儿童结节性胃炎幽门螺杆菌耐药性分析

目的分析儿童结节性胃炎幽门螺杆菌(H.pylori)的耐药情况,探讨H.pylori耐药菌株的抗生素合理使用方法。方法 2013年1月至2014年6月因上消化道症状就诊行胃镜检查的结节性胃炎患儿473例,收集患儿的胃窦黏膜2块,分别行H.pylori快速尿素酶试验和培养。用琼脂稀释法和E-test法检测H.pylori对阿莫西林、克拉霉素、甲硝唑、莫西沙星和左氧氟沙星的耐药情况。结果 473例结节性胃炎患儿,258例H.pylori培养阳性,H.pylori菌株对阿莫西林、克拉霉素、甲硝唑、莫西沙星、左氧氟沙星的耐药率分别为6.2%、34.9%、49.2%、8.9%、5.0%。对克拉霉素和甲硝唑双重耐药率为23.3%。473例患儿中,405例家长有H.pylori感染。结论结节性胃炎是儿童H.pylori感染的一种特殊征象。H.pylori感染有明显家族聚集性。儿童结节性胃炎H.pylori对阿莫西林的耐药率较低,应作为根除H.pylori的主要药物;克拉霉素的耐药率较高,在H.pylori高耐药地区,应在药敏结果指导下实施三联抗H.pylori治疗。     

婴幼儿幽门螺杆菌感染的临床及病理研究

目的为探讨婴幼儿慢性胃炎的幽门螺杆菌(H.pylori)感染与不同类型胃炎之间的关系及组织病理学的特征。方法评估5年内采用胃镜和胃粘膜病理组织学检查特征,及H.pylori检测的结果。结果152例婴幼儿慢性胃炎中H.pylori感染率为15.8%。各种不同类型的慢性胃炎中,以胃镜下结节性胃炎和消化性溃疡伴慢性胃炎组的H.pylori感染率为高,分别为33.3%和28.6%。中-重度粘膜炎症的病例H.pylori阳性组明显高于阴性组(P<0.05);H.pylori的菌量与胃粘膜的病理变化、炎症程度密切相关;H.pylori阳性组的家庭成员中13C?UBT检测阳性率为54%。结论H.pylori感染起始于婴幼儿,并与胃十二指肠疾病有一定关系,与胃镜下结节性胃炎和消化性溃疡最为密切;胃粘膜病理炎症程度与H.pylori的菌量密切相关;家庭成员中H.pylori感染可能是婴幼儿感染的来源。     

无锡地区散居儿童幽门螺杆菌感染及相关因素流行病学调查

目的了解无锡地区儿童人群中幽门螺杆菌(H．pylori)感染率，探讨影响H．pylori感染的因素。方法采用酶联免疫分析法检测1126例0—12岁健康儿童及其父母粪便中的幽门螺杆菌抗原(HpSA)。并对每位人选者进行问卷调查，对其平时有无消化道症状、生活环境、生活习惯及家族史等情况进行了解。结果本地区儿童平均H．pylori感染率为19．1％，其中男性为19．6％，女性为18．5％，两者差异无显著性。有症状组阳性率为26．％，无症状组为10．6％。城区儿童H．pylori感染率为12．5％，城郊结合部儿童为19．3％，郊区、农村儿童为24．9％。结论无锡地区儿童中H．pylori感染率较高．有随年龄递增的趋势。幽门螺杆菌感染为引起无锡地区儿童胃十二指肠疾病的主要原因。     

幽门螺杆菌毒力基因与致病性研究进展

幽门螺杆菌(H. pylori)感染是人类最常见的慢性细菌感染,感染了全球超过50%的人口。大部分H. pylori感染是在儿童期获得,与慢性萎缩性胃炎、消化性溃疡、胃黏膜相关淋巴组织(MALT)淋巴瘤、胃癌等疾病密切相关。此外,还可能参与多种胃肠外疾病,如缺铁性贫血、生长发育迟缓、特发性血小板减少性紫癜等。H. pylori感染给儿童健康带来极大的危害,其致病性的差异主要与其毒力基因型的多态性有关。文章综述H. pylori毒力基因的特征与致病性。     

过敏性紫癜伴幽门螺杆菌感染患儿肠道菌群变化的研究

目的 研究过敏性紫癜(HSP)伴有幽门螺杆菌(H.pylori)感染患儿肠道菌群的变化.方法 随机收集40例HSP患儿及40例正常儿童的粪便标本,先用快速免疫检测卡进行粪便幽门螺杆菌抗原(HpSA)检测,判定有无H.pylori感染.然后提取两组粪便标本目标细菌DNA,采用16SrRNA荧光定量PCR技术对两组粪便标本中的双歧杆菌和大肠杆菌进行定量分析和比较.并计算双歧杆菌/大肠杆菌(B/E)比值.结果 HSP患儿H.priori检出率为50.0%,正常儿童为27.5%(x2=4.266.P<0.05).双歧杆菌在HSP伴H.Pylori感染组和HSP非H.pylori感染组分别与正常儿童H.pylori感染组和非H.pylori感染组相比,数鼍明显减少(P<0.008 3);大肠杆菌在正常儿童H.pylori感染组和非H.pylori感染组分别与HSP非H.pylori感染组相比,数量明显升高(P<0.008 3),在HSP伴H.pylorii感染组与HSP非H.pylori感染组相比,数量明显升高(P<0.008 3).B/E值在HSP伴H.pylori感染组分别与HSP非H.pylori感染组、正常儿童H.priori感染组和正常儿童非H.pylon感染组相比,数值明显降低(P<0.008 3).结论 HSP患儿H.pylori检出率较正常儿童明显增多,HSP发病可能与H.pylori感染有关.HSP伴H.pylori感染和HSP非H.pylori感染患儿肠道双歧杆菌均较正常儿童减少,HSP伴H.pylori感染患儿肠道大肠杆菌较HSP非H.pylori感染息儿升高,HSP伴H.pylori感染患儿B/E值明显降低,提示HSP患儿肠道菌群失调明显.     

昆明地区儿童幽门螺杆菌感染状况及危险因素分析

目的了解和探讨昆明地区儿童幽门螺杆菌感染状况及其危险因素。方法随机抽取2008年1月至2010年6月在儿科就诊无消化道症状并做血清H.pylori抗体检测的儿童进行问卷调查。通过单因素配对资料χ2分析及多因素logistic回归分析,筛选出危险因素。结果共478例儿童中H.pylori IgG阳性238例,感染率为49.8%。其中1～3岁、4～7岁、8～14岁H.pylori IgG阳性率分别为24.3%、42.4%、58.3%。学龄期儿童(>7岁)占总感染人数的64.7%。而年龄、共用牙刷口杯、共用餐具、家庭人口数多、经济收入低、人均居住面积小及父母亲和照顾者有胃病史等为H.pylori感染的危险因素。结论 H.pylori感染在儿童中,尤其学龄儿童较为常见,与年龄相关。H.pylori感染危险因素的筛查为预防提供指导。     

无锡地区散居儿童粪便幽门螺杆菌抗原检测结果分析

自1983年由澳大利亚Warren和Marshail发现幽门螺杆菌(Helicobacter pylori, H. pylori)以来,成人和儿童的大量研究证实H. pylori已成为世界各地最常见的慢性感染性疾病的病原之一,与许多消化道疾病密切相关,包括慢性活动性胃炎、萎缩性胃炎、消化性溃疡、胃癌、胃粘膜相关淋巴样组     

儿童幽门螺杆菌感染研究进展

幽门螺杆菌(H.pylori)是引起儿童慢性胃炎、消化性溃疡、胃黏膜相关性淋巴样组织(MALT)淋巴瘤等相关疾病的重要病原微生物。H.pylori感染可能发生在儿童早期,如不给予根除治疗,可持续终身,甚至直接影响到成年期的健康。文章综述近年来关于儿童H.pylori感染情况、感染途径、感染的免疫特点及其与胃十二指肠外疾病的关系。     

儿童幽门螺杆菌感染与HLA-DQB1等位基因遗传多态性研究

目的　研究HLA -DQB1基因位点上是否存在幽门螺杆菌(H .pylori)感染及其相关胃炎的易感基因或抵抗基因,从免疫遗传角度探讨H .pylori感染后临床结局多样性的可能发生机制。方法　对1 999年9月至2 0 0 0年7月上海第二医科大学附属瑞金医院收治的1 3 3例慢性胃炎及80名健康儿童(对照组) ,进行H .pylori检测,应用PCR SSO杂交方法确定其HLA -DQB1等位基因型别。结果　80名对照组儿童中H .pylori阳性3 3名,H .pylori阴性47名;1 3 3例慢性胃炎患儿中,H .pylori阳性85例,H .pylori阴性48例。DQB1 0 3 0 3 2等位基因频率在血清学H .pylori阳性者中低于血清学H .pylori阴性的健康儿童( 1 0 . 61 %vs 2 5. 53 % ,P <0 . 0 5)。DQB1 0 60 2等位基因频率在H .pylori阳性胃炎患儿低于H .pylori阴性胃炎患儿( 4 . 71 %vs 1 2 . 50 % ,P <0 . 0 5)。结论　DQB1 0 3 0 3 2对H .pylori感染可能具有抵抗保护作用,DQB1 0 60 2缺乏可能是H .pylori相关性胃炎发生的宿主遗传因素。     

儿童幽门螺杆菌感染的临床表现、诊断及治疗

我国是幽门螺杆菌(Helicobacter pylori,H.pylori)感染率较高的国家。儿童H.pylori感染不仅与消化性溃疡、慢性胃炎、胃癌等胃肠道疾病密切相关,还可能与多种胃肠道外疾病有关。但目前H.pylori感染的多种诊断方法各有利弊,各种治疗药物在不同地区显示出不同程度的耐药性。文章回顾了近年国内外儿童H.pylori感染流行病学、临床表现、诊断方法及其治疗方案的最新研究进展。     

Helicobacter pylori - dependent intragastric urea biodegradation in children: Diagnostic and pathogenetic importance

Abstract The objective of the present work was to study the relationship between intragastric urea hydrolysis generated by Helicobacter pylori urease and acid-peptic disease in childhood. Intragastric urease activity was examined by urea and ammonia concentration measurement in gastric juice in 91 children with upper abdominal complaints. Helicobacter pylori infection was detected from 70 (76.9%) of 91 patients, including all of the 15 subjects with peptic ulcer disease. Helicobacter pylori -related gastritis in children was associated with a decrease of urea and an increase of ammonia in gastric juice ( P < 0.001) in comparison with H. pylori-negative children. The gastritis score was correlated with the concentrations of urea and ammonia in the gastric juice of patients infected with H. pylori. There was a significant correlation between the histologically detected dissemination of organisms and gastric ammonia levels. Similar results were obtained concerning correlation between gastric juice ammonia and anti- H. pylori specific immunoglobulin G versus highly purified antigen of H. pylori containing urease. Present findings prove that H. pylori plays an essential role in the pathogenesis of gastritis and that ammonia is one of the main pathogenic factors of acid-peptic disease.     

The role of Helicobacter pylori in abdominal pain in children]

Helicobacter pylori (H. pylori) colonizes the human stomach, especially during childhood. H. pylori gastritis, in the absence of duodenal ulcer, does not appear to be associated with specific symptoms. After eradication of H. pylori infection, abdominal pain is improved only in children with duodenal ulcer. Children with H. pylori gastritis cannot be distinguished from uninfected children on the basis of initial symptoms. However, although not demonstrated, a relationship between H. pylori and recurrent abdominal pain might exist since some studies showed that H. pylori-infected children present more frequent pain related to meals or ulcer-like symptoms. These discrepancies could be explained by the fact that H. pylori is probably not a frequent cause of recurrent abdominal pain. The use of refined clinical characteristics of abdominal pain could be of help identifying a subgroup of patients with abdominal pain in whom H. pylori infection needs to be sought and treated. Recent pediatric consensus conferences recommend testing for H. pylori infection by endoscopy only those patients presenting symptoms suggestive of an organic origin.     

Alpha-defensin expression in the gastric tissue of children with Helicobacter pylori-associated chronic gastritis: an immunohistochemical study

In this study, we evaluated the expression of alpha-defensin and its correlation with histological criteria in children with and without Helicobacter pylori-associated gastritis. Forty-five children were included. Immunohistochemical staining was performed and the relationship between alpha-defensin immunoscoring and H. pylori status and histological criteria was evaluated. Expression of alpha-defensin was significantly higher in the H. pylori-positive group (P < 0.001) and it was significantly associated with higher grades of chronic inflammation and neutrophil density (P < 0.001 for both). Our data show that alpha-defensin expression is increased in H. pylori infection in childhood and is associated with inflammatory tissue damage.     

Correlation between Helicobacter pylori infection and vitamin C levels in whole blood,plasma, and gastric juice,and the pH of gastric juice in Korean children

BACKGROUND: It is well known that chronic gastritis induced by Helicobacter pylori may be associated with hypochlorhydria and may also be accompanied by low levels of vitamin C in plasma and gastric juice in adults. This study investigates the relationship between H. pylori infection and vitamin C levels in the blood, plasma and gastric juice and the gastric juice pH of Korean children. METHODS: During a 5-year period, multiple gastric antral biopsies were taken from 452 children who underwent gastroduodenoscopy. The biopsy specimen was inoculated into phenol red buffered urea broth and incubated for 48 hours to detect color changes. The histopathologic findings were evaluated using the Sydney System. Concentrations of vitamin C in whole blood, plasma, and gastric juice aspirate were measured using the 2,4-dinitrophenylhydrazine method. RESULTS: Four hundred fifty-two patients (228 boys, 224 girls) aged 1 to 15 years were enrolled in this study. H. pylori was detected in 112 patients (24.8%) using histology, whereas it was found in 204 patients (45.1%) using the urease test. One hundred seven patients (23.7%) had active gastritis, and 421 patients (93.1%) had chronic gastritis. Vitamin C levels in whole blood, plasma, and gastric juice exhibited significant negative correlation with the age of patients, the histologic density of H. pylori, the degree of active and chronic gastritis, and the severity of H. pylori infection (based on urease positivity and histologic density of H. pylori). Gastric juice pH was correlated with the degree of chronic gastritis and was significantly higher in urease-positive patients. CONCLUSIONS: The data demonstrate that vitamin C levels in whole blood, plasma, and gastric juice and the gastric juice pH in Korean children are closely related to the severity of H. pylori infection and the histologic changes in the stomach. These data suggest that vitamin C may play a role in determining infection and progression, and vitamin C supplementation may be an important axis for the management of H. pylori infection in children.     

Gastric histopathology, iron status and iron deficiency anemia in children with Helicobacter pylori infection

OBJECTIVES: Helicobacter pylori has been established as a major cause of gastritis and peptic ulcer disease in adults and children. H. pylori infection may also have a role in the development of some extra-gastrointestinal diseases, including iron deficiency anemia. The aim of this study is to investigate H. pylori-related changes in gastric physiology and histology and the relationship of these changes to iron deficiency anemia in children. METHODS: Fifty-two patients with gastrointestinal complaints were studied. Hematologic parameters, 3-day vitamin C and iron consumption, serum gastrin levels, and gastric juice ascorbic acid levels were compared in patients with and without H. pylori infection. Dietary intake of vitamin C and iron, serum gastrin, gastric juice ascorbic acid content, and gastric histology were compared in patients with H. pylori infection and anemia and in patients with H pylori infection and no anemia. The CagA status of the H. pylori organisms was evaluated. RESULTS: Twenty-eight of 52 patients had H. pylori. Thirty-one patients had iron deficiency anemia. H. pylori infection was associated with low serum iron levels. H. pylori gastritis was associated with a decrease in the gastric juice ascorbic acid level. Infection with CagA-positive strains was associated with a greater decrease in gastric juice ascorbic acid than infection with CagA-negative strains. However, the gastric juice ascorbic acid levels of patients with H. pylori and anemia were not different from those of non-anemic patients with H. pylori. Among patients with H. pylori infection, pangastritis was twice as common in those with anemia than in those without anemia. CONCLUSIONS: H. pylori infection was associated with a decrease in gastric juice ascorbic acid concentration, and this effect was more pronounced in patients with the CagA-positive strain. Pangastritis was more common in patients whose H. pylori.infection was accompanied by anemia.     

Is Helicobacter pylori infection in childhood a risk factor for gastric cancer?

Helicobacter pylori infection is associated with chronic gastritis and peptic ulcer disease. Furthermore, the World Health Organization has classified this organism as a carcinogen for gastric cancer. H pylori infection is mainly acquired in childhood. Children with H pylori infection are asymptomatic except for a very small number that develop peptic ulcer disease. However, if H pylori gastritis is associated with gastric cancer, do pediatricians need to screen children for this infection and treat those who are infected? In an attempt to determine the significance of the association between H pylori and gastric cancer, we have reviewed all of the English language literature on this topic. H pylori infection seems to be associated with an increased risk of developing gastric cancer. However, only a small number of infected individuals (~1%) will develop gastric cancer. Furthermore, there are potential cofactors other than H pylori that could be equally important. The effect of the eradication of H pylori alone on the development of gastric cancer is unknown. Based on our knowledge to date, we suggest that it is not indicated to treat all children with H pylori infection because of the risk of developing gastric cancer or to institute a screening and treatment program.     

Helicobacter pylori infection and peptic ulcer in eastern Turkish children: is it more common than known?

Helicobacter pylori (H. pylori) infection is mainly acquired in childhood and is frequent in developing countries. The infection is associated with chronic gastritis in all infected children, but peptic ulcer disease develops in a small number of them. In our country, H. pylori infection and associated peptic ulcer disease are common. In eastern Turkey, we found peptic ulcer disease in 13.2% of children who underwent endoscopic examination. Peptic ulcers were mostly gastric ulcers and H. pylori-positive in the studied population, and most of the children were admitted due to abdominal pain. As there are no well-established criteria leading directly to diagnosis, pediatricians should include H. pylori infection and peptic ulcer disease in the differential diagnosis list when evaluating children with abdominal pain, failure to thrive and upper gastrointestinal system bleeding.     

Parietal cell antibodies and Helicobacter pylori in children

BACKGROUND: Gastric autoantibodies are common in Helicobacter pylori-infected adults, and the presence of these antibodies is associated with atrophic gastritis. The role of H. pylori in the autoimmune type of atrophic gastritis is unresolved, and it is not known at what stage the autoantibodies appear in serum during H. pylori infection. Therefore, we screened children with and without H. pylori infection for gastric parietal cell antibodies. METHODS: Seventy-one children with H. pylori infection verified by examination of gastric biopsy specimens (mean age, 9.4 years), 8 children with positive serology but negative histology for H. pylori (mean age, 11.6 years), and 130 children with negative serology for H. pylori (mean age, 7.7 years) were screened for the presence of gastric parietal cell antibodies in serum by indirect immunofluorescence. In addition, 61 children with celiac disease (mean age, 7.1 years) were screened for gastric parietal cell antibodies and H. pylori antibodies. RESULTS: None of the children with H. pylori infection had gastric parietal cell antibodies in serum. Only three positive parietal cell antibody reactions were found: a 14-year-old boy with positive serology for H. pylori but no other signs of infection (titer 5000), a 14-year-old girl with tuberculosis (titer 1250, seronegative for H. pylori) and a 10-year-old girl with insulin-dependent diabetes mellitus (titer 6250, seronegative for H. pylori). CONCLUSIONS: Although gastric autoantibodies are often found in adults with chronic H. pylori gastritis, it seems that H. pylori-infected children are not positive for gastric parietal cell antibodies. It remains to be studied in which H. pylori infections and at what stages gastric autoantibodies appear.     

Treatment of Helicobacter pylori gastritis improves dyspeptic symptoms in children

BACKGROUND: In adults, the treatment of Helicobacter pylori infection is only recommended for patients with active gastric or duodenal ulcers. It is not known whether similar guidelines can be applied to children because the prevalence of peptic ulcer disease in childhood is estimated to be much lower than in adults. The purpose of this study was to determine whether treatment of H. pylori gastritis would improve symptoms of dyspepsia in children. METHODS: Sixteen patients (5 boys, 11 girls) aged 14 +/- 1.2 years who had symptoms of dyspepsia were evaluated using upper gastrointestinal endoscopy with biopsies to establish the diagnosis of H. pylori gastritis. They were treated for 2 weeks with clarithromycin, amoxicillin, and a proton pump inhibitor. Dyspepsia symptoms were evaluated by a questionnaire before and after treatment of the infection. The effect of H. pylori treatment on the total symptom score was analyzed with use of the Student t test. Values are presented as mean +/- SEM. RESULTS: All patients had antral nodularity and chronic active gastritis with spiral-shaped organisms but no evidence of peptic ulcer disease. Mean total symptom score decreased significantly at 2 to 4 weeks after treatment (12.6 +/- 0.9 vs. 2.1 +/- 0.5 P < 0.001), and it remained low (2.9 +/- 0.7) at follow-up 9.7 +/- 1.4 months (range, 2-24 months later). CONCLUSION: These results suggest that the treatment of H. pylori gastritis can improve dyspeptic symptoms in children.     

Increased mucosal inflammatory cytokines in children with Helicobacter pylori-associated gastritis

The concentrations of tumour necrosis factor-alpha (TNF-α), interleukin-6 (IL-6) and IL-1-β in tissue homogenates of gastric mucosal biopsy specimens, and in gastric juice samples from Helicobacter pylori-positive and -negative children, were determined. The study population comprised 30 children with recurrent abdominal pain attending upper gastrointestinal endoscopy. Of these patients 18 were infected with H. pylori. Cytokine concentrations in gastric biopsy homogenate supernatants and in gastric juice were measured by enzyme-linked immunosorbent assay (ELISA). TNF-α levels in gastric juice and in gastric biopsy homogenate supernatants in patients with H. pylori-positive gastritis were found to be significantly higher than those in children without H. pylori infection. IL-6 levels were also higher in H. pylori -infected subjects, but the difference in IL-6 concentrations measured in gastric juice and biopsy homogenate supernatants did not reach statistical significance. IL-1-β concentrations in both specimens showed no significant difference between the two groups of children. It was suggested that increased levels of inflammatory cytokines, especially TNF-α and IL-6 generated locally within the gastric mucosa might be implicated in the pathogenesis of H. pylori-associated gastritis in childhood.