心房颤动与C反应蛋白

目的:探讨心房颤动(房颤)与C反应蛋白(CRP)的关系。方法:选择135例房颤患者为房颤组,另选取同期住院的非房颤患者111例作为对照组,用速率散射免疫比浊法测定CRP,采用非参数秩和检验。结果:房颤组与对照组在影响CRP的主要因素上相匹配。房颤组CRP中位数(1.44mg/dl)与对照组CRP中位数(1.50mg/dl)相比无明显差异,P>0.05。器质性房颤CRP中位数(1.76mg/dl)明显高于特发性房颤中位数(1.06mg/dl),P<0.01,有极显著性差异。阵发性房颤CRP中位数为1.37mg/dl,持续性房颤CRP中位数为1.33mg/dl,永久性房颤CRP中位数为2.57mg/dl;三者之间无显著差异。结论:本研究未发现CRP与房颤相关,器质性房颤的CRP高于特发性房颤可能与器质性疾病本身有关。     

老年不同类型房颤患者同型半胱氨酸及C反应蛋白水平的变化

目的观察不同类型老年房颤患者血浆同型半胱氨酸(Hcy)、C反应蛋白(CRP)水平,探讨其与房颤的关系。方法选择住院的老年房颤患者83例,其中30例阵发性房颤,28例持续性房颤,25例永久性房颤患者,窦性心律30例(对照组),分别检测患者血清中Hcy、CRP水平,同时应用超声心动图测定各组左心房内径(LAD),并对各指标作相关性分析。结果 1血清Hcy、CRP及LAD值永久性房颤、持续性房颤组、阵发性房颤组均高于对照组,永久性房颤组及持续性房颤组高于阵发性房颤组(均P0.05);2房颤患者LAD与Hcy、CRP呈正相关。结论炎症和氧化应激可能参与了左心房的电重构及结构重构,并促进了房颤的发生、发展。     

单纯疱疹病毒感染与心房颤动的相关性研究

目的观察单纯疱疹病毒(HSV)感染与心房颤动(房颤)的相关性。方法严格筛选103例孤立性房颤患者,分为阵发性房颤组74例和持续性房颤组29例,从流行病学对照研究队列中选取72例未合并房颤的健康人群作为对照组。空腹采集静脉血,用ELISA法按试剂盒标准流程检测血清HSV1 IgG抗体、HSV2 IgG抗体水平;运用相关分析探讨患者血清高敏C反应蛋白(hs-CRP)水平与HSV1 IgG抗体、HSV2 IgG抗体滴度的关系。结果对照组、阵发性房颤组和持续性房颤组的血清HSV1 IgG抗体水平分别为(217.95±53.18)μg/ml、(304.76±57.58)μg/ml和(322.99±60.35)μg/ml,血清HSV2 IgG抗体水平分别为(307.25±64.02)μg/ml、(407.22±59.1)μg/ml和(406.63±50.67)μg/ml,hs-CRP水平分别为(2.16±0.70)mg/L、(3.90±0.59)mg/L和(3.90±0.63)mg/L;对照组的血清HSV1 IgG抗体、HSV2 IgG抗体、hs-CRP水平均显著低于阵发性房颤组和持续性房颤组(均P0.001);阵发性房颤组与持续性房颤组的血清HSV1 IgG抗体、HSV2 IgG抗体、hs-CRP水平比较,差异均无统计学意义(均P0.05)。血清HSV IgG抗体水平与hs-CRP水平呈正相关关系(rHSV1=0.532,P0.001;r_(HSV2)=0.446,P0.001)。结论房颤患者的血清HSV IgG抗体水平显著升高,且与血清hs-CRP水平呈正相关。     

非瓣膜性心房颤动患者血清C-反应蛋白变化及其临床意义

目的测定非瓣膜性心房颤动(简称房颤)患者血清C-反应蛋白及外周血白细胞的变化,以探讨炎症机制在非瓣膜性房颤的发生发展中的作用。方法对135例房颤患者(房颤组)和120例非房颤患者(对照组),采用免疫比浊法测定其血清中CRP水平,用库尔特JT血球仪测定外周血白细胞数(WBC)、中性粒细胞百分率(N%)、中性粒细胞绝对值(N)、淋巴细胞百分率(L%)、淋巴细胞绝对值(L)。应用超声心动图诊断左室肥厚(LVH)及左房内径(LAD)。观察CRP及白细胞变化与房颤关系。结果房颤组血中CRP水平显著高于非房颤组(6.41±2.73mg/Lvs3.66±1.18mg/L;P<0.05)。其中房颤合并LVH较不合并LVH组CRP显著增高(7.51±3.32mg/Lvs5.76±2.92mg/L;,P<0.05)。四分位法研究表明房颤组血清CRP水平位于最高四分位者显著多于对照组;房颤组血清CRP水平位于最高四分位者较同组最低四分位者显著增加(P<0.05)。CRP位于最高四分位者LAD较位于最低四分位者显著增加(P<0.05)。两组WBC、N%、N、L%、L无显著性差异。结论慢性炎症反应在非瓣膜性房颤的发生发展中可能起到重要的作用。     

幽门螺杆菌感染与慢性阻塞性肺疾病的关系及其对肺功能的影响

目的观察幽门螺杆菌(Hp)感染与慢性阻塞性肺疾病(简称慢阻肺)的关系及其对肺功能的影响。方法选择稳定期慢阻肺患者200例,测定肺功能,检测血清抗Hp-IgG及抗CagA-IgG水平,并与120例正常人对照,观察COPD并发Hp感染情况及其对肺功能的影响。结果与健康对照组相比,慢阻肺患者抗Hp-IgG及抗Hp-CagAIgG阳性率及表达水平明显升高(P均0.05)。与未感染Hp的慢阻肺患者相比,感染Hp的慢阻肺患者第1秒用力呼气量(FEV_1)、FEV_1占预计值比值(FEV_1/pre)、第一秒用力呼气量占用力肺活量的比值(FEV_1/FVC)明显降低(P均0.05)。不同严重程度慢阻肺患者抗Hp-IgG、抗Hp-CagAIgG阳性率及表达水平差异有统计学意义(P均0.05)。结论 Hp感染与慢阻肺关系密切,可能是参与并加重慢阻肺的重要因素。     

心房颤动患者幽门螺旋杆菌感染的发生率及相关因素分析

目的探讨心房颤动(简称房颤)患者幽门螺旋杆菌(Hp)感染的情况及相关因素。分析超敏C反应蛋白(Hs-CRP)、白细胞介素-6(IL-6)、血脂(TC、TG、LDL-C、HDL-C)、胱抑素C(Cysc)以及左房内径(LAD)与房颤的相关性。方法选取房颤组患者69例,室上性心动过速(简称室上速)组患者50例,同时选取健康志愿者50例作为正常组,各组均行14C呼气试验,比较各组Hp阳性率。检测房颤组及室上速组两组Hs-CRP、IL-6、血脂、Cysc、LAD。结果房颤组Hp阳性率(56.5%,39/69)明显高于室上速组(34.0%,17/50)及正常组(30.0%,15/50)(P0.0167),室上速组与正常组比较Hp阳性率无显著差异(P0.05)。房颤组Hs-CRP(3.65 mg/L)、IL-6(6.66ng/L)、Cysc(1.33mg/L)中位数分别明显高于室上速组(1.06、2.77、0.97 mg/L)(P0.05),TC(3.69±0.97)、LDL-C(2.13±0.76)、HDL-C(中位数0.99mmol/L)均低于室上速组(4.31±0.96、2.43±0.73、1.09)(P0.05),LAD明显大于室上速组[(44.25±9.26)mm vs(28.87±4.85)mm,P0.05)],TG中位数与室上速组比较无显著差异(P0.05)。结论幽门螺旋杆菌感染、炎症、TC、LDL-C、HDL-C与房颤存在相关性。     

C反应蛋白与心房颤动的关系

目的探讨C反应蛋白(CRP)作为系统炎症因子在心房颤动发生和发展中的作用。方法入选98例患者将其分为正常对照组(n=34)、阵发性房颤组(n=31)和持续房颤组(n=33),比较各组C反应蛋白水平。结果心房颤动组CRP水平[(1.85±0.44)mg/d]比正常对照组的水平[(0.41±0.13)mg/d]高,P<0.01;在心房颤动组中持续房颤组血清中CRP[(2.02±0.54)mg/d]高于阵发性房颤组[(1.55±0.40)mg/d],P<0.01,阵发性房颤组[(2.02±0.54)mg/d]高于正常对照组(0.41±0.13)mg/dl,P<0.01。并且不同原因引起的房颤CRP不同,冠心病最高,其次为高血压,心肌病最低。结论CRP在心房颤动患者中明显升高,说明炎症状态在心房颤动的发生和持续中起一定作用。     

心房颤动发病相关因素的临床研究

目的探讨幽门螺杆菌(Helicobacter pylori,Hp)感染、高敏-CRP(High sensitivity C-reactiveprotein,Hs-CRP)水平、左心房内径(Lef tatriumdiameter,LAD)与房颤的相关性。方法回顾性分析2007年1月至2012年12月在我院住院治疗的房颤患者262例,非房颤患者115例;所有病例均行13C呼气试验测定、血浆幽门螺杆菌抗体(HpIgG)测定、Hs-CRP水平测定及超声心动检查。结果①心房颤动组13C呼气试验幽门螺杆菌、hs-CRP、左心房内径阳性率明显高于非心房颤动组(p<0.05);②心房颤动组13C呼气试验幽门螺杆菌感染δ值、hs-CRP以及左心房内径水平明显高于非心房颤动组(p<0.05);③首发房颤、阵发性房颤、持续性房颤、长程持续性房颤以及永久性房颤5个亚组分别两两比较:永久性房颤组Hpδ值高于初发房颤组、阵发性房颤组及持续性房颤组(p<0.05);永久性房颤组hs-CRP水平高于首发房颤组、阵发性房颤组及持续性房颤组(p<0.05);长程持续性房颤组hs-CRP水平高于首发房颤组、阵发性房颤组(p<0.05);永久性房颤组左心房内径水平高于首发房颤组、阵发性、持续性房颤组(p<0.05);④综合HP感染、hs-CRP、左心房内径及其他危险因素后,发现Hp≥4‰、hs-CRP>5mg/L以及左心房内径≥36mm与心房颤动较强的相关性(p<0.05)。结论 HP感染、hs-CRP升高、左心房内径增大均可反应房颤的发生率;Hp≥4‰、hs-CRP>5mg/L、左心房内径≥36mm均是患者心房颤动的敏感指标。     

原发性高血压患者颈动脉粥样硬化与幽门螺杆菌感染的相关性研究

目的探讨原发性高血压(EH)患者颈动脉粥样硬化(CAS)与幽门螺杆菌(Hp)感染的相关性。方法选择2012—2013年我院收治的EH患者150例为EH组,同期在我院体检健康者50例为对照组。检测两组受试者的颈动脉内膜中层厚度(CAIMT)、幽门螺杆菌抗体(Hp-IgG)、血脂及血清高敏C反应蛋白(hs-CRP)、同型半胱氨酸(HCY)水平。结果根据CAIMT和Hp-IgG检查结果将EH组患者分为CAIMT增厚组89例和CAIMT非增厚组61例,Hp感染组67例和Hp非感染组83例。EH组CAIMT1.0 mm者所占比例(59.3%)和Hp-IgG阳性者所占比例(44.7%)均高于对照组(12.0%,28.0%)(P0.05)。CAIMT增厚组Hp-IgG阳性者所占比例(55.1%)高于CAIMT非增厚组(29.5%)(P0.05),Hp感染组CAIMT1.0 mm者所占比例(73.1%)高于Hp非感染组(48.2%)(P0.05)。直线相关分析结果显示,CAIMT增厚与Hp感染率呈正相关(r=0.787,P0.01)。Hp感染组血清TG、TC、LDL-C、HCY、hs-CRP高于Hp非感染组,HDL-C水平低于Hp非感染组(P0.01)。结论 EH患者CAS的发生与Hp感染有关,Hp感染可能通过影响机体炎性反应、血脂代谢及HCY水平促进CAS的发生和发展,清除或预防Hp感染可能是防治EH患者发生CAS的策略之一。     

NLRP3炎症小体与心房颤动的相关性研究

目的:通过检测心房颤动(房颤)患者外周血NLRP3的表达水平,探讨NLRP3炎症小体与房颤的相关性。方法:选择2014-06至2016-03我院收治的房颤患者60例,其中阵发性房颤(PAF)组30例,非阵发性房颤(n PAF)组30例,26例健康体检者作为正常对照组。收集3组的临床资料,利用流式细胞术检测外周血单核淋巴细胞(PBMCs)中NLRP3表达水平,利用酶联免疫吸附法(ELISA)检测血清白细胞介素(IL)-1β、IL-6、C反应蛋白(CRP)及N末端B型利钠肽原(NT-pro BNP)水平。比较3组间各指标差异,通过线性回归进行指标的相关性分析。结果:(1)PAF组和n PAF组患者外周血PBMCs中NLRP3、IL-1β、IL-6、CRP水平均高于正常对照组(P均0.05),但PAF组和n PAF两组患者间NLRP3表达水平差异无统计学意义(P0.05)。(2)PAF组和n PAF组患者NT-pro BNP水平均高于正常对照组(P均0.05),PAF组和n PAF组间比较差异有统计学意义(P0.05)。(3)房颤患者(PAF组和n PAF组)外周血PBMCs中NLRP3水平与左心房内径(LAD)呈正相关(r=0.579,P0.05),与左心室射血分数(LVEF)呈负相关(r=-0.490,P0.05)。结论:(1)NLRP3炎症小体与房颤密切相关,可能为房颤临床治疗的重要干预靶点。(2)房颤与炎症反应关系密切。(3)可能通过NLRP3炎症小体的下游相关炎症因子产生炎症反应,导致心肌重构或电重构进而诱发房颤的产生、发展。     

人巨细胞病毒在冠心病发病中的意义及致病机制的研究

目的 :探讨人巨细胞病毒 (HCMV)在冠心病 (CHD)发病中的意义及可能的致病机制。方法 :对 CHD(80例 )包括急性冠状动脉事件患者 (A组 ,5 9例 )和症状稳定患者 (B组 ,2 1例 ) ,和非 CHD患者 (对照组 ,2 6例 )进行外周血 HCMV- Ig M、Ig G、C-反应蛋白 (CRP)检测。结果 :HCMV - Ig M阳性率、Ig G阳性率、CRP阳性率及CRP均值在 CHD组与对照组间差异有显著性意义 (P <0 .0 5 ) ,在 A组与对照组间差异有非常显著性意义 (P<0 .0 1) ,而 B组与对照组间差异无显著性意义 (P>0 .0 5 )。CRP均值在急性心肌梗死中明显高于不稳定心绞痛(P <0 .0 5 )。 A组中 HCMV- Ig M与 CRP间存在相关性 (r =0 .336 )。结论 :HCMV的感染与激活在 CHD的急性冠状动脉事件发病中具有一定意义 ,其发病机制与急性炎症反应有关。外周血 HCMV- Ig M及 CRP检测可作为急性冠状动脉事件早期诊断指标之一 ,定量 CRP检测可作为病情发展判断指标之一。     

C-Reactive protein elevation predicts the occurrence of atrial structural remodeling in patients with paroxysmal atrial fibrillation

It has been poorly understood whether inflammation may contribute to atrial structural remodeling and increase the propensity for atrial fibrillation (AF) to persist. We investigated the relationship between C-reactive protein (CRP) elevation and the development of atrial remodeling in AF. The study population comprised 50 consecutive paroxysmal AF (PAF) patients and 50 control patients without AF. All patients underwent echocardiography, and high-sensitivity CRP was routinely measured. C-Reactive protein was significantly higher in the patients with PAF than control patients (0.231 ± 0.176mg/dl vs 0.055 ± 0.041mg/dl, P < 0.001). Other predictors of elevated CRP included left ventricular mass (P < 0.05), left ventricular end-systolic diameter (P < 0.05), and left atrial (LA) diameter (P < 0.001). In a multivariate analysis, only CRP and LA diameter were independent predictors of PAF. Elevated CRP levels correlated with LA diameter (r = 0.489, P < 0.001). Left atrial diameter was increased in PAF patients compared with control patients (P < 0.001). We found that a longer duration of AF is associated with higher CRP levels and a larger LA diameter (duration <30 days: CRP 0.166 ± 0.139mg/dl, LA diameter 38.4 ± 8.0mm; duration >30 days: CRP 0.345 ± 0.181mg/dl, LA diameter 45.6 ± 6.6mm; P < 0.001). In conclusion, longer AF duration is associated with CRP elevation and atrial structural remodeling, as approximated by larger LA diameter. However, CRP elevation, while correlating with LA diameter, was not an independent predictor of atrial structural remodeling. Thus, it remains unclear whether CRP and the inflammatory state are contributory to LA remodeling or whether LA remodeling or AF induces elevation in CRP and inflammation.     

Helicobacter pylori and Alzheimer's disease: a possible link

BACKGROUND: Although serological findings indicate the presence of a relationship between Helicobacter pylori (HP) and vascular disease, no data have been reported about a possible association of HP with dementia. The aim of the present study was to determine whether chronic HP infection might play a role in Alzheimer's disease (AD). METHODS: Plasma homocysteine level, serum folate and vitamin B(12) concentrations, plasma pyridoxal phosphate level, IgG and IgA antibodies to HP, and C-reactive protein (CRP) were determined in 30 AD patients, 30 patients affected by vascular dementia (VaD), and 30 control subjects. All patients and control subjects were matched for age, educational level, and nutritional and socioeconomic status. None of the subjects had a history of chronic gastritis, peptic ulcer, gastric cancer, or major abdominal surgery. RESULTS: HP-IgG level was significantly increased in VaD patients as compared to controls and AD patients, while AD patients had HP-IgG levels higher than those of normal controls. HP-IgA levels were equally increased in both VaD and AD patients. CRP was higher in AD patients than in VaD patients and controls, although CRP levels in VaD patients were also significantly increased. CONCLUSIONS: The present study found an association between HP infection and AD. The question remains as to whether this association is due to the ubiquity of HP, or whether it contributes to the neuroinflammatory process in AD. The relationship between HP and AD, if confirmed by additional studies with a greater number of patients, may have important clinical and therapeutic implications.     

C-reactive protein and atrial fibrillation: "evidence for the presence of inflammation in the perpetuation of the arrhythmia"

BACKGROUND: Atrial fibrillation (AF) is associated to a high risk of systemic embolism. The mechanisms that contribute to thrombogenesis in these patients are still poorly understood. Systemic and/or local inflammation could be involved in the process of thrombogenesis and contribute to the perpetuation of the arrhythmia. The purpose of the study was to evaluate the role of inflammation and its relation to thrombogenesis and cardiac rhythm in AF. METHODS: We prospectively studied 130 patients with newly diagnosed non-valvular AF in absence of antithrombotic therapy. Determinations of C-reactive protein (CRP) and thrombin-antithrombin complex (TAT) plasma levels, along with a transesophageal echocardiogram were performed in all the patients at admission. RESULTS: Mean age of the group was 67+/-14 years. CRP levels were significantly elevated in AF patients versus controls (matched by age, gender and cardiovascular risk factors) (1.0+/-1.8 versus 0.3+/-0.4 mg/dl, respectively, p<0.01). Baseline TAT levels were also significantly elevated in AF patients but no correlation was found between CRP and TAT. At 1-year of follow-up, mean CRP levels were still elevated in patients that remained in AF compared to those who converted to sinus rhythm (1.2+/-1.8 compared to 0.5+/-1.5 mg/dl, p=0.03). CRP was the only biochemical predictor of sinus rhythm maintenance at 1-year follow-up independently of clinical (including adjustment for risk factors and antiarrhythmic drugs), biochemical and echo parameters. CONCLUSIONS: There is evidence for the presence of inflammation in patients with non-valvular AF, which is not related to activation of the coagulation cascade. The persistence of inflammation is associated with chronic AF at 1-year follow up.     

幽门螺杆菌感染及其毒力与急性心肌梗死、血浆纤维蛋白原及血栓素B2的关系

目的　探讨幽门螺杆菌 (Hp)感染及其不同毒力与心肌梗死的关系。 方法　测定 5 1例急性心肌梗死 (AMI组 )和 42例陈旧性心肌梗死 (OMI组 )患者及 3 1例冠脉造影正常者 (对照组 )的Hp特异性抗体 (HpIgG、HpIgM )及其细胞毒素相关蛋白特异性抗体浓度 ,并同步观察血浆纤维蛋白原 (Fg)、血栓素B2 (TXB2 )变化及其与Hp感染的相关性。结果　AMI组HpIgG、HpIgM阳性率及平均浓度 (或OD值 )明显高于对照组 (P <0 .0 5 ) ;校正冠心病危险因素前、后 ,HpIgG阳性与AMI均具有相关关系。AMI组Fg、TXB2 明显高于对照组、OMI组。AMI组中Hp阳性者Fg、TXB2 明显高于Hp阴性者 (P <0 .0 5 )和OMI组中Hp阳性者 (P <0 .0 0 1) ;调整冠心病的危险因素前、后 ,IgG与Fg均呈正相关 (P <0 .0 5 )。 结论　Hp感染与AMI、Fg、TXB2 之间存在明显的相关性 ,不同毒力的Hp感染与冠心病心肌梗死的关系无显著性差异     

The HMG-CoA reductase inhibitor atorvastatin prevents atrial fibrillation by inhibiting inflammation in a canine sterile pericarditis model

OBJECTIVE: It has been recently reported that AF is associated with tissue inflammation. Statins reduce C-reactive protein (CRP) levels. However, the effect of statin on atrial fibrillation (AF) is unclear. The purpose of the present study was to evaluate the effect of statin on AF in a canine sterile pericarditis model. METHODS: Sterile pericarditis was created in 20 dogs randomly assigned to two groups: a control group (10 dogs) and an atorvastatin treatment group (10 dogs). Atorvastatin was administered orally (2 mg/kg/day) beginning 1 week before the operation until the end of the study. Before and 2 days after the operation, CRP levels, the duration of induced AF, the atrial effective refractory period (AERP), and intra-atrial conduction time were determined. RESULTS: Before the operation, there were no significant differences in any of the parameters between the two groups. On the second postoperative day, the atorvastatin group had a lower CRP level (7.6+/-0.5 versus 11.7+/-1.3 mg/dl, P<0.0001), a shorter AF duration (177+/-57 versus 534+/-189 s, P<0.0001), a longer AERP (138+/-6 versus 130+/-6 ms, P<0.01), and a shorter intra-atrial conduction time (46+/-3 versus 51+/-5 ms, P<0.01) than the control group. CONCLUSIONS: Atorvastatin can prevent maintenance of AF by inhibiting inflammation in the canine sterile pericarditis model. Atorvastatin may thus be a novel therapeutic agent for AF.     

Relation between Helicobacter pylori infection, thyroid hormone levels and cardiovascular risk factors on blood donors

The aim of this study was to assess the relationship between Helicobacter pylori (Hp) infection, serum thyroid hormone levels and certain cardiovascular risk factors in normal volunteers. In 110 blood donors (85 men, 25 women, aged 35.6 +/- 9.76) the serum levels of IgG antibodies against Hp were estimated using a sensitive immunoassay. Serum estimation of T3, T4, TSH, FT3, FT4, thyroid (microsomial) autoantibodies, C-Reactive-Protein, a1-acid-glycoprotein, vitamin B12, folic acid, cholesterol, triglycerides, total lipids, HDL, LDL, and antibodies against hepatitis A, was also carried-out. In all subjects a number of clinicoepidemiological parameters including body mass index, smoking habits, educational level, number of siblings and presence of symptoms from the digestive system were carefully recorded. Statistical analyses were performed using the SPSS statistical package. Helicobacter pylori infection was found in 54 subjects (49.1%). On univariate analysis, significant differences between subjects positive and negative for Helicobacter pylori infection were found for FreeT3 (3.11 +/- 0.5 pmol/ vs. 3.42 +/- 0.8 pmol/l, P=0.025), FreeT4 (1.04 +/- 0.2 ng/dl vs. 1.17 +/- 0.3 ng/dl, P=0.025), and thyroid autoanti bodies (23.65 +/- 24 vs. 14.97 +/- 8, P=0.018). Significant differences were also found for Cholesterol (207.8 +/- 39 mg/dl vs. 193.3 +/- 40 md/dl, P=0.05), LDL (133.2 +/- 32 mg/dl vs. 119.6 +/- 40 mg/dl, P=0.05) and folic acid (7.66 +/- 3.7 ng/ml vs. 6.39 +/- 2.5 ng/ml, P=0.038). A significantly positive correlation of Hp infection with age and number of siblings and a negative one with educational level were noticed. No differences concerning the levels of acute phase proteins, vitamin B12, antibodies against hepatitis A, body mass index, and smoking habits were found. On logistic regression analysis, significant differences remained only for thyroid autoantibodies (Odds ratio for titer ?30: 7.8, P=0.012), age (Odds Ratio for those aged >40 years vs those aged <40 years: 3.8, P=0.022) and educational level (Odds ratio for elementary 8.7 and moderate 5.1 vs higher education, P=0.003 and P=0.011 respectively). It is concluded that a relationship exist between Hp infection and the presence of high titers of thyroid autoantibodies in blood donors. There are no indications of the existence of a relationship between Hp infection with thyroid hormone levels, lipid concentrations and other cardiovascular risk factors.     

The relationship between Helicobacter pylori IgG titre and coronary atherosclerosis

OBJECTIVES: The role of Helicobacter pylori (HP) in the progression of atherosclerosis is controversial. We investigated the relation between HP IgG antibody titres and severity and intensity of coronary atherosclerosis and also clinical presentation of coronary artery disease (CAD). METHODS: The patient group consisted of 353 patients with angiographically proven CAD, which contains 3 different subgroups: 163 patients with myocardial infarction (MI), 106 patients with unstable angina (USAP) and 84 patients with stable angina (SAP). Control group included 163 subjects with angiographically proven normal coronary arteries. Helicobacter pylori IgG antibody titres were measured by an enzyme immunoassay method in all patients. Gensini and Extent scores were used to evaluate the angiographic severity and extent of atherosclerosis. C-reactive protein levels were measured by Behring nephelometry system kits. RESULTS: Seropositivity rates for HP were similar between groups (82.7% in the patient group and 86.6% in the control group (P > 0.05)). Also HP-IgG levels were similar among the MI, USAP and SAP groups. No significant correlation was observed between CRP levels and HP-LgG level titres. There was no significant correlation between HP-IgG level (r = 0.086, P = 0.2) and Gensini score but a significant poor correlation was observed between HP-IgG level and Extent score (r = + 0.156, P = 0.03). CONCLUSIONS: Helicobacter pylori IgG titres do not play an important role in the presentation of CAD and do not increase systemic inflammatory response. However, Helicobacter pylori IgG antibody titres may be correlated with the extent of CAD.