老年男性恶性肿瘤患者高尿酸血症危险因素分析

目的分析老年男性恶性肿瘤患者发生高尿酸(UA)血症的常见危险因素。方法 201例老年男性恶性肿瘤患者依UA水平420μmol/L分为正常UA组(n=114)和高UA组(n=87),2组间年龄及肿瘤类型匹配,比较2组间高血压、高血糖、高血脂、肾功能不全及肿瘤转移发生率的差异,以吸烟状况、收缩压(SBP)、舒张压(DBP)、空腹血糖(FBG)、总胆固醇(TC)、三酰甘油(TG)、体质量指数(BMI)、肌酐(Scr)、尿素氮(BUN)、肿瘤转移为协变量进行单因素logistic回归分析,选择其中有统计学意义的变量为自变量,UA血症为因变量,进行多变量lo-gistic逐步回归分析。结果与正常UA组相比,高UA组肾功能不全的发生率显著增高(P<0.01)。logistic多元回归分析显示,UA水平与SBP(OR=1.038,P<0.05)、BUN(OR=1.187,P<0.01)、TG(OR=1.518,P<0.05)显著相关,与肿瘤转移无关。结论老年男性恶性肿瘤患者高UA血症主要与高血压、肾功能不全和高血脂有关,而与肿瘤转移关系不大。     

老年冠心病患者高尿酸血症与其他危险因素相关性分析

目的探讨老年冠心病高尿酸血症(HUA)与其他危险因素的相关性。方法收集2007—2009年在北京大学人民医院住院的300例老年冠心病患者,检测血尿酸(UA)、空腹血糖(FPG)、血压及血脂等指标,并记录年龄、性别、吸烟史、体重指数(BMI),分析HUA与冠心病其他危险因素的相关性。结果 300例冠心病患者中HUA的192例,尿酸正常的108例。Logistic多元回归结果表明,血尿酸与年龄、性别、血压及血脂水平、BMI均具有正相关性。HUA组冠心病患者的血压、血脂水平、BMI均明显高于尿酸正常组的冠心病患者。结论冠心病患者合并HUA的发病率高,后者常常与血压、血脂、血糖代谢异常并存,是冠心病的危险因素之一。     

男性高尿酸血症患者性腺功能减退的危险因素分析

目的 探讨男性高尿酸血症(HUA)患者合并性腺功能减退的危险因素.方法 入选HUA男性患者245例,均测量身高、体重、腰围、血压,测定空腹血尿酸、三酰甘油(TG)、总胆固醇、低密度脂蛋白胆固醇、高密度脂蛋白胆固醇、谷丙转氨酶(ALT)、谷草转氨酶、谷氨酰转肽酶、血尿素氮、肌酐、空腹血糖(FPG)、空腹胰岛素(FINS)...     

老年NIDDM伴高尿酸血症临床分析

老年ＮＩＤＤＭ伴高尿酸血症临床分析严锦平南京市红十字医院（２１０００１）自广泛开展血尿酸检查以来，老年非胰岛素依赖型糖尿病（ＮＩＤＤＭ）伴高尿酸血症日益受到临床重视。为了解老年ＮＩＤＤＭ伴高尿酸血症与高甘油三酯血症、高血压、糖尿病肾病（ＤＮ）的相互影...     

老年高尿酸血症106例临床分析

本文对1999年5月在本院体检的且资料完整的597例离休干部进行高尿酸血症及其相关疾病的分析,现报道如下。1　资料与方法1.1　资料与方法　597例均为1999年5月在本院进行健康体检的离休干部,其中男471例,女126例,年龄60～91岁,平均年龄(663±148)岁。所有人除测血压、称体重等全身体检外均查血尿酸(ＵＡ)、空腹血糖(ＧＬＵ)、胆固醇(ＴＣ)、甘油三酯(ＴＧ)、尿素氮(ＢＵＮ)、肌酐(Ｃｒ)、丙氨酸转氨酶(ＡＬＴ)、血尿常规等。血尿酸值采用尿酸酶过氧化物酶偶联法测定,因更年期后女性血尿酸值接近男性,故本组资料高尿酸血症标准男女均大于或等…     

不同年龄男性高尿酸血症危险因素分析

目的探讨不同年龄阶段男性高尿酸血症的危险因素。方法200例男性高尿酸血症患者和286例尿酸正常的男性对照按年龄分组,调查饮食和疾病史,检测生化指标,测量一般身体指标。结果49岁以下人群中,病例组肥胖、腹型肥胖、高血压、高血脂、空腹血糖异常升高率、吸烟量、白酒、啤酒量和嘌呤食物摄入量均高于对照组(P<0.05),而49岁及以上人群中,病例组高血压发生率、空腹血糖、肌酐、尿素氮异常升高率和啤酒摄入量较对照组升高(P<0.05)。Logis-tic回归显示,49岁以下男性发生高尿酸血症的危险因素为体重指数、甘油三酯、胆固醇、啤酒和嘌呤食物的摄入;49岁及以上男性发生高尿酸血症的危险因素为啤酒、血肌酐和血糖。结论49岁以下男性血尿酸升高的危险因素主要为不良的饮食结构和多种代谢紊乱,而49岁以上男性尿酸水平受到不良饮食结构的影响较少(啤酒除外),血糖、尿素氮、血肌酐异常升高与尿酸升高紧密关联。     

高尿酸血症一个未被重视的心血管病危险因素

高尿酸血症：尿酸（UA）是嘌呤的代谢产物，当体内的UA生成增多和（或）排泄减少时，血中UA含量增高。临床空腹血清尿酸（SUA）一般男性〉420μmol／L（4．0mg／dL），女性〉350μmol／L（6mg／dL）可确定为高尿酸血症（HUA）。服用利尿剂、小剂量阿司匹林及运动等均可影响尿酸水平。     

高尿酸血症一个未被重视的心血管病危险因素

高尿酸血症：尿酸（UA）是嘌呤的代谢产物，当体内的UA生成增多和（或）排泄减少时，血中UA含量增高。临床空腹血清尿酸（SUA）一般男性〉420μmol／L（4．0mg／dL），女性〉350μmol／L（6mg／dL）可确定为高尿酸血症（HUA）。服用利尿剂、小剂量阿司匹林及运动等均可影响尿酸水平。     

老年高尿酸血症与相关危险因素的临床观察

检测92例高尿酸血症(HUA)、88例正常的患者,对两组间的血糖、血脂、血压对比分析。结果老年HUA患者血清空腹血糖(FBG)、甘油三酯(TG)、总胆固醇(TC)、低密度脂蛋白(LDL-C)、血压均高于对照组,而血清高密度脂蛋白(HDL-C)低于对照组(P0.05)。结论高血压、糖尿病及血脂异常与HUA的发生密切相关。     

老年人肺部感染致多器官功能不全综合征的血糖分析

目的观察老年人肺部感染致多器官功能不全综合征(MODSE)患者的血糖变化,分析血糖变化与MODSE发病及其严重程度的相关性。方法对2005年1月至2014年12月在解放军白求恩国际和平医院住院的625例≥65岁的肺部感染患者进行回顾性调查,所有患者按是否有糖尿病分为糖尿病组和非糖尿病组;各组再按肺部感染是否诱发MODSE分为MODSE亚组和非MODSE亚组。分别比较糖尿病组中MODSE亚组与非MODSE亚组、以及非糖尿病组中MODSE亚组与非MODSE亚组的最高空腹血糖水平,采用Spearman等级相关分析血糖与MODSE发病及其严重程度的相关性。结果糖尿病组196例患者并发MODSE 89例,非糖尿病组429例患者并发MODSE 95例,糖尿病组中MODSE亚组和非MODSE亚组患者最高空腹血糖水平分别为(13.720±4.863)、(7.439±3.043)mmol/L,非糖尿病组中MODSE亚组和非MODSE亚组患者最高空腹血糖水平分别为(8.656±2.664)、(5.679±1.332)mmol/L,MODSE亚组最高空腹血糖水平均显著高于非MODSE亚组(P0.001)。老年肺部感染患者的最高空腹血糖水平与MODSE发病及其严重程度呈显著正相关(P0.001)。结论老年人肺部感染致MODSE患者的最高空腹血糖水平明显增高,并且空腹血糖变化与MODSE发病及其严重程度呈显著正相关。     

老年尿毒症患者脑血流动力学的分析

目的　探讨老年尿毒症患者脑血管血流动力学的变化及其影响因素。方法　采用经颅多谱勒超声 ,分别于血液透析 (血透 )和腹膜透析前后测量收缩期和舒张末期脑血管血流速度 (CABFV) ;监测血压变化 ;微盘测定法和放射免疫法分别检测血清一氧化氮 (NO)和内皮素 (ET)含量的变化 ,对CABFV与血压、血清NO和ET的关系进行分析。结果　老年尿毒症患者CABFV显著低于同龄正常老年人和中青年尿毒症患者 (收缩期 ,P <0 .0 1,舒张末期 ,P <0 .0 5 ) ;血透后CABFV在短期内进一步下降 (P <0 .0 1) ,腹膜透析前后CABFV没有显著变化 ;透析前后血压的变化没有统计学意义 ;血透可使血清NO和ET含量明显下降 (P <0 .0 0 1) ,但血透前血清NO和血透前后血清ET水平均明显高于正常老年人 (P <0 .0 0 1) ,而腹膜透析则对其没有影响 ;血透前收缩期CABFV的变化与血压和血清ET显著负相关 ,与血清NO显著正相关 (P <0 .0 0 1或 P <0 .0 1)。结论　老年尿毒症患者CABFV显著低于同龄正常老年人和中青年尿毒症患者 ,血透后短期内进一步下降 ;尿毒症患者血压、血清NO和ET水平均明显高于正常老年人 ;血透后血清NO和ET水平在一定时间内显著降低 ,而血压无明显改变 ;腹膜透析对上述指标无显著影响 ;血压、血清NO和ET的变化是导致老年尿毒症患者CA     

Developmental disruption of serotonin transporter function impairs cerebral responses to whisker stimulation in mice

There is growing evidence that serotonin (5-hydroxtryptamine, 5-HT) has major influences on brain development in mammals. Genetic and pharmacological disruption of 5-HT signaling during early postnatal development in rodents causes neuroanatomical cortical abnormalities, including malformations in the somatosensory cortex. Possible functional consequences of this developmental perturbation by 5-HT are not yet understood. We have examined the effects of deletion of the 5-HT transporter (5-HTT) gene on somatosensory responses to sensory stimulation in mice. Local cerebral glucose utilization (lCMR(glc)) was measured by the quantitative 2-deoxy[(14)C]glucose method during unilateral whisker stimulation in awake adult mice. lCMR(glc) was increased by stimulation but to a markedly lesser extent in 5-HTT(-/-) mice than in 5-HTT(+/+) controls in each of four major stations in the whisker-to-barrel cortex pathway (the spinal and principal sensory trigeminal nuclei, the ventral posteromedial thalamic nucleus, and the barrel region of the somatosensory cortex). Lowering brain 5-HT levels by administration of the selective tryptophan hydroxylase inhibitor p-chlorophenylalanine on postnatal days 0 and 1 restored the metabolic responses to functional activation in the whisker-to-barrel cortex pathway in adult 5-HTT(-/-) mice. These results indicate that functional deficits in this pathway in 5-HTT(-/-) mice may be due to excessive postnatal 5-HT activity. With or without postnatal p-chlorophenylalanine treatment, 5-HTT(-/-) mice exhibited lower resting (unstimulated) lCMR(glc) than did 5-HTT(+/+) controls in the whisker-to-barrel cortex pathway and throughout the brain. These findings have implications for understanding the potential long-term consequences of genetic and pharmacological disruption of 5-HT neurotransmission on cerebral functions during critical periods of postnatal development.     

Abnormalities of whole body protein turnover, muscle metabolism and levels of metabolic hormones in patients with chronic heart failure

OBJECTIVE: It is well known that chronic heart failure (CHF) is associated with insulin resistance and cachexia, but little is known about the underlying substrate metabolism. The present study was undertaken to identify disturbances of basal glucose, lipid and protein metabolism. DESIGN: We studied eight nondiabetic patients with CHF (ejection fraction 30 +/- 4%) and eight healthy controls. Protein metabolism (whole body and regional muscle fluxes) and total glucose turnover were isotopically assayed. Substrate oxidation were obtained by indirect calorimetry. The metabolic response to exercise was studied by bicycle ergometry exercise. RESULTS: Our data confirm that CHF patients have a decreased lean body mass. CHF patients are characterised by (i) decreased glucose oxidation [glucose oxidation (mg kg(-1) min(-1)): 1.25 +/- 0.09 (patients) vs. 1.55 +/- 0.09 (controls), P < 0.01] and muscle glucose uptake [a - v diff(glucose) (micromol L(-1)): -10 +/- 25 (patients) vs. 70 +/- 22 (controls), P < 0.01], (ii) elevated levels of free fatty acids (FFA) [FFA (mmol L(-1)): 0.72 +/- 0.05 (patients) vs. 0.48 +/- 0.03 (controls), P < 0.01] and 3-hydroxybutyrate and signs of elevated fat oxidation and muscle fat utilization [a - v diff(FFA) (mmol L(-1)): 0.12 +/- 0.02 (patients) vs. 0.05 +/- 0.01 (controls), P < 0.05] and (iii) elevated protein turnover and protein breakdown [phenylalanine flux (micromol kg(-1) h(-1)): 36.4 +/- 1.5 (patients) vs. 29.6 +/- 1.3 (controls), P < 0.01]. Patients had high circulating levels of noradrenaline, glucagon, and adiponectin, and low levels of ghrelin. We failed to observe any differences in metabolic responses between controls and patients during short-term exercise. CONCLUSIONS: In the basal fasting state patients with CHF are characterized by several metabolic abnormalities which may contribute to CHF pathophysiology and may provide a basis for targeted intervention.     

脑梗死患者血清抵抗素水平变化及与糖代谢的相关性分析

目的探讨血清抵抗素水平变化在脑梗死发病中的作用。方法采用ELISA法测定82例急性脑梗死患者（脑梗死组）及50例健康查体者（对照组）血清抵抗素、瘦素、胰岛素、空腹血糖（FBG）、TG、TC、HDL-C、LDL-C、超敏C反应蛋白（hs-CRP）,计算定量胰岛素敏感性检测指数（QUICKI）;测量身高、体质量、腰围、臀围,计算BMI及腰臀比（WHR）。对上述指标间的相关性进行统计学分析。结果①脑梗死组血清抵抗素、胰岛素、FBG、瘦素、LDL-C及hs-CRP均明显高于对照组（P〈0.05）,QUICKI和血清HDL-C均低于对照组（P均〈0.05）。②多因素Logistic回归分析显示,脑梗死与年龄、抵抗素、瘦素、hs-CRP、TG、LDL-C呈显著正相关（P均〈0.05）,与QUICKI呈显著负相关（P〈0.05）。③单因素直线相关分析显示,抵抗素与胰岛素、FBG呈显著正相关（P均〈0.05）,与QUICKI呈显著负相关（P〈0.05）。结论急性脑梗死患者血浆抵抗素水平升高与糖代谢指标密切相关;此可能在脑梗死发生过程中发挥重要作用。     

胰岛素抵抗与糖脂代谢

近些年,对胰岛素抵抗的认识逐渐增加,其在心脑血管疾病发展中所起的重要作用倍受关注.胰岛素抵抗时常伴有糖和脂代谢紊乱发生,通过异常的代谢途径最终使疾病向不可逆方向发展.因此,在改善胰岛素抵抗的同时,还要注重对糖和脂代谢的调节,即从整体对异常代谢环境进行治疗.     

江苏省机关老年人代谢综合征患病率及相关疾病的分析

目的调查江苏省机关老年人代谢综合征（MS）患病率及其与高尿酸血症（HUA）、非酒精性脂肪肝（NAFL）、心脑血管病的关系。方法选择7860例老年人健康体检资料进行MS患病情况与HUA、NAFL、心脑血管病患病率关系分析。结果 7860例老年人中MS 1931例,占24.57%。MS组HUA、NAFL和心脑血管病的患病率显著高于非MS组（P〈0.01）。结论老年人MS患病率高,患有MS的老年人NAFL、HUA、心脑血管病患病率增高,在不同年龄之间存在差异。     

老年高尿酸血症患者血清25（OH）D3水平变化及意义

目的 观察老年高尿酸血症患者血清25（OH）D3水平的变化,并探讨其意义.方法 选择高尿酸血症患者51例（A组）及血尿酸正常患者259例（B组）.采用酶免疫分析法测定两组的血清25（OH）D3水平.同时测量两组患者血压、身高、体质量,计算BMI,并检测TC、HDL-C、LDL-C、TG、空腹血糖（FBG）、血尿酸（UA）、钙、磷.结果 A组血清25（OH）D3水平为（33.02±11.60） nmol/l,B组为（37.77±14.51） nmol/l,两组比较P＜0.05;两组25（OH）D3不足与缺乏的构成比比较P均＜0.05.血尿酸水平与老年高尿酸血症患者的BMI、TG呈正相关（r分别为0.216、0.184,P均＜0.001）,与HDL-C、血清25（OH）D3水平呈负相关（r分别为-0.282、-0.114,P均＜0.05）.结论 老年高尿酸血症患者血清25（OH）D3水平低下,低水平血清25（OH）D3可能是高尿酸血症的危险因素.     

Oxytocin in metabolic homeostasis: implications for obesity and diabetes management

Oxytocin was once understood solely as a neuropeptide with a central role in social bonding, reproduction, parturition, lactation and appetite regulation. Recent evidence indicates that oxytocin enhances glucose uptake and lipid utilization in adipose tissue and skeletal muscle, suggesting that dysfunction of the oxytocin system could underlie the pathogenesis of insulin resistance and dyslipidaemia. Murine studies revealed that deficiencies in oxytocin signalling and oxytocin receptor expression lead to obesity despite normal food intake, motor activity and increased leptin levels. In addition, plasma oxytocin concentration is notably lower in obese individuals with diabetes, which may suggest an involvement of the oxytocin system in the pathogenesis of cardiometabolic disease. More recently, small scale studies demonstrated that intranasal administration of oxytocin was associated with significant weight loss as well as improvements in insulin sensitivity and pancreatic β‐cell responsivity in human subjects. The multi‐pronged effects of oxytocin signalling on improving peripheral insulin sensitivity, pancreatic function and lipid homeostasis strongly suggest a role for this system as a therapeutic target in obesity and diabetes management. The complexity of obesity aetiology and the pathogenesis of obesity‐related metabolic complications underscore the need for a systems approach to better understand the role of oxytocin in metabolic function.