昆明彝族儿童中HLA-DRB1和DQB1基因检出率与对幽门螺杆菌感染的易感性和抵抗力之间可能的关联

目的　探讨幽门螺杆菌 (Hp)感染的彝族儿童是否有HLA DRB1和DQB1易感和抵抗基因。方法　对 156名儿童以整群抽样的方法取静脉血,用ELISA金标免疫法检测各研究对象的血Hp抗体;根据血Hp抗体结果将儿童分为Hp抗体阳性组(61人)和Hp抗体阴性组(95人);从以上 2组中各随机抽取 40名儿童行13C尿素呼吸试验,两者均阳性者诊断为Hp感染,共 31名;两者均阴性者则为Hp无感染,共 39名;分别提取本组儿童的外周血基因组DNA,并应用聚合酶链反应 序列特异性引物(PCR SSP)方法行HLA DRB1、DQB1基因分型,并比较无感染组和感染组中的HLA DRB1和DQB1等位基因分布频率。结果　70名彝族儿童无感染的 39人,有感染的 31人。无感染组中的HLA DRB1* 12等位基因频率 ( 42. 31% )高于感染组 ( 14. 52% ) (P<0. 001,Pc<0 .012 );而HLA DRB1* 11等位基因频率无感染组 ( 3. 85% )低于感染组 ( 12. 9% ) (P< 0. 05,Pc> 0 .05 )。HLA DQB1* 0301等位基因频率无感染组(55. 13% )高于感染组 (32. 26% ) (P<0. 007,Pc<0. 05); HLA DQB1* 04等位基因频率无感染组 ( 2. 56% )低于感染组 ( 11. 29% ) (P<0. 05,Pc>0 .05 )。结论　HLA DRB1* 12和HLA DQB1* 0301等位基因可能是儿童抵抗Hp感染的保护基因;HLA DRB1* 11和HLA DQB1* 04等位基因是否为     

昆明白族儿童幽门螺杆菌感染与HLA-DR/DQB1的免疫遗传学分析

目的了解昆明白族儿童幽门螺杆菌感染与HLA-DR/DQB1等位基因的相关性。方法采用聚合酶链反应-序列特异性引物技术对符合流行病学诊断标准的36例H.pylori感染患儿及34例非感染儿童进行HLA-DR/DQB1基因分型。结果感染组检出15种DRB1等位基因,非感染组检出11种DRB1等位基因,两组均检出7种DQB1等位基因;组间各等位基因频率经检验,差异无统计学意义。结论白族儿童中H.pylori感染和非感染组的HLA-DR/DQB1等位基因频率无免疫遗传学差异;白族儿童H.pylori感染与HLA-DR/DQB1可能无关。     

彝族儿童幽门螺杆菌感染HLA-DQA1免疫遗传学特征分析

目的研究人类白细胞抗原(HLA)DQA1基因位点上是否存在H.pylori感染的易感基因或抵抗基因，探讨免疫遗传因素在H.pylori感染中的作用。方法用聚合酶链反应-序列特异性引物(PCR-SSP)技术对用血清学试验及^13C尿素呼气实验确诊的31例H．pylori感染的彝族儿童及39例无感染儿童进行HLA．DQA1基因分型。结果感染组HLA-DQA1*0102等位基因频率明显高于对照组(14．52％vs3．85％，P=0．025，Pc=0．35)，OR=4．245(95％CI：1．097～16．428)；感染组HLA-DQA1*0302等位基因频率低于对照组(0 vs12．82％，P=0．003，Pc=0．042)，OR=1．147(95％CI：1．053-1．249)。结论在HLA-DQA1位点上，H．pflori感染的彝族儿童与对照组儿童存在免疫遗传学差异，HLA-DQA1*0102基因可能是彝族H．pylori感染的易感基因，而HLA-DQA1*0302基因则可能是抵抗基因和具有免疫抵抗作用。     

人类白细胞抗原-DQB1与儿童十二指肠溃疡和幽门螺杆菌感染的相关性研究

目的探讨人类白细胞抗原(HLA)-DQB1等位基因与儿童十二指肠溃疡(DU)和幽门螺杆菌(H.pylori)感染的遗传关联性。方法采用非同位素标记的聚合酶链反应-序列特异性寡核苷酸探针(PCR-SSO)杂交的方法,对上海地区汉族健康儿童80例、DU患儿58例的HLA-DQB1等位基因进行分型;并同时检测DU患儿H.pylori感染情况。结果在DU患儿中,HLA-DQB1×05031等位基因频率明显高于正常健康儿童(分别为:6.02%、0.63%,P<0.05,RR=9),而在H.pylori阳性和H.pylori阴性DU组之间差异无显著性。结论HLA-DQB1×05031与DU呈正相关,DU患儿与正常对照组儿童之间存在着遗传学的差异;虽然H.pylori感染是DU的重要致病因素,但HLA-DQB1×05031并不是通过H.pylori感染而影响DU的遗传易感性。     

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。     

儿童尿液幽门螺杆菌抗体检测的临床应用

目的 评估尿液中幽门螺杆菌(H.pylori)抗体检测对H.pylori感染的诊断应用价值.方法 应用金标渗滤法检测238例胃肠疾病患儿尿液H.pylon抗体,并以血清学为标准进行χ2检验对比.结果 238例患儿尿H.pylori抗体阳性96例,血抗体阳性103例,差别无统计学意义(χ2=2.8824,P＞0.05).血、尿抗体结果相符221例,不符17例,其中5例尿抗体阳性而血抗体阴性,12例尿抗体阴性而血抗体阳性.以血清学为标准,尿液抗体检测的敏感性88.35%、特异性96.30%、阳性预测值94.79%、阴性预测值91.55%.结论 尿液H.pylori抗体检测是一种方便、敏感、实用的诊断H.pylori感染的方法.     

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。     

幽门螺杆菌感染与儿童功能性消化不良的关系

目的探讨幽门螺杆菌(H.pylori)感染对功能性消化不良(FD)儿童症状、病理及胃排空的影响。方法FD儿童110例,H.pylori阴性组30例,H.pylori阳性组80例,H.pylori阳性组按不同的治疗方案分A组(吗丁啉组)30例,B组(H.pylori根除 吗丁啉治疗后复查H.pylori转阴者)42例。比较各组症状积分、胃窦粘膜病理积分和胃液体排空情况。结果H.pylori阳性组饱胀和食欲下降症状重于阴性组(P<0.05),根除H.pylori后上述症状明显改善。H.pylori阳性组胃窦液体排空慢于阴性组,根除H.pylori后排空加快(P<0.05)。结论H.pylori感染是FD患儿的致病因素之一,H.pylori感染可能影响FD儿童的胃排空,根除H.pylori可改善胃排空从而减轻临床症状。     

广西壮族、仫佬族和越南中部京族儿童幽门螺杆菌感染与HLA-DQA1相关性的研究

目的 探讨广西罗城县壮族、仫佬族儿童与越南中部京族儿童间幽门螺杆菌(helicobacter pylori,Hp)感染与人类白细胞抗原DQAl(HLA-DQAl)等位基因位点的关系。方法(1)广西罗城县壮族儿童54名,仫佬族儿童76名,平均年龄11岁;京族儿童109名,平均年龄13岁。采用间接酶联免疫吸附法(ELISA)检测血清抗Hp—IgG抗体,采用免疫印迹法检测血清中Hp空泡毒素、毒素相关蛋白及尿素酶抗体;(2)采用聚合酶链反应-序列特异引物(PCR-SSP)方法对3个民族儿童的HLA—DQAl等位基因进行检测,并采用疾病关联分析法进行HLA-DQAl等位基因分布与Hp感染检测结果相关性分析。结果 (1)越南中部京族儿童Hp阳性率(39％)明显低于广西壮族及仫佬族儿童(65％、58％,P<0.01);(2)广西壮族、仫佬族儿童及越南京族儿童HLA-DQAl*0104等位基因频率在Hp阳性儿童人群均高于Hp阴性儿童(P<0.01),相对风险度分别为5.57、4.18及3.45。结论(1)广西壮族、仫佬族儿童的Hp感染率高于越南中部京族儿童;(2)3个民族的Hp阳性和阴性儿童在HLA—DQAl*0104等位基因上存在差异,HLA—DQAl*0104等位基因可能是Hp感染的易感基因。     

儿童发作性睡病的诊断及人类白细胞抗原在诊断中的意义

目的　　探讨儿童发作性睡病的诊断依据和人类白细胞抗原 (HLA)Ⅱ类等位基因在诊断中的意义。方法　对 4 0例发作性睡病患儿的临床资料进行分析。所有患儿接受了多次小睡潜伏时间试验 (MSLT)。应用PCR序列特异性引物体外基因扩增 (PCR -SSP)方法测定HLA -DRB1及DQB1等位基因 ,并与本室对北京地区 91名正常人检测的数据进行比较。结果　本组 4 0例 ,平均病程 6 5个月 ,≤ 3个月者 14例 ( 30 % )。 4 0例患儿均有过度或发作性睡眠 ,37例伴猝倒 ,2 2例伴入睡幻觉 ,6例伴睡眠瘫痪。本组MSLT平均睡眠潜伏期 <5min ,异常快速眼动 (REM )睡眠平均 2～ 5( 4 33± 0 2 6 )次。异常REM睡眠潜伏期为 0 2 5～ 4 9( 4 0± 1 8)min。本组HLA -DRB1 15 0 1阳性率为 0 4 38,较对照组 ( 0 115 )高 ,DQB1 0 6 0 1阳性率为 0 0 2 5 ,较对照组 ( 0 0 93)低。本组 35例为DRB1 15 0 1及DQB1 0 6 0 2均阳性 ,2例为DRB1 15 0 2及DQB1 0 6 0 1均阳性 ,余 3例患儿DRB1 15和DQB1 0 6均为阴性。结论　本病诊断可依据其临床表现 ,MSLT测试结果 ,并除外其他可解释这些症状的躯体或精神方面疾病。DRB1 15 0 1及DQB1 0 6 0 2为发作性睡病易感基因 ,HLA-DRB1 15检测结果阴性者 ,不能排除本病     

Five- to 7-year-old children with Helicobacter pylori infection are smaller than Helicobacter-negative children: a cross-sectional population-based study of 3,315 children.

OBJECTIVE: To test whether Helicobacter pylori-positive children are smaller and weigh less than H pylori-negative children. DESIGN: Cross-sectional population-based study. PARTICIPANTS: In 3,315 5-to 7-year-old preschool and school children, the putative influence of H pylori infection on growth was investigated. Standing height and weight were analyzed in relation to H pylori infection. The diagnosis of H pylori infection was established by 13C-urea-breath test. RESULTS: The prevalence of H pylori infection in boys was 7.2% (95% confidence interval, 5.9-8.9; n = 1,550) and in girls was 6.1% (95% confidence interval, 4.9-7.3; n = 1,552) H pylori-positive children were smaller than noninfected children (117.6 +/- 5.5 cm vs. 118.9 +/- 5.7 cm; P < 0.01). Although H pylori-positive boys were 2.06 cm smaller than H pylori-negative boys (117.4 +/- 5.6 cm vs. 119.5 +/- 5.7 cm; P < 0.001), the difference in girls was not significant (117.9 +/- 5.3 cm vs. 118.4 +/- 5.7 cm). When standing height was adjusted for age, the found differences were more pronounced. Differences between the infected and noninfected children with regard to body weight were not significant (22.4 +/- 4.0 kg vs. 22.1 +/- 4.0 kg), nor was there a significant difference with regard to body-mass index. However, boys with H pylori infection had a lower weight than noninfected boys (21.6 +/- 3.3 kg vs. 22.6 +/- 4.0 kg; P < 0.01), but in girls, these differences were not observed (22.2 +/- 4.0 vs. 22.8 +/- 4.6 kg, respectively). When weight was adjusted for age, H pylori -positive children also had a lower weight than H pylori -negative children because of the lower weight of boys. CONCLUSIONS: H pylori infection is associated with growth delay, growth retardation, or both in affected children.     

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目的探讨儿童幽门螺杆菌vacA基因型并分析各基因亚型与胃十二指肠疾病的关系。方法对80例H·pylori感染的儿童,采用PCR法扩增胃黏膜vacA基因亚型。结果南宁儿童H·pylorivacA基因型有s1a/m1和s1a/m2两种组合,基因频率分别为3·75%、66·25%。vacA基因各亚型在慢性浅表性胃炎及消化性溃疡中的检出率差异无显著性(P>0·05)。结论s1a/m2为南宁地区儿童幽门螺杆菌的vacA优势基因型。部分患儿同时感染多株不同vacA基因型H·pylori。vacA基因各亚型不能作为南宁地区儿童H·pylori菌株毒力强弱的指标。     

Endoscopic nodular gastritis: an endoscopic indicator of high-grade bacterial colonization and severe gastritis in children with Helicobacter pylori

OBJECTIVE: To investigate the significance of endoscopic nodular gastritis associated with Helicobacter pylori infection. METHODS: This prospective study included 185 children (50.8% boys) aged 1 to 12 years (mean, 6.9 +/- 3.0 years) who underwent upper intestinal endoscopy during evaluation of chronic abdominal pain. The authors assessed the endoscopic appearance of the stomach, noting those patients with endoscopic nodular gastritis. Urease activity of gastric mucosal biopsies was measured. With histologic examination, the presence and density of H. pylori organisms, the presence of follicular gastritis, the nature of inflammation, and the gastritis activity grade and overall gastritis score were assessed. RESULTS: H. pylori infection was identified in 50 children (27%). Endoscopic nodular gastritis was significantly associated with active chronic gastritis and follicular gastritis. Nodularity in the stomach showed a high specificity (98.5%) and positive predictive value (91.7%) for the diagnosis of H. pylori infection and was observed in 22 of 50 (44%) H. pylori-positive patients and in 2 of 135 (1.5%) H. pylori-negative patients. A significant association was observed between older age and the prevalence of this finding (P< 0.001). There was a significant increase in endoscopic nodular gastritis with increased H. pylori density and a positive correlation (Pearson coefficient = 0.97) with increased gastritis score on histologic examination. Increase in gastritis score was dependent on increased H. pylori density in patients with gastric nodularity; this finding was independent of age. CONCLUSIONS: Endoscopic findings of antral nodularity in children suggest the presence of H. pylori infection and follicular gastritis and may identify cases of severe gastritis and marked bacterial colonization.     

Testing for serum IgG antibodies to Helicobacter pylori cytotoxin-associated protein detects children with higher grades of gastric inflammation.

BACKGROUND: Little information is available about the relationships between Helicobacter pylori cytotoxin-associated protein (CagA) and clinicopathologic features in children. The purpose of this study was to test whether determining serum IgG antibodies to CagA is a useful tool for detecting more severe disease. METHODS: One hundred twenty-seven consecutive children (age range, 0.75-17.8 years; median, 9.4 years) referred for gastroscopy were included in the study. Antral and corpus biopsies were taken for gastric histology and H. pylori detection. Major symptoms and endoscopic findings were recorded. A serum sample was drawn from each child and assayed for IgG antibodies CagA by a commercial enzyme-linked immunosorbent assay. RESULTS: Sixty-three (50%) children had no evidence of H. pylori infection, 28 (22%) were H. pylori positive/CagA positive, and 36 (28%) were H. pylori positive/CagA negative. There were no differences in clinical diagnosis and occurrence of any predominant symptom according to H. pylori and CagA status. Findings of antral nodularity were more frequent (p = 0.003) in H. pylori-positive/CagA-positive children than in H. pylori-positive/CagA-negative children. The gastritis score was significantly higher in H. pylori-positive/CagA-positive children than in H. pylori-positive/CagA-negative children (5.7 +/- 1.9 vs. 3.8 +/- 1.6, respectively; p = 0.0003), either in the antral (p = 0.0002) or in the corpus (p = 0.001) mucosa. Inflammation (p = 0.0001) and activity (p = 0.0001) scores were both higher in H. pylori-positive/CagA-positive children than in H. pylori-positive/CagA-negative children, but the H. pylori density score was not significantly different (p = NS). In no case was normal gastric mucosa found in H. pylori-positive/ CagA-positive children. Lymphocytic gastritis (p = 0.0008) and lymphoid follicles (p = 0.000003) were a more frequent finding in H. pylori-positive children than in H. pylori negative children, irrespective of CagA status. CONCLUSION: Testing for serum IgG to CagA detects higher grades of gastric inflammation among children with H. pylori infection. It may be useful in targeting H. pylori-positive/ CagA-positive children for antimicrobial therapy while reducing the need for endoscopy and gastric biopsy.     

The association between Helicobacter pylori infection and height in children from an urban community in north-east Brazil

BACKGROUND: An association between Helicobacter pylori infection and short stature in children has been described recently. AIM: To describe differences in stature between H. pylori-infected and non-infected children in a low-income community in north-east Brazil. METHODS: H. pylori status was evaluated by 13C-urea-breath test; centile values for weight and height were calculated for each child. RESULTS: The prevalence of H. pyloni was 55.8% (197/353) and increased with age. Of 197 H. pylori-positive children, 62% were below the 25th centile for height compared with 48% of H. pylori-negative children (75/156) [AOR (adjusted odds ratio) 1.61, 95% CI 1.04-2.49, p=0.03] after adjustment for variables with p < 0.25 in univariate analysis (gender, number of residents, of children per household and of persons per bed). These results were significant only when older children were included. Thus, in children aged 8-14 years, 80% (89/111) of H. pylori-positive were <25th centile for height compared with 63% (35/56) of H. pylori-negative children (p=0.01). Compared with children with a height >25th centile, the AOR for H. pylori infection increased from 2.42 in the crude analysis to 6.62 after adjustment (p=0.006). CONCLUSIONS: H. pylori is associated with short stature in older children living in a poor urban community in Brazil.     

Alleles of HLA-DQB1 and familial aggregation of type 1 diabetes

The HLA complex, located on the short arm of chromosome 6, is the strongest genetic marker for type 1 diabetes (T1DM). In previous study we demonstrated association between genes HLA-DRB1 and HLA-DQB1 and T1DM in the Polish population. There is a strong-independent association of alleles HLA-DRB1*0401 and DQB1*302, despite population linkage disequilibrium among alleles of these genes. The aim of the current study was to verify a hypothesis that some alleles or haplotypes of HLA-DRB1, DQA1 and DQB1 genes increase the risk for familiar aggregation of T1DM. We analysed 507 patients with IDDM derived from 80 multiplex and 325 patients from simplex families. PCR and hybridisation with SSO probes performed HLA typing for DRB1, DQA1 and DQB1 alleles. Genetic analysis demonstrated strong association of allele HLA-DQB1*0302 with T1DM in the Polish population in families with single (DM1) and more numerous cases (DM2) cases, compared with healthy cases (n=103). The HLA-DQB1*302 allele frequencies were 27.8% vs 8.7%; Pc<10(-5); OR(95%CI)=4,03(3.80-4.25) and 16.3% vs 8.7%; Pc<0.04; OR(95%CI)=2.04(1.79-2.89), respectively. The presence of allele HLA-DQB1*0602 has a strong protective effect from T1DM in both studied groups (1.46% vs. 13.6%; Pc<10(-5); OR(95%CI)=0.09(-0.25-0.44) and 0.98% vs. 13.6%; Pc<10(-5); OR(95%CI)=0.06(-0.46-0.58), respectively. Interestingly, HLA-DRB1*04 allele more often co-segregated with DM2 families as comparing the DM1 group (31.0% vs. 15.8%, respectively; Pc<10(-5)). However in both cases differences remain significant as compared to controls: Pc<10(-5), OR (95%CI)=3.52(3.33-3.70) and Pc<10(-5) OR(95%CI)=6.17(5.97-6.37), for DM1 and DM2 respectively. Subtyping of HLA-DRB1*04 alleles demonstrated that the strongest predisposing effect has been identified with DRB1*0401. Moreover, difference in frequencies of the protective allele HLA-DQB1*0301 among DM1 and DM2 group was revealed (8.8% vs. 13.7%, respectively; Pc<10(-5)) and the protective effect of this allele remained only significant in DM1 group: 8.8% vs. 19.9%; Pc<10(-5); OR(95%CI)=0.39(0.19-0.58). The results suggest that it is likely that familial aggregation of T1DM is associated with lower frequency of protective alleles of HLA-DQB1 gene.     

Helicobacter pylori antigens in stool specimens of gastritis children before and after treatment

BACKGROUND: Various testing methods are successfully applied to the diagnosis of Helicobacter pylori infection, but noninvasive techniques are still needed for therapeutic monitoring, especially in children. In the search for new noninvasive techniques for the diagnosis of H. pylori infection, the authors evaluated an enzyme immunoassay for the detection of H. pylori antigen in stool (HpSA). METHODS: The authors studied 62 H. pylori-positive children with chronic gastritis and 45 control subjects. H. pylori infection was diagnosed using cultures and histology of gastric biopsy specimens and a stool antigen test before treatment (clarithromycin, amoxicillin, omeprazole for 7 days) and 4 weeks to 6 weeks after treatment. RESULTS: Before therapy, antigen in stool was detected in 55 of 62 H. pylori-positive patients, which indicates that the sensitivity of the HpSA test was 88.7%. Of the 45 control subjects (with negative culture and histology results), 43 had negative results for H. pylori in the stool test (specificity, 95.5%). After completion of therapy, eradication was obtained (and confirmed by culture and histology) in 53 of the 62 H. pylori-positive children (85.5%). Four weeks to 6 weeks after eradication therapy, the sensitivity, specificity, positive predictive value, and negative predictive value of the stool antigen (HpSA) test were 88.9%, 96.2%, 80%, and 98%, respectively. CONCLUSIONS: The accuracy of the HpSA test for the detection of H. pylori in human stool 4 weeks to 6 weeks after treatment is comparable with the accuracy of the culture results. The stool antigen (HpSA) test was found to be a useful method for posttreatment eradication testing of infection in children.