高效液相色谱法测定氟维司群原料药有关物质

为建立高效液相色谱法测定氟维司群原料药中有关物质的方法,采用Waters Symmetry C8(150 mm×4.6 mm,3.5μm)色谱柱,以水-乙腈-甲醇(41∶32∶27)为流动相A,以水-乙腈-甲醇(10∶49∶41)为流动相B,流速为2.0 mL·min-1进行梯度洗脱,柱温为40℃;检测波长为225 nm;样品温度为8℃;进样体积为10μL.结果表明:系统适应性试验氟维司群主峰和杂质A的分离度为3.03,大于1.5的标准要求;供试品溶液分别经强酸、强碱、高温、氧化、强光等条件破坏,主峰的纯度角均小于纯度阈值,主峰与相邻峰之间的最小分离度均大于1.5、杂质质量守恒均在在95%~105%之间;已知杂质B、C、D、F定量限分别为4.080、1.940、1.355、1.160μg·mL-1,小于报告阈值0.05%对应的样品浓度;所测单个未知杂质质量分数和总杂质量分数在小于0.1%的情况,重复性和中间精密度RSD分别为9.84%和12.49%;供试品在48 h内稳定.

甲羟戊酸逆转氟伐他汀钠对舌鳞癌细胞的抑制作用

目的:探究甲羟戊酸(MEV)及氟伐他汀钠(FS)对舌鳞癌细胞的抑制作用。方法:不同浓度的FS和MEV分别或联合处理舌鳞癌细胞HSC-4。用CCK-8、流式细胞术、划痕实验、免疫荧光和Western blot技术分别检测细胞增殖、凋亡、迁移以及RAS同源基因家族成员A(RHOA)、组织因子(TF)和BAX蛋白的表达情况。结果:FS抑制HSC-4细胞的增殖和迁移,降低细胞内RHOA和TF的表达,促进BAX表达。MEV逆转FS对HSC-4细胞的抑制作用,促进细胞内RHOA和TF的表达(P<0.05)。结论:MEV体外逆转FS对舌鳞癌细胞HSC-4的抑制作用。

氟伐他汀钠对斑马鱼肝抗氧化体系及肝功能的影响

目的研究氟伐他汀钠(FLU)对斑马鱼肝内抗氧化体系和肝功能的影响。方法采用半静态暴露法,以氟伐他汀钠为研究对象,选取斑马鱼为指示生物,将斑马鱼分别暴露在空白对照组和0.004、0.04、0.4 mg/L的氟伐他汀钠溶液中,于暴露48 h后,取样检测氟伐他汀钠对斑马鱼肝内ROS含量和抗氧化酶SOD、CAT、GPx、GST的活性,同时检测肝功能指标ALT、AST的活性。结果与对照组相比,氟伐他汀钠暴露48 h后,中、高浓度的氟伐他汀钠会造成ROS含量显著性升高(P<0.01),CAT、SOD、CuZn-SOD、GPx的活性变化具有同步性,但低浓度的氟伐他汀钠对所有的抗氧化酶均无显著的激活或抑制作用。中浓度的氟伐他汀钠对CAT、SOD具有激活作用(P<0.01),高浓度的氟伐他汀钠对抗氧化酶SOD、CAT、GPx、GST都有激活作用(P<0.05,P<0.01),同时对ALT和AST也具有显著性的激活作用(P<0.01)。分子对接结果表明氟伐他汀钠能够与斑马鱼CAT蛋白对接,最佳对接位点为Met392,对接能量为-4.63 kcal/mol。结论随着药物浓度的升高,氟伐他汀钠能够对斑马鱼肝内抗氧化体系和肝功能造成影响。

Inhibitory effect of fluvastatin on ileal ulcer formation in rats induced by nonsteroidal antiinflammatory drug

AIM: Nonsteroidal anti-inflammatory drugs (NSAIDs)cause gastrointestinal damage as one of their side effects in humans and experimental animals. Lipid peroxidation plays an important role in NSAID-induced ulceration. The aim of this study was to investigate the inhibitory effect of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA)reductase inhibitors on the ulceration in small intestines of rats.METHODS: The effects of three HMG-CoA reductase inhibitors, fluvastatin, pravastatin and atorvastatin on ileal ulcer formation in 5-bromo-2-(4-fluorophenyl)-3-(4-methylsulfonylphenyl) thiophene (BFMeT)-treated rats were examined. Antioxidative activity of the inhibitors was measured by a redox-linked colorimetric method.RESULTS: Fluvastatin, which was reported to have antioxidative activity, repressed the ileal ulcer formation in rats treated with BFMeT an NSAIDs. However, the other HMG-CoA reductase inhibitors (pravastatin and atorvastatin)did not repress the ileal ulcer formation. Among these HMG-CoA reductase inhibitors, fluvastatin showed a significantly stronger reducing power than the others(pravastatin, atorvastatin).CONCLUSION: Fluvastatin having the antioxidaitive activity suppresses ulcer formation in rats induced by NSAIDs.

Expression of Serum and Glucocorticoid-inducible Kinase1 in Diabetic Rats and Its Modulation by Fluvastatin

The expression of serum and glucocorticoid-induced protein kinase in the renal cortex of diabetic rats was examined, and the function of signal transduction mediated by SGK1 in diabetic nephropathy and its modulation by fluvastatin were also investigated. 24 male Wistar rats were randomly divided into normal control group （n = 8）, diabetic nephropathy group （n = 8） and fluvastatin-treated diabetic nephropathy group （15 mg/kg/d, n=8）. The metabolic parameters were measured at the 8th week. The expression of transforming growth factor β1 （TGF-β1） and fibronectin （FN） was immunohistochemically examined. The expression of SGK1 was detected by RT-PCR and Western blot, and CTGF mRNA was assessed by RT-PCR. As compared to DN, blood glucose, 24-h urinary protein, Cer and kidney weight index were all decreased and the weight was increased obviously in group F. At the same time, mesangial cells and extracellular matrix proliferation were relieved significantly. The levels of cortex SGK1 mRNA and protein were up-regulated, and both TGF-β1 and FN were down-regulated by fluvastatin. The mRNA of SGK1 was positively correlated with the CTGF, TGF-β1 and FN. SGK1 expression is markedly up-regulated in the renal cortex of DN group and plays an important role in the development and progress of diabetic nephropathy by means of signal transduction. Fluvastatin suppressed the increased SGKlmRNA expression in renal cortex and postponed the development of diabetic nephropathy.

The influence of genetic polymorphisms in drug metabolism enzymes and transporters on the pharmacokinetics of different fluvastatin formulations

The purpose of the present study was to investigate the impact of genetic polymorphism on fluvastatin pharmacokinetics.In addition,we compared the fluvastatin pharmacokinetics differences between extended-release(ER)80 mg tablet and immediate-release(IR)40 mg capsule in terms of drug metabolism enzyme and transporter genetic polymorphisms.In this open-label,randomized,two-period,two-treatment,crossover study(n=24),effects of ABCG2,SLCO1B1,ABCB1,CYP2C9 and CYP3A5 polymorphisms on the pharmacokinetics of fluvastatin were analyzed.The administration dosage for IR 40 mg and ER 80 mg were twice and once daily,respectively,for total 7 d.Blood samples for pharmacokinetic evaluation were taken on the 1st and 7th d.The lower exposure following ER was observed.For ER tablets,SLCO1B1 T521C genotype correlated with AUC 0-24 of repeat doses(P=0.010).SLCO1B1 T521C genotype had no statistically significant effect on AUC 0-24 of IR capsule of fluvastatin after single or repeated doses.In vitro study demonstrated that when the concentration of fluvastatin was low(<1μmol/l),the uptake of fluvastatin in the HEK293-OATP1B1 with SLCO1B1521TT(K m=0.18μmol/l)was faster than that with SLCO1B1521CC(K m=0.49μmol/l),On the other hand,when concentration reached to higher level(>1μmol/l),transport velocity of fluvastatin by HEK293-OATP1B1 with SLCO1B1521TT(K m=11.4μmol/l)and with SLCO1B1521TCC(K m=15.1μmol/l)tend to be the same.It suggests that the increased effect of SLCO1B1 T521C genotype on ER formulation of fluvastatin was mainly caused by lower blood concentrations.We recommend that formulation should be incorporated into future pharmacogenomics studies.

Inhibitory Effects of NO-Fluvastatin on Proliferation of Human Lens Epithelial Cells in vitro by Modulating Cell Cycle Regulatory Proteins

The effects of NO-Fluvastatin on proliferation of human lens epithelial cells （HLECs） and the action mechanism were investigated. Cell proliferation was assessed by MTT assay. Cell cycle was analyzed by flow cytometry. The expression of cell cycle regulatory proteins CyclinE mRNA and P21waf1 mRNA was detected by reverse transcription polymerase chain reaction （RT-PCR）. MTT staining colorimetry showed that HLECs proliferation was markedly inhibited by NO-Fluvastatin and the effect was dependently related to time （24, 48 and 72 h） and dosage （1, 5 and 20 μmol/L）. Flow cytometry revealed that NO-Fluvastatin could significantly block HLECs in the G0/G1 phase, resulting in the increased cells in the G0/G1 phase and decreased in the S phase （P〈0.05）. RT-PCR showed that NO-Fluvastatin could obviously inhibit the CyclinE mRNA expression and induce the P21waf1 mRNA expression as compared with the negative control groups （P〈0.05）. This experiment suggested that NO-Fluvastatin could suppress the proliferation of HLECs by regulating cell cycle regulatory proteins （inhibiting the expression of CyclinE mRNA and inducing the expression of P21waf1 mRNA）, resulting in the arrest of HLECs in the G0/G1 phase, which can offer theory basis for NO-Fluvastatin in treating posterior capsular opacification in clinic practice.

INHIBITORY EFFECT OF FLUVASTATIN ON AORTIC INTIMAL THICKENING IN NORMOCHOLESTEROLEMIC RABBITS

The anti atherosclerotic effect of fluvastatin at doses insufficient to lower serum cholesterol on the catheter induced intimal thickening and possible mechanism were investigated in abdominal aorta of rabbits. Methods.Fifty six rabbits were randomly divided into eight groups(n=7,each).Fluvastatin was given mixed with food at daily dose of8mg/kg starting 5 days before catheterization.Light microscope,immunohistochemistry,transmission electron microscope and RT PCR assay were applied to assess vascular smooth muscle cell (VSMC)proliferation and apoptosis, as well as oncogene expression in vascular wall. Results.At day 10 and day 15 after catheter induced denudation intima/media(I/M)thickness ratio was obviously higher, and also the percentage of PCNA positive cells and TUNEL positive cells in media was significantly higher compared with controls.The intimal hyperplasia was mostly composed of α SM actin positive cells.In rabbits given fluvastatin I/M ratio and the percentage of these positive cells significantly decreased compared with those without fluvastatin.The overexpression of proto oncogene H ras mRNA and decreased expression of anti oncogene p53 mRNA were found after vascular injury,whereas fluvastatin significantly reduced H ras mRNA and increased p53 mRNA expression. Conclusion.Proliferation of VSMC in the media and the migration to the intima can be inhibited,and apoptosis of VSMC be induced by short term use of fluvastatin after balloon catheter denudation,independent of serum lipid change.The underlying mechanism is presumably associated with the influence of fluvastatin on oncogene expression in the injured vascular wall.

Silencing of Bcl-2 gene expression by siRNA transfection in- hibits the protective effect of fluvastatin against cell apoptosis in human aortic endothelial cells

Objective To study the protective effect of fluvastatin,one of the HMG-CoA reductase inhibitors (statins),against oxygen radical-induced oxidative damages in human aortic endothelial cell,and the role of Bcl-2 in this protection.Methods Human aortic endothelial cells with or without Bcl-2 siRNA transfection were subjected to 1-100 nM of fluvastatin and 100 la hydrogen peroxide for 24 hours.Bcl-2 mRNA and protein expression were measured by Taqman quantitative PCR and Western blotting.Cell apoptosis was measured by normal and fluorescent microscopy and Cell Death Detection ELISA.Results In the Bcl-2-expressed cells,fluvastatin significantly reversed hydrogen peroxide-induced microscopic apoptosis and apoptotic DNA fragmentation,which were accompanied by a markedly upregulation of Bcl-2 expression by fluvastatin.However,the endothelial protection by fluvastatin was completely lost in Bcl-2 siRNA transfected cells.Conclusion Fluvastatin protects human endothelial cells against oxygen radical-induced cell apoptosis in vitro,and this protection seemed to be mediated in a Bcl-2 dependent pathway.(J Geriatr Cardil 12008;5:33-38)

Influence of genetic polymorphisms in drug metabolism enzymes and transporters on pharmacokinetics of different fluvastatin formulations

OBJECTIVE The purpose of the present study was to investigate the impact of fluvas.tatin formulation on the pharmacokinetics-genetic polymorphis relationship.METHODS We compared the difference between the pharmacokinetics of fluvastatin as an extended-release(ER) 80 mg tablet and an immediate-release(IR) 40 mg capsule in terms of drug metabolism enzyme and transporter ge.netic polymorphisms.In this open-label,randomized,two-period,two-treatment,crossover study,ef.fects of BCRP,SLCO1B1,MDR1,CYP2C9,and CYP3A5 polymorphisms on the pharmacokinetics of fluvastatin were analyzed in 24 healthy individuals.Each treatment duration was 7 days with a washout period of 7 days between the crossover.Serum concentration of fluvastatin was evaluated using highperformance liquid chromatography-tandem mass spectrometry.RESULTS The SLCO1 B1 T521 C genotype had no statistically significant effect on IR 40 mg capsule of fluvastatinafter single or repeated doses.However,for the ER 80 mg tablet,the SLCO1 B1 T521 C genotype correlated with the AUC_(0-24) of repeat doses(P=0.01).The CYP2C9*3 genotype correlated with the AUC_(0-24) after the first dose IR40 mg capsule(P<0.05);however,the difference between CYP2C9*1/*1 and CYP2 C9*1/*3 was not statistically significant after repeated doses.CONCLUSION The effect of SLCO1B1T521C on fluvas.tatin exposure was observed and was more profound in ER and repeated dose administration than in IR and single dose administration.We recommend that formulation should be incorporated into future pharmacogenomics studies and clinical implication guidelines.

Effect of fluvastatin combined with β-receptor-blockers on cardiac function and peripheral blood NF-κB and sST2 in patients with coronary heart disease complicated with heart failure

Objective: To investigate the effects of fluvastatin combined with β-receptor-blockers on cardiac function and peripheral blood NF-κB and sST2 in patients with coronary heart disease (CHD) complicated with heart failure. Methods: A total of 90 CHD patients complicated with heart failure from September 2016 to September 2017 were selected and randomly divided into the control group and the observation group, with 45 cases in each group. The control group was treated with arotinolol and the observation group was treated with arotinolol combined with fluvastatin. The clinical efficacy of the two groups after treatment was compared. The cardiac function index, blood lipid index, inflammatory factor and serum NF-κB and sST2 levels were detected and compared between the two groups. Results: The effective rate of the observation group was significantly higher than that of the control group (P<0.05). After treatment, the cardiac function indexes of the two groups were significantly improved (P<0.05). The LVEF and LVFS of the observation group were significantly higher than those of the control group, and LVEDD and LVESD of the observation group were significantly lower those of the control group (P<0.05). The serum lipid index and inflammatory factors of the two groups were significantly decreased after treatment. The hs-CRP, TNF-α, TC and LDL-C of the observation group were significantly lower than those of the control group after treatment (P<0.05). After treatment, the serum NF-κB and sST2 were significantly decreased in both groups, and the serum NF-κB and sST2 in the observation group were significantly lower than those in the control group. There was no significant difference in the incidence of adverse reactions between the two groups (P<0.05). Conclusions: Fluvastatin combined with β-receptor-blockers can reduce the level of blood lipid and inflammatory factors more effectively and improve the clinical efficacy of the CHD patients complicated with heart failure. It can effectively reduce serum NF-κB and sST2 more effectively and improve prognosis.

高效液相色谱法测定氟伐他汀钠缓释片的有关物质

目的 建立氟伐他汀钠缓释片有关物质的高效液相色谱(HPLC)测定方法,为建立氟伐他汀钠缓释片的质量控制标准提供参考。方法 色谱柱为ZORBAX Eclipse Plus C18Rapid Resolution(75 mm×4.6 mm, 3.5μm);流动相A:pH值7.2缓冲液-甲醇乙腈混合液(体积比90:10),流动相B:pH值7.2缓冲液-甲醇乙腈混合液(体积比10:90),梯度洗脱;流速:2.0 mL·min^(-1);柱温:35℃;检测波长:305,365 nm;进样量:25μL。结果 主峰与各杂质峰均能达到完全分离;杂质A、B、C、D、E、F、G的检测限分别是0.069 5,0.032 5,0.059 3,0.074 0,0.050 3,0.048 6,0.026 3μg·mL^(-1),杂质A、B、C、D、E、F、G的定量限分别是0.2318,0.108 3,0.197 8,0.246 6,0.167 6,0.162 1,0.087 6μg·mL^(-1);在研究的浓度范围内与各自峰面积呈良好的线性关系,杂质A、B、C、D、E、F、G的线性浓度范围分别是0.231 8~6.0,0.108 3~1.2,0.197 8~1.2,0.246 6~3.0,0.167 6~1.2,0.162 1~3.0,0.087 6~1.2μg·mL^(-1);回收率89.8%~103.5%;供试品溶液在5℃中保存54 h稳定。结论 该方法简单、准确、可靠,能满足氟伐他汀钠缓释片有关物质的检测要求。

氟伐他汀钠通过下调lncRNA PTPRG-AS1表达对结直肠癌SW620细胞增殖凋亡的影响

目的:探究氟伐他汀钠对结直肠癌SW620细胞增殖、凋亡的影响及可能机制。方法:体外培养SW620细胞、正常结直肠上皮FHC细胞,qRT-PCR法检测细胞中lncRNA PTPRG-AS1表达。SW620细胞分为对照组、氟伐他汀钠-低、中、高组、si-PTPRG-AS1组、si-NC组、氟伐他汀钠+pcDNA-PTPRG-AS1组、氟伐他汀钠+pcDNA组。CCK-8法、克隆形成实验、流式细胞术分别检测细胞活性、克隆形成数、凋亡率,Western blot法检测凋亡相关蛋白(cleaved-caspase3、cleaved-caspase9)表达。结果:结直肠癌SW620细胞中lncRNA PTPRG-AS1表达量高于FHC细胞(4.38±0.31 vs 1.00±0.00,P<0.05);氟伐他汀钠-低、中、高组细胞活性、克隆形成数均低于对照组(P<0.05),细胞凋亡率、蛋白(cleaved-caspase3、cleaved-caspase9)表达均高于对照组(P<0.05),且lncRNA PTPRG-AS1表达量低于对照组(P<0.05);si-PTPRG-AS1组细胞活性、克隆形成数均低于si-NC组(P<0.05),细胞凋亡率、蛋白(cleaved-caspase3、cleaved-caspase9)表达均高于si-NC组(P<0.05);氟伐他汀钠+pcDNA-PTPRG-AS1组细胞活性、克隆形成数均高于氟伐他汀钠+pcDNA组(P<0.05),细胞凋亡率、蛋白(cleaved-caspase3、cleaved-caspase9)表达均低于氟伐他汀钠+pcDNA组(P<0.05)。结论:氟伐他汀钠可能通过下调lncRNA PTPRG-AS1表达抑制结直肠癌SW620细胞增殖,并促进其凋亡。

氯吡格雷联合氟伐他汀在脑梗塞标准化治疗中的临床疗效分析

目的:探究对于脑梗塞患者在标准化治疗中应用氯吡格雷与氟伐他汀联合治疗的作用效果。方法:本次以随机方式将我院起止时间为2021年3月-2022年3月接收的93例脑梗塞患者区分为两组,试验组与参照组分别纳入47例和46例,参照组在标准化治疗中应用氯吡格雷,试验组在参照组基础上应用氟伐他汀,对比两组临床各项指标。结果:试验组LDL-C、TG及TC均低于参照组,HDL-C高于参照组,两组患者在NIHSS评分方面比较,试验组更低,两组患者在FMA评分与ADL评分方面比较,试验组更高,临床疗效(97.87%)优于参照组(82.61%),P<0.05,组间数值符合统计学意义;两组患者用药后不良反应相比较无显著差异,P>0.05,组间数值不符合统计学意义。结论:脑梗塞在标准化治疗中应用氯吡格雷与氟伐他汀联合治疗能有效降低改善血脂水平,减轻神经功能缺损,提高运动功能与活动能力,提升治疗效果,且具有一定安全性。

氯吡格雷+氟伐他汀治疗脑梗死的效果观察及生活能力评分影响分析

目的 探究氯吡格雷+氟伐他汀治疗脑梗死的效果。方法 方便选择2021年1—12月聊城市退役军人医院收治的脑梗死患者98例作为研究对象。采取随机数表法分成对照组(氯吡格雷)和研究组(氯吡格雷+氟伐他汀)各49例。比较疗效、血脂、炎症指标、神经功能、生活能力、不良反应。结果 研究组有效率为93.88%,高于对照组的79.59%,差异有统计学意义(χ^(2)=4.346,P=0.037)。治疗前两组TC、TG、LDL-C、HDL-C水平比较,差异无统计学意义(P>0.05);治疗后两组TC、TG、LDL-C水平均下降,HDL-C水平提升,且研究组优于对照组,差异有统计学意义(P<0.05)。治疗前两组Lp-PLA2、sVCAM-1水平比较,差异无统计学意义(P>0.05);治疗后两组Lp-PLA2、sVCAM-1水平均降低,且研究组优于对照组,差异有统计学意义(P<0.05)。治疗前两组NIHSS量表、Barthel量表得分比较,差异无统计学意义(P>0.05);治疗后两组NIHSS量表得分减少,Barthel量表得分增加,且研究组优于对照组,差异有统计意义(P<0.05)。两组不良反应发生率比较,差异无统计学意义(P>0.05)。结论 氯吡格雷与氟伐他汀联合使用治疗脑梗死的效果理想,值得推广。

氟伐他汀联合氯吡格雷治疗脑梗死患者的效果

目的:观察氟伐他汀联合氯吡格雷治疗脑梗死患者的效果。方法:选取2019年1月至2022年2月该院收治的96例脑梗死患者进行前瞻性研究,按照随机数字表法将其分为对照组和观察组各48例。对照组采用氯吡格雷治疗,观察组在对照组基础上联合氟伐他汀治疗,比较两组临床疗效、治疗前后炎性因子[C反应蛋白(CRP)、白细胞介素-6(IL-6)]水平、血脂指标[总胆固醇(TC)、三酰甘油(TG)]水平、神经功能缺损[美国国立卫生研究院卒中量表(NIHSS)]评分、日常生活能力[日常生活能力量表(ADL)]评分和不良反应发生率。结果:观察组治疗总有效率为95.83%(46/48),高于对照组的72.92%(35/48),差异有统计学意义(P<0.05);治疗后,两组CRP、IL-6、TC、TG水平均低于治疗前,且观察组低于对照组,差异有统计学意义(P<0.05);治疗后,两组NIHSS评分均低于治疗前,且观察组低于对照组,两组ADL评分均高于治疗前,且观察组高于对照组,差异有统计学意义(P<0.05);两组不良反应发生率比较,差异无统计学意义(P>0.05)。结论:氟伐他汀联合氯吡格雷治疗脑梗死患者可提高治疗总有效率和日常生活能力评分,改善炎性因子和血脂指标水平,降低神经功能缺损评分,效果优于单纯氯吡格雷治疗。

联合应用氯吡格雷和氟伐他汀治疗脑梗死的疗效及对患者生存质量的影响

目的探究联合应用氯吡格雷和氟伐他汀治疗脑梗死的疗效及对患者生存质量的影响。方法选择南阳市中心医院2020年10月至2022年10月收治的72例脑梗死患者,采用随机数字表法将其分为参照组(氯吡格雷治疗)和试验组(氯吡格雷联合氟伐他汀治疗)各36例,观察两组患者治疗效果、生活质量、血清炎性因子水平、纤维蛋白原和中枢神经特异性蛋白水平。结果试验组治疗有效率高于参照组(80.56%),差异有统计学意义(P<0.05)。用药前,两组患者的ADL评分比较,差异无统计学意义(P>0.05);用药后,试验组日常生活能力表(ADL)评分低于参照组,差异有统计学意义(P<0.05);用药前,两组患者各炎性因子指标浓度差异无统计学意义(P>0.05);用药后,试验组血清中各炎性因子指标浓度低于参照组,差异有统计学意义(P<0.05)。用药前,两组患者纤维蛋白原(FIB)、中枢神经特异性蛋白(S100-β)水平差异无统计学意义(P>0.05);用药后,试验组血清中FIB、S100β浓度低于参照组,差异有统计学意义(P<0.05)。结论氟伐他汀联合氯吡格雷可显著改善患者临床症状,加快神经功能缺损的恢复,改善炎性因子,值得应用。

氟维司群联合阿那曲唑治疗雌激素受体阳性的晚期乳腺癌的临床疗效

目的:探讨氟维司群联合阿那曲唑治疗雌激素受体(Estrogen receptor,ER)阳性的晚期乳腺癌(Advanced breast cancer,ABC)患者的临床疗效。方法:选取2012年1月至2022年1月三门峡市中心医院收治的232例ER阳性ABC患者作为研究对象进行回顾性分析,根据治疗方案不同,分为阿那曲唑组和氟维司群联合组,各116例。比较两组患者的疗效、中位无进展生存期(Progression free survival,PFS)、总生存期(Overall survival,OS)、不良反应发生率。结果:氟维司群联合组的临床获益率(Clinical benefit rate,CBR)、PFS和OS明显高于阿那曲唑组(P<0.05);两组客观缓解率(Objective response rate,ORR)和不良反应发生率无明显差异(P>0.05)。结论:氟维司群联合阿那曲唑治疗ER阳性ABC患者,可显著提升CBR,延长PFS和OS,但未显著增加不良反应,具有较高的用药安全性。