An examination of sex and racial/ethnic differences in the metabolic syndrome among adults: A confirmatory factor analysis and a resulting continuous severity score

Objective

The metabolic syndrome (MetS) is typically diagnosed based on abnormalities in specific clustered clinical measures that are associated with increased risk for coronary heart disease (CHD) and Type 2 diabetes mellitus (T2DM). However, current MetS criteria result in racial/ethnic discrepancies. Our goals were to use confirmatory factor analysis (CFA) to delineate differential contributions to MetS by sub-group, and if contributions were discovered, develop sex and racial/ethnic-specific equations to calculate MetS severity.

Research Design and Methods

Using data on adults from the National Health and Nutrition Examination Survey 1999–2010, we performed a CFA of a single MetS factor that allowed differential loadings across groups, resulting in a sex and race/ethnicity-specific continuous MetS severity score.

Results

Loadings to the single MetS factor differed by sub-group for each MetS component (p < 0.001), with lower factor loadings among non-Hispanic-blacks for triglycerides and among Hispanics for waist circumference. Systolic blood pressure exhibited low factor loadings among all groups. MetS severity scores were correlated with biomarkers of future disease (high-sensitivity C-reactive-protein, uric acid, insulin resistance). Non-Hispanic-black-males with diabetics had a low prevalence of MetS but high MetS severity scores that were not significantly different from other racial/ethnic groups.

Conclusions

This analysis among adults uniquely demonstrated differences between sexes and racial/ethnic groups regarding contributions of traditional MetS components to an assumed single factor. The resulting equations provide a clinically-accessible and interpretable continuous measure of MetS for potential use in identifying adults at higher risk for MetS-related diseases and following changes within individuals over time. These equations hold potential to be a powerful new outcome for use in MetS-focused research and interventions.     

原发性t(10;11)易位白血病CALM和AF10融合转录检测及其体外化疗敏感性分析

为了研究CALM和AF10融合转录在原发性t( 10 ;11)易位白血病形成和治疗中的作用 ,采用RT PCR技术检测了 5例原发性t( 10 ;11)易位白血病患者CALM AF10融合转录 ,体外MTT法检测了其白血病细胞体外化疗敏感性。结果表明 :在 5例原发性t( 10 ;11)易位白血病患者中检测到 5种分子量的AF10 CALM融合转录和 4种分子量的CALM AF10融合转录 ;MTT法显示 5例原发性t( 10 ;11)易位白血病患者的白血病细胞有 2例对体外化疗敏感 ( 60 % ) ,3 6例非t( 10 ;11)易位白血病细胞有 3 1例对体外化疗敏感 ( 86% ) ,统计分析有显著差异 (P <0 0 1) ,与临床治疗结果一致。化疗药物处理 72小时 ,t( 10 ;11)白血病细胞的凋亡率为 ( 16.3 7± 2 .5 6) % ,而非t( 10 ;11)白血病细胞的为 ( 3 3 .75± 5 .5 9) % ,差异有显著性 (P <0 .0 1)。结论 :CALM AF10是t( 10 ;11)易位白血病的常见特点之一 ,可能与该白血病发生密切相关 ,且t( 10 ;11)易位白血病患者预后较差。     

床边敏感性肌钙蛋白Ⅰ对急性心肌梗死的早期诊断价值

目的 评估床边敏感性肌钙蛋白Ⅰ(point-of-care testing for sensitive cardiac troponin Ⅰ,POCT-cTnⅠ)对早期诊断急性心肌梗死(acute myocardial infarction,AMI)的分析性能.方法 检测中山大学附属第一医院急诊科收治的127例疑诊AMI的急诊胸痛患者在入院3个不同时间点(入院即刻、入院后3h和6h)POCT-cTnI和中心实验室高敏肌钙蛋T(central laboratory testing for high sensitive cardiac troponin T,CLT-hscTnT)水平,由两名临床医师根据90 d内所获得的全部临床资料各自独立地给出胸痛病因的最终诊断,并将患者分为AMI组和非AMI组.应用受试者工作特征曲线(receiver operating characteristic curve,ROC曲线)比较POCT-cTnI和CLT-hscTnT两种检测方法对AMI的诊断性能,采用DeLong检验比较ROC曲线下面积(area under the curve,AUC);并计算使用不同诊断界值时的敏感性、特异性、阴性预测值(negative predictive value,NPV)和阳性预测值(positive predictive value,PPV).结果 127例胸痛患者中,有40例(31.5％)最终诊断为AMI.POCT-cTnI和CLT-hscTnT在入院即刻水平诊断AMI的准确性用AUC表示,分别为0.901 (95％CI:0.901～0.947)和0.907 (95％CI:0.842～0.951),两者差异无统计学意义(Z=0.235,P=0.745).POCT-cTn在入院后3h的AUC增加至0.931,与入院即刻相比(AUC,0.858)差异有统计学意义(Z=-2.038,P=0.042),但较入院后6 h(AUC,0.949)差异无统计学意义(Z=-1.435,P=0.151).POCT-cTn使用正常人群参考范围上限的第99百分位数为诊断界值(0.023 ng/mL),入院即刻水平的诊断敏感性为77.5％,特异性为94.2％;入院后3h诊断特性进一步提高,敏感性为96.4％,特异性为92.0％,NPV为98.6％,PPV为81.8％.而CLT-hscTnT使用第99百分位数为诊断界值(0.014 ng/mL),在入院3h水平的NPV为100％.结论 POCT-cTnI可在急诊胸痛患者入院后3h快速准确地识别或除外AMI,诊断性能与CLT-hscTnT相近.     

Amélioration de la perfusion des organes vitaux par la valve d’impédance inspiratoire et le concept de pompe respiratoire : rationnel physiologique et application clinique

Objective

In this article, we review the effects of the respiratory pump to improve vital organ perfusion by the use of an inspiratory threshold device.

Data sources

Medline and MeSH database.

Study selection

All papers with a level of proof of I to III have been used.

Data extraction

The analysis of the papers has focused on the physiological modifications induced by intrathoracic pressure regulation.

Data synthesis

Primary function of breathing is to provide gas exchange. Studies of the mechanisms involved in animals and humans provide the physiological underpinnings for “the other side of breathing”: to increase circulation to the heart and brain. We describe studies that focus on the fundamental relationship between the generation of negative intrathoracic pressure during inspiration through a low-level of resistance created by an impedance threshold device and the physiologic effects of a respiratory pump. A decrease in intrathoracic pressure during inspiration through a fixed resistance resulting in an intrathoracic pressure of −7 cmH₂O has multiple physiological benefits including: enhanced venous return, cardiac stroke volume and aortic blood pressure; lower intracranial pressure; resetting of the cardiac baroreflex; elevated cerebral blood flow oscillations and increased tissue blood flow/pressure gradient.

Conclusion

The clinical and animal studies support the use of the intrathoracic pump to treat different clinical conditions: hemorrhagic shock, orthostatic hypotension, septic shock, and cardiac arrest.     

Syndrome post-arrêt cardiaque : aspects physiopathologiques,cliniques et thérapeutiques

Objective

This review aims at providing an update on post-cardiac arrest syndrome, from pathophysiology to treatment.

Data sources

Medline database.

Data extraction

All data on pathophysiology, clinical manifestations and therapeutic management, with focus on the publications of the 5 last years.

Data synthesis

Care of the patients after cardiac arrest is a medical challenge, in face of “post-cardiac arrest syndrome”, which culminates into multi-organ failure. This syndrome mimics sepsis-related dysfunctions, with all clinical and biological manifestations related to the phenomenon of global ischemia-reperfusion. Acute cardiocirculatory dysfunction is usually controlled through pharmacological and mechanical support. Meanwhile, as a majority of cardiac arrest is related to myocardial infarction, early angiographic exploration should then be discussed when there is no obvious extracardiac cause, percutaneous coronary revascularization being associated with improved short and long-term prognosis. Therapeutic hypothermia is the cornerstone of neuroprotective armamentarium, beyond hemodynamic stabilization and metabolic maintenance.

Conclusion

If ongoing evaluations should shed light on potential efficiency of new therapeutic drugs, a multidisciplinary approach of the post-cardiac arrest syndrome in expertise centre is essential.     

High Prevalence of Undiagnosed Kidney Disease in Those Presenting with Troponin Positive Acute Coronary Syndrome

Aim: The aim of this study is to assess the prevalence and knowledge of chronic kidney disease (CKD) in those presenting to a District General Hospital (DGH) in the United Kingdom with troponin positive acute coronary syndrome (ACS) as compared to a sample of the general population. Methods: A retrospective observational study. Data were collected from ProForma completed during the 18-month period from 1 November 2007 to 30 April 2009. The stage of CKD and the proportion of undocumented CKD at presentation were calculated and the mean stage was compared with the general practice population (of similar demographics) sampled by de Lusignan et al. (Identifying patients with chronic kidney disease from general practice computer records. Fam Pract. 2005;22:234–241.) using the t-test statistics. Results: A total of 936 patients (600 men and 336 women) presented with troponin positive ACS; their mean stage of CKD = 2.874 ± 0.024. This was significantly different from the mean stage of CKD = 1.999 ± 0.004 found within the general population (p < 0.001). About 58.6% of patients with CKD stages 4 or 5 had no knowledge or documentation of their renal impairment. Conclusions: Among those presenting to hospital with troponin positive ACS were many patients with undocumented severe renal impairment, emphasizing the need for general practitioners to screen for renal disease and refer to specialist nephrology services where appropriate. Joint renal and cardiac clinics may offer better care for this group of patients’ long-term care.     

Predictive markers of asymptomatic atherosclerosis in end-stage renal disease patients

Objective: Uremia is associated with accelerated atherosclerosis and increased cardiovascular mortality in patients with end-stage renal disease (ESRD). Cardiac injury markers, such as myoglobin, creatine kinase-MB (CK-MB), or troponins, frequently used to recognize acute coronary events, may be falsely elevated in this patient group. In this study, our aim was to (i) test serum levels of myoglobin, CK-MB, and troponin I (cTnI) in ESRD patients without coronary artery disease (CAD) and compare the results with healthy controls and (ii) to investigate the association between these markers and carotid artery intima–media thickness (CA–IMT), high-sensitive C-reactive protein (hs-CRP), and serum uric acid (SUA) levels in ESRD patients. Materials and methods: Fifty-two ESRD patients (25 hemodialysis and 27 peritoneal dialysis) and 17 healthy controls were included in the study. Serum levels of myoglobin, CK-MB, and cTnI were measured and ultrasonographic CA–IMT was determined in all participants. SUA and hs-CRP levels were only measured in the ESRD group. Results: Serum myoglobin, CK-MB levels, and the mean CA–IMT were significantly higher in ESRD group (p < 0.01), whereas cTnI levels were not different compared to healthy controls (p = 0.70). There was also a positive correlation between CA–IMT and cTnI levels (p = 0.003, r = 0.35) and CA–IMT and hs-CRP (p = 0.03, r = 0.30) or SUA levels (p = 0.003, r = 0.43). Conclusion: cTnI may serve as a more sensitive marker in detecting cardiovascular events in patients with renal failure. Besides the traditional risk factors of atherosclerosis, cTnI, hs-CRP, and SUA may have a predictive role in recognizing premature atherosclerosis in ESRD patients.     

美托洛尔、尼卡地平对手术期间高血压患者心肌的保护作用

目的高血压患者因其本身的病理生理改变,手术期间心肌缺血损伤的发生率高于正常人,通过观察美托洛尔、尼卡地平干预对高血压患者非心脏手术前后心肌钙蛋白I(CTnI)的影响及心率血压变化,以探讨其对心肌的保护作用。方法选择ASAⅠ～Ⅱ级高血压病史5～20年择期行上腹部或胸部手术患者60例,采用抽签法随机分为对照组(Ⅰ)和美托洛尔(Ⅱ)、尼卡地平(Ⅲ)治疗组。在手术前后采静脉血,测心肌钙蛋白I同时观察围插管期心率血压变化。结果Ⅰ组术后CTnI浓度明显高于术前(F=126.79,P<0.01);而Ⅱ、Ⅲ组CTnI浓度术后轻度升高与手术前比较无统计学差异。心率血压方面插管即刻Ⅱ组、Ⅲ组与术前无明显变化与Ⅰ组比较有显著差异(F=19.26,P<0.01)。插管后5min,血压、心率基本平稳。结论美托洛尔、尼卡地平不但能有效抑制全麻诱导气管插管所致的心血管反应,而且对原发性高血压患者非心脏手术手术期间心肌缺血损伤也具有良好的保护作用。     

我国患者多重耐药乙肝病毒感染的基因型和表型特点

目的分析我国大样本来源的慢性乙肝病毒(HBV)感染患者多重耐药HBV的基因型和表型特点。方法回顾性分析11 800例慢性乙肝患者血清中HBV反转录酶(RT)区与核苷(酸)类似物耐药相关的突变类型及频率,采用PCR产物直接测序法和克隆测序法(≥20个克隆/样本)对其中的46例多重耐药HBV突变株进行鉴定。采用体外表型耐药分析法检测核苷类与核苷酸类联合处理对多重耐药HBV的抑制效果。分析临床治疗方案在多重耐药HBV感染的发生及控制中的作用。结果在11 800例慢性HBV感染者中,共3658例(31.0%)检出核苷(酸)类耐药相关突变,其中拉米夫定(LAM)耐药突变2592例(70.9%),阿德福韦酯(ADV)耐药突变665例(18.2%),恩替卡韦(ETV)耐药突变293例(8.0%),替比夫定(LdT)耐药突变62例(1.7%),同时针对核苷类和核苷酸类的多重耐药(MDR)突变46例(1.3%)。对46例多重耐药感染样本的克隆测序显示,40例样本在同一病毒基因组上检出MDR突变,其他6例样本的MDR突变则存在于不同的HBV基因组中。基因型分析显示共有15种病毒变异形式,同时耐LAM(或LdT)和ADV,以及同时耐ETV和ADV的MDR株分别为10种和5种。体外表型耐药分析结果显示,ETV(或LAM)和ADV联合用药可有效抑制HepG2细胞内MDR HBV的复制,但对野生株无类似效果。临床用药方案分析显示,多重耐药HBV感染常出现在LAM(或)LdT、ADV、ETV序贯治疗的患者,以LAM→ADV(22例)和LAM→ADV→ETV(10例)最多见,发生多重耐药后大多出现病毒学和(或)生化学突破。LAM+ADV或ETV+ADV联合挽救治疗可成功将大多数多重耐药HBV的DNA复制控制在检测不到的水平。结论我国MDR HBV株具有多样性和复杂性,表型分析和临床观察均证实核苷与核苷酸类似物联合使用可有效控制MDR HBV复制。多重耐药HBV感染的发生与临床长期应用核苷(酸)类似物序贯治疗有关,密切监测病毒应答及耐药突变对于临床尽早制定最优的抗病毒策略具有重要意义。     

伴t(8;21)M2型急性髓系白血病患者c-kit和JAK2基因突变分析

目的 研究伴t(8;21)M2型成人急性髓系白血病(AML)患者蛋向酪氨酸激酶家族中c-kit和JAK2基因突变的发生情况、临床特征与预后的关系.方法 采用PCR扩增产物直接测序法检测78例伴t(8;21)M2患者中c-kit基因8号与17号外显子的突变情况;采用等位基因特异性PCR方法 检测患者JAK2 V617F的发生情况.结果 ①78例伴t(8;21)M2患者中27例(34.6%)检测出c-kit基因突变(mac-kit),6例(7.7%)检出JAK2 V617F突变,未见同一患者同时发生mac-kit和JAK2V617F突变. ②c-kit/JAK2 V617F突变型患者的外周血白细胞中位数为23.0(4.4～167.0)×109/L,明显高于野生型c-kit和JAK2患者[14.4(1.6-97.4)×109/L](P<0.05),两组的血红蛋白水平、血小板计数、骨髓原始细胞比例、CD117表达水平以及年龄、性别差异均无统计学意义(P>0.05);c-kit突变型组患者的外周血白细胞中位数为23.1(4.4-167.0)×109/L,与野生型组[16.0(1.6-97.4)×109/L]患者相比,差异有统计学意义(P<0.05);由于JAK2 V617F突变患者仅6例,未单独进行统计学分析. ③c-kit/JAK2 V617F突变组患者的完全缓解率与野生型组相近(分别69.6%与80.0%,P>0.05),但c-kit/JAK2 V617F突变组患者的2年持续完全缓解(CCR)率低于野生型组(分别26.7%与56.1%,P<0.05);两组患者2年总生存率的差异无统计学意义(分别为34.8%与58.6%,P>0.05).结论 蛋白酪氨酸激酶家族的c-kit和JAK2基因突变在伴t(8;21)M2型AML患者中较常见,并且与白细胞数量增高相关;其中c-kit突变更为频繁,但同一类的两种突变一般不会同时出现于同一患者;伴有此类基因突变的患者复发率高,预后较差;筛查此类基凶突变对于今后的靶向治疗以及了解临床预后将有重要意义.