地塞米松冲击疗法治疗成人原发免疫性血小板减少症的疗效观察

目的：观察地塞米松冲击疗法治疗成人原发免疫性血小板减少症（ITP）的临床疗效。方法：自2006年7月-2013年9月间笔者所在医院收治成人ITP患者38例,患者均给予胸腺肽α1联合大剂量维生素C治疗,其中19例同时应用4 d地塞米松冲击治疗,观察临床症状、血小板计数和不良反应。结果：胸腺肽α1＋大剂量维生素C治疗组总有效率78.9%,平均起效时间（16.8±3.2）d;胸腺肽α1＋大剂量维生素C联合地塞米松冲击治疗组总有效率84.2%,平均起效时间（6.7±2.7）d。两种治疗方案的不良反应均较轻微。结论：胸腺肽α1联合大剂量维生素C与冲击量地塞米松联合应用治疗成人ITP疗效较好,副作用少,可缩短起效时间。     

Films based on the biopolymer poly(3-hydroxybutyrate) as platforms for the controlled release of dexamethasone

Controlled drug delivery aims to achieve an effective drug concentration in the action site for a desired period of time, while minimizing side effects. In this contribution, biodegradable poly(3-hydroxybutyrate) films were evaluated as a reservoir platform for dexamethasone controlled release. These systems were morphological and physicochemically characterized. In vitro release assays were performed for five different percentages of drug in the films and data were fitted by a mathematical model developed and validated by our research group. When the profiles were normalized, a single curve properly fitted all the experimental data. Using this unique curve, the dissolution efficiency (DE), the time to release a given amount of drug (t_X%), and the mean dissolution time were calculated. Furthermore, the dissolution rate, the initial dissolution rate (a%) and the intrinsic dissolution rate were determined. The a% mean value was 1.968 × 10^?2% released/min, t_80% was about 14 days, and the DE was 59.6% at 14 days and 66.5% at 20 days. After 2 days, when approximately 40% of the drug was released, the dissolution rate decreased about 60% respect to the initial value. The poly(3-hydroxybutyrate) platforms behaved as an appropriate system to release and control the dexamethasone delivery, suggesting that they could be an alternative to improve drug therapy.     

地塞米松联合尿激酶治疗结核性胸膜炎的临床疗效

目的：探讨地塞米松联合尿激酶治疗结核性胸膜炎的临床疗效。方法结核性胸膜炎120例根据入院单双号顺序平分为治疗组与对照组各60例,两组都采用中心静脉导管胸腔置入术,对照组胸腔内注入地塞米松治疗,治疗组胸腔内注入地塞米松联合尿激酶治疗。结果治疗组与对照组的有效率分别为83.3%、66.7%,组间对比有明显差异（P＜0.05）。治疗后治疗组的躯体评分、心理功能、症状与副作用、社会功能评分明显高于对照组,差异有统计学意义（P＜0.05）。结论地塞米松联合尿激酶治疗结核性胸膜炎有很好的疗效,可有效改善患者的生活质量,有很好的临床推广价值。     

周围神经阻滞局麻药中添加右美托咪定或地塞米松对阻滞效果的影响

如何改善周围神经阻滞的效果,一直以来是麻醉医生积极探索的方向。近年来,周围神经阻滞局麻药中添加佐剂右美托咪定和地塞米松的研究日渐增多,故本文就局麻药中添加地塞米松、右美托咪定在各个神经部位的应用以及各研究观察得到的相关风险进行综述,旨在为周围神经阻滞麻醉的实践提供参考。     

高效液相色谱法测定氯霉素地塞米松搽剂中二组份的含量

目的建立一种快速、准确的高效液相色谱法测定氯霉素地塞米松搽剂中的氯霉素和醋酸地塞米松含量的方法。方法色谱柱岛津VP-ODS(5μm,150mm×4.6mm)流动相:甲醇-水(70∶30);流速:1mL.m in-1;检测波长:240nm;柱温:室温;进样量:20μL。结果氯霉素进样量在5.00μg~30.00μg范围内线性良好,r=0.99999。平均回收率为99.70%,RSD=0.68%(n=9);醋酸地塞米松进样量在0.13μg~0.75μg范围内线性良好,r=0.99999。平均回收率为99.97%,RSD=1.38%(n=9)结论试验结果表明本法简便快速,重现性好,结果准确可靠,可以作为氯霉素地塞米松搽剂中氯霉素和醋酸地塞米松含量测定的方法。     

地塞米松混合丁卡因表面麻醉对病人拔管心血管反应和咽喉炎的影响

目的:评价气管插管前应用地塞米松混合丁卡因用于咽喉、气管内表面麻醉后对术后病人清醒时耐管效果、拔管心血管反应及拔管后咽喉炎发病率的影响。方法:将60例病人随机等分为丁卡因混合地塞米松组(试验组)和对照组。在诱导成功后:试验组后用地塞米松5mg加1%地卡因3m l对咽喉、气管内充分表面喷雾麻醉,面罩给氧3m in后插入气管导管。对照组在麻醉诱导成功后用生理盐水3m l对咽喉部、气管内表面喷雾,面罩给氧3m in后插入气管导管。观察记录各组:①术后病人清醒时的耐管效果。②拔管前、拔管即刻、拔管后1、3、5m in的平均动脉压(MAP)、心率(HR)。③术后24h咽喉炎发生程度和发病率。结果:全部手术在2h内完成,试验组病例清醒时的耐管效果显著优于对照组(P<0.01)。对照组病例在吸痰拔管后即刻出现MAP升高、HR加快,并延续至拔管后3m in,与拔管前相比差异有显著性(P<0.05),5m in时恢复正常。而实验组病例在各时间点的MAP和HR与拔管前相比差异无显著性。对照组拔管后即刻、1m in、3m in时的HR、MAP与实验组同时点相比差异有显著性(P<0.05)。拔管后24h咽喉炎发病率显示试验组显著低于对照组(P<0.01)。结论:气管插管前应用地塞米松混合地卡因于咽喉、气管内表面麻醉能显著增强短时手术病人术后清醒时的耐管效果,并能预防拔管时引起的心血管反应,同时减少拔管后咽喉炎的发病率。     

鼓室注射地塞米松原位凝胶的体内分布及药动学研究

目的研究鼓室注射（intratympanic injection,IT）地塞米松磷酸钠（DSP）温度敏感原位凝胶的体内分布特征,探讨载药凝胶经圆窗膜吸收的规律,为其临床应用提供理论依据。方法制备DSP温度敏感原位凝胶。建立在外淋巴（perilymph,PL）、脑脊液（cerebrospinal fluid,CSF）和血中DSP及地塞米松（Dex）的HPLC测定方法。经鼓室注射DSP凝胶,并与溶液剂相比较,测定药物的体内分布和在PL中的药代动力学参数。结果鼓室注射DSP原位凝胶,Dex在内耳组织的局部生物利用度显著提高,AUC是静脉注射溶液的593．7倍,药物作用时间明显延长,同鼓室注射溶液相比,t1／2高28．6倍,MRT增加了近5倍。而且,当采用鼓室注射时,药物在体内其他部位分布甚少,在血和CSF中的浓度均远远低于PL。结论经鼓室给药的DSP原位凝胶对耳蜗具有明显的定位释药作用和缓释效果。     

地塞米松治疗重症胰腺炎并发急性呼吸窘迫综合征的临床疗效分析

目的 评估地塞米松治疗重症急性胰腺炎并发急性呼吸窘迫综合症患者的有效性和安全性.方法 58例重症急性胰腺炎患者按收住时间随机分成两组,治疗组除采用常规组的治疗措施外,加用大剂量地塞米松.比较两组急性呼吸窘迫综合症(ARDS)的发生率和病死率.结果 58例患者中,常规治疗组有17例(占65.4%)并发ARDS,死亡1 0例(占38.2%);地塞米松治疗组有10例(占35.7%)并发ARDS,死亡2例(占7.1%),组间差异有统计学意义,但在腹痛缓解时间、首次排便时间、消化道出血发生率及平均住院天数上,组间差异无统计学意义.结论 地塞米松对重症急性胰腺炎并发ARDS的疗效显著,能降低其病死率.     

Intranasal Dexamethasone Reduces Mortality and Brain Damage in a Mouse Experimental Ischemic Stroke Model

Neuroinflammation triggered by the expression of damaged-associated molecular patterns released from dying cells plays a critical role in the pathogenesis of ischemic stroke. However, the benefits from the control of neuroinflammation in the clinical outcome have not been established. In this study, the effectiveness of intranasal, a highly efficient route to reach the central nervous system, and intraperitoneal dexamethasone administration in the treatment of neuroinflammation was evaluated in a 60-min middle cerebral artery occlusion (MCAO) model in C57BL/6 male mice. We performed a side-by-side comparison using intranasal versus intraperitoneal dexamethasone, a timecourse including immediate (0 h) or 4 or 12 h poststroke intranasal administration, as well as 4 intranasal doses of dexamethasone beginning 12 h after the MCAO versus a single dose at 12 h to identify the most effective conditions to treat neuroinflammation in MCAO mice. The best results were obtained 12 h after MCAO and when mice received a single dose of dexamethasone (0.25 mg/kg) intranasally. This treatment significantly reduced mortality, neurological deficits, infarct volume size, blood–brain barrier permeability in the somatosensory cortex, inflammatory cell infiltration, and glial activation. Our results demonstrate that a single low dose of intranasal dexamethasone has neuroprotective therapeutic effects in the MCAO model, showing a better clinical outcome than the intraperitoneal administration. Based on these results, we propose a new therapeutic approach for the treatment of the damage process that accompanies ischemic stroke.Electronic supplementary materialThe online version of this article (10.1007/s13311-020-00884-9) contains supplementary material, which is available to authorized users.     

Sudden sensorineural hearing loss – A contemporary review of management issues

Sudden sensorineural hearing loss (SSNHL) is an enigmatic entity, with obscure pathophysiology and debatable efficacy of the treatment agents used. An underlying cause is identified in only 10–15% of cases. The management of the remaining patients, classified as ‘idiopathic’, is empirical, and is conventionally with systemic steroids, vasodilator therapy, rheological agents, and antioxidants, to list a few amongst the host of the agents employed for the treatment. The availability of conflicting outcomes and lack of conclusive evidence has resulted in the propagation of consensus-based treatment protocols. In the present review, we discuss the various controversial issues and newer developments in the management of idiopathic SSNHL. The current review aims to present a narrative outlook of the updated evidence base available from PUBMED, augmented with relevant designated publications.