血塞通软胶囊联合比索洛尔治疗2型糖尿病合并左室舒张功能减退临床观察

目的探讨血塞通软胶囊联合比索洛尔治疗2型糖尿病合并左室舒张功能减退的临床效果。方法选择2017年8月-2018年8月治疗的2型糖尿病合并左室舒张功能减退的患者120例,依据随机数字的方法分为对照组(60例)和观察组(60例),患者入院后均常规治疗,对照组在常规治疗基础上给予比索洛尔,观察组在对照组治疗方法基础上给予血塞通软胶囊。对两组治疗前后的空腹血糖(FPG),餐后2 h血糖(2hPG),糖化血红蛋白(HbA1c),E波峰值流速/A波峰值流速(E/A),E峰减速时间(EDT),左心室容舒张时间(IVRT),血清B型尿钠肽(BNP)浓度进行比较。对两组的治疗效果进行比较。对治疗过程中的不良反应进行对比。结果经过治疗后,对照组的FPG从(7.85±0.67)mmol/L降低到(6.45±0.48)mmol/L,2 hPG从(12.21±1.23)mmol/L降低到(9.35±1.45)mmol/L,HbA1c从(9.31±0.95)%降低到(8.22±0.68)%,观察组的FPG从(7.89±0.71)mmol/L降低到(5.88±0.23)mmol/L,2hPG从(12.37±1.35)mmol/L降低到(8.27±1.34)mmol/L,HbA1c从(9.38±0.88)%降低到(7.14±0.71)%,观察组的变化幅度大于对照组,数据差异均具有统计学意义(t=8.295,4.237,8.509,P<0.05),经过治疗后,对照组的E/A从(0.83±0.13)升高到(0.98±0.17),EDT从(80.51±5.47)ms升高到(92.81±6.23)ms,IVRT从(121.48±7.79)ms升高到(131.51±7.66)ms,观察组的E/A从(0.84±0.12)升高到(1.18±0.21),EDT从(81.65±5.67)ms升高到(98.57±6.72)ms,IVRT从(120.98±7.81)ms升高到(139.25±6.81)ms,观察组的变化幅度大于对照组,数据差异均具有统计学意义(t=-5.734,-4.869,-5.849,P<0.05),经过治疗后,对照组的血清BNP浓度从(222.56±43.25)ng/L降低到(167.11±27.61)ng/L,观察组的血清BNP浓度从(228.92±44.91)ng/L降低到(131.25±25.07)ng/L,观察组的变化幅度大于对照组,数据差异均具有统计学意义(t=7.448,P<0.05),观察组治疗效果优于对照组,数据差异具有统计学意义(z=-2.184,P<0.05),两组的头晕[8.33%(5/60)vs.5.00%(3/60)],水肿[3.33%(2/60)vs.6.67%(4/60)],面部潮红[11.67%(7/60)vs.8.33%(5/60)],头痛[5.00%(3/60)vs.1.67%(1/60)],发生率数据差异均不具有统计学意义(χ^2=0.134,0.175,0.370,0.259,P>0.05)。结论利用血塞通软胶囊联合比索洛尔治疗2型糖尿病合并左室舒张功能减退的患者,可以改善血糖指标和心室功能指标,提升治疗效果,安全性良好。     

经皮肺动脉瓣植入术在肺动脉瓣反流患者中的临床应用

经皮肺动脉瓣植入术(PPVI)在我国作为一种新兴的技术,开展相对较晚,但随着我国医疗水平的不断提高以及临床对于右心室流出道梗阻的先天性心脏病患者术后出现重度肺动脉瓣反流的不断重视,PPVI在我国得到了飞速发展。近十几年来,欧美国家已在临床成熟应用PPVI,相对于传统外科手术而言其具有微创、可重复性、术后疗效好等优点。现对PPVI在肺动脉瓣反流患者中的临床应用进行叙述。     

Clinical and molecular spectrum of Wiedemann-Steiner syndrome,an emerging member of the chromatinopathy family

Wiedemann-Steiner syndrome (OMIM #605130) is a rare congenital malformation syndrome characterized by hypertrichosis cubiti associated with short stature; consistent facial features, including long eyelashes, thick or arched eyebrows with a lateral flare, wide nasal bridge, and downslanting and vertically narrow palpebral fissures; mild to moderate intellectual disability; behavioral difficulties; and hypertrichosis on the back. It is caused by heterozygous pathogenic variants in KMT2A. This gene has an established role in histone methylation, which explains the overlap of Wiedemann-Steiner syndrome with other chromatinopathies, a heterogeneous group of syndromic conditions that share a common trigger: The disruption of one of the genes involved in chromatin modification, leading to dysfunction of the epigenetic machinery.