股骨头缺血性坏死骨髓水肿MRI研究

目的通过核磁共振(MRI)影像学探讨股骨头缺血性坏死(ONFH)患者骨髓水肿的程度与坏死分期、髋关节液体量、临床症状之间的相关性,以提高骨髓水肿表现在股骨头缺血性坏死中临床意义的认识。方法回顾性分析经MRI扫描的ONFH病例117例、173髋次,根据MRI表现将骨髓水肿分为0～3级、将坏死分为Ⅰ～Ⅳ期、将髋关节液体量分为1～4型,另外将临床表现分为0～3级,分别统计分析不同等级的骨髓水肿在各个坏死分期、各型关节液体量、各级别临床症状下的分布情况。结果 173髋次MRI扫描中,骨髓水肿112髋次(64.7%),其中1级水肿27髋次(24.1%)、2级水肿44髋次(39.3%)、3级水肿41髋次(36.6%)。随骨髓水肿分级加重,坏死分期、髋关节液体量分型和临床症状分级均有不同程度的加重。结论骨髓水肿是ONFH的重要伴随征象,与坏死分期、髋关节液体量、临床症状密切相关;3级骨髓水肿多出现于ONFH的中晚期,提示病情进展、预后不良;骨髓水肿程度可作为评价ONFH进展情况的重要指标。     

股骨头缺血坏死的介入治疗

目的探讨经导灌注药物治疗股骨头缺血坏死的疗效。方法对11例股骨头缺血坏死患者,采用穿刺插管的方法,将药物直接灌注至患侧股骨头的供血动脉内。结果介入治疗后,疼痛消失6例,减轻4例,无明显改善1例。结论介入方法治疗股骨头缺血坏死有一定价值。     

股骨头缺血坏死的MRI诊断

目的：探讨MRI在成年人股骨头缺血性坏死（ANFH）中的诊断价值。方法：对62例成年ANFH患者行双侧股骨头MRI检查．分析其对ANFH的显示能力。结果：62例患者（84个股骨头1均存在骨坏死表现。其中10个股骨头MRI表现为,股骨头形态正常,头内仅可见持重区骨小梁模糊或局限性斑点状及线条状长T1、长T2信号影;21个股骨头表现为,股骨头形态正常,关节间隙正常,头内可见斑片状、囊状或不规则形状长T1、长T2信号影,相应部位STIR序列呈高信号：35个股骨头表现为,股骨头轻度变形,关节间隙基本正常,关节腔大量积液,头内表现为较大片状或较宽条带样长T1、长T2信号影,STIR序列可见相应区域骨髓腔明显水肿;18个股骨头表现为,股骨头塌陷变形,关节间隙增宽或变窄,关节腔内大量积液,头内呈现大片状长T1、长T2信号影,并伴有骨质吸收,STIR序列呈大片高信号影。结论：MRI诊断ANFH具有高度敏感性,能准确反映股骨头坏死部位和分期,可达到早期诊断的目的。     

激素性股骨头缺血坏死的治疗进展

股骨头坏死（osteonecrosis of the femoral head，0NFH）是一种破坏性退干行性疾病，病情进展可以引起软骨下骨和关节面软骨的塌陷，该病多发生于青壮年，平均发病年龄38岁。激素性股骨头坏死占非创伤性股骨头坏死的首位，激素性股骨头缺血性坏死是指因大剂量应用激素而造成股骨头活性成分（骨细胞、骨髓造血细胞和脂肪细胞）死亡所引起的病理过程。     

股骨头缺血坏死的介入疗效评价

成人股骨头缺血性坏死(avascular necrosis of the femoral head,ANTH)又称为无菌性坏死、骨软骨病等,发病率和致残率较高。由于其发病原因复杂,病变可累及整个髋关节,导致关节软骨破坏、股骨头坏死、塌陷性改变,从而引起髋关节功能障碍甚至功能丧失。本文探讨成人股骨头缺血坏死的影像诊断、临床治疗时机、治疗方法的有效性等。     

股骨头缺血坏死介入治疗22例探讨

目的探讨介入治疗股骨头缺血坏死的临床疗效。方法第1步,患髋减压术。于患侧股骨粗隆外侧壁施行骨钻钻孔1～2个,以期达到股骨头微静脉压力下降,改善股骨头微循环。第2步,采用Sedinger技术经对侧股动脉穿刺插管,选择至患侧旋股内侧动脉、旋股外侧动脉及闭孔动脉,分别灌注尿激酶、罂粟碱、低分子右旋糖酐溶解微小血栓,疏通改善股骨头血供。第3步,术后尿激酶、复方党参注射液或血塞通维持治疗1周。第4步,较长期服用小剂量阿司匹林,3个月内不做激烈活动及负重劳动。第5步,视情况重复上述第1～3步骤治疗程序。结果 22例患髋均不同程度疼痛缓解,临床症状明显改善,有效率达100%。结论股骨头缺血坏死的介入治疗是一种非常有效的方法,在众多治疗方法中,介入治疗值得肯定。     

活血通络汤治疗股骨头缺血坏死的临床观察

目的 本文介绍活血通络汤治疗股骨头缺血坏死的临床观察。方法 口服活血通络汤六个月。结果 治愈80％、好转13.33％、无效6．67％。结论 活血通络汤治疗股骨头缺血坏死中、早期效果显著。     

髋关节退行性骨关节病误诊股骨头缺血坏死5例分析

目的通过对5例髋关节退行性骨关节病误诊为股骨头缺血坏死的X线分析,探讨二者相似点及鉴别点,防止误诊发生。方法回顾性分析5例髋关节退行性骨关节病误诊为股骨头坏死X线片,核对MR I检查。结果5例患者X线下分别表现为关节间隙变窄、股骨头密度不均、股骨头变扁等改变。结论髋关节退行性骨关节病与股骨头缺血性坏死均可存在股骨头骨质密度、形态等相似改变,可能造成误诊。X线片分析时注意细节的分析,必要时行MR I检查明确诊断。     

早期股骨头缺血坏死的MRI与SPECT临床研究

股骨头缺血性坏死(ANFH)是由不同病因引起的股骨头血液供应破坏或细胞变性导致骨的有活力成分(骨细胞、骨髓造血细胞和脂肪细胞)死亡引起的病理过程,是一种多发病,且致残率高,只有早期治疗才能防止疾病进展。本研究通过对疾病不同阶段同时进行MRI和SPECT检查,比较这两种方法在早期诊断治疗该病中的敏感性、应用价值和各自的优缺点,探讨早期诊断的最佳影像学检查途径。     

Overview of the clinical pharmacokinetics of oxcarbazepine

Oxcarbazepine (GP 47680, 10,11-dihydro-10-oxo-5H-dibenz[b,f]azepine- 5-carboxamide) is an antiepileptic drug registered worldwide by Novartis under the trade name Trileptal((R)). Trileptal((R))is approved as adjunctive therapy or monotherapy for the treatment of partial seizures in adults and in children. In the US, Trileptal((R)) is approved as adjunctive therapy in adults and in children >/=4 years of age and as monotherapy in adults and in children.Trileptal((R))is currently marketed as 150, 300 and 600mg film-coated tablets for oral administration. A 60 mg/mL (6%) oral suspension formulation has also been registered worldwide.Oxcarbazepine and its pharmacologically active metabolite, 10-monohydroxy derivative (MHD; 10,11-dihydro-10-hydro-carbamazepine; GP 47779) show potent antiepileptic activity in animal models comparable to that of carbamazepine (Tegretol((R))) and phenytoin. Oxcarbazepine and MHD have been shown to exert antiepileptic activity by blockade of voltage-dependent sodium channels in the brain.Oxcarbazepine is rapidly reduced by cytosolic enzymes in the liver to MHD, which is responsible for the pharmacological effect of the drug. This step is mediated by cytosolic arylketone reductases. MHD is eliminated by conjugation with glucuronic acid. Minor amounts (4% of the dose) are oxidised to the pharmacologically inactive dihydroxy derivative (DHD). The absorption of oxcarbazepine is complete. In plasma after a single oral administration of oxcarbazepine the mean apparent elimination half-life (t((1/2))) of MHD in adults was 8-9h. Food has no effect on the bioavailability of the highest strength of the final market image tablet (600mg). At steady state MHD displays predictable linear pharmacokinetics at doses ranging from 300 to 2400mg. In children with normal renal function, renal clearance of MHD is higher than in adults, with a corresponding reduction in the terminal t((1/2)) of MHD. Consequently, although no special dose recommendation is needed, an increase in the dose of oxcarbazepine may be necessary to achieve similar plasma levels to those in adults. In patients with moderate to severe renal impairment (creatinine clearance <30 mL/min), the elimination t((1/2)) of MHD is prolonged with a corresponding 2-fold increase in area under the concentration-time curve. Therefore, a dose reduction of at least 50% and a prolongation of the titration period is necessary in these patients. Mild-to-moderate hepatic impairment does not affect the pharmacokinetics of MHD. Based on in vitro and in vivo findings and compared with antiepileptic drugs such as carbamazepine, phenytoin and phenobarbital, oxcarbazepine has a low propensity for drug-drug interactions. In vitro, MHD inhibits the cytochrome P450 (CYP) 2C19 (ki [inhibition constant] = 88 micromol/L). At oxcarbazepine doses above 1.2g, a 40% increase in the concentration of phenytoin and a 15% increase in phenobarbital levels were observed. Oxcarbazepine/MHD at high doses may slightly increase phenobarbital and phenytoin plasma concentrations. Therefore, when using high doses of oxcarbazepine an adjustment in the dose of phenytoin may be required. In vitro, MHD is only a weak inducer of uridine diphospate (UDP)-glucuronyltransferase (UDPGT) and therefore is unlikely to have an effect on drugs that are mainly eliminated by conjugation through the UDPGT enzymes (e.g. valproic acid and lamotrigine). Weak interactions between MHD and antiepileptic drugs that are strong inducers of CYP enzymes have been identified. Carbamazepine, phenobarbital and phenytoin have been shown to reduce MHD levels by 30-40% when coadministered with oxcarbazepine, with no decrease in efficacy. Oxcarbazepine decreases the plasma hormone levels (ethinylestradiol and levonorgestrel) of oral contraceptives and may therefore have the potential to cause oral contraception failure.     

中药鉴定方法及其发展概况

目的：对中药的传统与现代鉴别技术进行综述,以期为中药鉴定方法的开发与中药质控标准的提升提供参考与借鉴。方法：对中药的传统鉴定方法、中药的现代鉴定方法、DNA条形码鉴定技术、基于DNA条形码的SNP分型方法、下一代测序（NGS）技术在中药鉴定中的应用等几个方面进行了梳理。结果：中药鉴定学在传统鉴别技术的基础上逐步形成与植物系统分类学、植物化学、生物化学、分子生物学、细胞生物学及现代仪器分析等多学科的知识和技术的大融合,为中药真伪的鉴别提供了更广泛的选择。结论：中药的应用历史源远流长,同时中药在漫长的历史沿革与传承中也存在严重的混伪、代用现象。中药鉴定是促进中药应用国际化和质控标准化的基础,是保障人民用药安全的重要前提。     

优洛芬临床应用概况

目的了解优洛芬(KPF)的临床应用情况。方法通过文献法收集有关优洛芬的临床应用资料。结果优洛芬是强效非甾类抗炎药,对治疗各种疾病引起的疼痛起到了重要作用。结论随着临床作用机制和药物新剂型的研究开发,优洛芬应用范围将越来越广。     

Overview of FTY720 clinical pharmacokinetics and pharmacology

Drug discovery programs are actively exploring for therapeutic agents targeting enzymes and receptors regulating sphingolipid metabolism and biologic functions. FTY720 is a close structural analogue of sphingosine with immunomodulatory properties. After oral administration, FTY720 is phosphorylated by sphingosine kinase to form the active moiety FTY720-phosphate, which subsequently binds to the sphingosine-1-phosphate receptor. In characterizing the safety and pharmacological effects of FTY720, detailed clinical pharmacology studies in healthy subjects and renal transplant recipients have focused on cardiac responses and lymphocyte trafficking. After the first dose, FTY720 causes a mild, transient decrease in heart rate that returns to baseline in approximately 1 to 2 weeks despite continued administration of the drug. FTY720 elicits a prompt and dose-dependent decrease in peripheral blood lymphocytes by redirecting them from the circulation to the lymph nodes without impairing lymphocyte functions. An association among FTY720 blood concentration, decrease in lymphocyte counts, and freedom from acute rejection episodes has been observed in early clinical development trials in de novo kidney transplantation.     

洛匹那韦/利托那韦临床应用概述

洛匹那韦/利托那韦是复方制剂,洛匹那韦与病毒蛋白酶催化部位结合干扰病毒装配过程,低剂量利托那韦抑制人体CYP3A介导洛匹那韦代谢,提高生物利用度,提高血浆中洛匹那韦药物浓度。本文对洛匹那韦/利托那韦在病毒感染性疾病的临床应用、不良反应、药物相互作用等进行介绍。     

伊沙匹隆的耐药性与临床研究进展

伊沙匹隆(ixabepilone)是一类治疗乳腺癌的新型微管蛋白抑制剂、半合成埃博霉素B类似物,可作为单一用药或与卡培他滨联用治疗对蒽环类、紫杉醇类耐药的转移性或局部严重性乳腺癌。临床结果显示,伊沙匹隆可以治疗多种肿瘤,与单用卡培他滨疗法相比,伊沙匹隆与卡培他滨合用可以显著延长乳腺癌患者的病情无进展生存期。本文就伊沙匹隆的耐药性、临床单一用药和联合用药的研究进行概述。     

Overview of clinical trials employing antibody-targeted superantigens

Two Phase I clinical trials have been conducted using PNU-214565, a recombinant fusion protein of C242Fab and staphylococcal enterotoxin A (SEA). The initial escalating single dose trial was performed to determine safety and define toxicities. Cumulative doses determined to be safe as single doses were incorporated in an escalating, repeated dose regimen. Twenty-one patients were treated in the single dose and 27 in the repeated dose trials. Patient demographics were equivalent in both, as were the toxicities encountered - primarily fever and hypotension. Three patients in the single dose regimen treated at 0.5 ng/kg experienced grade 3 fever and/or hypotension, and one patient in the repeated dose trial had a dose-limiting grade 4 hypotension (2.75 ng/kg). TNFalpha and IL-2 induction in circulating blood preceded the development of clinical symptoms. One partial response was observed in the repeated dose trial. Pre-existing anti-SEA plasma antibodies protect patients against toxicity at a given drug dose. Based on these findings, a pharmacodynamically-based dosing scheme is currently being tested in a new repeated dose trial.     

硝普钠的临床应用及稳定性研究概况

硝普钠为快速短效血管扩张剂。本文综述了硝普钠的临床应用及稳定性研究进展,以期为临床合理用药提供参考。     

曲克芦丁的药理作用和常见临床应用概述

曲克芦丁是一种半合成黄酮类化合物,具有多种有效的药理活性,在慢性静脉功能不全、缺血性脑卒中(cerebral ischemic stroke,CIS)、痔及微循环回流障碍等血管性疾病的治疗中具有较广泛的应用,并取得了良好的效果.本文对曲克芦丁主要药理活性及其临床应用研究进行综述,旨在探讨该药物的临床应用意义和前景.     

海洛因依赖脱毒用药概述和临床评价

脱毒是戒毒过程重要的第一步。本文概述海洛因依赖者脱毒的药物选择、使用方法和临床评价。总体上脱毒药物治疗国内外趋向一致,阿片受体激动剂美沙酮替代递减疗法唱主角,为临床广泛使用。阿片受体部分激动剂丁丙诺啡国外推荐积极,国内用户不多。可乐定仅适用戒断反应不严重者,阿片受体竞争拮抗剂（纳洛酮、纳曲酮）主要用于快速脱毒和预防复吸,用于维持治疗仅为一种选择。我国社区维持治疗均用美沙酮,为减轻危害近年来积极推广。中西医结合脱毒是我国戒毒特色。