (98.75%) were also negative after 1 year. The Hp recurrence rate is very low (1.25%) in a 1-year period. The symptoms were relieved shortly after eradication therapy in the majority of patients with ulcer disease or erosive lesions. However, significantly smaller portion of the patients with gastroduodenitis became symptom-free. Only about one third of the treated patients remained symptom-free 1 year after the eradication.     

胆汁反流性胃炎134例临床分析

目的:探讨胆汁反流性胃炎的病因及其临床治疗效果。方法:回顾性性分析134例反流性胃炎患者的临床症状、胃镜检查、幽门螺杆菌(Hp)检测和治疗结果。结果:胆汁反流性胃炎的主要由胃切除手术、胆结石、胆囊炎、糖尿病、消化性溃疡、肝炎、肝硬化、消化道肿瘤和胰腺炎等诱发,但Hp感染率并不高,134例均在四周内治愈。结论:胆汁反流性胃炎是胆汁、胰液和肠液等反流入胃引起的胃黏膜损害造成,治疗上要以减少反流物的损害作用和改善胃肠动力为主。     

Functional variability of cagA gene in Japanese isolates of Helicobacter pylori

CagA protein of Helicobacter pylori is injected into the epithelium, where CagA undergoes tyrosine phosphorylation and activates proliferation signals. However, the importance of these CagA activities for pathogenesis has yet to be resolved. The aim of this study is to analyze the genetic and functional variability of cagA gene of clinical strains in relation to gastric diseases. Thirty-six H. pylori strains were isolated from Japanese patients with various gastric diseases and examined. All 36 strains were found to contain cagA and cagE gene and to induce CagA phosphorylation upon infection. The intensity of CagA phosphorylation expressed in HeLa cells by transfection was highly correlated to the number of R1 region. The phosphorylation intensity was slightly higher in strains from chronic atrophic gastritis (CG); however, the differences were not statistically significant. These CagA proteins also activated the serum response element (SRE) reporter by 5- to 14-fold, above the level of the control. CagA proteins which lack R2 or R3 region exhibited smaller ability for SRE activation. The average of SRE activation was slightly higher in strains from cases of gastric cancer (GC; 11.4+/-1.6), MALT lymphoma (ML; 10.7+/-1.0), and chronic atrophic gastritis (CG; 11.2+/-1.6) than in those of duodenal ulcer (DU; 8.3+/-1.9) or gastric ulcer (GU; 9.0+/-1.1). In summary, most Japanese H. pylori strains contained CagA transport system and induced CagA phosphorylation, and the levels of the intensity of phosphorylation and the ability to induce SRE varied among strains. Although the association between CagA activities and disease outcome shown in this study is not very strong, variety of CagA structure, which induces variable activities, may be one of the reasons why H. pylori induces distinct diseases on host.     

Antral nodularity and positive CagA serology are distinct and relevant markers of severe gastric inflammation in children with Helicobacter pylori infection

Background. The aim of this study was to assess whether the endoscopic finding of antral nodularity and serum IgG antibodies to CagA are associated with higher grades of gastric inflammation. Materials and methods. The comprehensive data of two previously published trials were reanalysed. One hundred and fifty‐three children (median age 9.5 years) who underwent gastroscopy were included. Biopsy specimens from the antrum and corpus were taken to assess Helicobacter pylori status, gastritis score and lymphoid follicles. During endoscopy, antral nodularity was noted. Serum samples were assayed for IgG antibodies to CagA. Results. The presence of antral nodularity (nod+) and positive CagA serology (CagA+) were each found in 32 of the 77 (41.5%) children who had evidence of H. pylori infection. Crosstabulation showed that 20 children (26%) were nod+/CagA+, 12 (15.5%) nod+/CagA?, 12 (15.5%) nod‐/CagA+ and 33 (43%) nod?/CagA?. Gastritis score was significantly lower in nod?/CagA?children than in nod+/CagA? (p = .004), nod?/CagA+ (p = .002) and nod+/CagA+ (p < .001), both in the antrum and corpus. Completely normal gastric histology was only found in the nod?/CagA?subgroup of H. pylori‐infected children (eight of 33, 24%). Regression analysis showed that antral nodularity and positive CagA serology were related to severe gastric inflammation independently of each other and age. Separate analysis showed that inflammation (p < .001), activity (p < .001) and H. pylori density (p = .002) scores were significantly lower in nod?/CagA?children compared with nod+/CagA+ children. The number of lymphoid follicles in the gastric mucosa was related to antral nodularity (p = .003) and positive CagA serology (p = .043), independently of each other. Conclusions. Antral nodularity and positive CagA serology are distinct and relevant markers of severe gastric inflammation in children with H. pylori infection. The lack of both findings in the same child reflects low‐grade or no gastritis.     

Characteristics of Helicobacter pylori-induced gastritis and the effect of H. pylori eradication in patients with chronic idiopathic thrombocytopenic purpura

BACKGROUND: The association between Helicobacter pylori infection and idiopathic thrombocytopenic purpura (ITP) has been reported widely. We investigated the prevalence of H. pylori infection, its virulence profile and the effectiveness of its eradication in patients with ITP. MATERIALS AND METHODS: Twenty patients with ITP, 20 with peptic ulcer (10 gastric ulcer (GU), 10 duodenal ulcer (DU)) and 20 with NUD were studied. The virulence profile of the strains was assessed by genotyping for cagA, vacA, iceA, and hpyIIIR/hrgA and by assaying for IL-8 and DNA fragmentation after incubation with AGS cells. Infected patients and two uninfected ITP patients received triple therapy and platelets were counted before and 1 month, 6 months, 1 year, and 2 years after eradication therapy. RESULTS: H. pylori infection was found in 17 ITP (85%), 20 ulcer (100%) and 13 NUD (65%) patients. Biopsies and strains were collected from five ITP, 20 ulcer and 13 NUD patients. The ITP patients had a pangastritis or corpus-predominant gastritis pattern. All H. pylori isolates, from ITP, ulcer and NUD patients, were cagA(+) and vacA s1/m1, and did not differ in levels of IL-8 induction or DNA fragmentation. Fifteen ITP (88%) and 17 ulcer (85%) patients had successful eradication of H. pylori. Ten of these 15 (67%) H. pylori-eradicated ITP patients had platelet recovery. There was no significant change in platelet count in the two ITP patients in whom eradication failed or in the two originally H. pylori-uninfected ITP patients, or in the treated ulcer patients. Age at onset of ITP was the main determinant of platelet recovery: 100% of patients diagnosed after the age of 60 recovered compared with only 22% of those diagnosed before 50. CONCLUSIONS: H. pylori-infected ITP patients have a corpus-predominant pattern of gastritis but the virulence profile of their strains does not differ from that of ulcer or NUD patients. Eradication of H. pylori infection is a good therapeutic option for some patients with chronic ITP, especially for those who develop ITP in older age.     

Association of Helicobacter pylori infection with coronary heart disease.

The role of Helicobacter pylori (HP) as the main etiological factor in gastritis and peptic ulcer disease is undisputable. Gastric mucosal damage caused by HP involves various bacterial and host-dependent toxic substances that have been recently associated with an increased risk of coronary artery disease (CAD), possibly through the activation acute phase response and of procoagulant hemostatic factors. Recent studies showed a close and strong correlation between plasma increments of some cytokines such as IL-6 or TNFalpha and cardiovascular diseases. HP infection induces platelet activation and aggregation that could be the pathogenic explanation of the association between HP infection and CAD. The aim of this study was to determine the seroprevalence of HP infection and antibodies to CagA, an antigen that is expressed by the most virulent HP strains inducing an enhanced gastric inflammatory response, in patients undergoing routine coronary artery examination. We studied 76 patients with CAD and 81 healthy controls patients without significant change in coronary circulation. Angiograms were read by two independent experienced cardiologists blinded to the results of HP status. The presence of serum IgG antibodies to HP and to CagA and plasma interleukin-8 (IL-8) levels was measured by ELISA. In addition plasma C-reactive protein fibrinogen, total cholesterol and lipids levels were measured in all studied patients. Seropositivity to HP was found in 81.5 % of cases and in 51% of controls and the difference in prevalence was statistically significant, the odds ratio being 4.3 for Hp patients. Antibody to CagA protein was detected in 47.3% of CAD but only in 28% of healthy controls (OR = 2.3 vs OR = 10). C-reactive protein, plasma fibrinogen and total cholesterol were, respectively higher in patients with CAD than in controls. Present data show that there is significant link between CAD and HP infection. The HP infection significantly increases the risk of CAD, especially when both the anti-HP IgG and anti-CagA IgG are considered. Higher prevalence of cytotoxic HP strains might enhance the atherosclerotic process by inducing a persistent, low grade inflammatory response in arterial wall with enhanced synthesis of acute phase reactants.     

放大染色内镜对结节性胃炎、胃粘膜相关组织淋巴瘤的诊断

目的：探讨放大染色内镜对结节性胃炎、胃粘膜相关组织淋巴瘤诊断的可行性。方法：选择哈尔滨医科大学第四临床医学院2007年5月～2010年7月诊断的结节性胃炎、疑诊胃粘膜相关组织淋巴瘤患者,观察临床、内镜、病理表现、幽门螺杆菌感染情况和根除治疗的效果。并应用日本FUJINONEG-590ZW型放大内镜对患者进行检查,观察根除幽门螺杆菌前后结节性胃炎、胃粘膜相关组织淋巴瘤的改变。结果：纳入分析的100例成人患者,男25例,女75例,年龄19-68岁,平均年龄39．2岁。主要临床表现为上腹痛和消化不良症状。内镜下表现为胃窦部为主,可扩展至胃体部的色泽均匀的结节样或颗粒样改变。病理检查显示胃窦部活检标本中有伴生发中心的淋巴滤泡增生。所有患者均有幽门螺杆菌感染,经根除治疗后,症状缓解率达92．0％。结论：结节性胃炎、胃粘膜相关组织淋巴瘤发生与幽门螺杆菌感染相关,放大染色内镜对结节性胃炎有诊断意义。     

胆汁反流性胃炎134例临床分析

目的：探讨胆汁反流性胃炎的病因及其临床治疗效果。方法i回顾性性分析134例反流性胃炎患者的临床症状、胃镜检查、幽门螺杆菌（Hp）检测和治疗结果。结果：胆汁反流性胃炎的主要由胃切除手术、胆结石、胆囊炎、糖尿病、消化性溃疡、肝炎、肝硬化、消化道肿瘤和胰腺炎等诱发,但Hp感染率并不高,134例均在四周内治愈。结论：胆汁反流性胃炎是胆汁、胰液和肠液等反流入胃引起的胃黏膜损害造成,治疗上要以减少反流物的损害作用和改善胃肠动力为主。     

The influence of the different morphological changes on gastric mucosa on somatostatin cell number in antrum mucosa and serum somatostatin

The aim of our paper was to investigate the influence of the different morphological changes on gastric mucosa on somatostatin D-cell number in antral mucosa and serum Somatostatin. We analyzed according to Sydney classification to what extent the severity of gastritis affect the observed hormonal values. somatostatin D-cell number in antral mucosa and serum Somatostatin values were compared between three groups of patients; mild, moderate and severe chronic gastritis. The average number of somatostatin cell in biopsy sample of antrum mucosa was 30.41 +/- 35.38 (N = 17) in the case of middle form, 18.69 +/- 26.65 (N = 56) in moderate and in severe case of chronic gastritis 5.23 +/- 5.93 (N = 7) cells in mm2 of mucosa. The level of somatostatin in the serum of middle form gastritis were 26.43 +/- 28.76, moderate 19.95 +/- 35.93 and severe 17.88 +/- 17.66 pg/mL. In order to determine the number of somatostatin cells in antrum mucosa and serum somatostatin with present morphological changes of mucosa, it might helpful to exclude the patients with non-ulcer dyspepsia, but with the higher risk of premalignant and malignant changes.     

Oxidative damage of the gastric mucosa in Helicobacter pylori positive chronic atrophic and nonatrophic gastritis, before and after eradication

Background. Helicobacter pylori is the main cause of gastritis and a primary carcinogen. The aim of this study was to assess oxidative damage in mucosal compartments of gastric mucosa in H. pylori positive and negative atrophic and nonatrophic gastritis. Materials and methods. Five groups of 10 patients each were identified according to H. pylori positive or negative chronic atrophic (Hp‐CAG and CAG, respectively) and nonatrophic gastritis (Hp‐CG and CG, respectively), and H. pylori negative normal mucosa (controls). Oxidative damage was evaluated by nitrotyrosine immunohistochemistry in the whole mucosa and in each compartment at baseline and at 2 and 12 months after eradication. Types of intestinal metaplasia were classified by histochemistry. Results. Total nitrotyrosine levels appeared significantly higher in H. pylori positive than in negative patients, and in Hp‐CAG than in Hp‐CG (p < .001); no differences were found between H. pylori negative gastritis and normal mucosa. Nitrotyrosine were found in foveolae and intestinal metaplasia only in Hp‐CAG. At 12 months after H. pylori eradication, total nitrotyrosine levels showed a trend toward a decrease in Hp‐CG and decreased significantly in Hp‐CAG (p = .002), disappearing from the foveolae (p = .002), but remaining unchanged in intestinal metaplasia. Type I and II of intestinal metaplasia were present with the same prevalence in Hp‐CAG and CAG, and did not change after H. pylori eradication. Conclusions. Oxidative damage of the gastric mucosa increases from Hp‐CG to Hp‐CAG, involving the foveolae and intestinal metaplasia. H. pylori eradication induces a complete healing of foveolae but not of intestinal metaplasia, reducing the overall oxidative damage in the mucosa.     

益生菌抑制幽门螺杆菌的作用机制及研究进展

幽门螺杆菌在胃部疾病的发病过程中起着重要作用,是导致胃炎、胃溃疡,甚至胃癌的关键因素之一。随着胃部疾病患者幽门螺杆菌阳性检出率的不断升高,人们对于胃病和幽门螺杆菌的相关性研究也有了一定进展。如今,对于幽门螺杆菌阳性患者根除治疗的必要性,以及抗生素治疗耐药性等问题已引起广泛关注。在这种情况下,益生菌作为相对安全的天然微生物,在抑制幽门螺杆菌并促进胃部健康的益生功能方面具有重要的研究潜力。本综述对幽门螺杆菌的致病机理、不同基因分型的致病程度等方面进行了总结,并对益生菌抑制幽门螺杆菌的机制进行了探讨。建议在治疗幽门螺杆菌感染时,应与常规的治疗手段结合应用,不仅会增加幽门螺杆菌的根除率,还能减少治疗相关的副作用。     

Inducible nitric oxide synthase expression before and after eradication of Helicobacter pylori in different forms of gastritis

An increased expression of inducible nitric oxide synthase (iNOS) has been observed in the inflamed human gastric mucosa as well as in some tumors. This observation suggests a pathobiological role of elevated NO production. The purpose of this study was to compare the immunohistochemical iNOS expression in the different kinds of gastritis before and after the eradication of Helicobacter pylori. We performed iNOS and H. pylori immunohistochemical staining and counted iNOS positive cells. We detected elevated expression of iNOS around sites infected with H. pylori. iNOS expression in chemical gastritis was strongly elevated in mucosal glands. After treatment, we found a significant difference in iNOS expression in patients with classical H. pylori-induced antrum predominant gastritis and in patients with active autoimmune gastritis. In the special case of progressed gastritis with intestinal metaplasia we found persistence of intestinal metaplasia, and we could not find a significant difference in the number of positive iNOS cells before and after treatment. The persistence of IM as a possibly precancerous lesion is probably at least in the antrum a source of continuous iNOS induction even after H. pylori eradication.     

CagA and VacA: Virulence Factors of Helicobacter pylori in Thai patients with Gastroduodenal Diseases

Background. The aim of this study was to assess the seroprevalence of cytotoxin-associated gene A ( cag A) and vacuolating cytotoxin gene A ( vac A) of Helicobacter pylori in selected Thai populations with specific gastroduodenal diseases.
Materials and Methods. The immunoblot assay was used to detect serum antibodies against CagA and VacA obtained from the following patients: 87 cases of nonulcer dyspepsia (NUD), 61 cases of duodenal ulcer (DU), 49 cases of gastric ulcer (GU), and 10 cases of gastric cancer (GC).
Results. Serum antibodies to CagA were detected in 75.4% of all patients (70.1% of NUD, 78.7% of DU, 77.6% of GU, and 90% of GC). Although the prevalence of CagA seropositivity in GC patients was higher than in the other three groups, the difference was not statistically significant ( p > .05).
Conclusions. The high seroprevalence of the CagA-positive H. pylori strain in patients with peptic ulcer, GC, and NUD indicates that this strain is common in Thai patients with gastroduodenal diseases. Furthermore, phenotypic classification of H. pylori into type 1 (CagA-positive, VacA-positive) and type 2 (CagA-negative, VacA-negative) is not a useful marker for screening patients with severe forms of gastroduodenal diseases.     

Decrease of erythropoietin level by human recombinant tumour necrosis factor alpha (hrec TNFalpha) in patients with advanced cancer

Anaemia is a frequent complication of chronic inflammation, infectious diseases and cancer. Inappropriate erythropoietin production is regarded as one of the main causative factors responsible for the occurrence of anaemia. The pathogenesis of TNFalpha induced-anaemia has not been fully clarified yet and its influence on hematopoiesis has been suggested. We performed a clinical study to access the influence of hrec TNFalpha administration on plasma EPO concentration and the degree of anaemia in patients with advanced solid tumours for whom no other kind of therapy but palliative treatment was available. All these patients exposed mild anaemia (HT 36.1 +/- 1.0%). Plasma EPO was estimated at 8 a.m. before and after 5 days of TNFalpha therapy with a dose of 75 pg/day iv (cycle I). Two weeks later plasma EPO was estimated again before and after 5 days of TNFalpha administration of a double dose (150 microg/day) (cycle II). The control group comprised 8 non-cancer patients (5M/3F, age 48.5 +/- 6yr) with the same degree of anaemia (HT 36 +/- 1.1%) due to haemorrhage. In the control group the plasma EPO level was significantly higher (54.2 +/- 8 mU/ml) than in cancer patients before cycle I (17.1 +/- 2.5 mU/ml) and II (14.6 +/- 3.8 mU/ml) respectively.TNF administration was followed by a significant decline of plasma EPO both after the first (17.1 +/- 2.5 vs 9.0 +/- 1.5 mU/ml) and second cycle (14.6 +/- 3.8 vs 8.4 +/- 2.0 mU/ml) of TNF treatment. CONCLUSIONS: Patients with solid cancer and mild anaemia are characterised by inappropriate low plasma EPO concentration. Therapy with TNFalpha exerts a suppressive effect on EPO secretion in these patients.