Drug-induced musculoskeletal disorders.

Drug-induced musculoskeletal disorders represent a broad clinical spectrum, from asymptomatic biological abnormalities to severe and even life-threatening diseases. Since an increasing number of drugs have been implicated in inducing rheumatic symptoms and/or syndromes, this review is not meant to be exhaustive, bearing in mind that the development of any musculoskeletal disorder should be considered as possibly related to a medication. The purpose of this article is to provide an overview of the more frequent drug-induced musculoskeletal disorders. These include: (i) arthralgias and arthropathies, including chondropathies and inflammatory arthritis; (ii) connective tissue diseases, especially lupus-like syndromes; (iii) periarticular disorders, including tendinopathies, enthesopathies and frozen shoulder; (iii) bone diseases, such as osteoporosis, osteomalacia and osteonecrosis; and (iv) myopathies. Although virtually all drug classes may induce musculoskeletal disorders, a significant part of them are related to corticosteroids, vaccines, antibacterials and lipid-lowering agents. Knowledge of drug-induced musculoskeletal disorders avoids carrying out unnecessary investigations, and allows optimal management of the patients, i.e. early discontinuation of the offending agent, adequate treatment monitoring and/or intervention with appropriate preventive actions.     

药源性视力损害的文献分析

目的：探讨药源性视力损害的一般规律和特点，为临床安全用药提供参考。方法：检索中国知网、万方数据库、维普中文数据库中药物致视力损害的个案报道，对收集到的137篇文献进行统计和分析。结果：药源性视力损害共收集到159例，抗微生物药物58例，占36.48%；其次为麻醉药物19例，占11.95%；消化系统药物15例，占9.43%；内分泌系统药物13例，占8.18%，其他类药物54例，占33.96%。临床表现以双眼损害为主，中、轻度视力损害占69.81%，严重的视力损害占30.19%。结论：临床应重视药源性视力损害，加强用药监护并及时对症处理。     

他汀类与核苷类药物所致横纹肌溶解症及其防治

本文列举了他汀类和核苷类药物中可诱发药源性横纹肌溶解症的相关药物,介绍药源性横纹肌溶解症的防治措施.通过对横纹肌溶解症的发生机制及诱发该不良反应的药物应用进行分析,并结合临床诊断及治疗进行阐述.认为临床上应该慎用可能诱发药源性横纹肌溶解症的药物,观察到横纹肌溶解症出现的初始症状及时停用相关药物,避免横纹肌溶解症的发生,促进临床合理用药.     

住院患者药物性肝病的危险因素和可疑药物分析

目的探讨药物性肝病在住院患者人群中的发生率、危险因素和可疑药物。方法基于上海市医院住院患者用药数据库中拥有2次及以上ALT记录的患者人群,以用药后ALT〉60U·L^-1为药物性肝病的评价标准,采用逐步Logistic回归方法分析年龄、性别、服药种类、住院时间和基线ALT值对药物性肝病发生率的影响,并计算引起药物性肝病的可疑药物的似然比。结果：纳入研究的3030例患者中药物性肝病有171例,占5．6l％。服药种类是其危险因素。药物性肝病的可疑药物涉及各个类别的药物,以中药出现的频次最高,其次为主要抗菌药物。有220种可疑药物可能与药物性肝病有关,其中磺胺甲嘿唑、氯胺酮等似然比较高。结论住院患者在合并使用多种药物和应用磺胺甲口恶唑等具有肝毒性药物时应加强肝功能监测,以避免药物性肝病的发生。     

药源性眼部损伤967例分析

目的 :回顾分析药源性眼部损伤的发生情况与药物品种及给药方法的关系。方法 :查阅1960年～2000年国内公开发行的医药学期刊上有关药物所致眼部损伤病例的报道 ,并进行统计分析。结果 :154种药物引起眼部损伤967例 ,临床表现包括眼部色素沉着、视力障碍、失明及角膜、结膜、视神经、视网膜、视乳头的损伤等 ;诱发药物以抗微生物药、中枢神经系统药及循环系统药占的比例较大 ,氯丙嗪、奋乃静、胺碘酮、乙胺丁醇等诱发病例最多。结论 :全身给药所致眼部损伤多为正常用法、用量下的药物不良反应 ,而眼部用药所致眼部损伤则有错误用药、错误操作、眼部手术中及手术后用药不当等原因     

药物所致贫血性疾病的因素分析

目的:旨在回顾药物所致贫血性疾病的致病因素,以期为临床合理用药提供参考。方法:检索和采用中、外相关文献进行分析。结果与结论:药物所致的贫血性疾病发病机制各异,临床表现也不尽相同,临床应用中应充分了解药物的作用机制,合理应用,尽可能规避其不良反应。     

我院药品不良反应报告的特点分析

目的了解该院上报全国药品不良反应（ADR）监测网络中心的报告特点,促进ADR监测工作的全面开展,提高ADR报表质量。方法对该院的149例ADR报告分别从给药途径、涉及药品种类、临床表现及报告人职业等方面进行统计分析。结果以静脉滴注给药方式引发的ADR较多（93.9%）;抗菌药物引发的ADR比例最高（42.3%）;ADR的临床表现以皮肤损害为主（50.3%）。结论抗菌药物是不良反应监测的重点,应进一步加强药品不良反应监测,确保用药安全。     

药物性肝损害162例临床分析

目的探讨药物性肝损害发生机制及防治措施。方法回顾性分析162例药物性肝损害患者的年龄、损肝药物、临床表现、治疗及转归。结果导致肝损害的药物常见的有利福平（17．3％,28／162）、消渴丸（16．7％,27／162）、非诺贝特（9．9％,16／162）、白癣皮（8．6％,14／162）及环磷酰胺（7．4％,12／162）等;药物性肝病临床表现为纳差、乏力、恶心、呕吐、皮肤黄疸等;治疗后158例治愈,1例好转,3例死亡。结论使用可能损肝的药物时应加强监测,定期复查肝功能。     

药物性肝炎344例临床分析

目的:探讨药物性肝炎的病因、临床特点及治疗.方法:回顾性分析我院2004～2009年收治的药物性肝炎344例的临床资料,通过对基础病、用药种类、临床表现、实验室检查及临床转归等总结其发病规律及特点.结果:引起药物性肝炎的基础病主要为肺结核、糖尿病、甲亢、风湿性关节炎、精神性疾病等;引发药物性肝炎的药物种类较多,主要以中药、抗结核药、抗生素为主;临床表现乏力、纳差、尿黄、眼黄、身黄、恶心、皮肤瘙痒等;停药及保肝治疗后治愈率93.9%,肝衰竭发生率6.1%,死亡率0.9%,发生肝衰竭以抗结核药为主,其次为中药.人工肝支持治疗药物性肝炎,可明显降低病死率,缩短病程.结论:应高度重视药物性肝炎,注意了解药物的成分、适应证、禁忌证,影响药物性肝炎的因素主要有用药种类、用药时间及是否合并乙肝等.     

我院100例药品不良反应报告分析

目的分析我院药品不良反应（ADR）发生的特点及其规律,确保临床用药的合理、安全。方法采用回顾性方法,对我院2007—2008年报的100份ADR报告,按患者年龄、性别、给药途径、引起ADR的药品种类、涉及器官或系统以及临床表现等进行统计、分析。结果静脉给药较其他给药途径更易发生ADR（占68．0％）;抗感染药物引发ADR的比例最高（占51．0％）,其次为神经系统与心血管系统药物。结论加强ADR监控意识,并完善相关报告分析制度,以确保临床用药的安全、有效。     

54例药物性肝炎调查分析

目的：探讨及分析药物性肝炎患者的病因和临床特征,评价可疑药物与疾病的相关性,为该疾病的临床诊治提供依据.方法：回顾性总结我院的54例急性药物性肝炎患者的临床资料,分析其临床表现、实验室检查、用药情况和预后.结果：药物性肝炎的主要临床表现为乏力、发热等全身症状,食欲减退、恶心、呕吐、上腹胀等消化道症状,以及皮肤和巩膜黄染等肝病特征症状,并可伴有其他症状.易诱发药物性肝炎的药物中,以抗结核药、抗菌药及中药所致肝损害为多见,占66.7％;而其他如降血糖、降血脂及激素类药物所致肝损害者亦时有发生.结论：药物性肝炎的临床症状和实验室检查不具特征性,各年龄段均可罹患此病,发病与药物具有极大相关性.     

The significance of mitochondrial toxicity testing in drug development

Mitochondrial dysfunction is increasingly implicated in the etiology of drug-induced toxicities. Members of diverse drug classes undermine mitochondrial function, and among the most potent are drugs that have been withdrawn from the market, or have received Black Box warnings from the FDA. To avoid mitochondrial liabilities, routine screens need to be positioned within the drug-development process. Assays for mitochondrial function, cell models that better report mitochondrial impairment, and new animal models that more faithfully reflect clinical manifestations of mitochondrial dysfunction are discussed in the context of how such data can reduce late stage attrition of drug candidates and can yield safer drugs in the future.     

Drug-induced rheumatic disorders: incidence, prevention and management.

The purpose of this article is to review the causes, the clinical manifestations and the management of the more frequent drug-induced rheumatic disorders. These include: (i) articular and periarticular manifestations induced by fluoroquinolones, nonsteroidal anti-inflammatory drugs, injections of corticosteroids, and retinoids; (ii) multisystemic manifestations such as drug-induced lupus and arthritis induced by vaccination, Bacillus Calmette-Guerin therapy and cytokines; (iii) drug-induced disorders of bone metabolism (corticosteroid-induced osteoporosis, drug-induced osteomalacia and osteonecrosis); and (iv) iatrogenic complex regional pain syndromes. Disorders caused by nonpharmacological and rarely used treatments have been deliberately excluded. Knowledge of these drug-induced clinical symptoms or syndromes allows an earlier diagnosis and treatment, and earlier drug withdrawal if necessary. With the introduction of new medications such as the recombinant cytokines and antiretroviral treatments, the number of drug-induced rheumatic disorders is likely to increase.     

Drug-induced renal calculi: epidemiology, prevention and management

Drug-induced calculi represent 1-2% of all renal calculi. The drugs reported to produce calculi formation may be divided into two groups. The first one includes poorly soluble drugs with high urine excretion that favours crystallisation in the urine. Among poorly soluble molecules, triamterene was the leading cause of drug-containing urinary calculi in the 1970s, and it is still currently responsible for a significant number of calculi. In the last decade, drugs used for the treatment of HIV-infected patients, namely indinavir and sulfadiazine, have become the most frequent cause of drug-containing urinary calculi. Besides these drugs, about twenty other molecules may induce nephrolithiasis in patients receiving long-term treatment or high doses. Calculi analysis by physical methods, including infrared spectroscopy or x-ray diffraction, is needed to demonstrate the presence of the drug or its metabolites within the calculi. The second group includes drugs that provoke urinary calculi as a consequence of their metabolic effects. Here, diagnosis relies on careful clinical inquiry because physical methods are ineffective to differentiate between urinary calculi induced by the metabolic effects of a drug and common metabolic calculi. The incidence of such calculi, especially those resulting from calcium/vitamin D supplementation, is probably underestimated. Although drug-induced urinary calculi most often complicate high-dose, long-duration drug treatments, there also exist specific patient risk factors in relation to urine pH, urine output and other parameters, which provide a basis for preventive or curative treatment of calculi. Better awareness of the possible occurrence of lithogenic complications, preventive measures based on drug solubility characteristics and close surveillance of patients on long-term treatment with drugs with lithogenic potential, especially those with a history of urolithiasis, should reduce the incidence of drug-induced nephrolithiasis.     

Drug effects on clinical laboratory tests

Drugs and xenobiotics can affect clinical laboratory test results either by interfering with the analytical systems themselves, or by influencing endogenous constituents. National and international bodies have brought widespread recognition to this problem and have proposed protocols for its thorough scientific study. In this survey the authors discuss studies in their laboratories concerning the effects of drugs on thousands of patients undergoing a routine clinical screen. A database is described for storing both patient information and a detailed analysis of the published literature on drug effects. Analytical interferences in clinical tests must be examined in validating the procedure. However, highly specific analytical techniques are increasingly helping to reduce such interferences. Biological effects can be classified as physiological, pharmacological or toxicological. In some cases, biological effects can be used to advantage in monitoring treatment by potentially hazardous drugs, such as the cardiac glycosides. The requirement for a well-defined reference population for each drug and for access to all clinical and medical data for each patient is discussed. The need for greater awareness of the influence of drugs on clinical laboratory results is considered, together with the suggestion that the health professions should try to exploit such effects in monitoring possible toxicity problems, in defining genetic constitution and in designing medication programmes.     

《中国药学文摘》收录的抗菌药物致不良反应统计分析

目的:统计分析抗菌药物引起药品不良反应(ADR)的情况,以有效预防和减少ADR的危害,提高ADR的监测能力。方法:对2008-2009年《中国药学文摘》收录的抗菌药物致ADR文献进行检索。通过Excel电子表对发生ADR的药品种类、给药途径、累及器官或系统及临床表现、ADR发生例数居前10位药品进行回顾性统计、分析。结果:抗菌药物致ADR报道篇数1249篇,病例656例,涉及药品123种。以头孢菌素类(18.90%)发生例次最多,其次为喹诺酮类(16.16%)、青霉素类(14.18%);静脉滴注最易导致ADR(81.10%);ADR临床主要表现为皮肤及其附件损害(19.05%),其次为消化系统损害(16.31%)和中枢或外周神经系统损害(14.63%);左氧氟沙星的ADR发生率最高(89例)。结论:临床应加强对抗菌药物致ADR的重视和监测工作,以保证用药的安全性。     

162例药物性肝损害不良反应/事件报告分析

目的探讨药物性肝损害不良反应/事件发生的临床特点和规律,为临床合理用药提供参考。方法采用回顾性研究的方法,从安徽省2012年药品不良反应/事件数据库中筛选出162例药物性肝损害病例,并行整理、统计与分析。结果统计数据显示药物性肝损害中,年龄≥60岁的老年患者发生率最高,占35.80%。涉及10大类药物,西药引起例次较多,占89.20%,其中以抗肿瘤药所占比重最大,其次为抗菌药、质子泵抑制剂和抗脑血管病药;中成药以中药注射剂引起例次最多,占8.92%。发生药物性肝损害的最常见给药途径是静脉滴注,占71.83%。肝损害发生时间差异较大,最短的1天,最长的175天。临床表现与实验室检查无明显特异性,大部分病例在停药和对症治疗后好转。结论临床医务人员应该提高对药物性肝损害的认识,一旦确诊为药物性肝损害,积极采取对症治疗,同时要加强不良反应监测,提高合理用药水平。     

药源性耳聋防治研究进展

为进一步了解耳毒性药物的种类和致聋机理,探讨预防和治疗耳聋的策略,对国内外近些年来报道的药源性耳聋相关文献进行整理、总结,药物的耳毒性与遗传、用药剂量、用药时间、给药途径、患者年龄和身体状况等有关。耳毒性药物涉及品种众多,造成的后果严重,应引起II缶床重视,加强临床合理用药,以预防为主,早发现,早治疗,减轻患者痛苦。     

抗新型冠状病毒药物致QT间期延长的文献复习及药学监护

本文对新型冠状病毒肺炎患者临床用药方案涉及的抗病毒药物致QT间期延长的文献报道情况进行复习。根据目前文献复习结果可知,洛匹那韦/利托那韦和磷酸氯喹存在引起QT间期延长进而引发尖端扭转型室速的潜在风险。在新型冠状病毒肺炎患者中使用此类药物需关注由此带来的用药风险,熟悉临床上常用的可引起QT间期延长的药物,提高识别患者QT间期延长的易感因素和药物相互作用的能力,重视心电图、电解质管理来预防临床潜在的药物致急性心律失常事件,以降低新型冠状病毒肺炎患者的药物不良反应,避免药源性损害。     

我院105例药品不良反应报告分析

目的了解我院药品不良反应（ADR）发生的特点,为临床合理用药提供参考。方法对我院2007～2008年收集的105例ADR报告分别从患者年龄、性别、给药途径、引起ADR的药品种类、涉及器官或系统以及临床表现等方面进行统计分析。结果105例ADR涉及的药品有47种,其中抗感染药物所致ADR居首位（占35.24%）,其次是中药制剂（占25.71%）;给药途径以静脉给药引发ADR为主（占74.29%）;ADR临床表现以皮肤粘膜损害最常见（占24.76%）。结论应加强ADR的监测,合理使用药物,避免ADR的重复发生。