结核分枝杆菌黏附素(HBHA)对小鼠结核病免疫治疗作用的实验研究

目的 探讨结核分枝杆菌粘附素(HBHA)对小鼠结核病实验模型的免疫治疗作用.方法 取在改良罗氏培养基上生长良好的结核分枝杆菌H37Rv两周培养物,制备成均匀菌悬液,每只小鼠尾静脉注射菌量为106 CFU.于感染2周后,分别对CPG组30 ug、HBHA组5 ug、CpG+ HBHA组(CpG 30 ug和HBHA 5 ug)及对照组腹腔注射生理盐水.于感染后4周脱颈处死小鼠,称取小鼠体重、肺脏和脾脏重量,对肺和脾组织进行菌落计数,观察肺病理改变.结果 各实验组肺组织的重量与体重和对照组相比稍有偏大,菌落计数中发现HBHA免疫治疗组明显优于空白对照组,在病理切片中对照组小鼠肺组织有大片肉芽肿形成,病理损害严重.其它各组肺部病变呈弥散分布,但病变程度明显轻于对照组,在抗酸染色中空白对照组有大量的抗酸杆菌存在,其它各组相对明显减少.结论 实验结果表明HBHA对治疗小鼠结核病变模型起一定的作用.     

不同感染途径和接种菌量对建立SD大鼠结核菌感染模型的影响

目的探讨建立SD大鼠结核病模型的方法,比较不同感染途径和接种菌量在建立SD大鼠结核病动物模型的影响。方法用标准人型结核菌株H_(37)Rv 0.1、1、10 mg 3种接种菌量分别经尾静脉和腹腔途径注入SD大鼠。6周后剖杀大鼠,并比较肺、肝、脾的脏器质量指数,观察肺、肝、脾大体病变和镜下特点,肺、肝、脾的组织匀浆涂片做抗酸染色及结核菌培养。结果肺、肝、脾组织切片HE染色见不同程度增殖性结核结节。随着接种量的增加,其脏器组织病理改变越显著。肺、肝、脾组织切片抗酸染色见炎性结节及多核巨细胞内散乱排列的红色短小抗酸杆菌。接种菌量一致的情况下,尾静脉感染组肺、肝、脾组织病理改变较腹腔感染组显著,肺、肝、脾组织匀浆的结核分枝杆菌培养阳性率较腹腔感染组高(P<0.05)。结论建立SD大鼠肝、脾、肺结核杆菌感染模型,尾静脉感染途径优于腹腔感染途径。SD大鼠对结核菌敏感,可作为结核病实验的动物模型。     

不同感染途径和接种菌量对建立SD大鼠结核菌感染模型的影响

目的　探讨建立SD大鼠结核病模型的方法 ,比较不同感染途径和接种菌量在建立SD大鼠结核病动物模型的影响。方法 用标准人型结核菌株H₃₇Rv 0.1、1、10 mg 3种接种菌量分别经尾静脉和腹腔途径注入SD大鼠。6周后剖杀大鼠,并比较肺、肝、脾的脏器质量指数,观察肺、肝、脾大体病变和镜下特点,肺、肝、脾的组织匀浆涂片做抗酸染色及结核菌培养。结果 肺、肝、脾组织切片HE染色见不同程度增殖性结核结节。随着接种量的增加,其脏器组织病理改变越显著。肺、肝、脾组织切片抗酸染色见炎性结节及多核巨细胞内散乱排列的红色短小抗酸杆菌。接种菌量一致的情况下,尾静脉感染组肺、肝、脾组织病理改变较腹腔感染组显著,肺、肝、脾组织匀浆的结核分枝杆菌培养阳性率较腹腔感染组高（P<0.05）。结论 建立SD大鼠肝、脾、肺结核杆菌感染模型,尾静脉感染途径优于腹腔感染途径。SD大鼠对结核菌敏感,可作为结核病实验的动物模型。     

结核分枝杆菌L型的垂直感染及其对子代小鼠的影响

目的　研究结核分枝杆菌L型的垂直感染及其对子代小鼠的影响。方法　将C5 7BL/ 6N小鼠 (雌∶雄 3∶2 )随机分成 4组 ,分别用自肺癌患者血中分离的结核分枝杆菌L型 (B组 ) ,牛型分枝杆菌 (A组 )及其L型 (C组 )经尾静脉进行感染 ,并用生理盐水注射组作为对照 ,观察感染鼠子代新生鼠和子代成年鼠的病理学改变 ,同时采用培养法、IK抗酸染色和免疫组织化学技术检查组织内的抗酸杆菌及其L型。结果　感染鼠的肺、肝、肾、脑、心等主要脏器组织均发生间质性炎症 ,并有多只小鼠伴有肝脏和卵巢的瘤样增生。新生子鼠中 ,A和B组有间质性炎症表现 ,B组有一例肝瘤样增生 ,C组有一例畸胎 ,组织内有多种形态的分枝杆菌L型 ;成年子鼠中A组有两只良性畸胎瘤。结论　血源性结核分枝杆菌L型和牛型分枝杆菌L型仍有一定的致病性并可能诱导肿瘤发生。通过垂直感染 ,结核分枝杆菌L型可导致子代小鼠的病变。     

母牛分枝杆菌菌苗预防老龄小鼠肺结核的动物实验研究

目的探讨母牛分枝杆菌菌苗对实验性老龄小鼠肺结核的免疫预防作用。方法老龄C57BL/6J小鼠30只,随机法分为3组:即无免疫保护组、母牛分枝杆菌菌苗预防组(微卡组)、卡介苗(BCG)预防组,分别给予生理盐水0.1ml、母牛分枝杆菌菌苗22.5μg、BCG 0.1 mg皮内注射。4周后将浓度为5×10⁵/ml的H37Rv标准菌株0.2ml经小鼠尾静脉给予攻毒。感染6周后处死小鼠,流式细胞仪测定小鼠外周血T淋巴细胞亚群、观察肺脏肺泡巨噬细胞内结核分枝杆菌数、肺脏中活结核分枝杆菌定量培养及肺组织病理学分析。结果微卡组和卡介苗组的CD4T淋巴细胞、CD4/CD8比值分别为(48.81±3.10、3.84±0.37),(48.08±3.72、4.16±0.24)均较无免疫保护组(38.97±3.03、3.25±0.26)显著升高(p<0.01)。而微卡组CD4/CD8比值则低于卡介苗组(p<0.05)。微卡组和卡介苗组的肺脏肺泡巨噬细胞内结核分枝杆菌数、肺脏中活结核分枝杆菌定量培养分别为(2.3±0.5(、1.06±0.25)×10⁵cfu),(2.7±0.6(、1.21±0.37)×10⁵cfu)无免疫保护组(5.4±0.9、(4.07±0.97)×10⁵cfu)减少(p<0.01)。组织病理学显示微卡组和卡介苗组肺脏结核病变以增殖性结核结节为主,无坏死结节;无免疫保护组肺脏则以淋巴细胞结节、坏死结节为主。结论母牛分枝杆菌菌苗可增强CD4T淋巴细胞活性,对实验性老龄小鼠肺结核有较好的预防作用。     

沿海地区11例手部分枝杆菌感染分析

目的探讨沿海地区手部非结核分枝杆菌感染的体外培养技术和要领,为临床确诊,治疗提供直接证据。方法对2001年6月—2004年9月收治的28例可疑手部分枝杆菌感染作组织块匀浆后的涂片抗酸染色,分枝杆菌培养,分枝杆菌生化分型,分枝杆菌的核酸测序分型。结果分枝杆菌培养阳性11例,具体为海分枝杆菌占8例,偶发1例,鸟1例,结核1例,其中直接抗酸染色检查阳性2例。结论手部慢性可疑分枝杆菌感染患者应同时做抗酸染色及分枝杆菌培养。非结核分枝杆菌感染尤其是海分枝杆菌远比结核分枝杆菌常见,是沿海地区手部非典型感染的主要致病因素。在分枝杆菌培养时必须同时在30℃、35℃两种温度下进行培养。     

结核分枝杆菌感染小鼠模型的建立与评价

目的建立结核分枝杆菌感染的小鼠模型,分析感染小鼠重量指数、组织荷菌量、组织病理改变随感染时间的变化。方法以1.1×10^5菌落形成单位（CFU）的结核分枝杆菌标准株H37Rv经尾静脉感染50只雌性BALB/c小鼠,于感染后1、2、3、4、8周杀鼠,每个时间点剖杀10只,观察肺组织病理改变并称重,计算重量指数,同时做肺和肝菌落计数。结果感染1、2、3、4、8周小鼠的肺脏器重量指数分别为0.0112±0.0036、0.0101±0.0071、0.0112±0.0046、0.0151±0.0057和0.0198±0.0069,差异有统计学意义（F=4.24,P〈0.01）;肝脏器重量指数分别为0.0558±0.0059、0.0591±0.0094、0.0569±0.0076、0.0582±0.0030和0.0619±0.0079,差异无统计学意义（F=0.86,P〉0.05）;脾脏器重量指数分别为0.0107±0.0034、0.0146±0.0060、0.018±0.0034、0.0174±0.0026和0.0204±0.0066,差异有统计学意义（F=4.01,P〉0.05）;肺菌落数分别为（4.472±0.504）log、（5.539±0.429）log、（6.294±0.478）log、（6.250±0.315）log和（6.836±0.196）log,差异有统计学意义（F=43.90,P〈0.01）。感染后1周小鼠肺组织可见病理改变,且随着感染时间的增加病变范围逐渐扩大,病变程度逐渐严重。结论成功建立了结核分枝杆菌感染小鼠模型,该模型可用于结核疫苗和药物研究。     

CpG寡脱氧核苷酸促进小鼠清除体内结核分枝杆菌的机制

目的 探讨CpG寡脱氧核苷酸(CpG-ODN)增强小鼠体内结核分枝杆菌清除能力的可能机制.方法 将雌性BALB/c小鼠随机分为免疫组36只和对照组24只,并分别腹腔注射CpG-ODN 30 μg(溶于200 μl生理盐水)和200 μl生理盐水.2周后每只小鼠经尾静脉注射结核分枝杆菌H37Rv 1×106 CFU.感染后3周和4周每组分别处死12只小鼠,免疫组小鼠饲养至感染后6周处死.肺和脾组织进行菌落计数,观察肺和脾组织的病理学变化.用实时定量聚合酶链反应方法检测肺和脾组织γ-干扰素、白细胞介素(IL)-4、IL-10、IL-12、IL-18和诱导型一氧化氮合酶(iNOS)mRNA表达的相对含量.组间比较采用t检验.结果 感染后3周,免疫组小鼠的肺和脾组织经培养后无结核分枝杆菌生长.感染后4周,免疫组小鼠的肺和脾组织培养后有结核分枝杆菌生长,但明显少于对照组;肺组织中IL-18、γ-干扰素和iNOS的mRNA表达的相对含量分别为(3.6±0.5、0.32±0.14和23.2±4.7),均明显高于对照组的(1.6±1.1、0.20±0.10和16.2±5.1),IL-12p40 mRNA表达的相对含量(5.7±0.6)明显低于对照组(14.5±1.9),IL-4和IL-10 mRNA表达的相对含量(0.30±0.09和0.28±0.05)与对照组(0.26±0.05和0.29±0.08)无明显差别;脾组织中IL-18、γ-干扰素和iNOS mRNA表达的相对含量(5.5±1.3、0.52±0.07和9.1±1.8)明显高于对照组(0.8±0.4、0.21±0.06和6.0±1.4),IL-12p40、IL-4和IL-10 mRNA表达的相对含量(2.1±0.3、0.23 ±0.10和0.10±0.04)明显低于对照组(5.1±0.4、1.21±0.26和0.57±0.13).与感染后4周比较,免疫组小鼠感染后6周,肺组织γ-干扰素mRNA表达的相对含量(0.95±0.27)明显增高,IL-18、IL-4和IL-10 mRNA表达的相对含量(3.51±0.86、0.45±0.35和0.24±0.21)无明显变化,IL-12p40和iNOS mRNA表达的相对含量(1.72±1.41和1.1±0.5)明显降低;脾组织IL-12p40和IL-18 mRNA表达的相对含量(0.08±0.02)和(0.11±0.03)明显降低,IL-10 mRNA表达的相对含量(0.39±0.11)明显增高,γ-干扰素、IL-4和iNOS mRNA表达的相对含量(0.63±0.32、0.30±0.16和8.4±2.7)无明显变化.结论 CpG-ODN增强小鼠清除体内结核分枝杆菌的能力与IL-18、γ-干扰素和iNOS的表达增强及IL-4和IL-10的表达抑制密切相关.     

结核分枝杆菌低剂量感染小鼠模型的建立与分析

目的 建立结核分枝杆菌低剂量感染的小鼠模型,分析感染小鼠组织荷菌量、组织病理随感染时间的动态变化。 方法 以100 菌落形成单位(CFU)的结核分枝杆菌标准株H37Rv经尾静脉途径感染雌性C57BL/6J小鼠40只,于感染后1、3、5、8、12、16、20、24周取材,每个时间点5只小鼠,脾、肺组织匀浆培养检测脾脏组织的荷菌量,脾脏、肺脏及肝脏组织经HE染色分析病理变化。 结果 小鼠感染后3周脾脏荷菌量达到（4.97±0.19）lg CFU,在感染后5周下降至（3.64±0.22）lg CFU,至感染后8周降到最低的（2.75±0.23）lg CFU;感染后3周肝、脾、肺等脏器出现病理改变,感染5周时病变加重,感染8周时病变自然减轻。 结论 成功建立了结核分枝杆菌低剂量感染小鼠模型,为结核分枝杆菌慢性持续感染或潜伏感染的研究可提供有用的工具。     

沿海地区11例手部分枝杆菌感染分析

目的探讨沿海地区手部非结核分枝杆菌感染的体外培养技术和要领，为临床确诊，治疗提供直接证据。方法对2001年6月－2004年9月收治的28例可疑手部分枝杆菌感染作组织块匀浆后的涂片抗酸染色，分枝杆菌培养，分枝杆菌生化分型，分枝杆菌的核酸测序分型。结果分枝杆菌培养阳性11例，具体为海分枝杆菌占8例，偶发1例，鸟1例，结核1例，其中直接抗酸染色检查阳性2例。结论手部慢性可疑分枝杆菌感染患者应同时做抗酸染色及分枝杆菌培养。非结核分枝杆菌感染尤其是海分枝杆菌远比结核分枝杆菌常见，是沿海地区手部非典型感染的主要致病因素。在分枝杆菌培养时必须同时在30℃、35℃两种温度下进行培养。     

Autophagic flux without a block differentiates varicella-zoster virus infection from herpes simplex virus infection

Autophagy is a process by which misfolded and damaged proteins are sequestered into autophagosomes, before degradation in and recycling from lysosomes. We have extensively studied the role of autophagy in varicella-zoster virus (VZV) infection, and have observed that vesicular cells are filled with >100 autophagosomes that are easily detectable after immunolabeling for the LC3 protein. To confirm our hypothesis that increased autophagosome formation was not secondary to a block, we examined all conditions of VZV infection as well as carrying out two assessments of autophagic flux. We first investigated autophagy in human skin xenografts in the severe combined immunodeficiency (SCID) mouse model of VZV pathogenesis, and observed that autophagosomes were abundant in infected human skin tissues. We next investigated autophagy following infection with sonically prepared cell-free virus in cultured cells. Under these conditions, autophagy was detected in a majority of infected cells, but was much less than that seen after an infected-cell inoculum. In other words, inoculation with lower-titered cell-free virus did not reflect the level of stress to the VZV-infected cell that was seen after inoculation of human skin in the SCID mouse model or monolayers with higher-titered infected cells. Finally, we investigated VZV-induced autophagic flux by two different methods (radiolabeling proteins and a dual-colored LC3 plasmid); both showed no evidence of a block in autophagy. Overall, therefore, autophagy within a VZV-infected cell was remarkably different from autophagy within an HSV-infected cell, whose genome contains two modifiers of autophagy, ICP34.5 and US11, not present in VZV.VZV induces macroautophagy (hereafter referred to as autophagy) in skin cells within the typical exanthem associated with either primary VZV infection (varicella or chickenpox) or VZV reactivation (herpes zoster or shingles). During prior studies, the extent of autophagy was gauged by enumeration of autophagosomes by both 2D and 3D microscopy (1, 2). The usual number of autophagosomes seen by 3D animation was 100 per infected cell, but sometimes approached 200 per cell. In contrast, a typical nonstressed cell usually has fewer than 4 autophagosomes (3, 4). When monolayers were inoculated with VZV-infected cells, the traditional method for VZV infection, autophagy was again easily seen after enumeration of autophagosomes and immunoblotting for the LC3-phosphatidylethanolamine conjugate (LC3-II). Again these results suggested that autophagic flux was present during VZV infection in cultured cells.As part of a more extensive assessment of autophagy after VZV-induced cellular stress, we have now investigated autophagy in infected human skin xenografts from the SCID mouse model of VZV infection. This model is the most accurate representation of the skin manifestation of varicella in the human host (5, 6). Finally, we addressed an important point about the nature of VZV-induced autophagy. Because the number of autophagosomes seen in the human vesicle cells from varicella and herpes zoster patients is so high, the question has arisen whether there is a late block in the maturation of autophagosomes to autolysosomes. In this report, we demonstrate that (i) autophagy induced by VZV infection is related to the overall stress to the cell, namely, a higher inoculum leads to greater autophagy; and that (ii) autophagosomes induced during VZV infection mature into autolysosomes without an obvious block before final maturation. The autophagic flux assay results confirm that VZV infection induces autophagy that proceeds to completion, possibly allowing the cell to alleviate the cellular stress caused by the viral infection (7). In previous work, we showed that inhibition of autophagy led to a significant decrease in VZV titer. Overall, therefore, autophagy within a VZV-infected cell is remarkably different from autophagy within an HSV-infected cell, an alphaherpesvirus whose genome contains two modifiers of autophagy, ICP34.5 and US11 (8–13). In contrast, autophagy appears to be proviral in the life cycle of VZV.     

Delta-agent infection in Taiwan

Based on observations of a limited number of patients, delta (δ) infection has been reported to be infrequent in Taiwan. To further evaluate the role of δ-infection in patients with hepatitis B virus (HBV) infection, serum samples of 493 subjects with acute and chronic HBV infections collected in 1976–85 were studied for anti-δ by radioimmunoassay. Intrahepatic δ-antigen was also studied by immunofluorescence in 12 anti-δ-positive patients. The overall prevalence of δ-infection was 4.7%, consistent with previous studies. δ-Infection had an even yearly distribution in the last decade. However, there were four groups with significantly higher frequencies: (i) 24% of 41 anti-HBe-positive patients with chronic active hepatitis (CAH); (ii) 21% of 14 HBsAg carriers with prominent lobular hepatitis; (iii) two of three HBsAg carriers with intravenous drug abuse; and (iv) two of seven with fulminant hepatitis. On the other hand, δ-infection was uncommon in patients with chronic persistent hepatitis, cirrhosis, hepatocellular carcinoma, classical type B hepatitis, submassive necrosis and asymptomatic HBsAg carriers. δ-Antigen was found in only two patients with CAH; one progressed to cirrhosis, and the other had disease regression on follow-up. Overall, at least half of the δ-superinfected HBsAg-positive patients had a non-progressive course on follow-up.
It was concluded that δ-agent was introduced to Taiwan before 1976. Although it has played a role in some clinical settings of HBV infections, it is generally infrequent in Taiwan. The δ-superinfection apparent in half the patients studied seems to have a non-progressive course.     

Helicobacter pylori infection and drugs malabsorption

Drug absorption represents an important factor affecting the efficacy of oral drug treatment.Gastric secretion and motility seem to be critical for drug absorption.A causal relationship between impaired absorption of orally administered drugs and Helicobacter pylori(H.pylori)infection has been proposed.Associations have been reported between poor bioavailability of l-thyroxine and l-dopa and H.pylori infection.According to the Maastricht Florence Consensus Report on the management of H.pylori infection,H.pylori treatment improves the bioavailability of both these drugs,whereas the direct clinical benefits to patients still await to be established.Less strong seems the association between H.pylori infection and other drugs malabsorption,such as delavirdine and ketoconazole.The exact mechanisms forming the basis of the relationship between H.pylori infection and impaired drugs absorption and/or bioavailability are not fully elucidated.H.pylori infection may trigger a chronic inflammation of the gastric mucosa,and impaired gastric acid secretion often follows.The reduction of acid secretion closely relates with the wideness and the severity of the damage and may affect drug absorption.This minireview focuses on the evidence of H.pylori infection associated with impaired drug absorption.     

Prevention of Helicobacter pylori infection in childhood

Helicobacter pylori(H.pylori)infection is one of the most common infections worldwide.Although infection rates are falling in the developed and developing countries,H.pylori is still widespread in the world.This article has reviewed the important publications on H.pylori in childhood with a focus on its evolving transmission route and the source of infection and preventive strategies in childhood,PubMed was searched up to identify eligible studies.Relevant publications were searched using the following.     

Helicobacter pylori infection in older people

Since the discovery of Helicobacter pylori(H.pylori)infection as the major cause of gastroduodenal disorders three decades ago,H.pylori has been the focus of active research and debate in the scientific community.Its linkage to several diseases,such as peptic ulcer disease,gastritis and gastric malignancy is incontestable.In particular,it has been noticed that,as the aged population is increasing worldwide,older people are at increased risk of developing several gastroduodenal diseases and related complications.At the same time,gastric cancer is definitely more frequent in elderly than in adult and young people.In addition,it has been showed that peptic ulcer and related complications occur much more commonly in aged individuals than in young people,resulting in a significantly higher mortality.Although this infection plays a crucial role in gastrointestinal disorders affecting all age groups and in particular older people,only a few studies have been published regarding the latter.This article presents an overview of the epidemiology,diagnosis,clinical manifestations and therapy of H.pylori infection in elderly people.     

Review: Diagnosis of Helicobacter pylori infection

A number of diagnostic tests have been developed for the detection of H. pylori. Diagnostic techniques can be divided into invasive and noninvasive methods. The invasive methods require upper gastrointestinal endoscopy and involve culture of gastric biopsy specimens, examination of stained biopsies and detection of urease activity in the biopsies themselves. In addition, we have developed endoscopic diagnosis of H. pylori infection in gastric mucosa using phenol red dye-spraying. The noninvasive methods include urea breath test and serological techniques. Although there has been considerable improvement in the techniques, a combination of at least two different techniques should be used in order to optimize the diagnostic yield. We recommend the use of one rapid test in the combination. The rapid urease test, cytology and the phenol red dye-spraying endoscopy give results available before the patient leaves the endoscopy suite.     

Prediction of Plasmodium falciparum placental infection according to the time of infection during pregnancy

Malarial infection during pregnancy leads to placental infection, a known risk factor for low birth weight. Whether the stage of pregnancy at infection has a differential influence on these effects is not clearly known, but may be of importance for prevention strategies, including intermittent preventive treatment of pregnant women. Malaria infection during early (before 20 weeks), middle (20-28 weeks), or late (after 28 weeks) pregnancy was evaluated by logistic regression and receiver operating characteristics analysis in relation to placental infection in pregnant Senegalese women. Plasmodium falciparum infections during late pregnancy are strongly related to placental infection, as well as those that occur in middle pregnancy. Knowledge of parasitological events over the entire duration of pregnancy permits a highly accurate prediction of placental infection. Not only malaria infections during late pregnancy increase the likelihood of placental infection. The current policy of intermittent preventive treatment of pregnant women, which implies an initial antimalarial cure after 20 weeks of pregnancy, will not avoid early infections. An earlier initiation of malaria prevention might improve its efficacy.     

Helicobacter pylori infection - recent developments in diagnosis

Considering the recommended indications for Helicobacter pylori (H. pylori) eradication therapy and the broad spectrum of available diagnostic methods, a reliable diagnosis is mandatory both before and after eradication therapy. Only highly accurate tests should be used in clinical practice, and the sensitivity and specificity of an adequate test should exceed 90%. The choice of tests should take into account clinical circumstances, the likelihood ratio of positive and negative tests, the cost-effectiveness of the testing strategy and the availability of the tests. This review concerns some of the most recent developments in diagnostic methods of H. pylori infection, namely the contribution of novel endoscopic evaluation methodologies for the diagnosis of H. pylori infection, such as magnifying endoscopy techniques and chromoendoscopy. In addition, the diagnostic contribution of histology and the urea breath test was explored recently in specific clinical settings and patient groups. Recent studies recommend enhancing the number of biopsy fragments for the rapid urease test. Bacterial culture from the gastric biopsy is the gold standard technique, and is recommended for antibiotic susceptibility test. Serology is used for initial screening and the stool antigen test is particularly used when the urea breath test is not available, while molecular methods have gained attention mostly for detecting antibiotic resistance.     

Consequences of Helicobacter pylori infection in children

Although evidence is emerging that the prevalence of Helicobacter pylori (H. pylori) is declining in all age groups, the understanding of its disease spectrum continues to evolve. If untreated, H. pylori infection is lifelong. Although H. pylori typically colonizes the hu-man stomach for many decades without adverse con-sequences, children infected with H. pylori can manifest gastrointestinal diseases. Controversy persists regarding testing (and treating) for H. pylori infection in children with recurrent a...     

Metabolic consequences of Helicobacter pylori infection and eradication

Helicobacter pylori(H.pylori)is still the most prevalent infection of the world.Colonization of the stomach by this agent will invariably induce chronic gastritis which is a low-grade inflammatory state leading to local complications(peptic ulcer,gastric cancer,lymphoma)and remote manifestations.While H.pylori does not enter circulation,these extragastric manifestations are probably mediated by the cytokines and acute phase proteins produced by the inflammed mucosa.The epidemiologic link between the H.pylori infection and metabolic changes is inconstant and controversial.Growth delay was described mainly in low-income regions with high prevalence of the infection,where probably other nutritional and social factors contribute to it.The timely eradication of the infection will lead to a more healthy development of the young population,along with preventing peptic ulcers and gastric cancer An increase of total,low density lipoprotein and high density liporotein cholesterol levels in some infected people creates an atherogenic lipid profile which could promote atherosclerosis with its complications,myocardial infarction,stroke and peripheral vascular disease.Well designed and adequately powered long-term studies are required to see whether eradication of the infection will prevent these conditions.In case of glucose metabolism,the most consistent association was found between H.pylori and insulin resistance:again,proof that eradication prevents this common metabolic disturbance is expected.The results of eradication with standard regimens in diabetics are significantly worse than in non-diabetic patients,thus,more active regimens must be found to obtain better results.Successful eradication itself led to an increase of body mass index and cholesterol levels in some populations,while in others no such changes were encountered.Uncertainities of the metabolic consequences of H.pylori infection must be clarified in the future.