药物导致的获得性长QT综合征诊断与治疗

药物导致的获得性长QT综合征是由药物引起的可逆性的QT间期延长的综合征,其主要机制是药物通过对IKr的阻断作用,导致动作电位3期快速复极延迟,表现为QT间期延长。在临床上,许多结构上无关的药物,包括抗精神病药物均可以导致QT间期的延长。药物导致的获得性长QT综合征容易导致尖端扭转性室性心动过速（TdP）,临床上可以通过Tp-e和Tp-e/QT比值、巨大T-U波、QRS缓慢上升支和QT间期短期变异可以预测TdP的风险。治疗获得性长QT综合征,最根本的是识别和停用导致QT间期延长的药物并积极的纠正代谢异常,如低钾血症或低镁血症。大多数TdP的发作是短暂的,并可自行终止。然而,长时间发作会导致血流动力学紊乱,需要立即进行电复律。     

氯氮平致周期性麻痹综合征1例

<正> 抗精神病药物和氯丙嗪、氟哌啶醇等可导致血清钾代谢紊乱,产生周期性麻痹综合征文献已有报道,而氯氮平引起周期性麻痹综合征尚未见报告。现报道1例既有氯丙嗪又有氯氮平导致低血钾而产生周期性麻痹综合征。     

抗癫痫药致药物超敏反应综合征引发消化道出血和感染性休克死亡一例

分析1例癫痫患者使用抗癫痫药物后出现药物超敏反应综合征,后引发消化道出血和感染性休克死亡的病例,从药物因素、发生机制和不良反应发生与药物关联性等多方面论证抗癫痫药物引起患者药物超敏反应综合征的关联性。同时分析、总结患者救治过程中的经验教训,为后期药物超敏反应综合征患者救治提供参考。     

高渗性药物导致骨筋膜间室综合征的因素与预防

高渗性药物临床应用相当广泛,由于药物高渗的浓度和微粒,医疗护理操作不当,故导致骨筋膜间室综合征.近年来,各种杂志关于高渗药物导致骨筋膜间室综合征的报道日趋增多,我们通过几年来的临床观察,就其发生的原因与预防综述如下.     

引起锥体外系综合征的药物分析

在临床医疗过程中,部分药物可导致锥体外系综合征,如帕金森综合征、急性肌张力障碍、迟发性运动障碍、静坐不能等.这些患者服药前无锥体外系征,服药后几周或更长时间出现症状并进行性加重,停药后逐渐消失,重复用药后又出现;或原有帕金森病服用这些药物后症状加重,停药后好转.这些药物可作用于中枢神经递质,使其失去平衡,还可以阻断突触后受体,或使突触前神经终末的多巴胺枯竭,或造成大脑相关部位损伤,而导致上述症状出现.我们检索近20年以来的医疗文献,有相关报道54篇.这些报道较集中于抗精神类药和甲氧氯普胺等多巴胺受体阻断剂,对其他药物报道相对较少.本文根据文献和临床资料,列出鲻可引起锥体外系综合征的药物,并加以分析,以加强防范,注意鉴别,避免发生不良后果.     

1例抗癫痫药物高敏综合征的病例分析

目的：探讨含苯环的芳香族抗癫痫药物临床应用发生高敏综合症的特点。方法通过介绍1例癫痫患儿在应用含苯环的芳香族抗癫痫药物治疗过程中发生高敏综合征的病例,结合相关资料阐明含苯环的芳香族抗癫痫药物引起的高敏综合征病例的成因及预防、治疗措施。结果使用含苯环的芳香族抗癫痫药物会导致儿童患者出现高敏综合征,临床工作人员应高度注意,并最大程度地减少药源性伤害。结论抗癫痫药物高敏综合征对儿童危害大,临床工作人员有必要及早识别、诊断,及时治疗并停用可疑抗癫痫药物。     

1例疑似神经阻滞剂恶性综合征患儿不良反应及分析

目的：通过分析1例抽动症患儿使用氟哌啶醇导致神经阻滞剂恶性综合征的不良反应,为合理用药提供参考建议。方法：判断该神经阻滞剂恶性综合征和氟哌啶醇的相关性,并分析发生的原因和易感因素。结果：氟哌啶醇很可能是引起了该患儿神经阻滞剂恶性综合征的药物,经过药物的调整,病情已得到控制。结论：在使用氟哌啶醇中应密切监测症状体征,避免过快调整剂量,以免发生严重不良反应。     

5-羟色胺综合征的临床特征、诊断及防治

5-羟色胺综合征是一种由治疗药物引起的可能危及生命的不良反应。发生机制为5-羟色胺(5-HT)在神经系统内积蓄,过度激活突触后5-HT受体,导致5-HT能神经系统活动增强,其临床特征为精神障碍、自主神经功能亢进及神经肌肉功能异常。本综合征常发生于抗抑郁药联用或与其他药物联用时,主要依据临床表现诊断。治疗包括停撤可疑药物、密切观察、控制激越行为、给予5-HT拮抗剂、对症治疗、并发症的处理等。本综合征重在预防。     

经导管射频消融去肾交感神经术的作用机制及临床应用进展

高血压是最常见的慢性疾病之一,被认为是一个由多种病因引起的处于不断进展状态的心血管综合征,可导致心脏和血管功能与结构的改变。尤其是难治性高血压,患者在生活方式改善的基础上规律服用3种或3种以上足量的不同作用机制的降压药物（其中之一为利尿剂）,血压仍不能达标,往往导致多种并发症的发生,预后极差。     

氟哌啶醇癸酸酯与氯氮平合用致阿-斯综合征1例

<正> 抗精神病药物可影响心脏功能,严重时可引起室性心动过速和心室扑动、颤动,导致阿-斯综合征发生。现将氟哌啶醇癸酸酯(HD)和氯氮平合用所致阿-斯综合征1例,报道如下。 患者女性,41yr,已婚,工人,精神异常已20yr。主要表现为猜疑,耳闻人语,反复自杀等症状,曾3次住院治疗,诊断为精神分裂症。本次因上述症状加剧,于1989年7月19日入院,诊断同前。既往曾因跳楼致骨盆骨折、右股骨颈骨折,无其他严重     

Topical henna for capecitabine induced hand–foot syndrome

Summary Capecitabine is a chemotherapeutic drug for use in cancers. Hand–foot syndrome (HFS) is side effect of capecitabine which can lead the cessation of the therapy or dose reduction. Henna (Lawsonia inermis) is a traditionally used plant of Middle-East that is applied on hands and feet. Some of cancer patients in capecitabine treatment who developed HFS, we recommended to apply henna. In these patients, six patients were grade 3 HFS and four were grade 2 HFS. Complete response (CR) were seen in four of grade 3 HFS and all of grade 2; two grade 3 HFS improved to grade 1. So far, in the chemotherapy, there was no need of dose reduction and also no side effect of henna seen. Clinical improvement in these patients may relate to anti-inflammatory, antipyretic and analgesic effects of henna. Prospective studies are needed to show this therapeutic effect of henna.     

Capecitabine and hand-foot syndrome

Hand-foot syndrome (HFS), or palmar-plantar erythrodysesthesia, is a common side effect in patients taking long-term 5-fluorouracil treatment and is the most frequently reported side effect of oral capecitabine therapy (≥ 50% of patients). Although the pathogenesis of HFS is not fully understood, it may be due to damaged deep capillaries in the soles of the feet and palms of the hands, leading to a COX inflammatory-type reaction, or related to enzymes involved in the metabolism of capecitabine, namely, thymidine phosphorylase and dihydropyrimidine dehydrogenase. Ethnic variations in the clinical manifestation of HFS warrant further attention, and an alternative system for grading HFS in non-white patients has been proposed. In addition to treatment interruption and dose reduction, supportive treatments can help alleviate symptoms. Because capecitabine is an oral therapy administered at home, it is crucial that patients understand the importance of complying with treatment, be aware of the possibility of HFS, and inform the doctor or nurse immediately if symptoms of HFS develop. Several cases of HFS are presented.     

抗反转录病毒治疗及机会感染治疗中的药物相互作用

目前有30余种药物用于艾滋病毒感染治疗。3种及以上抗病毒药物联合应用显著提高了抗反转录病毒治疗的疗效,但也存在多种药物相互作用。同时,艾滋病患者常因机会感染接受治疗,而抗感染药物,尤其是抗结核、抗真菌药物的使用会使药物相互作用更加复杂。药物相互作用可能导致治疗疗效下降和(或)增加不良反应风险。本文主要介绍抗反转录病毒治疗和机会感染治疗中的重要药物相互作用以及与此有关的配伍禁忌和剂量调整。     

From ultrasocial to antisocial: a role for oxytocin in the acute reinforcing effects and long-term adverse consequences of drug use?

Addictive drugs can profoundly affect social behaviour both acutely and in the long-term. Effects range from the artificial sociability imbued by various intoxicating agents to the depressed and socially withdrawn state frequently observed in chronic drug users. Understanding such effects is of great potential significance in addiction neurobiology. In this review we focus on the 'social neuropeptide' oxytocin and its possible role in acute and long-term effects of commonly used drugs. Oxytocin regulates social affiliation and social recognition in many species and modulates anxiety, mood and aggression. Recent evidence suggests that popular party drugs such as MDMA and gamma-hydroxybutyrate (GHB) may preferentially activate brain oxytocin systems to produce their characteristic prosocial and prosexual effects. Oxytocin interacts with the mesolimbic dopamine system to facilitate sexual and social behaviour, and this oxytocin-dopamine interaction may also influence the acquisition and expression of drug-seeking behaviour. An increasing body of evidence from animal models suggests that even brief exposure to drugs such as MDMA, cannabinoids, methamphetamine and phencyclidine can cause long lasting deficits in social behaviour. We discuss preliminary evidence that these adverse effects may reflect long-term neuroadaptations in brain oxytocin systems. Laboratory studies and preliminary clinical studies also indicate that raising brain oxytocin levels may ameliorate acute drug withdrawal symptoms. It is concluded that oxytocin may play an important, yet largely unexplored, role in drug addiction. Greater understanding of this role may ultimately lead to novel therapeutics for addiction that can improve mood and facilitate the recovery of persons with drug use disorders.     

Methadone—metabolism, pharmacokinetics and interactions

The pharmacokinetics of methadone varies greatly from person to person; so, after the administration of the same dose, considerably different concentrations are obtained in different subjects, and the pharmacological effect may be too small in some patients, too strong and prolonged in others. Methadone is mostly metabolised in the liver; the main step consists in the N-demethylation by CYP3A4 to EDDP (2-ethylidene-1,5-dimethyl-3,3-diphenylpyrrolidine), an inactive metabolite. The activity of CYP3A4 varies considerably among individuals, and such variability is the responsible for the large differences in methadone bioavailability. CYP2D6 and probably CYP1A2 are also involved in methadone metabolism. During maintenance treatment with methadone, treatment with other drugs may be necessary due to the frequent comorbidity of drug addicts: psychotropic drugs, antibiotics, anticonvulsants and antiretroviral drugs, which can cause pharmacokinetic interactions. In particular, antiretrovirals, which are CYP3A4 inducers, can decrease the levels of methadone, so causing withdrawal symptoms. Buprenorphine, too, is metabolised by CYP3A4, and may undergo the same interactions as methadone. Since it is impossible to foresee the time-lapse from the administration of another drug to the appearing of withdrawal symptoms, nor how much the daily dose of methadone should be increased in order to prevent them, patients taking combined drug treatments must be carefully monitored. The so far known pharmacokinetic drug-drug interactions of methadone do not have life-threatening consequences for the patients, but they usually cause a decrease of the concentrations and of the effects of the drug, which in turn can cause symptoms of withdrawal and increase the risk of relapse into heroin abuse.     

Cytochrome P450-mediated cardiovascular drug interactions

INTRODUCTION: There are numerous drug-drug interactions (DDIs) related to cardiovascular medications and many of these are mediated via the cytochrome P450 (CYP) system. Some of these may lead to serious adverse events and it is, therefore, essential that clinicians are aware of the important interactions that occur. AREAS COVERED: An extensive literature search was performed to analyze the CYP-mediated cardiovascular DDIs that lead to a loss of efficacy or potential toxicity. Cardiovascular drugs may be victims or act as perpetrators of DDIs. The paper analyzes CYP-mediated drug interactions concerning anticoagulants, antiplatelet agents, antiarrhythmics, β-blockers, calcium antagonists, antihypertensive medications, lipid-lowering drugs and oral antidiabetic agents. EXPERT OPINION: Cardiovascular DDIs involving the CYP system are numerous. Additionally, the spectrum of drugs prescribed is constantly changing, particularly with cardiovascular diseases and it is not necessarily the case that drugs that had shown safety earlier will always show safety. Clinicians are encouraged to develop their knowledge of CYP-mediated DDIs so that they can choose safe drug combination regimens, adjust drug dosages appropriately and conduct therapeutic drug monitoring for drugs with narrow therapeutic indices.     

阿托伐他汀致相关性肌病的回顾性分析

目的 探讨阿托伐他汀致相关性肌病的特点、影响因素、临床转归情况,促进临床合理用药。方法 检索中国知网全文数据库和万方数据库,统计分析他汀相关性肌病的药物不良反应（adverse drug reaction,ADR）,并统计患者的年龄、性别、服用日剂量、发生ADR时服药时间、合并用药、基础疾病以及ADR临床表现、肌酸激酶（creatine kinase,CK）的变化、转归情况。结果 检索到38篇阿托伐他汀导致肌病发生的相关病例报告,共计41例。男性的发生率（60.98%）明显高于女性;>70岁老人（68.29%）是肌病发生的高危人群;初次服药或既往服用阿托伐他汀正常患者在服用阿托伐他汀过程中新增合并用药的前2个月内是肌病发生的危险期;肌病始发症状多见乏力、肌痛,偶见血尿/褐色尿/棕红色尿,恶心/食欲不振、抽搐、皮肤黄染,少见发热、心慌、局部肿胀。结论 阿托伐他汀致相关性肌病发生严重时可导致致死性事件;加强用药教育,避免自行添加药物,注意肌病发生的症状,用药后1~2个月密切监护肝肾功能及CK的变化,一旦出现肌病症状或CK升高,及时就医,避免致死性事件的发生。     

A型肉毒毒素治疗偏侧面肌痉挛临床分析

目的观察国产及进口A型肉毒毒素(BTX-A)治疗偏侧面肌痉挛(HFS)的临床效果。方法总结2013年5月至2015年11月就诊于我院门诊的215例HFS患者及39例接受BTX-A治疗HFS患者的临床特点,包括性别、面部受累部位、病情程度、发病年龄及病程等特点;比较注射保妥适32例次和衡力20例次的肉毒素用量、治疗效果、疗效持续时间及不良反应,总结重复注射及药物互换时的疗效,总结注射部位与常规注射部位的变化。结果 215例HFS中,女性154例,占71.63%;面部受累左侧略占优势;平均发病年龄45岁,平均病程24个月;病情程度中及重度169例。在接受BTX-A治疗的39例中,女性、受累左侧面部和病情程度重居多,重复治疗7例,共注射52例次。保妥适组和衡力组间肉毒素用量比较差异无统计学意义(P=0.087),治疗效果亦无显著差异(P=1.000),治疗平均有效时间组间差异无统计学意义(P=0.309),不良反应无明显差异(P=0.849)。重复注射及药物互换时无疗效减退。根据痉挛肌肉受累部位不同,注射部位在常规部位上增加了耳后镫骨肌和颈部颈阔肌。结论局部注射国产和进口BTX-A治疗HFS同样疗效显著,毒副作用少、安全性高,可重复使用。并且重复注射时,进口和国产BTX-A可以互换,注射部位增加了镫骨肌和颈阔肌,能更好改善痉挛肌肉群症状。     

北京市药品检验体系发展与技术能力提升研究

目的为促进北京市药品检验体系发展,提升技术能力提供参考。方法由市药检所牵头,采取调查问卷、实地调研、召开专题座谈会等方法 ,对北京市药品检验体系主要工作数据进行对比与分析,提出了解决方案和构建三级药品检验机构的设想。结果与结论 北京市药品检验体系由市药检所与区县药检所构成,必须在检验术语、应急检验机制、人员编制与仪器设备、检验方法等方面进行规范及改进创新,才能实现检验体系的发展与技术能力的提升。     

氟喹诺酮类药物的不良反应

目的为熟悉掌握氟喹诺酮类药物的不良反应和用药安全,协助临床合理用药。方法通过查阅文献和本院不良反应报告进行分类综述。结果氟喹诺酮类药物是一类疗效确切,应用广泛的抗菌药,用药过程应严密监视其不良反应,及时采取措施治疗。结论通过合理使用可以避免或减轻不良反应及耐药性的发生,提高疗效。