胃十二指肠疾病幽门螺杆菌检出的意义

目的:研究幽门螺杆菌(Hp)与消化性溃疡及慢性胃炎致病的关系。方法:因胃十二指肠疾病而做胃镜的患者,采取胃粘膜进行组织快速检菌,一分钟尿素酶(1min UT)试验和血清间接免疫荧光法进行检菌分析。结果:对5000例胃及十二指肠疾病Hp的组织检出率为88.1％。1min UT阳性率为62.9％,两种检菌法有显著差异(P<0.01)。十二指肠溃疡Hp检出为96.0％,胃癌和萎缩性胃炎Hp感染率为50.0％和59.2％,而1min UT只有41.5％阳性率。结论:胃癌和萎缩性胃炎均有粘膜层萎缩,腺体减少、粘液分泌功能降低,Hp茵不能适应强酸环境下生存。十二指肠溃疡和慢性胃炎多伴引起幽门口水肿和幽门变型,胃排空减缓。是导致Hp茵高检出率的重要因素。     

Peptic ulcer and gastritis in uraemia, with particular reference to the effect of Helicobacter pylori infection

AIMS: To determine: (i) the prevalence of histological gastritis and peptic ulcer; and (ii) the clinical features of peptic ulcer, in patients with end-stage renal failure. METHODS: Upper endoscopy was performed by a single observer in 268 patients with end-stage renal failure over a 6-year period. Gastric histology and Helicobacter pylori status were studied in 40 consecutive subjects in whom there were no contraindications for gastric biopsy and who had not used antibacterial drugs in the preceding 4 weeks. As there are only limited data for healthy volunteers in Singapore, 33 age-, sex- and race-matched patients with functional dyspepsia from an earlier drug trial and 18 healthy volunteers who were not age-matched were used as controls. The clinical features of 43 consecutive uraemic patients with peptic ulcer were compared with those of 118 consecutive non-uraemic peptic ulcer patients seen by the same author. RESULTS: Among uraemic patients, histological gastritis was less common, compared with healthy volunteers and functional dyspepsia patients. Helicobacter pylori infection as assessed by histology was also less common among uraemic patients compared with functional dyspepsia patients, but the difference was not statistically significant on serological assessment. Uraemic patients with ulcer had an equal sex ratio, in contrast to a male preponderance among peptic ulcer patients with normal renal function. Uraemic patients with ulcer were more likely to be pain-free, to present with haemorrhage, to have multiple ulcers and postbulbar duodenal ulcers, but were less likely to have H. pylori infection. Among uraemic subjects, the prevalence of H. pylori infection was similar whether or not peptic ulcer was present. CONCLUSIONS: The prevalence of histological gastritis was lower in uraemic patients when compared with patients with functional dyspepsia and healthy volunteers. Peptic ulcers in uraemic subjects have different clinical characteristics from peptic ulcer in non-uraemic subjects.     

幽门螺杆菌不是慢性胃病的主要致病因素——附378例临床调查报告

[目的]验证幽门螺杆菌（Hp）是否为慢性胃病的主致病因素。[方法]用概率、构成比、相对比对378例慢性胃病患者进行统计分析。[结果]慢性活动性胃炎213例,Hp阳性概率为0．2535,Hp阳性例数构成比为25．35％;Hp阴性概率为o．7465,Hp阴性例数构成比为74．65％,Hp阴性例数与Hp阳性例数的相对比为2．94（倍）。溃疡病（A1期）165例,Hp阳性概率为0．4061,Hp阳性例数构成比为40．61％;Hp阴性概率为0．5939,Hp阴性例数构成比为59．39％,Hp阴性例数与Hp阳性例数的相对比为1．46（倍）。[结论]Hp不是胃炎及溃疡病的主致病因素,Hp可能对胃黏膜屏障起保护作用。     

Helicobacter pylori eradication in the healing of atrophic gastritis: A one-year prospective study

Objective. Whether gastric atrophy or intestinal metaplasia heals after successful treatment of Helicobacter pylori (H. pylori) infection is still a matter of controversy. The aim of this article was to clarify whether, after one year, H. pylori eradication is associated with healing in glandular atrophy and intestinal metaplasia in the corpus and antrum. Material and methods. Ninety-two H. pylori-positive peptic ulcer patients with atrophic gastritis (panatrophy, antral or corpus predominant) participated in the baseline study, 1-year prospective follow-up data being available from 76 patients. Mean age was 58±12.6 years (mean±SD) and the male/female ratio 2/1. The patients participated in an H. pylori eradication study in which they randomly received active eradication therapy. Endoscopy was performed before H. pylori eradication therapy and after 8 and 52 weeks, with specimens examined according to the Sydney system. Results. Of the 92 patients, 8 (9%) had panatrophy, 58 (63%) had antral- and 26 (28%) had corpus-predominant atrophic gastritis. After H. pylori eradication, the mean atrophy score declined in patients with antral-predominant atrophy from 1.5 (mean) to 0.7 (p<0.05), in corpus-predominant atrophy from 1.7 to 0.2 (p=NS) and in patients with panatrophy from 1.2 to 0.8 (p=NS). Atrophy healing was seen in 55% of antral-predominant atrophy patients who had successful H. pylori eradication.The mean antral atrophic score in one year declined in patients with duodenal ulcer (from 1.0 mean to 0.4) whereas it remained the same (1.3) in those with gastric ulcer (p<0.05). Conclusions. Atrophy can diminish or even disappear, especially in the antrum, during a 1-year follow-up after eradication of infection. Atrophy progression seems milder in patients with duodenal ulcer than in patients with gastric ulcer.     

雷、环、痢方案根治幽门螺杆菌感染临床疗效观察(附134例报告)

目的　观察雷尼替丁、环丙沙星、痢特灵三联对幽门螺杆菌 (Hp)阳性的消化性溃疡、慢性胃炎患者的Hp根除率及对消化性溃疡的治疗效果。方法　经快速尿素酶试验及胃粘膜活检均确认有Hp感染的消化性溃疡、慢性胃炎患者共 15 5例 ,用雷尼替丁、环丙沙星、痢特灵三联与改良的经典三联 (果胶铋、四环素、痢特灵 )作随机对照治疗。治疗组进入临床试验病例 79例 ,疗效评价 6 8例。对照组进入试验病例 76例 ,疗效评价 6 6例。结果　治疗组与对照组Hp根除率分别为 88 2 % ( 6 0 /6 8)与 84 8% ( 5 6 /6 6 )。消化性溃疡临床愈合率分别为 81 7%与 6 5 6 % ,总有效率分别为 97 2 %与81 3 %。不良反应发生率分别为 4 4%与 14 9% ,上述结果经统计学比较Hp根除率两组差异无显著性 (P >0 0 5 ) ,消化性溃疡愈合率及总有效率、不良反应发生率差异有显著性 (P <0 0 5 )。结论　雷尼替丁、环丙沙星、痢特灵三联为一效好、价廉、不良反应少的治疗方案。     

广州胃病患者幽门螺杆菌多株感染的研究

目的了解我国Ｈｐ感染人群中的多株感染状况．方法取因上腹不适行内镜检查的２０例Ｈｐ阳性患者（胃溃疡６例,十二指肠溃疡８例,慢性胃炎６例）的胃窦和胃体粘膜组织,进行Ｈｐ培养．初代培养后,分别取胃窦和胃体各１０个菌落进行传代,抽提各菌落ＤＮＡ,应用聚合酶链反应随机引物扩增的ＤＮＡ多态指模技术［ＲＡＰＤＰＣＲ］进行菌株鉴定．结果ＰＣＲ扩增产物电泳分析显示有１８例患者胃窦和胃体的ＨｐＤＮＡ指模一致,提示这１８例患者均是单株感染;另有２例胃体菌株表现为两种指模形态,提示为２株Ｈｐ感染．结论广州地区存在Ｈｐ多株感染,但不普遍．     

Clinical significance of PCR in Helicobacter pylori DNA detection in human gastric disorders

ＣｌｉｎｉｃａｌｓｉｇｎｉｆｉｃａｎｃｅｏｆＰＣＲｉｎＨｅｌｉｃｏｂａｃｔｅｒｐｙｌｏｒｉＤＮＡｄｅｔｅｃｔｉｏｎｉｎｈｕｍａｎｇａｓｔｒｉｃｄｉｓｏｒｄｅｒｓＸＵＧｕｏＭｉｎｇ，ＪＩＸｕＨｕａｉ，ＬＩＺｈａｏＳｈｅｎ，ＭＡＮＸｉａｏＨｕａ...     

Novel combination therapy for the eradication of Helicobacter pylori infection in a mouse model

Abstract

Objective. Recently, several publications in adults have shown an increased incidence of non-Helicobacter pylori (HP), non-non-steroidal anti-inflammatory drug (NSAID) peptic disease (PD). There are only a few case reports linking celiac disease (CD) to PD. We therefore aimed to review our experience of CD presenting with PD. Material and methods. We retrospectively reviewed all the endoscopies performed for children and young adults diagnosed with CD between 1 January, 2004 and 31 October, 2008. The diagnosis of CD was based on accepted guidelines. Patients with a doubtful diagnosis of CD were excluded. Results. We had 240 patients with the diagnosis of CD. We had 29 (12.0%) patients [15 males (52%), 14 females (48%)] for whom the diagnosis of PD was ascertained. The age range was 1–50 years (mean 16.9 ± 12.1 years). Twenty-three of the 29 patients (79%) were HP-negative. Duodenal PD was noted in 22 patients (76%) and 16 (73%) were HP-negative. Gastric PD was noted in eight patients (28%) and 7 (87%) were HP-negative. The PD group was significantly older at diagnosis (p < 0.001) compared to the whole CD group. Conclusions. PD is not uncommon in the presentation of CD. It is more likely to be found in the second decade of life. CD should be included in the differential diagnosis of patients with non-HP PD and we suggest routine CD serology and small bowel biopsy in patients with unexplained PD.     

Helicobacter pylori infection in Icelandic children

Objective: The prevalence of Helicobacter pylori (HP) infection is decreasing in the western world. The seroprevalence among 25–50-year-old Icelandic adults was recently shown to be 30–40%. Information on the seroprevalence in Nordic children is limited. We aimed at ascertaining the infection prevalence among healthy Icelandic children.

Methods: The infection status in stored frozen blood samples from two cross-sectional studies on the health of 7–9-year-old children (n?=?125) and 16–18-year-old adolescents (n?=?80) was determined by enzyme-linked immunosorbent assay (ELISA). Information on family demographics and GI symptoms was obtained by standardized questionnaires.

Results: Overall, 3.4% (7/205) of the children were infected with H. pylori. The prevalence was 2.6% (5/190), missing data n?=?3, among children with both parents born in a low prevalence country compared to 17% (2/12) among those with at least one parent born in a high prevalence area (p?=?.026). When at least one parent was born in a high prevalence country, the odds ratio for being H. pylori seropositive was 2.2 (95% CI, 1.02–54.67), when adjusted for the educational status of the mother. There was no significant association between H. pylori infection and gastrointestinal symptoms.

Conclusion: Prevalence of H. pylori infection in Iceland has become very low, suggesting a great reduction in transmission from older generations. There was an association between H. pylori infection and origin from high prevalence areas but not with gastrointestinal symptoms. The results mirror recent studies of children of Scandinavian ancestry.     

Treatment of Helicobacter pylori

INTRODUCTION Using an evidence-based approach this review discusses the current treatment of Helicobacter pylori infection in patients with peptic ulcer disease, functional (non-ulcer)dyspepsia or gastro-oesophageal reflux disease (GORD).It also briefly addresses the potential role of eradication of H . pylori in preventing gastric cancer .     

Lansoprazole and amoxycillin: Observations on the treatment of Helicobacter pylori infection

Symptomatic patients (n=101) with Helicobacter pylori infection were enrolled into a double-blind, double-dummy study to assess the efficacy of lansoprazole plus amoxycillin in the treatment of H. pylori infection. Patients were randomized to either lansoprazole 30 mg once daily (days 0-28) together with placebo (matched to amoxycillin) three times a day (days 0-14) followed by either placebo or amoxycillin 500 mg three times daily (days 15-28). Biopsy specimens for culture and histology were collected on days 0 and 56 or upon symptomatic relapse. Blood for serology was collected at days 0, 56 and 168. A [¹⁴C]-urea breath test was performed on day 168. Eighty-one (80.2%) patients completed the 56 day assessment. Of patients treated with lansoprazole plus amoxycillin, 35.1% (13/37) were cured of infection as assessed at day 56 (26.5% on an intention-to-treat basis), compared with 4.8% (2/42) of the placebo group (4% on an intention-to-treat basis). Recrudescence/re-infection occurred in one patient upon re-evaluation at day 168. Analysis of prognostic factors indicated that smoking and alcohol intake had little impact on the treatment outcome. Inflammation (both acute and chronic) improved in patients treated with lansoprazole plus amoxycillin. The relatively low efficacy of the treatment may relate to a single daily dose of lansoprazole (30 mg) being prescribed, treatment with amoxycillin being commenced 2 weeks after the initiation of lansoprazole or accurate assessment of treatment efficacy (both antral and body biopsy specimens taken).     

Helicobacter pylori: Past, present and future

Abstract Much has been achieved in Helicobacter pylori research, to the point that the growth of new knowledge is bound to slow down. However, expectations for further developments remain high. Knowledge about the characteristic organism and behaviour is already extensive. Particularly intriguing are the differences in genetic make-up in the various geographical regions. Sadly, detailed knowledge on how the organism spreads is still lacking. The spectrum of clinical presentation in humans is largely known. Helicobacter pylori is disappearing worldwide, allowing the relative frequency of H. pylori n-egative ulcer disease to increase. The extent to which H. pylori disappearance and eradication is responsible for decreasing prevalence of gastric cancer remains speculative. Antimicrobial therapy is dominated by proton pump inhibitor triple therapy as first line therapy, with quadruple therapy as second rescue line therapy. The long-term consequences of the rising resistance to the 'key' antimicrobials are so far unknown, because few data are available on therapeutic outcomes in routine practice outside pharmaceutical trials.     

幽门螺杆菌阴性消化性溃疡与出血关系的多中心对照研究

目的明确中国大陆地区幽门螺杆菌（Hp）阴性消化性溃疡与出血的关系。方法拟定于2006年4月至2007年3月期间在国内14个研究中心中进行,每个中心预期调查30例经急诊内镜诊断为胃溃疡和（或）十二指肠溃疡合并出血的患者（PUB组）,同时调查30例不伴出血的胃溃疡和（或）十二指肠溃疡患者作为对照（PU组）。共拟人选840例患者,消化性溃疡合并及不合并出血组各420例。在内镜检查中采用快速尿素酶试验和病理检测却感染,并对初次检查却阴性者于1个月后进行尿素呼气试验复查。结果共617例患者纳入分析,其中PUB组263例、PU组354例,2组在性别比、平均年龄等一般状况方面差异无统计学意义（P均〉0．05）。PUB组却阳性率61．2％（161／263）显著低于PU组的87．9％（311／354）（P〈0．001）;PUB组跏阳性的溃疡出血发生复合溃疡的比例7．5％（12／161）显著高于Hp阴性溃疡出血者1．0％（1／102）（P=0．018）,但两者在平均发病年龄、性别比、呕血发生率、十二指肠球部溃疡发生率、胃溃疡发生率及溃疡平均直径方面差异无统计学意义（P均〉0．05）。对于初次tip阴性的溃疡出血患者,1个月后的呼气试验复查未发现阳性病例。结论目前中国大陆缉,阴性溃疡在消化性溃疡出血中的比例较高,坳阴性溃疡可能更容易并发消化道出血,需要引起消化专科医生的重视。     

Efficacy of 7 day lansoprazole-based triple therapy for Helicobacter pylori infection in elderly patients

BACKGROUND: The prevalence of Helicobacter pylori increases with age. However, data regarding the effects of anti-H. pylori treatments in the elderly are very scarce. METHODS: To evaluate the effect of three lansoprazole-based, 7 day, triple-therapy regimens on H. pylori eradication rates, symptomatology, chronic gastritis activity and serological markers of H. pylori infection in elderly subjects, we studied 150 symptomatic patients over 60 years of age with H. pylori-positive duodenal ulcer (DU, n = 34), gastric ulcer (GU, n= 19) or chronic gastritis (CG, n = 97). Patients were consecutively treated with one of the following regimens: (A) lansoprazole (LNS) 30 mg b.i.d. + clarithromycin (CLR) 250 mg b.i.d. + metronidazole (MTR) 250 mg q.i.d.; (B) LNS 30mg b.i.d. + amoxycillin (AMOX) 1 g b.i.d. + MTR 250 mg q.i.d.; and (C) LNS 30 mg b.i.d. + CLR 250 mg b.i.d. + AMOX 1 g b.i.d. RESULTS: Two months after therapy, the eradication rates of the three treatments, expressed using both intention-to-treat and per-protocol analyses were, respectively; group A, 86 and 91.5%; group B, 80 and 87%; group C, 82 and 89.1%. After therapy, a significant reduction in epigastric pain (P<0.001), heartburn (P=0.02), dyspepsia (P<0.001) and vomiting (P< 0.005) was observed independently of the success of H. pylori eradication. A significantly higher percentage of asymptomatic patients were in the GU-DU group than in CG group (87.7 vs 70.0%, P= 0.032). After therapy, 33 subjects still suffered from symptoms. Persistence of symptoms was significantly associated with an endoscopic diagnosis of oesophagitis and not with H. pylori infection. Patients cured of H. pylori infection showed a significant decrease in the histological activity of both antral and body gastritis (P< 0.0001), a significant drop in immunoglobulin (Ig) G anti-H. pylori antibodies (P< 0.0001) and pepsinogen (PG) C (P<0.0001) and an increase in the PGA/PGC ratio (P<0.0001). CONCLUSIONS: The 7 day, lansoprazole-based triple therapy was well tolerated and highly effective in the cure of H. pylori infection, the reduction of symptoms, chronic gastritis activity and serum levels of IgG anti-H. pylori antibodies and PGC. Persistence of symptoms after therapy was significantly higher in CG than GU and DU patients and was significantly associated with oesophagitis.     

十二指肠胃化生与幽门螺杆菌感染

本文调查了155例十二指肠溃疡旁粘膜的组织病理学变化,并与对照组相比较。结果显示:溃疡旁组织炎症、胃化生和Hp检出率分别为69.7％、75.5％和24.5％,显著高于对照组的18.8％、10.4％和4.2％(P<0.01)。Hp在胃化生组织中的检出率为32.8％,81例不伴胃化生的粘膜中均未检出Hp(P<0.01)。透射电镜观察胃化生有其特征性改变。提示胃化生可能是溃疡形成的基础,Hp在化生区定植并非是产生溃疡的唯一直接因素,还可能通过其他复杂环节间接起作用。     

Review: Eradication of Helicobacter pylori. Problems and recommendations

The successful isolation of Helicobacter pylori from the stomachs of patients with gastritis and peptic ulcer has revolutionized our concepts of the pathogenesis of gastritis, peptic ulcer, gastric cancer and gastric B cell lymphoma. Eradication of H. pylori heals gastritis and H. pylori-related peptic ulcer. After a successful cure of H. pylori infection, virtually no recurrence of duodenal ulcer is seen. However, treatment to cure the infection has proved difficult. Numerous clinical trials have been attempted, but as yet no ideal regimen has been identified. Monotherapies have many drawbacks and should be avoided. Dual therapies combining a proton pump inhibitor (PPI) and an antimicrobial agent provide higher eradication rates than those involving two antimicrobial agents. Bismuth-based triple therapies are more effective than dual therapies in eradicating H. pylori infection. However, poor compliance and frequent adverse effects have made these combinations less favourable in clinical practice. Proton pump inhibitor-based triple therapies have shown more consistent and higher eradication rates with a short duration of treatment, good patient compliance, fewer side effects, prompt symptom relief and fast ulcer healing. Results from PPI-based quadruple therapies are promising; however, large multicentre clinical trials are needed to confirm the effect and the complex regimen again may compromise compliance outside of the clinical trial setting. Eradication of H. pylori infection is cost-effective in the long-term management of peptic ulcer disease compared with maintenance therapy with antisecretory drugs.     

Helicobacter pylori: host genetics and disease outcomes

Helicobacter pylori infection is the most common chronic bacterial infection worldwide and is associated with divergent clinical outcomes that range from simple asymptomatic gastritis to more serious conditions, such as peptic ulcer disease and gastric cancer. The key determinants of these outcomes are the severity and distribution of H. pylori-induced gastritis. Host genetic factors play an important role in influencing disease risk, but identifying candidate genes is a major challenge that has to stem from a profound understanding of the pathophysiology of the disease. In the case of H. pylori, the most promising candidate genes are ones that attenuate gastric acid secretion and lead to a destructive chronic inflammatory response against the infection. In particular, certain cytokine and innate immune response gene polymorphisms appear to influence risk of gastric cancer and its precursor conditions. There are currently no convincing genetic risk markers for acquisition of H. pylori infection or risk of developing peptic ulcer disease. Future research agendas should focus on identifying the full genetic risk profile for H. pylori-induced gastric neoplasia. This will help to target the population most at risk by directing eradication therapy and closer follow-up to the affected individuals.     

Persistence of Helicobacter pylori infection in patients with peptic ulcer perforation

Objective. In patients with perforated peptic ulcer (PPU) the convergence between the high eradication rate of Helicobacter pylori infection and low rates of ulcer relapse after treatment has been associated with reinfection by non-virulent strains. The objective of this study was to evaluate the persistence of infection by virulent H. pylori strains and ulcer recurrence in 33 patients with PPU one year after surgery and antimicrobial treatment. Material and methods. The histological evaluation and molecular detection of H. pylori cagA and ureA genes, vacA allelic types and the polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) analyses of the glmM gene products from antral mucosa specimens were performed initially, 2–5 months and 1 year after therapy. Results. The density of H. pylori colonization was temporarily decreased (p<0.05) 2–5 months after therapy. After one year, complete eradication was achieved in only 7 patients (23%) at histological examination and recurrent ulcers were found in 3/33 (9%) patients. The vacA s1a allelic type of cagA-positive strains persisted in 19/33 (58%) PPU patients with identical PCR-RFLP fingerprints in 8/9 (89%) of the patients. Conclusions. In PPU patients with a low eradication rate of H. pylori infection after surgical and antimicrobial treatment, the frequent recrudescence of the infection is mostly caused by the persisting virulent strains of the cagA and vacA s1a subtypes. In the 1-year follow-up period the recurrent ulceration can be postponed just by the lowered colonization density of H. pylori after eradicative therapy.     

Beta-2-microglobulin and Helicobacter pylori infection in uraemic dialysed patients

Chronic gastritis in patients with chronic renal failure may have different causes and mechanisms. Recent observations suggest that severe gastritis often found in uraemic patients might be related to Helicobacter pylori (HP) infection. In chronic gastritis HP has been found in the mucus and on the epithelial cell surface of gastric foveolas. Significant infiltration of the subepithelial gastric layer by polymorphonuclear leucocytes has been described. Moreover, beta-2-microglobulin deposits have been found by immunohistochemical methods in the subepithelial layer of gastric mucosa of uraemic dialysed patients with active chronic gastritis and HP infection. Similar findings have also been demonstrated in gastric biopsies from patients with HP positive active chronic gastritis and normal renal function. Since HP infection is associated with significant leucocyte infiltration, it is hypothesized that the inflammatory process causes the release of beta-2-M from the surface of the leucocytes and its subsequent deposition at gastric level.