胃幽门螺杆菌感染与口臭的相关性研究

目的:探讨胃幽门螺杆菌感染与口臭发生的相关性。方法:选取48例口臭患者为研究对象,另选取96例无口臭的健康志愿者为无口臭组,通过13C呼气试验检测所有研究对象幽门螺杆菌的感染情况,比较两组幽门螺杆菌的感染率。根据是否感染幽门螺杆菌分为感染组和无感染组,比较两组口臭的发生率,分析幽门螺杆菌感染与口臭发生的相关性。结果:口臭组和非口臭组患者幽门螺杆菌的感染率分别为79.17%,27.08%,口臭组显著高于无口臭组,差异有统计学意义(x2=35.16,P0.05)。口臭与幽门螺杆菌的感染显著相关(r=0.4)。幽门螺杆菌感染组患者和未感染组口臭的发生率分别为70.31%和3.75%,感染组显著高于未感染组,差异有统计学意义(x2=70.89,P0.05)。幽门螺杆菌的感染与口臭的发生率显著相关(r=0.69)。结论:幽门螺杆菌感染与口臭的发生有密切的相关性,是引起口臭的一个重要因素。     

慢性乙型肝炎及乙肝肝硬化合并消化性溃疡患者与幽门螺杆菌感染的相关性研究

目的研究慢性乙型肝炎及乙肝肝硬化合并消化性溃疡患者与幽门螺杆菌(Helicobacter pylori,H.pylori)感染的相关关系。方法选择2012年1月至2014年12月宣汉县人民医院收治的慢性乙型肝炎合并消化性溃疡患者108例作为A组,选择同期收治的乙肝肝硬化合并消化性溃疡患者65例作为B组。以快速尿素酶方法检测H.pylori。应用免疫印迹法急性H.pylori抗体分型。结果 A组患者H.pylori阳性率为67.6%,B组患者H.pylori阳性率为24.6%。A组胃溃疡患者H.pylori阳性率为11.4%,十二指肠溃疡患者H.pylori阳性率为94.5%;B组胃溃疡患者H.pylori阳性率为11.5%,十二指肠溃疡患者H.pylori阳性率为33.3%。A组及B组患者中十二指肠溃疡H.pylori感染率均显著高于胃溃疡H.pylori感染率(P0.05)。两组胃溃疡患者的H.pylori阳性率比较差异无统计学意义(P0.05),十二指肠患者的H.pylori阳性率在A、B两组间差异有统计学意义(χ2=48.528,P0.01)。两组患者H.pylori抗体血清分型表达阳性率比较差异无统计学意义(χ2=0.464,P0.05)。结论 H.pylori感染可能是慢性乙肝、乙肝肝硬化消化性溃疡发生的始动因素,尤其在慢性乙肝合并十二指肠溃疡的发病中可能起重要作用,在乙肝肝硬化合并十二指肠溃疡疾病的发病中可能只是其中因素之一。     

幽门螺杆菌感染对冠心病患者血清炎症因子及 颈动脉硬化的影响

目的探讨幽门螺杆菌感染对冠心病患者血清炎症因子及颈动脉硬化的影响。方法选取2015年6月至2017年2月在安康市中心医院治疗的幽门螺杆菌感染冠心病患者(感染组)50例,以及同时期未被幽门螺杆菌感染的冠心病患者(非感染组)50例。对两组患者血清炎症因子及颈动脉硬化程度进行评估。结果幽门螺杆菌感染组患者TC、TG及LDL水平均显著高于非感染组,HDL水平显著低于非感染组,差异均有统计学意义(P0.05);幽门螺杆菌感染组患者TNF-α、IL-8及Hs-CRP水平均显著高于非感染组,差异均有统计学意义(P0.05)。感染组患者颈动脉膜厚度指标CCA-IMT、CB-IMT及CCT-IMT均显著大于非感染组,差异有统计学意义(P0.05)。感染组与非感染组患者稳定斑块的检出率分别为12.00%和10.00%,差异无统计学意义(P0.05),感染组患者不稳定斑块的检出率为48.00%,显著高于非感染组的24.00%,差异有统计学意义(P0.05)。结论幽门螺杆菌感染能显著升高冠心病患者血脂水平,加重机体炎症反应,并增加患者颈动脉中膜厚度及斑块的不稳定性。     

含米诺环素和奥硝唑的四联疗法联合双歧杆菌乳杆菌三联活菌片根除幽门螺杆菌的效果

目的研究含米诺环素及奥硝唑的四联疗法的有效性和安全性,并分析双歧杆菌乳杆菌三联活菌片(金双歧)在幽门螺杆菌根除治疗中的效果,指导临床实践。方法回顾性分析2018年5月至2019年5月福建省立医院收治的101例幽门螺杆菌阳性患者,所有患者均采用艾司奥美拉唑+米诺环素+奥硝唑+铋剂四联方案,其中51例患者联合金双歧治疗,比较各类患者治疗效果及不良反应。通过~(13)C尿素呼气试验评估幽门螺杆菌根除情况。不良反应及临床症状缓解情况通过访谈进行评估。结果 101例患者幽门螺杆菌总根除率为94.06%(95%CI:87.01%～97.56%),共出现不良反应19例,不良反应率为18.81%(95%CI:11.98%～28.07%)。90.10%的患者依从性良好。联合和不联合金双歧的患者其幽门螺杆菌根除率差异无统计学意义(92.2%vs 96.0%,P=0.678 0),临床症状缓解情况差异也无统计学意义(P=0.444 0),但联合金双歧可减少治疗不良反应发生率(P=0.005 0)。结论含米诺环素和奥硝唑的四联疗法是根除幽门螺杆菌有效且耐受性良好的方案。补充金双歧不能提高患者根除率,但可以减少治疗时的不良反应。     

小儿幽门螺旋杆菌感染与缺铁性贫血的相关性分析

目的:分析并探讨小儿幽门螺杆菌感染与缺铁性贫血的相关性。方法:选择2012年2月至2013年2月本院门诊患儿412例,行血常规、血清铁、血清铁蛋白、HP-IgG抗体检测。结果:HP感染患儿IDA26例,IDA患病率为20.4%(26/127),HP未感染患儿IDA19例,IDA患病率为6.7%(19/285)。两者比较差异有统计学意义(x2=17.21,P=0.00)。对比两组患儿MCV、MCH、MCHC指标,差异具有显著性(P均0.05)。45例IDA患儿中26例有HP感染,感染率为57.8%(26/45),367例非IDA患儿中有101例HP感染,感染率为27.5%(101/367)。两者比较差异有统计学意义(x2=17.21,P=0.00)。结论:HP感染同IDA发病有显著相关性,HP感染可以是导致IDA的原因。     

幽门螺杆菌根除治疗对消化性溃疡患者血清胃泌素水平的影响

目的观察幽门螺杆菌(H.pylori)根除治疗对消化性溃疡患者血清胃泌素水平的影响,为该病治疗提供参考。方法选择我院2017年8月至2019年8月收治的120例H.pylori感染的消化性溃疡患者作为观察组,根据H.pylori分型结果进一步分为HPⅠ型组和HPⅡ型组,观察组患者接受根除幽门螺杆菌治疗。选择同期入院的40例非幽门螺杆菌感染消化性溃疡患者作为对照组,对照组患者接受常规治疗。比较两组患者治疗效果、胃镜检查结果、H.pylori清除情况及血清胃泌素、IL-10、IL-17水平。结果HPⅠ型组、HPⅡ型组和对照组患者临床总有效率差异无统计学意义(92.75%、96.08%、97.50%,χ²=1.384,P=0.051)。HPⅠ型组、HPⅡ型组、对照组患者胃镜检查总有效率差异无统计学意义(91.30%,96.08%,97.50%,χ²=1.384,P=0.051)。HPⅡ型组患者幽门螺杆菌根除率高于HPⅠ型组(98.04%vs 85.51%,χ²=4.129,P=0.042)。HPⅠ型组患者治疗后血清胃泌素、IL-10、IL-17水平均高于对照组(均P<0.05)。HPⅠ型组患者治疗后血清IL-10、IL-17水平均高于HPⅡ型组(均P<0.05)。HPⅠ型组与HPⅡ型组患者治疗后血清胃泌素差异无统计学意义(t=1.918,P=0.058)。HPⅡ型组患者治疗后血清IL-10、IL-17水平均高于对照组(均P<0.05)。HPⅡ型组与对照组患者治疗后血清胃泌素差异无统计学意义(t=1.382,P=0.170)。结论不同类型H.pylori感染消化性溃疡患者行幽门螺杆菌根除治疗后临床效果无显著差异。幽门螺杆菌根除治疗可降低消化性溃疡患者血清胃泌素、IL-10、IL-17水平。     

抗病毒治疗乙型肝炎相关慢加急性肝衰竭患者的临床研究

目的:探讨抗病毒治疗乙型肝炎相关慢加急性肝衰竭(acute on chronic liver failure,ACLF)的临床意义。方法:回顾性分析2007年8月~2013年8月我院收治的乙型肝炎相关慢加急性肝衰竭的住院患者80例,按照患者有无接受抗病毒治疗分为抗病毒治疗组(A组)50例和未抗病毒治疗组(B组)30例,分析患者接受治疗后的近期与远期疗效、并发症及生存率。结果:1出院时A组好转率70%;B组好转率33.3%。两组比较差异有统计学意义(x2=10.243,P=0.0010.05)。2治疗14周后A组乙肝病毒DNA阴转率72%;B组阴转率30%,两组比较差异有统计学意义(x2=13.440,P=0.0000.05)。3A组出现细菌感染45例,电解质紊乱41例,消化道出血5例,肝性脑病10例,肝肾综合征10例,B组出现细菌感染30例,电解质紊乱27例,消化道出血6例,肝性脑病10例,肝肾综合征12例,两组比较差异无统计学意义(x2=2.755,P=0.0970.05)。4随访5年,A组存活36例,死亡14例,12、36和60个月累积生存率分别为78.5%、71.2%、71.2%,B组存活5例,死亡25例,12、36和60个月累积生存率分别为35.4%、27.5%、27.5%,两组比较差异有统计学意义(P0.05)。结论:对乙型肝炎相关慢加急性肝衰竭患者给予抗病毒治疗可明显改善预后,提高生存率。     

不同剂量埃索美拉唑三联疗法根除幽门螺杆菌中的疗效观察

目的:研究不同剂量埃索美拉唑的三联疗法根治幽门螺杆菌的临床疗效。方法:选取2012年12月到2014年12月我院收治的幽门螺杆菌阳性胃炎患者100例,按照随机数字表法将患者分为高剂量组(n=50)和低剂量组(n=50),低剂量组给予阿莫西林(1 g/次)+克拉霉素(0.5 g/次)+埃索美拉唑(20 mg/次)治疗,而高剂量组埃索美拉唑改为40 mg/次,疗程均1个月。比较两组幽门螺杆菌清除率,及治疗前后发生反酸、上腹痛和腹胀的临床症状评分以及治疗后不良反应发生情况。结果:高剂量组患者的幽门螺杆菌清除率为92.0%,显著高于低剂量组的70.0%(P0.05);治疗后两组临床症状评分均显著低于治疗前(P0.05),且高剂量组显著低于低剂量组(P0.05);两组不良反应发生率比较差异无统计学意义(P0.05)。结论:高剂量较低剂量埃索美拉唑三联疗法能更有效根除幽门螺杆菌,改善患者的临床症状,且不会增加不良反应,值得在临床上借鉴。     

幽门螺杆菌感染对肝硬化患者高氨血症的影响

目的探讨幽门螺杆菌(Hp)感染对肝硬化患者血氨浓度的影响.方法 51例确诊为Hp阳性的肝硬化患者为阳性组,27例Hp阴性的肝硬化患者为阴性组,40例Hp阳性的消化性溃疡或胃炎患者为对照组.分别检验3组的血氨浓度并进行比较,应用三联法治疗1周,于4周后再测定3组的血氨并进行比较.结果阳性组与阴性组、对照组血氨浓度相比差异有显著性(P＜0.01).阴性组与对照组相比差异无显著性(P＞0.05),阳性组治疗前后血氨浓度变化差异有显著性(P＜0.01).阳性组不同肝功能分级组血氨浓度之间差异有显著性(P＜0.05);阴性组不同肝功能分级组血氨浓度之间差异无显著性(P＞0.05).结论幽门螺杆菌感染可导致肝硬化患者血氨的升高,根除Hp后可使血氨水平明显下降.     

MIF mRNA在胃窦胃癌组织中的表达及其与幽门螺杆菌感染的关系

目的:探讨胃窦胃癌组织中人巨噬细胞移动抑制因子MIF mRNA的表达,并分析其与幽门螺杆菌感染的关系,分析二者在胃窦胃癌发生中的相关性。方法:选取2013年1月至2014年12月于我院收治的胃窦胃癌患者30例作为观察组,另随机选择10例胃窦胃炎患者作为对照组,采用14C-尿素呼气试验(UBT)检测各组患者有无幽门螺杆菌感染,定量逆转录PCR检测观察组患者及对照组患者组织中MIF mRNA表达。统计分析不同组织中MIF mRNA表达与幽门螺杆菌感染之间的关系。结果:观察组组织中MIF mRNA的表达为(1.09±0.11),高于对照组组织的(0.21±0.08),差异具有统计学意义(P0.05)。进一步亚组分析,观察组合并幽门螺杆菌感染组织中MIF mRNA的表达为(1.24±0.14),高于非幽门螺杆菌感染者的(1.09±0.11),差异具有统计学意义(P0.05)。结论:MIF mRNA在胃窦胃癌组织中高表达,幽门螺杆菌感染促进了MIF mRNA的表达,共同促进了胃窦胃癌的发生发展。     

幽门螺杆菌感染与门脉高压性胃病的发病关系

为了解门脉高压性胃病 (portalhypertensivegastropathyPHG)与幽门螺杆菌 (HP)感染的关系 ,选门脉高压性胃病胃窦粘膜 30例 ,免疫组化SP法 (链霉菌抗生物素蛋白—过氧化酶法 ,Streplavidin Peroxidase,SP)抗HP抗体染色 ,并以慢性乙型肝炎并胃病 2 0例及非肝病胃病 2 1例胃窦粘膜作对照。结果显示 ,30例门脉高压性胃病阳性2 2例 ,占 73.3% ;2 0例慢乙肝组阳性 11例 ,占 5 5 % ;2 1例非肝病组阳性 11例 ,占 5 2 .38%。门脉高压组HP感染阳性率与慢乙肝组、非肝病组相比差异无显著性 (P >0 .0 5 )。可见HP感染虽不是门脉高压性胃病的发生原因 ,但在治疗中短期加用杀HP的药物是必要的。     

Helicobacter pylori infection and coronary artery disease

The aim of this investigation was to determine the seroprevalence of H. pylori in patients with coronary artery disease (CAD). Patients with coronary artery disease (n = 90) and control group (n = 90) were enrolled into this randomized, multi-centre study. CAD risk factors analyzed included age, male gender, diabetes mellitus, systemic hypertension, cigarette smoking, hypercholesterolemia and socioeconomic status. The results of this study showed a higher seroprevalence of Helicobacter pylori infection in patients with CAD compared to controls (78.8% versus 58.3%, p < 0.05). However, Helicobacter pylori seropositivity was not associated with coronary artery risk factors (smoking, body mass index, diabetes mellitus, hypertension, total cholesterol and socioeconomic status) either in the whole study population or in the patients and control subjects analyzed separately (P > 0.05). Further study are needed to clarify the precise role of Helicobacter pylori infection on the development of coronary artery disease.     

Effect of H. pylori Infection on Cytokine Profiles and Oxidative Balance in Subjects with Chronic Alcohol Ingestion

Different amounts of ingested alcohol can have distinct effects on the human body. However, there is limited research on chronic alcohol consumption with Helicobacter pylori infection. We sought to investigate the relationship between the cytokine profile, oxidative balance and H. pylori infection in subjects with chronic alcohol consumption. A total of 142 subjects were divided into three groups: 59 subjects with chronic alcohol ingestion and H. pylori infection (group A); 53 subjects with chronic alcohol ingestion without H. pylori infection (group B); and 30 control subjects (group C). The serum levels of CagA, interleukin (IL)-10, E-selectin, TNF-α, malondialdehyde (MDA) and superoxide dismutase (SOD) activity were measured by enzyme-linked immunosorbent assay (ELISA). We found that the ages and serum H. pylori CagA levels among the three groups, as well as both the mean drinking age and the mean daily alcohol consumption between groups A and B, were matched and comparable. Comparing the BMIs among the three groups, the BMI differences were found to be statistically significant (F=3.921, P<0.05). Compared with group C, the BMIs in groups A and B were significantly higher (P<0.001 and P<0.01, respectively); however, the BMI differences between group A and group B were not statistically significant (P>0.05). Additionally, no differences in the serum CagA levels were found in comparisons among the groups (all P>0.05). The serum IL-10 and E-selectin levels in group A were significantly lower than those in group B (serum IL-10: P<0.05; E-selectin: P<0.05). The serum IL-10 in group A was significantly higher than that in group C (P<0.01); the serum E-selectin levels in group A did not significantly differ compared with those in group C (P>0.05). Furthermore, the serum IL-10 and E-selectin levels in group B were significantly higher than those in group C (serum IL-10: P<0.001; E-selectin: P<0.05); however, the serum TNF-α levels did not differ among groups (all P>0.05). Although the serum levels of MDA and SOD in groups A and B were slightly lower than those in group C, there were no significant differences among groups (all P>0.05). In conclusion, we believe that H. pylori infection might cause a significant inhibition of certain cytokine profiles in subjects with chronic alcohol ingestion. Moreover, chronically ingested alcohol may exert an adjusted inflammatory effect, but there was no association between H. pylori infection, chronic alcohol consumption and oxidative balance.     

Detection of serum antibodies against Helicobacter pylori using a chromatographic immunoassay in outpatients

OBJECTIVES: The presence of the antibodies against Helicobacter pylori was tested in 163 subjects (children and adults) in the outpatient department, in the years 2005 and 2006. METHODS: Of the 163 investigated patients 108 (66.3%) were females and 55 (33.7%) were males. The antibodies against Helicobacter pylori were determined by "One Step Helicobacter pylori Test Device (Serum/Plasma)" (ACON Laboratories, Inc.), a rapid, high quality chromatographic immunoassay using human antibodies against IgG immobilized and particles covered with Helicobacter pylori antigen, in contact with the serum of the tested subjects. RESULTS: Of the 163 investigated subjects, 60 (36.8%) presented a positive test suggesting the passage through the infection with Helicobacter pylori. The positive tests were found in adults, 1 case was a boy of 12 years and 5 cases were teenagers between 16 and 18 years. The incidence of the antibodies increased with age. Only 40% of the patients with positive test had a clinical diagnosis of gastritis or gastro-duodenal ulcer, the remaining patients presenting symptoms of chronic hepatitis, cholecystitis or urticaria. CONCLUSIONS: Antibody assay is considered by many authors as a simple, noninvasive, rapid method, applicable in the diagnosis of Helicobacter pylori infection. Other authors asserted that the performance of these assays is less satisfactory and the results should be confirmed by other tests, such as ureea breath test. High levels of antibodies against Helicobacter spp. were encountered in liver and biliary chronic diseases, suggesting a possible role of these bacteria in the development of hepatitis or cholecystitis.     

布拉酵母菌联合奥美拉唑阿莫西林克拉霉素治疗顽固性幽门螺杆菌感染的临床研究

目的 探讨布拉酵母菌联合奥美拉唑阿莫西林克拉霉素三联疗法对幽门螺杆菌(Helicobacter pylori,H.pylori)顽固性感染的治疗效果.方法 将120例H.pylori顽固性感染患者分成两组,分别采用奥美拉唑的三联疗法和布拉酵母菌联合奥美拉唑三联疗法治疗14 d.结果 两组患者治疗14d后,奥美拉唑三联组和布拉酵母菌联合奥美拉唑三联组的H.pylori清除率分别是94.6％和96.6％,两组间差异无统计学意义;在不良反应方面,奥美拉唑三联治疗组中发生16例,明显高于布拉酵母菌联合奥美拉唑三联组的5例(P＜0.05).结论 布拉酵母菌联合奥美拉唑三联治疗方案不仅具有良好的H.pylori清除效果,而且不良反应少,是治疗顽固性H.pylori感染患者比较好的方法.     

复方嗜酸乳杆菌片联合三联方案根除幽门螺杆菌的临床研究

目的探讨复方嗜酸乳杆菌片联合三联方案根除幽门螺杆菌(Helicobacter pylori,H.pylori)的疗效及不良反应。方法将143例H.pylori检测阳性的患者随机分为A1组(48例)、A2组(46例)和B组(49例)。B组给予三联方案(埃索美拉唑、阿莫西林、克拉霉素)根除H.pylori治疗,疗程10d。A1组、A2组分别在上述三联方案的基础上同时加用10d、20d的复方嗜酸乳杆菌片。治疗过程中观察并记录上述三组的不良反应发生情况,停药4周后查13 C呼气试验判别H.pylori根除是否成功。结果共133例患者完成治疗和随访,A1组、A2组、B组根除率按方案(PP)分析分别为65.9%、69.8%、63.0%,按意向性(ITT)分析分别为60.4%、65.2%、59.2%,无论按方案分析还是意向性分析三组根除率差异均无统计学意义(P0.05)。纳入三组的共143例患者均完成不良反应的随访,A1组、A2组、B组不良反应发生率分别为10.4%、8.7%、30.6%,三组相比差异有统计学意义(P0.05),其中A1组、A2组分别与B组相比差异有统计学意义(P0.05),A1组与A2组相比差异无统计学意义(P0.05)。结论三联方案加用10d、20d的复方嗜酸乳杆菌片未能提高H.pylori根除率,但可降低不良反应发生率。     

Molecular assessment of c-H-ras p21 expression in Helicobacter pylori-mediated gastric carcinogenesis

Helicobacter pylori (H. pylori) infection plays a significant role in causing gastric cancer; the exact molecular mechanisms of gastric carcinogenesis have not yet been fully determined. Therefore, this study was planned to examine the role of c-H-ras p21 expression in H. pylori infection at different stages of disease progression from precursor lesions to gastric carcinoma. This study was carried out in 200 patients, consisting of normal gastric mucosa (n = 20), mucosa with chronic gastritis (n = 63), intestinal metaplasia (n = 20), dysplasia (n = 11), and gastric adenocarcinoma (n = 86), in which the H. pylori status have been analysed. The expression of c-H-ras p21 was studied at mRNA as well as protein level using RT-PCR and western blotting, respectively. The localization of c-H-ras p21 was also studied semiquantitatively by immunohistochemistry. The RT-PCR and western blotting results of c-H-ras p21 mRNA and protein expressions were significantly increased in chronic gastritis, intestinal metaplasia, dysplasia, and gastric adenocarcinoma patients, respectively. Immunohistochemical study also showed the increased expression of c-H-ras p21 in the similar way. Overexpression of c-H-ras p21 might be due to H-ras mutation at codon 12 of ras gene family in H. pylori infection. The rate of expression of ras p21 was higher in the H. pylori-infected precursor lesions, chronic gastritis 49/56 (87.5%), intestinal metaplasia 16/17 (94%), and dysplasia 9/11(82%) whereas in the case of H. pylori negative cases these groups, show 12.5, 5.9, and 18.2%, respectively. The data suggested that H. pylori infection may increase the expression of c-H-ras p21 early in the process of gastric carcinogenesis.     

Leiden mutation (as genetic) and environmental (retinoids) sequences in the acute and chronic inflammatory and premalignant colon disease in human gastrointestinal tract.

BACKGROUND: Tumor, calor, dolor, pallor and functio laesa are together involved in the different acute and chronic inflammatory processes. The processes involved in the inflammation are determined by differently acquired and hereditary factors. Recently the presence of a new genetic marker (Leiden point mutation) was found in Crohn's disease and ulcerative colitis. On the other hand, the GI mucosal integrity was proven on gastrointestinal mucosal damage to be produced by different chemicals, xenobiotics, drugs. In human observations, the serum level of retinoids (vitamin A, lutein, zeaxanthin, alpha-, beta-carotene) was proven in patients with chronic gastrointestinal inflammatory bowel disease. The aims of this study were (1) to measure the prevalence of Leiden mutation; (2) to identify the changes in the serum retinoid level in patients with Helicobacter pylori infection of the stomach (n=24), hepatitis C infection (n=75), ileitis terminalis (Crohn's disease; n=49), ulcerative colitis (n=35), colon polyposis (n=59) and adenocarcinoma in colon polyps (n=9), and 57 healthy persons were used in the control group; (3) to compare the directions of the changes in the measured parameters in the acute (H. pylori and hepatitis C infections), chronic (ileitis terminalis, ulcerative colitis) GI inflammatory diseases and in colon polyposis without and with malignisation. METHODS: The Leiden mutation was measured by the method of polymerase chain reaction, the retinoid level in the patient's serum was measured by high liquid cromathografic method (HPCL). RESULTS: (1) It has been found that the prevalence of Leiden mutation increased significantly in patients with ileitis terminalis (P<0.001), ulcerative colitis (P<0.001), colon polyposis (P<0.001) and with colon polyps with malignisation (P<0.01). (2) Serum level of vitamin A and zeaxantin were decreased significantly in all group of patients except for the group with H. pylori infections. (3) alpha- and beta-carotenes were found to be practically at the same level as those in the control groups, except in patients of colon polyps with malignisation. (4) The vitamin A, lutein, zeaxantin, alpha- and beta-carotenes were decreased in patients with ileitis terminalis. CONCLUSIONS: (1) The essential role of retinoids (carotenoids) as environmental factors are suggested for keeping GI mucosal integrity in human healthy subjects and patients. (2) Leiden mutation, as a genetic marker, can be used in the screening of patients with ileitis terminalis, ulcerative colitis and colon polyposis (without and with malignisation). (3) An opposite direction can be found between the increased prevalence of Leiden mutation and decrease of serum levels of retinoids in group of patients with ileitis terminalis, ulcerative colitis and colon polyposis (without and with malignisation).     

Helicobacter pylori Infection in Congestive Gastropathy

Background. This study determines the prevalence and significance of Helicobacter pylori infection in portal hypertensive patients.
Materials and Methods. Patients numbered 118 and consisted of 90 patients with portal hypertension (66 men; 24 women; mean age, 49.1 ± 2.1 years) and 28 noncirrhotic patients with nonucler dyspepsia, (12 men; 16 women; mean age, 47.6 ± 2.8 years), who made up the control group. In all patients, diagnostic upper endoscopy was performed, and gastric biopsies were taken for histological examination and diagnosis of H. pylori.
Results. Of the portal hypertensive patients, 42 (47%) had congestive gastropathy, 11 (26%) of whom were positive for H. pylori. and 48 (53%) did not have gastropathy, 12 (25%) of whom were positive for H. pylori. In the control group, 15 of 28 (54%) were positive for H. pylori. H. Pylori was found less frequently in congestive gastropathy patients than in the control group. We found also that the presence and severity of congestive gastropathy is independent of H. pylori status.
Conclusions. We conclude that the role of H. pylori in the pathogenesis of congestive gastropathy is unlikely, and we suggest that there is no need for its routine eradication in cirrhotic patients.     

Role of noninvasive tests (C-urea breath test and stool antigen test) as additional tools in diagnosis of Helicobacter pylori infection in patients with atrophic body gastritis

BACKGROUND: Detection of Helicobacter pylori infection in atrophic body gastritis (ABG) is difficult, as during progression of body atrophy, H. pylori disappears. AIM: To increase the diagnostic yield of detection of active H. pylori infection in atrophic body gastritis patients by using noninvasive tests such as (13)C-Urea Breath Test ((13)C-UBT) and H. pylori stool antigen test (HpSA) would be useful. PATIENTS: 27 consecutive patients with newly-diagnosed atrophic body gastritis (19F/7M, age 27-73 years). METHODS: Gastroscopy with biopsies (antrum n = 3, body n = 3) and histology according to updated Sydney system, H. pylori IgG serology, (13)C-UBT, and HpSA. RESULTS: All tests used in the diagnosis of H. pylori infection were in agreement in 9/27 atrophic body gastritis patients (33.3%), being all positive in four (14.8%) and all negative in five patients (18.5%). Ten of the 27 (37%) patients were Giemsa stain-positive and serology-positive (group I). Seventeen of the 27 (63%) patients were Giemsa stain-negative: 5/17 with positive serology (group II) and 12/17 with negative serology (group III). In group I, 5/10 (50%) were (13)C-UBT positive and 4/10 (40%) HpSA positive. In group II, two patients were (13)C-UBT positive, but all were HpSA negative. Also in group III, all patients were HpSA negative, but one had a positive (13)C-UBT. CONCLUSIONS: In atrophic body gastritis patients, neither (13)C-UBT nor HpSA per se add useful information regarding active H. pylori infection, but these noninvasive tests may be important in combination with histology and serology to define the H. pylori status in some atrophic body gastritis patients.