依折麦布联合辛伐他汀治疗脑梗死合并高胆固醇血症的疗效和安全性

目的 观察依折麦布联合辛伐他汀对脑梗死合并高胆固醇血症患者的疗效与安全性。方法 脑梗死合并高胆固醇血症患者141例,随机分为三组,依折麦布组、辛伐他汀组和依折麦布与辛伐他汀联合组(联合组)进行12周的治疗。分别使用依折麦布10 mg/d、辛伐他汀20 mg/d、依折麦布10 mg/d与辛伐他汀20 mg/d联合治疗,比较三组患者治疗前后的低密度脂蛋白达标率,血脂其他参数的变化率及药物不良反应发生率。结果 治疗后联合组总胆固醇(TC)、低密度脂蛋白胆固醇(LDL-C)、三酰甘油(TG)有进一步下降,其中TC、LDL-C的变化率与依折麦布组、辛伐他汀组比较,差异有显著性统计学意义(P<0.01);联合组疗效明显高于依折麦布组、辛伐他汀组。不良反应发生率三组间比较差异无统计学意义(P>0.05)。结论 依折麦布联合辛伐他汀具有较好的调节胆固醇代谢的作用,优于单独使用,其安全性较好。     

依折麦布联合舒洛地特对高龄冠心病和糖尿病患者调脂、抗炎作用的临床观察

目的探讨依折麦布联合舒洛地特对高龄冠心病和糖尿病患者全面调脂、抗炎降低肿瘤坏死因子-α(TNF-α)、C反应蛋白(CRP)的作用及安全性。方法选取高龄冠心病、糖尿病患者180例,随机均分为三组。试验组:依折麦布/舒洛地特组(依/舒组),给予依折麦布片10 mg口服,1次/d,舒洛地特胶囊250LSU口服,2次/d;对照组一:依折麦布/辛伐他汀组(依/辛组),给予依折麦布片10 mg口服,1次/d,辛伐他汀片20 mg口服,1次/d;对照组二:辛伐他汀组(辛组),给予辛伐他汀片20 mg口服,1次/d。所有患者在治疗前及治疗后4周、12周末空腹采血,检测总胆固醇(TC)、低密度脂蛋白胆固醇(LDL-C)、高密度脂蛋白胆固醇(HDL-C)、三酰甘油(TG)。在治疗前及治疗12周末空腹采血测定血浆TNF-α、CRP。结果①治疗后三组TC、LDL-C均明显下降(P<0.05)。12周末,依/辛组较依/舒组、依/舒组较辛组TC、LDL-C变化显著(P<0.05)。②12周末,依/舒组HDL-C明显升高(P<0.05)。③4周、12周末,依/舒组、依/辛组TG明显下降(P<0.05),依/舒组较依/辛组,TG下降显著(P<0.05)。④12周末,依/舒组TC、LDL-C、HDL-C、TG的达标率皆优于辛组(P<0.05),TG的达标率优于依/辛组。依/辛组TC、LDL-C达标率在三组中最高,皆为100%。⑤三组在12周末血浆TNF-α、CRP较基线水平明显降低(P<0.05),彼此之间无显著差异。结论依折麦布、舒洛地特联用于冠心病、2型糖尿病高龄患者,有良好的全面调脂、抗炎作用,安全性佳,还能发挥舒洛地特的经典临床药理作用,是一种有前途的临床用药方案。     

依折麦布联合阿托伐他汀对高残粒样微粒胆固醇血症患者的疗效

目的探讨增加阿托伐他汀剂量或联合依折麦布对基础剂量阿托伐他汀治疗后出现高残粒样微粒胆固醇(RLP-C)血症患者的疗效。方法选取常规剂量阿托伐他汀(10 mg·d-1)治疗后出现高RLP-C(≥0.13 mmol·L-1)的稳定性冠心病患者共75例,随机分为双倍剂量阿托伐他汀组(20 mg·d-1,n=38)和联合药物组(阿托伐他汀10 mg·d-1+依折麦布10 mg·d-1,n=37)。比较两组进入研究时及6个月治疗后血脂水平及肱动脉血流介导的血管舒张反应(FMD)的变化。结果两治疗组患者血清总胆固醇(TC)、三酰甘油(TG)、低密度脂蛋白胆固醇(LDL-C)、RLP-C及C反应蛋白水平均较6月前明显降低;依折麦布联合阿托伐他汀比双倍剂量阿托伐他汀能更有效地降低RLP-C[分别为(-47.7±18.2)%和(-33.3±24.3)%,P<0.01]和提高FMD[分别为(48.5±45.2)%和(28.9±27.8)%,P=0.03]。结论对常规剂量阿托伐他汀治疗后出现高RLP-C血症的患者添加依折麦布有助于降低RLP-C和改善FMD。     

依折麦布联合辛伐他汀对经皮腔内冠状动脉介入术后低密度脂蛋白胆固醇和C反应蛋白水平的影响

目的 观察依折麦布联合辛伐他汀对冠心病经皮腔内冠状动脉介入术(PCI)后患者低密度脂蛋白胆固醇(LDL-C)和C反应蛋白(CRP)的影响.方法 80例冠心病PCI术后患者采用数字表法随机分为两组,联合治疗组40例:基础治疗+依折麦布+辛伐他汀;对照组40例:基础治疗+辛伐他汀.分别检测两组治疗前和治疗12周后LDL-C和CRP水平,并评估临床疗效及安全性.结果 联合治疗组患者LDL-C和CRP水平明显低于对照组(t=10.06、12.59,均P＜0.05).联合治疗组临床收益率(90％)明显优于对照组(80％)(x2=6.38,P＜0.05),不良反应发生率明显低于对照组.结论 与单用辛伐他汀相比,依折麦布联合辛伐他汀可显著降低冠心病PCI术后患者的LDL-C和CRP水平,提高临床疗效,并且具有很好的安全性.     

阿托伐他汀钙联合新型依折麦布药物治疗冠心病的效果与临床安全性分析

目的分析冠心病患者应用阿托伐他汀钙联合新型依折麦布药物治疗的效果与临床安全性。方法96例冠心病患者,采用双盲法分为常规组和试验组,每组48例。常规组患者行阿托伐他汀钙治疗,试验组患者行阿托伐他汀钙联合新型依折麦布药物治疗。对比两组患者治疗效果、不良反应发生情况、血脂指标[低密度脂蛋白胆固醇(LDL-C)、高密度脂蛋白胆固醇(HDL-C)、血清甘油三酯(TG)、总胆固醇(TC)]水平。结果试验组治疗总有效率97.92%高于常规组的87.50%,差异有统计学意义(P<0.05)。治疗后,试验组患者的LDL-C(2.02±0.33)mmol/L、HDL-C(1.44±0.37)mmol/L、TG(1.81±0.17)mmol/L、TC(4.14±0.66)mmol/L优于常规组的(2.86±0.24)、(1.30±0.23)、(2.25±0.24)、(4.97±1.13)mmol/L,差异有统计学意义(P<0.05)。试验组不良反应发生率2.08%低于常规组的14.58%,差异有统计学意义(P<0.05)。结论对冠心病患者实施阿托伐他汀钙联合新型依折麦布药物治疗,能够优化患者血脂水平,改善患者临床症状,值得广泛应用。     

依折麦布联合辛伐他汀治疗高脂血症的临床疗效分析

目的探讨依折麦布联合辛伐他汀治疗高脂血症的临床疗效。方法选取我院2009年10月至2011年10月收治148例高脂血症的患者,随机分为观察组和对照组各74例,观察组使用依折麦布联合辛伐他汀治疗,对照组单纯使用辛伐他汀治疗,比较两组在治疗后1个月内血浆中的低密度脂蛋白胆固醇(LDL-C)与总胆固醇(TC)的变化情况。结果观察组在治疗后1个月内血浆中的LDL-C与TC均低于对照组,P<0.05,具有统计学意义。结论依折麦布联合辛伐他汀治疗高脂血症的临床疗效显著,值得临床推广应用。     

依折麦布联合阿托伐他汀钙治疗冠心病的效果分析

目的 分析在冠心病患者的临床治疗中联合应用依折麦布与阿托伐他汀钙的临床效果。方法 120例冠心病患者,以数字抽签法分为实验组与参照组,各60例。实验组采取阿托伐他汀钙联合依折麦布治疗,参照组采取阿托伐他汀钙单独治疗。比较两组治疗前后的血脂[甘油三酯(TG)、总胆固醇(TC)、低密度脂蛋白胆固醇(LDL-C)]水平、不良反应发生情况。结果 治疗后,实验组TG、TC、LDL-C分别为(1.92±0.24)、(4.21±0.76)、(2.14±0.41)mmol/L,低于参照组的(2.33±0.39)、(4.88±1.22)、(2.96±0.35)mmol/L,差异有统计学意义(P<0.05)。实验组不良反应发生率1.67%低于参照组的11.67%,差异有统计学意义(P<0.05)。结论 在冠心病患者的临床治疗中,采用阿托伐他汀钙联合依折麦布治疗的效果更为显著,患者用药后血脂水平得以改善,同时药物安全性也较高,值得推广。     

HPLC测定依折麦布辛伐他汀片中6-氧代辛伐他汀含量

目的建立高效液相色谱法测定依折麦布辛伐他汀片中6-氧代辛伐他汀的含量。方法采用Phenomenex Luna Phenyl Hexyl柱(150×4.6mm,3μm),流动相A为0.025mol/L磷酸二氢钠溶液-乙腈(80:20),流动相B为乙腈,进行梯度洗脱,流速为1.5mL/min,检测波长为290nm,柱温为30℃,进样量为100μL。结果6-氧代辛伐他汀在0.02μg/mL~8μg/mL范围内与其峰面积成良好的线性关系(r=0.99998,n=6),平均回收率为98.27%,RSD为4%。结论该方法简便,准确,重复性好,可用于依折麦布辛伐他汀片中6-氧代辛伐他汀的质量控制。     

依折麦布联合辛伐他汀治疗高脂血症临床疗效分析

目的分析依折麦布联合辛伐他汀治疗高脂血症临床疗效。方法选取笔者所在医院2010年3月～2012年2月收治的高脂血症患者69例随机分为两组,治疗组37例给予依折麦布联合辛伐他汀进行治疗,对照组32例单用辛伐他汀进行治疗。经12周的治疗后,分别对两组患者的血脂水平进行复查,对比治疗前后两组患者血脂变化情况,以及治疗后血脂达标率。结果经治疗,治疗组的总胆固醇、甘油三酯水平明显低于对照组,高密度脂蛋白胆固醇水平高于对照组。治疗组血清中总胆固醇、甘油三酯、高密度脂蛋白胆固醇3项检测的达标率明显高于对照组。结论依折麦布联合辛伐他汀治疗高脂血症安全有效,且临床疗效优于单用辛伐他汀进行治疗。     

氯吡格雷联合依折麦布治疗冠心病心绞痛的疗效及对血清VEGF、NO、ET-1水平的影响研究

目的 探究氯吡格雷联合依折麦布治疗冠心病心绞痛的疗效及对血清血管内皮生长因子(VEGF)、一氧化氮(NO)、内皮素-1(ET-1)水平的影响。方法 100例冠心病心绞痛患者,采用随机数字表法分为研究组和对照组,各50例。对照组患者采用氯吡格雷进行治疗,研究组采用氯吡格雷联合依折麦布进行治疗。比较两组患者临床疗效及治疗前后血清VEGF、NO、ET-1水平。结果 研究组患者治疗总有效率96%明显高于对照组的74%,差异有统计学意义(P<0.05)。治疗后,两组患者血清VEGF、NO水平均明显高于本组治疗前, ET-1水平明显低于本组治疗前,且研究组患者血清VEGF(130.51±15.68)ng/L、NO(87.88±9.86)μmol/L均明显高于对照组的(108.66±12.71)ng/L、(76.28±8.91)μmol/L, ET-1(51.35±6.75)ng/L明显低于对照组的(61.23±7.53)ng/L,差异具有统计学意义(P<0.05)。结论 氯吡格雷联合依折麦布治疗冠心病心绞痛疗效确切,对血管内皮细胞有保护作用,值得临床推广。     

偏头痛患者听功能及前庭功能状态的临床研究

目的:探讨偏头痛患者听功能及前庭功能表现与原发病的关系。方法:随机选择31例偏头痛患者及31例对照组患者,收集详细病史,并测定其纯音听阈和声导抗以及视频眼震图。结果:偏头痛患者中有2例(3耳)出现听阈上升,均为感音神经性耳聋,声导抗无明显异常。偏头痛患者中有10例出现眩晕症状(对照组无明显眩晕症状)。偏头痛组视频眼震图各参数与对照组相比有不同程度的差异。结论:偏头痛患者有听功能的下降,无中耳传音功能的异常。一部分偏头痛患者出现眩晕,与偏头痛发作有密切关系。偏头痛患者不仅有周围性前庭功能的异常,也可以有中枢性前庭功能的异常。偏头痛患者进行前庭功能的检查,有助于该病的诊断和治疗。     

Lead and immune function

The heavy metal lead is a widely deposited environmental toxicant known to impact numerous physiological systems, including the reproductive, neurological, hepatic, renal, and immune systems. Studies illustrating the capacity of lead to impair immune function and/or host resistance to disease date back to at least the 1960s. However, it has only been in recent years that lead has been recognized among a new category of immunotoxicants-those that dramatically shift immune functional capacity while producing only modest changes to immune cell populations and lymphoid organs. These relatively noncytotoxic immunomodulating chemicals and drugs represent the immunotoxic hazards most difficult to identify and problematic for risk assessment using historic approaches. As a result, such environmental factors are also among the most likely to contribute to chronic immune-related disease at relevant exposure levels. This review considers the animal and human evidence that lead exposure can produce a stark shift in immune functional capacity with a skewing predicted to elevate the risk of atopic and certain autoimmune diseases. At the same time, host defenses against infectious agents and cancer may be reduced. Age-based exposure studies also suggest that levels of blood lead previously thought to be safe, that is, below 10 microg/dl, may be associated with later life immune alterations.     

Septum and adrenocortical function

Dorsal septum is an intermediary centre in between the hippocampus and hypothalamus and it has got inhibitory influence over the hypothalamo-pituitary-adrenal axis. Stimulation of the dorsal septum manifested with fall in adrenocortical output whereas its lesion has opposite response. Ventral septum is a facilitatory area regarding activation of the hypothalamo-pituitary-adrenal axis. It is a balancing centre lying in between the higher central nervous system structures and the hypothalamus. Stimulation and lesion of the ventral septum led to rise and fall in adrenal venous 17-OHCS output respectively. Adrenocortical response to stress of burn was not blocked or inhibited following lesion of the dorsal as well as ventall septum.     

Beta-blockers and renal function

alpha-, beta 1- and beta 2-adrenergic receptors in the kidney mediate vasoconstriction, renin secretion and vasodilatation, respectively. Blockade of beta-receptors may therefore be expected to influence renal blood flow and possibly glomerular filtration rate by intrarenal effects as well as by reducing cardiac output and blood pressure. Since the various beta-adrenergic blocking drugs available differ in the degree to which they block beta 2-receptors (cardioselectivity) and also in their intrinsic sympathomimetic activity, they would be expected to have different effects on renal function. The acute administration of beta-blockers usually results in a reduction in effective renal plasma flow and glomerular filtration rate, whether or not the drug is cardioselective or has intrinsic sympathomimetic activity, with the exceptions of nadolol, which has actually increased effective renal plasma flow in some studies and of tolamolol. With chronic oral administration, the non-cardioselective beta-blockers reduced glomerular filtration rate and effective renal plasma flow. The cardioselective drugs do not usually produce significant reductions in glomerular filtration rate or effective renal plasma flow, although small increases in serum urea during treatment do occur. Interestingly, in contrast to findings with intravenous administration, orally administered nadolol produced a slight reduction in glomerular filtration rate in 1 study, so the effect of this agent on renal function under clinical conditions remains uncertain. It seems likely that beta-blockers reduce renal function predominantly by blocking beta 2-receptors in the kidney. To keep area of discussion in perspective, it is important to realise that although there have been isolated reports of serious deterioration in renal function coinciding with beta-blocker treatment, the great majority of reports are of reduction in glomerular filtration rate which are not of clinical significance, even in patients with pre-existing impairment of renal function. The beta-blockers with low lipid solubility-i.e. atenolol, nadolol and sotalol-are not metabolised, and their dose must be reduced in renal failure. Propranolol has active metabolites and its dose must also be reduced slightly in uraemia.     

Estrogen and vascular function

The effects of estrogen on the female reproductive system are well known. In contrast, comparatively recent research has demonstrated that estrogen also exerts specific effects on the cardiovascular system--particularly the vasculature. This review summarizes some of the current ideas of how estrogen regulates and modulates vascular function, and focuses primarily on potential mechanisms of estrogen-induced vasodilation. Although many studies indicate estrogen exerts beneficial effects on the circulatory system, the overall conclusions from clinical studies remain somewhat equivocal. In contrast, it is clear that estrogen reduces atherosclerosis by reducing low-density lipoproteins (LDL) and inflammatory processes in the vasculature, and may also act as an antioxidant; however, these effects account for only a portion of the total cardiovascular benefit of estrogen. Estrogen is also a vasodilator and hypotensive agent, and can induce vascular relaxation by stimulating release of endothelium-derived vasodilatory substances (e.g., nitric oxide [NO]) or by acting directly on the vascular smooth muscle (VSM). Recent evidence indicates that calcium and potassium channels in VSM cells play an important role in mediating estrogen-induced relaxation of many vascular beds, but elucidating the signal transduction mechanisms coupling estrogen receptor (ER alpha and/or ER beta) activation to generation of second messengers and effector mechanisms remains an area of intense study. Not surprisingly, it is becoming apparent that the molecular basis of estrogen's influence on vascular function is multifactorial. A better understanding of these signaling mechanisms should lead to the development of powerful therapeutic agents which can maximize the many beneficial effects of estrogen action, while helping minimize the harmful (and sometimes lethal) side effects.