共查询到19条相似文献，搜索用时 109 毫秒
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为进一步加强龙口市药品的安全监管，提高药品经营、使用单位对药品不良反应报告和监测工作的认识水平和重视程度，减少龙口市药品不良反应的发生。龙口市食品药品监督管理局会同龙口市卫生局于2005年5月27日召开了全市药品不良反应报告和监测工作会议，龙口市各级医疗机构的分管领导、主要负责人和监测站成员参加了会议。 相似文献
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上海市儿童药品不良反应监测状况分析 总被引：1，自引：0，他引：1
目的分析儿童药品不良反应（ADR）监测工作存在的问题,找出解决方法,为做好儿童ADR监测工作提供依据。方法采用发放调查问卷的方式,就儿童ADR监测状况的相关问题对上海市儿童主要就诊医院的医务人员进行调查分析。结果大多数医务人员能正确理解和认识ADR定义,医务人员学历、ADR诊断经历、填写ADR报告的知晓程度和ADR知识培训教育情况与上报ADR史有统计学意义,医务人员对儿童新的ADR关注度较低。结论加强和深入医疗机构进行ADR培训教育对做好儿童ADR监测工作具有重要意义。 相似文献
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转变观念,提高认识,努力做好药品不良反应监测管理工作--在全国药品不良反应监测工作会议上的讲话 总被引：1，自引：1，他引：0
邵明立 《药物流行病学杂志》2000,9(3)
同志们: 今天, 国家药品监督管理局与卫生部在这里联合召开2000年全国药品不良反应监测工作会议. 本次会议的主要任务是: 学习、贯彻<药品不良反应监测管理办法>, 交流药品不良反应监测工作经验, 安排今明两年药品不良反应监测管理工作计划. 下面, 我代表国家药品监督管理局谈谈我国药品不良反应监测工作状况; 实施药品不良反应报告制度的意义和做好药品不良反应监测工作的要求, 供同志们参考. 相似文献
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近日,北京市药品监督管理局西城分局召开了2009年度药品不良反应监测工作会。西城区卫生局有关领导及辖区50余家医院、门诊部、药品生产经营企业相关人员参加了会议。北京市药品不良反应监测中心主任张黎明在会上进行了相关知识讲座。 相似文献
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3月5～6日,国家药品监管局在上海召开互联网药品信息服务监管座谈会。国家药品监管局和各省、自治区、直辖市药品监管局负责互联网药品信息服务监管工作的人员及药品电子商务试点单位的负责人共70多人参加了会议。国家药品监管局副局长张文周出席了会议并作重要讲话。 这次会议学习了关于互联网药品信息服务的政策法规文件,研究了加强监管的方式和手段;组织药品电子商务试点单位开展经验交流,对如何促进互联网药品信息服务健康发展进行了研讨;还听取了关于网络基础知识和药品电子商务认证监测的报告。代表们普遍认为,这次会议对于规范互联网药品信息服务活动,促进互联网药品信息服务健 相似文献
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摘 要 目的：研究住院患者使用白蛋白结合型紫杉醇致相关药品不良反应（ADR）的发生率及相关因素。方法：采用回顾性分析,利用“医疗机构ADE主动监测与智能评估警示系统”,筛选我院2015年10月1日～2016年9月30日使用白蛋白结合型紫杉醇化疗的住院患者作为研究对象,研究其相关ADR发生率,并对血液系统ADR相关因素进行分析。结果：系统共监测病例1 667 例,白细胞减少、中性粒细胞减少、血小板减少、贫血、肝功能异常及急性肾损伤的阳性报警率分别为94.24%,98.67%,91.78%,83.61%,70.33%和15.38%。血液系统ADR的总体发生率为39.06%,其中白细胞减少、中性粒细胞减少、血小板减少及贫血的发生率分别为29.26%,18.55%,7.39%和13.57%;肝功能异常发生率为14.53%;急性肾损伤发生率为0.38%。研究显示白蛋白结合型紫杉醇致血液系统ADR组与未致ADR组比较,在患者性别、年龄及住院次数方面差异无统计学意义（P>0.05）,但ADR组患者体重指数更低（P<0.05）。结论：借助专项系统能够高效、精准的对目标药物实行自动监测,警示临床用药方案,减少ADR发生风险。白蛋白结合型紫杉醇在临床使用过程中,要密切监测血液学指标及肝肾功能,做好防范。 相似文献
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上海医药行业协会第十六次技术工作年会于4月19～20日在青浦朱家角的虹珠苑召开.出席这次会议的领导有:上海市工业经济联合会常务副会长兼秘书长朱国梁、副秘书长余正华,上海市经委企管处处长王晓元、副处长蒋菊仙,上海医药(集团)有限公司副总裁黄彦正、杨苏鸣,上海医药行业协会会长陈统辉、副会长刘铭君和吴建文等.来自上海医药行业协会会员单位的负责人、总工程师及技术、质量、研究室有关负责人180余人出席了这次一年一度的盛会. 相似文献
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《Hospital pharmacy》2013,48(2):100-103
The purpose of this feature is to heighten awareness of specific adverse drug reactions (ADRs), discuss methods of prevention, and promote reporting of ADRs to the US Food and Drug Administration’s (FDA’s) MedWatch program (800-FDA-1088). If you have reported an interesting, preventable ADR to MedWatch, please consider sharing the account with our readers. Write to Dr. Shuster at ISMP, 200 Lakeside Drive, Suite 200, Horsham, PA 19044 (phone: 215-947-7797; fax: 215-914-1492; e-mail: ude.elpmet@retsuhs.leoj). Your report will be published anonymously unless otherwise requested. This feature is provided by the Institute for Safe Medication Practices (ISMP) in cooperation with the FDA’s MedWatch program and Temple University School of Pharmacy. ISMP is an FDA MedWatch partner. 2013 Feb; 48(2): 100–103. Published online 2013 Feb 1. doi: 10.1310/hpj4802-100
Aspirin/Clopidogrel-Induced Spontaneous Liver Hematoma
Joel Shuster, PharmD, BCPP*Joel Shuster
*Clinical Professor of Pharmacy Practice, Temple University School of Pharmacy, Philadelphia, Pennsylvania; Clinical Consultant, Episcopal Hospital, Philadelphia, Pennsylvania; Clinical Advisor, Institute for Safe Medication Practices, Horsham, PennsylvaniaFind articles by Joel ShusterAuthor information Copyright and License information Disclaimer*Clinical Professor of Pharmacy Practice, Temple University School of Pharmacy, Philadelphia, Pennsylvania; Clinical Consultant, Episcopal Hospital, Philadelphia, Pennsylvania; Clinical Advisor, Institute for Safe Medication Practices, Horsham, PennsylvaniaCopyright notice A 76-year-old man presented to his local emergency department (ED) with a day-long complaint of right upper quadrant pain. He stated that he had not had any trauma. His physical examination was essentially normal except for “mild tenderness in the epigastric area and 2+ pitting edema in both legs.” His medical history included the placement of drug eluting stents after a myocardial infarction 8 years earlier and 3 years after that for unstable angina. One of the stents was coated with heparin and the other was coated with paclitaxel. Other comorbidities included sarcoidosis, pulmonary hypertension, diabetes, and essential hypertension. His medications included aspirin, clopidogrel, glipizide, benazepril, rosuvastatin, allopurinol, prednisone, and omeprazole. He was also using a variety of inhalers for his pulmonary symptoms. He had been taking the clopidogrel and aspirin for 5 years. He did not use nonsteroidal anti-inflammatory drugs.Laboratory testing revealed the hemoglobin and hematocrit to be slightly below normal, while the platelet count was fine. Abdominal ultrasound and follow-up computed tomography (CT) of the abdomen showed a “large hypodense” mass in the right side of the liver. The patient was admitted to the hospital. Because of a suspected hemorrhage, the aspirin and clopidogrel were discontinued. By the following morning, the patient’s hemoglobin had dropped to 8.6 g/dL from 13 g/dL on admission (reference range, 14-18 g/dL), and he was given 2 units of packed red blood cells. The liver transaminases had also increased 5-fold in the first 24 hours. A few days later, a repeat CT scan showed that the first liver lesion had resolved, while a new hypodense lesion had developed. Because of a high white blood cell count, a liver abscess was suspected. “CT-guided aspiration of the lesion revealed 21 mL of dark blood.” The patient was treated with an additional unit of whole blood and was discharged a few days later with a “diagnosis of subcapsular liver hematoma while receiving dual antiplatelet therapy.” The clopidogrel and aspirin were not restarted upon discharge from the hospital, but the patient was placed back on aspirin alone a month later and had no further problems up to a 1-year follow-up.The authors state that liver hematoma from antiplatelet therapy is rare, but we must be cautious in using dual therapy for more than the recommended periods of time after stent placements.Darwish OS, Iqbal E. Dual antiplatelet agent-induced spontaneous liver hematoma. Ann Pharmacother. 2012;46(11):e33. 2013 Feb; 48(2): 100–103. Published online 2013 Feb 1. doi: 10.1310/hpj4802-100Adenosine-Induced Severe Bronchospasm in a Patient Without Pulmonary Disease
Copyright and License information DisclaimerCopyright notice An obese 29-year-old man developed frequent episodes of palpitations that were short and self-limiting. When he developed another episode of palpitations that lasted nearly 2 hours, he presented to his local ED. On physical examination, the patient’s heart rate was 210 beats per minute and his blood pressure was 140/90 mm Hg. He complained of “mild chest discomfort” but did not have any difficulty breathing. The electrocardiogram “showed a regular wide QRS tachycardia with a left bundle-branch block morphology, consistent with aberrant supraventricular tachycardia.” The patient underwent carotid massage with no effect. The patient was then given a 6 mg intravenous (IV) bolus of adenosine, which also had no effect. A 12 mg bolus was then administered without effect, but the patient developed a mild cough. Another 12 mg IV bolus of adenosine was given, which “cardioverted the patient to sinus tachycardia.” The patient immediately developed trouble breathing, and his pulse oximetry showed that he was hypoxic at 83% oxygen saturation on room air. Auscultation revealed “diffuse bronchospasm.” An arterial blood gas specimen revealed “hypocapnic respiratory failure,” whereas a chest x-ray was normal. He was treated with oxygen and inhaled beclomethasone, along with an IV bolus of methylprednisolone. When this did not help, an IV infusion of aminophylline was started, which relieved the bronchospasm but caused a recurrence of the supraventricular tachycardia (at a rate of 180 beats per minute). Intravenous flecainide halted the new arrhythmia, and the patient had no further problems with bronchospasm or abnormal rhythms. An accessory pathway was later discovered during electrophysiological studies, and the patient was treated with a radiofrequency ablation procedure.The authors remind us that adenosine is known to cause dyspneic symptoms during cardiac studies, but the symptoms are usually “transient and benign.” There are documented cases of severe bronchoconstriction occurring in patients with prior lung disease, but this is apparently the first such case in a patient with normal pulmonary status.Coli S, Mantovani F, Ferro J, Gonzi G, Zardini M, Ardissino D. Adenosine-induced severe bronchospasm in a patient without pulmonary disease. Am J Emerg Med. 2012;30(9):2082.e3-2082.e5. 2013 Feb; 48(2): 100–103. Published online 2013 Feb 1. doi: 10.1310/hpj4802-100Paclitaxel-Induced Acral Erythema
Copyright and License information DisclaimerCopyright notice A 66-year-old woman was started on paclitaxel as neoadjuvant therapy for ductal breast cancer. After receiving 3 IV doses at 80 mg/m2, the patient developed “a nonpruritic, 1-cm confluent erythematous patch over several metacarpophalangeal joints” bilaterally. Continued treatment with the antineoplastic agent caused new areas of discomfort. The new lesions were seen “primarily over her right lateral heel and toes.” The erythematous areas became “tender yellow plaques with scaling.” Even though there was a reduction in the dose of paclitaxel, the patient presented with pain and swelling in the right foot after the 11th dose. She had developed multiple lesions and had significant swelling of toes on both feet that caused significant pain. A biopsy of a lesion on the patient’s right foot showed “epithelial acanthosis with prominent compact orthokeratotic hyperkeratosis and areas of parakeratosis.” She was treated with topical silver sulfadiazine for the open wound areas and received triamcinolone and emollients to the right foot. All lesions and plaques were completely resolved a month after the paclitaxel therapy had been completed.The authors state that skin rashes are common with paclitaxel, but this type of acral erythema, pertaining to peripheral parts of the body, is not commonly seen. Acral lesions are more commonly seen with other chemotherapeutic agents, such as fluorouracil, cytarabine, or doxorubicin.Richards KN, Ivan D, Rashid RM, Chon SY. Paclitaxel-induced acral erythema. Arch Dermatol. 2012;148(11):1333-1334. 2013 Feb; 48(2): 100–103. Published online 2013 Feb 1. doi: 10.1310/hpj4802-100Acute Laryngeal Dystonia Associated with Aripiprazole
Copyright and License information DisclaimerCopyright notice A 16-year-old girl with a history of rape, sexual molestation, aggressive behaviors, and cutting was admitted to a psychiatric hospital after getting into a fight at school with a female peer. The admitting diagnosis was bipolar disorder not otherwise specified with borderline traits.Four months before admission, she was given aripiprazole 5 mg daily that had been added to topiramate 25 mg twice daily, which was being used for mood lability. She had been treated in the past with a variety of medications that caused weight gain, oversedation, or other adverse effects that caused her to stop taking the medications. She was also getting naproxen 375 mg twice daily for pain caused by recent cutting attempts. Three days before admission to the hospital, her dose of aripiprazole was increased to 10 mg daily. She was continued on the aripiprazole, topiramate, and naproxen upon admission.On the third hospital day, 6 days after the increase in dose of the aripiprazole, the woman was found on the floor of the hospital gymnasium “with dyspnea, dysphonia, tongue and throat tightening, cogwheel rigidity, and dizziness.” The oxygen saturation varied from 92% to 100%. She was treated with a stat dose of benztropine 2 mg intramuscularly and oral diazepam 5 mg, which caused rapid improvement of her breathing and rigidity. The aripiprazole was halted. Over the next 3 days, benztropine was used orally and there was not a recurrence of symptoms.The patient had an acute dystonic reaction involving her laryngeal musculature, which was easily treated with the anticholinergic agent, benztropine. The authors state that this is only the second published report of acute laryngeal dystonia occurring with the “newer” or “atypical” antipsychotic agents marketed over the past 20 years or so. It is likely that many such cases have not been reported. With the increased use of some of the antipsychotic agents as adjuncts to antidepressant therapy, we must be aware of such possible episodes of extrapyramidal side effects.Goga JK, Seidel L, Walters JK, Khushalani S, Kaplan D. Acute laryngeal dystonia associated with aripiprazole. J Clin Psychopharmacol. 2012;32(6):837-839. 2013 Feb; 48(2): 100–103. Published online 2013 Feb 1. doi: 10.1310/hpj4802-100Incidence of Thrombocytopenia During Heparin Prophylaxis
Copyright and License information DisclaimerCopyright notice This report is a follow-up to a study published in 2008 that showed that patients receiving prolonged unfractionated heparin for a variety of reasons developed thrombocytopenia at an extremely high rate of 33%.1 In this new report, a total of 1,017 patients were included in the analysis of patients receiving heparin solely for prophylaxis of venous thromboembolism. The investigation showed that 190 patients (18.7%) developed thrombocytopenia as a result of being placed on heparin prophylaxis. Thrombocytopenia “was defined as a nadir platelet count <150 x 109/L or a platelet count decrease ≥50% from admission levels.” Half of the patients had only nadir counts below 150 x 109/L, while 11% of the patients saw their admitting platelet counts fall below 50% of the first measured values. The other 39% of the patients had platelet counts below the cutoff point, and their counts were more than halved from admission. Forty percent of the cases of thrombocytopenia were caused by low-molecular-weight heparins, although the risk was certainly smaller with these agents.The authors conclude that almost 1 in 5 patients develop thrombocytopenia during heparin prophylaxis, and this high number still seems to be “under-recognized.” They suggest more vigilant platelet monitoring, especially in patients at higher risk.Wang TY, Honeycutt EF, Tapson VF, Moll S, Granger CB, Ohman EM. Incidence of thrombocytopenia among patients receiving heparin venous thromboembolism prophylaxis. Am J Med. 2012;125(12):1214-1221. 2013 Feb; 48(2): 100–103. Published online 2013 Feb 1. doi: 10.1310/hpj4802-100Oral Fluoroquinolones and the Risk of Retinal Detachment
Copyright and License information DisclaimerCopyright notice An article was published in the JAMA in early April 2012 that concluded that treatment with oral fluoroquinolone antibiotics caused an increased risk of retinal detachment.2 “The absolute risk in the risk of a retinal detachment was 4 per 10,000 person-years (number needed to harm = 2500 computed for any use of fluoroquinolones).”2 I had not seen that original publication, but I recently found this editorial in the American Journal of Ophthalmology that pointed out some potential problems with just a superficial observation of the original analysis.The authors discuss the fact that tendinitis and/or tendon ruptures may occur in 1 out of 1,000 patients treated with fluoroquinolones, yet we still use the fluoroquinolones in all manner of patients. Is the risk of a rhegmatogenous retinal detachment something to be feared? Please take a look at both of these publications, which may be used for a good discussion in a journal club.Albini TA, Karakousis PC, Abbey AM, Bartlett JG, Flynn HW. Association between oral fluoroquinolones and retinal detachment. Am J Ophthalmol. 2012;154(6):919-921. 2013 Feb; 48(2): 100–103. Published online 2013 Feb 1. doi: 10.1310/hpj4802-100Prenatal Exposure to Antidepressants: How Safe are They?
Copyright and License information DisclaimerCopyright notice A prospectively collected database looked at 4 groups of children. Two of the groups included women who took either venlafaxine or selective serotonin reuptake inhibitors (SSRIs) during their pregnancies. Another group included depressed pregnant women who were not treated, and the final group was made up of nondepressed, healthy women. The children of these women were followed to ages 3.5 to 6 years and were given intelligence tests and other tests for neurodevelopment.The study showed that exposure to antidepressants did not affect the children’s intellectual or behavioral outcomes. Untreated depression certainly led to a much higher risk of postpartum depression. The data also showed “that fetal and childhood exposure to maternal depression were significant predictors of child behavior problems and may represent risk for long-term child psychopathology.”A well-referenced accompanying editorial in the same issue of the American Journal of Psychiatry looks at other reports where prenatal exposure to antidepressants was studied.3Nulman I, Koren G, Rovet J, et al. Neurodevelopment of children following prenatal exposure to venlafaxine, selective serotonin reuptake inhibitors, or untreated maternal depression. Am J Psychiatry. 2012;169(11):1165-1174. 2013 Feb; 48(2): 100–103. Published online 2013 Feb 1. doi: 10.1310/hpj4802-100Proton Pump Inhibitors: The Good, The Bad, and The Unwanted
Copyright and License information DisclaimerCopyright notice This column has previously reported on uncommon adverse effects associated with proton pump inhibitors (PPIs). Last month (January 2013), we reviewed a case of agranulocytosis brought on by exposure to PPIs.4This report is a 60-reference review of adverse effects associated with PPIs. A good discussion is included about “usage issues” with this class of drugs. Too many hospitalized patients are placed on these agents without good reason. The takeaway lesson from this review is that PPIs should only be used for accepted indications and their long-term use should be reevaluated on a regular basis.Chubineh S, Birk J. Proton pump inhibitors: the good, the bad, and the unwanted. Southern Med J. 2012;105(11):613-618. 相似文献15.
目的分析老年人药品不良反应/事件(ADR/ADE)的发生情况、特点及相关因素。方法收集2011年我市食品药品监督管理局上报的60～85岁老年人ADR/ADE共232例,按照国家药品不良反应监测中心制定的标准进行分析,总结ADR/ADE发生的原因。结果在232例ADR/ADE中,抗生素、中药引起的ADR较多,以皮损及其附件损伤常见,ADR累及人体各系统。结论应加强对老年人用药的关注,合理用药,减少ADR/ADE的发生。 相似文献
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《Hospital pharmacy》2013,48(4):270-273
The purpose of this feature is to heighten awareness of specific adverse drug reactions (ADRs), discuss methods of prevention, and promote reporting of ADRs to the US Food and Drug Administration’s (FDA’s) MedWatch program (800-FDA-1088). If you have reported an interesting, preventable ADR to MedWatch, please consider sharing the account with our readers. Write to Dr. Mancano at ISMP, 200 Lakeside Drive, Suite 200, Horsham, PA 19044 (phone: 215-707-4936; e-mail: ude.elpmet@onacnamm). Your report will be published anonymously unless otherwise requested. This feature is provided by the Institute for Safe Medication Practices (ISMP) in cooperation with the FDA’s MedWatch program and Temple University School of Pharmacy. ISMP is an FDA MedWatch partner. 2013 Apr; 48(4): 270–273. Published online 2013 Apr 3. doi: 10.1310/hpj4804-270
Statin-Induced Lung Injury
Michael A. Mancano, PharmD*Michael A. Mancano
*Chair and Clinical Professor, Department of Pharmacy Practice, Temple University School of Pharmacy, Philadelphia, Pennsylvania; Clinical Advisor, Institute for Safe Medication Practices, Horsham, PennsylvaniaFind articles by Michael A. MancanoAuthor information Copyright and License information Disclaimer*Chair and Clinical Professor, Department of Pharmacy Practice, Temple University School of Pharmacy, Philadelphia, Pennsylvania; Clinical Advisor, Institute for Safe Medication Practices, Horsham, PennsylvaniaCopyright notice Statin-induced lung injury (SILI) is an uncommon but serious pulmonary complication of statin therapy. SILI was initially reported in the medical literature in 19951 and additional case reports followed. In 2007 an analysis of the US Food and Drug Administration (FDA) Adverse Reporting System data concerning statin use and SILI was performed.2 The findings demonstrated a group of disorders with similar pathological findings including cellular infiltration, scarring and/or architectural disruption of the pulmonary parenchyma involving alveolar lining cells, small and large airways, endothelial basement membranes, and occasionally the pleura. This group of pulmonary effects was found to occur in 0.01% to 0.4% of patients treated with statins and demonstrates that the clinical features of SILI vary widely.The authors completed an investigation of 12 previously reported cases of SILI as well as 4 cases diagnosed at their institution. The authors’ analysis demonstrated that simvastatin was the most common statin reported to cause lung injury; however, of the 4 patients at their institution, 3 patients received rosuvastatin and 1 received atorvastatin. The most common symptoms patients reported were fever, dyspnea, and cough. The onset of lung injury varied widely from the start of statin treatment, ranging from 0.25 to 120 months. Upon onset of symptoms, statins were discontinued and steroids were administered in 15 of the 16 patients. Clinical or radiologic improvement was noted in 10 patients receiving steroids. Because of severe lung injury, rechallenge with statins was not performed. However, 1 patient experienced increased dyspnea 1 week after inadvertent re-administration of rosuvastatin prescribed by a physician with no knowledge of the patient’s history of SILI. Of the remaining 6 patients with unfavorable outcome, 2 had slowly progressive disease complicated by persistent dyspnea. Four patients died from respiratory or cardiac failure, including 1 patient who received continuous simvastatin therapy.The authors’ analysis indicates that the patients with clinical symptoms of cough and/or fever had a favorable outcome. It may be that the presence of such acute symptoms prompts the patient to seek medical help and avoid delay in diagnosis and treatment. However, these clinical symptoms, in addition to thoracic radiological findings, may mimic pulmonary infection and confuse physicians who are unaware of SILI. The authors recommend a high index of suspicion of SILI; the presence of pulmonary phospholipidosis, shown by a foamy appearance of the majority of alveolar macrophages which stain positive for Sudan black in bronchoalveolar lavage fluid, may be of considerable value in diagnosing SILI. In addition, the high-resolution CT (HRCT) findings in SILI are nonspecific but may be of prognostic value. Alveolar infiltrates, especially ground-glass opacity, indicate favorable outcome, whereas fibrosis shown on HRCT suggests an unfavorable outcome.The authors outline the current research questions concerning SILI that remain: What are the underlying mechanisms of SILI? What are the risk factors for the occurrence of SILI? How can health care professionals become more aware of SILI in their clinical practice?Huang LK, Tsai MJ, Tsai HC, et al. Statin-induced lung injury: diagnostic clues and outcome. Postgrad Med. 2013;89:14-19. 2013 Apr; 48(4): 270–273. Published online 2013 Apr 3. doi: 10.1310/hpj4804-270Colchicine-Induced Rhabdomyolysis Caused by Interaction with Clarithromycin
Copyright and License information DisclaimerCopyright notice A 59-year-old man with a history of pulmonary tuberculosis about 40 years prior presented with generalized myalgia and fever. Behçet disease had been diagnosed 15 months prior, and the patient was treated with methotrexate and colchicine (0.6 mg every 12 hours). Behçet’s disease is a triad of aphthous ulcers, genital ulcerations, and ocular inflammation. Three months prior to his admission, methotrexate was discontinued because of elevated liver enzymes, and his liver function had normalized within 2 months. The patient developed nasal congestion and chronic cough as well as rhinosinusitis. Clarithromycin 500 mg every 12 hours was initiated. Nine days after starting treatment, he developed myalgia and weakness in both legs along with a febrile sensation. Despite treatment with analgesics, his myalgia had worsened and involved other extremities.Upon admission, his liver enzymes were elevated (aspartate aminotransferase, 227 IU/L; alanine aminotransferase, 564 IU/L), but neither cytopenia nor renal impairment was observed. The patient’s creatinine kinase and myoglobin concentrations were markedly elevated at 766 IU/L and 1,393 ng/mL, respectively. After conservative management, his subsequent liver enzymes, myoglobin, and creatinine kinase concentrations decreased while his muscle pain and weakness gradually disappeared within 2 weeks. The patient was discharged without colchicine therapy.According to the FDA’s safety data for colchicine-related deaths, 117 of the 169 fatal cases were within the therapeutic dosage range and more than half were reported in patients concomitantly using clarithromycin.3 Clarithromycin can increase the oral bioavailability of colchicine by increasing its absorption by inhibiting P-glycoprotein in enterocytes and can increase colchicine accumulation by decreasing the activity of CYP3A4, which is involved in colchicine metabolism. The authors warn that pharmacologic interactions between colchicine and clarithromycin and other drugs that inhibit CYP3A4 and/or P-glycoprotein can cause serious adverse reactions. Health professionals should be vigilant for these potentially life-threatening interactions.Kim JB, Kim S, Yoon SY, et al. Colchicine-induced rhabdomyolysis caused by interaction with clarithromycin in a patient with Behçet disease. J Clin Rheumatol. 2012;18(8):453-454. 2013 Apr; 48(4): 270–273. Published online 2013 Apr 3. doi: 10.1310/hpj4804-270Disulfiram Ethanol Reaction Mimicking Anaphylactic, Cardiogenic, and Septic Shock
Copyright and License information DisclaimerCopyright notice A 65-year-old man was admitted to the intensive care unit (ICU) for shock. The patient had no pertinent past medical history except for alcohol abuse and was asymptomatic until midday when he consumed 500 mL of wine. Within 30 minutes he fainted and was taken to the emergency department. Upon admission, the patient’s consciousness returned to normal but his blood pressure was 80/60 mm Hg, heart rate 110 beats per minute (bpm), respiratory rate 25 breaths per minute, oxygen saturation of 99% on room air, and a temperature of 36°C (96.8°F). The patient displayed diffuse erythema on his chest and face, without mucosal swelling or pruritus. Anaphylaxis was suspected, and the patient immediately received 0.1 mg of intravenous epinephrine along with aggressive fluid resuscitation. Worsening circulatory failure warranted high-dose norepinephrine (0.8 mcg/kg/min) infusion. ECG was suggestive of an acute myocardial infarction but coronary angiography was normal. Because of hypothermia (35.5°C [95.9°F]) and intense shivering, toxic shock syndrome was suspected and intravenous broad-spectrum antibiotics were initiated (ceftriaxone and clindamycin). Upon his admission to the ICU, lab results revealed metabolic acidosis (pH 7.33, bicarbonate 17.2 mmol/L, and arterial blood lactate 8.7 mmol/L), but procalcitonin, high-sensitivity troponin, and other routine lab tests were within normal limits. Blood ethanol concentration was 0.9 g/L measured 6 hours after ingestion.Additional history was elicited from the patient, and it was discovered that he erratically self-medicated with disulfiram and that he had ingested 500 mg of disulfiram 1 hour before his alcohol intake. Within 2 hours after ICU admission, his circulatory status dramatically improved and he was gradually weaned off of norepinephrine. Cutaneous manifestations, lactic acidosis, and ECG abnormalities also resolved within 6 hours. All cultures remained sterile, and antibiotics were discontinued. The patient was discharged to home the next day without any medications. The diagnosis was severe disulfiram ethanol reaction.The disulfiram ethanol reaction is widely known, but the manifestation is expected to be mild but unpleasant with the patient experiencing headache, flushing, and nausea as a deterrent to further ethanol ingestion. Severe vasodilatory shock has been reported rarely in the literature, with only 1 case describing ST-segment depression. This case is unique; the patient experienced effects that mimicked anaphylactic, cardiogenic, and septic shock that resolved relatively rapidly after ICU admission.Moachon L, Arnould MA, Perruche F, et al. Disulfiram ethanol reaction mimicking anaphylactic, cardiogenic and septic shock. Am J Emerg Med. 2013;31(1):270.e1-270.e3. 2013 Apr; 48(4): 270–273. Published online 2013 Apr 3. doi: 10.1310/hpj4804-270Weight Gain with Abdominal Enlargement in a Patient Receiving Tocilizumab
Copyright and License information DisclaimerCopyright notice A 56-year-old woman with rheumatoid arthritis (RA) and Sjögren syndrome was initiated on tocilizumab in November 2010 after a long course of disease and failure (due to lack of efficacy or unacceptable adverse effects) of numerous synthetic disease-modifying antirheumatic drugs, 3 anti–tumor necrosis factor (TNF) drugs, and rituximab. Upon initiation of therapy with tocilizumab (Actemra) 320 mg, the patient weighed 43 kg (94.8 lbs; body mass index [BMI] 16.8). The patient also received prednisone 10 mg daily, which had been part of her long-term background regimen. In February 2011, the patient complained of persistent abdominal distention and pain. Abdominal ultrasound, CT, gastroscopy, and colonoscopy did not reveal a cause for the pain. The patient reported no change in her appetite or eating habits and her weight was 52 kg (114.6 lbs; BMI 20.3). The patient experienced moderate improvement in RA activity, and tocilizumab therapy was continued.In May 2011, the patient presented with worsening diffuse abdominal pain and her appearance had changed dramatically. Prominent trunk fat deposition was now apparent and her weight was now 56 kg (123.5 lbs; BMI 21.9). Her anterior abdominal wall was tender and her skin was distended. Ultrasound of the abdominal wall revealed significant diffuse fat deposition in the subcutaneous area. Tocilizumab was discontinued at this time. Three months later (August 2011), the patient noted significant improvement in her abdominal pain and distention and her weight had decreased by 5 kg (11 lbs). However the patient required an increase in her prednisone dose to 20 mg daily to treat her RA. Because of worsening joint disease, the patient agreed to receive another infusion of tocilizumab in November 2011. Two weeks after administration, she presented again with abdominal pain and new weight gain of 3 kg (6.6 lbs). She refused further tocilizumab treatment and was then maintained on prednisone 10 mg/daily. During follow-up, the patient’s abdominal distention gradually diminished and pain disappeared, however her weight did not decrease significantly and remained at 52 kg (114.6 lbs; BMI 20.3) as of September 2012.Tocilizumab is a humanized monoclonal antibody to the interleukin-6 (IL-6) receptor. Although weight gain has been thought to be a potential adverse effect of IL-6 receptor blockade, it has not been reported in patients receiving tocilizumab. This case represents a patient who gained more than 30% of her initial weight as well as significant abdominal fat accumulation. The weight gain also reoccurred upon reintroduction of tocilizumab therapy.Younis S, Rosner I, Rimar D, et al. Interleukin 6 blockade-associated weight gain with abdominal enlargement in a patient with rheumatoid arthritis. J Clin Rheum. 2013;19(1):48-49. 2013 Apr; 48(4): 270–273. Published online 2013 Apr 3. doi: 10.1310/hpj4804-270Nilotinib-Associated Acute Pancreatitis
Copyright and License information DisclaimerCopyright notice A 69-year-old Caucasian male was admitted to the hospital for abdominal pain. Six days prior to admission, he began treatment with nilotinib for recently diagnosed chronic myelogenous leukemia (CML). He had been receiving nilotinib 300 mg twice daily. He had no history of smoking or alcohol abuse and no known allergies. He had been receiving simvastatin, aspirin, and enalapril for at least the last 5 years. His abdominal pain had begun after the first dose of nilotinib and gradually worsened prior to admission. The patient denied recent alcohol use or abdominal trauma. Lab test results revealed elevated white blood cell (WBC) count of 33,370/μL, amylase 152 IU/L, serum lipase 308 IU/L, and serum lactate dehydrogenase 308 IU/L. The patient had baseline serum amylase and lipase determined prior to nilotinib inhibition, and they were within normal limits. Serum bilirubin levels were slightly elevated at 1.7 mg/dL and serum triglyceride levels were within normal limits at 121 mg/dL. An abdominal CT scan demonstrated normal liver, a slightly enlarged spleen with normal appearance, and thickening of the pancreatic tail with infiltration of the surrounding fat. All of these findings are consistent with pancreatitis. Nilotinib was immediately discontinued, and the patient had no oral intake for a day and was treated with intravenous fluids and analgesics. The next day, the abdominal pain decreased and serum amylase, lipase, and bilirubin all decreased and returned to normal 2 weeks later.Nilotinib is a second-generation tyrosine kinase inhibitor (TKI). TKI administration has been associated with an increase in serum amylase and/or lipase. This case report describes acute pancreatitis, which was confirmed by clinical, radiologic, and laboratory studies after initiation of nilotinib. Even though the patient had been receiving simvastatin and enalapril and these agents are associated with pancreatitis, it is unlikely that these agents played a part in the development of pancreatitis. He had been receiving these drugs for at least 5 years and was reinitiated on these agents without incident.The authors state that nilotinib should be considered as capable of causing acute pancreatitis. The determination of baseline amylase and lipase serum levels prior to nilotinib initiation should be the standard of care, and clinicians should be alert for this rare phenomenon.Engel T, Justo D, Amitai M, et al. Nilotinib-associated acute pancreatitis. Ann Pharmacother. 2013;47(1):e3. 相似文献17.
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《Hospital pharmacy》2013,48(7):542-549
The purpose of this feature is to heighten awareness of specific adverse drug reactions (ADRs), discuss methods of prevention, and promote reporting of ADRs to the US Food and Drug Administration’s (FDA’s) MedWatch program (800-FDA-1088). If you have reported an interesting, preventable ADR to MedWatch, please consider sharing the account with our readers. Write to Dr. Mancano at ISMP, 200 Lakeside Drive, Suite 200, Horsham, PA 19044 (phone: 215-707-4936; e-mail: ude.elpmet@onacnamm). Your report will be published anonymously unless otherwise requested. This feature is provided by the Institute for Safe Medication Practices (ISMP) in cooperation with the FDA’s MedWatch program and Temple University School of Pharmacy. ISMP is an FDA MedWatch partner. 2013 Jul-Aug; 48(7): 542–549. Published online 2013 Jul 9. doi: 10.1310/hpj4870-542
Rash Associated with Dabigatran
Michael A. Mancano, PharmD*Michael A. Mancano
*Chair and Clinical Professor, Department of Pharmacy Practice, Temple University School of Pharmacy, Philadelphia, Pennsylvania; Clinical Advisor, Institute for Safe Medication Practices, Horsham, PennsylvaniaFind articles by Michael A. MancanoAuthor information Copyright and License information Disclaimer*Chair and Clinical Professor, Department of Pharmacy Practice, Temple University School of Pharmacy, Philadelphia, Pennsylvania; Clinical Advisor, Institute for Safe Medication Practices, Horsham, PennsylvaniaCopyright notice A 59-year-old male was admitted to the hospital and diagnosed with new-onset atrial flutter 10 weeks following a successful bilateral lung transplant. The patient was discharged in normal sinus rhythm, but during cardiac rehabilitation the patient’s atrial flutter returned. The patient was then started on dabigatran etexilate (Pradaxa) 150 mg twice daily for anticoagulation with an elective cardioversion to follow. For unknown reasons, the patient never initiated dabigatran therapy. The patient was hospitalized shortly thereafter with symptomatic heart failure; during the course of this hospital stay, dabigatran etexilate 150 mg twice daily was started. Five days later, the patient noticed a diffuse, nonpruritic rash on his trunk and lower extremities. The patient then self-discontinued dabigatran and refused the use of any products to relieve the rash.Six days after discovery of the rash, the patient was readmitted with atrial flutter. On admission, the physician noted a maculopapular rash isolated only to the patient’s trunk. Because the rash had improved without therapeutic intervention, no additional therapy for the rash was needed. The rash ultimately resolved 2 days after his recent hospitalization and 7 days after drug discontinuation.The patient was receiving a number of chronic medications, but the only new medication initiated (other than dabigatran) was furosemide, which was initiated 2 weeks prior to discovery of the rash. The rash resolved, even though the patient continued to receive furosemide. The authors state that current product labeling for dabigatran indicates a frequency of 0.1% for rash, pruritus, and urticaria, with additional clinical trial data revealing the occurrence of cutaneous reactions but none with a frequency of greater than 0.03%.The authors warn that although the incidence of rash is rare with dabigatran, practitioners and patients should be aware of the potential for rash as an adverse effect of dabigatran therapy.To K, Reynolds C, Spinler SA. Rash associated with dabigatran etexilate. Pharmacotherapy. 2013;33(3):e23-e27. 2013 Jul-Aug; 48(7): 542–549. Published online 2013 Jul 9. doi: 10.1310/hpj4870-542Skin Necrosis Induced by Generic Enoxaparin
Copyright and License information DisclaimerCopyright notice Heparin-induced skin necrosis (HISN) is a rare complication of heparin or low-molecular-weight heparin (LMWH) therapy. Cases of HISN are generally associated with antibodies to the heparin:platelet factor 4 complex and/or heparin-induced thrombocytopenia (HIT). The authors cited a recent review that described 25 cases of skin necrosis associated with LMWH therapy through May 2009.1 The authors report on 4 cases of HISN, all occurring at their institution since the formulary switch from enoxaparin (Lovenox) to generic enoxaparin manufactured by Sandoz.The first case is a 67-year-old female who had been receiving Lovenox for over 3 weeks for treatment of a deep vein thrombosis (DVT). Within 24 hours of transitioning to generic enoxaparin, the patient developed HISN at the injection site with scarring persisting for 6 months. Her heparin-dependent antibody (HDA) test was negative. The second case is a 49-year-old male who developed HISN after the first 3 doses of generic enoxaparin. The patient had been exposed to unfractionated heparin in the past and his HDA assay was strongly positive, however the patient did not develop thrombocytopenia or thrombosis.The third case is a 57-year-old female who was receiving postoperative prophylaxis with generic enoxaparin. On day 13 of prophylaxis, the patient developed 2 local skin necrosis reactions. The HDA assay was positive as was the serotonin release assay, however the patient did not develop thrombocytopenia or thrombosis. The fourth case is a 30-year-old woman who received generic enoxaparin for treatment of a proximal DVT. On day 3 of treatment, she developed inflamed injection site reactions that progressed to subsequent necrosis over several days; this led to hyperpigmented skin changes that persisted beyond 6 months. Her HDA assay was negative.None of the patients developed thrombocytopenia, new thrombosis, or clinical HIT and only 2 of the 4 cases exhibited a positive HDA assay. In 2 cases, the skin necrosis developed outside the usual time frame of HIT of 5 to 15 days of exposure. The authors note that this fact suggests a novel mechanism of pathology. They include a brief discussion of the facts surrounding the approval of generic enoxaparin by the US Food and Drug Administration (FDA). The generic product was approved after only in vitro analysis, and immunogenicity studies were conducted in healthy volunteers with limited human clinical trial experience.Gucalp A, Parameswaran R, Lacouture M, et al. Skin necrosis induced by generic enoxaparin. Am J Hematol. 2013;88(4):339. 2013 Jul-Aug; 48(7): 542–549. Published online 2013 Jul 9. doi: 10.1310/hpj4870-542Serotonin Syndrome with Concomitant Use of Tapentadol and Venlafaxine
Copyright and License information DisclaimerCopyright notice A 39-year-old male was admitted to the hospital twice within 12 days for symptoms of total body tremors, anxiety, and excessive sedation. The total body tremors were not apparent seizures, and the patient remained conscious throughout these episodes. The patient did have a history of seizures as a child, but he could not recall many details of the experiences.During the first admission, the patient complained of chills, diarrhea, and a severe headache. He had taken venlafaxine (Effexor XR) 75 mg daily for many years; his medication history also revealed zolpidem 10 mg as needed at bedtime, ranitidine 150 mg twice daily, and tapentadol ER (Nucynta ER) 100 mg twice daily. The patient had recently been switched from oxycodone/acetaminophen to tapentadol for the management of chronic back pain. During this first admission, tapentadol was discontinued and morphine sustained release 45 mg twice daily was initiated. An EKG, CT of the head, chest x-ray, and Cardiolite stress test were all normal. Urine and blood cultures were also negative. The patient was discharged 2 days after admission and was told to resume his previous home medications.The second admission occurred 10 days later when the patient presented with the same symptoms of total body tremors, anxiety, and excessive sedation. A drug interaction between tapentadol and venlafaxine was suspected; both drugs were discontinued, and the patient was placed on morphine sustained release 30 mg twice daily for his back pain. The patient improved following discontinuation of both medications and was discharged 2 days later. He was discharged on morphine, which was then transitioned to 1 to 3 tablets per day of oxycodone/acetaminophen 5/325 and cyclobenzaprine 10 mg 3 times daily.The authors conclude that this is a possible case of serotonin syndrome induced by the additive serotoninergic effects of tapentadol and venlafaxine. Tapentadol is a synthetic, centrally active analgesic, which is structurally and pharmacologically related to tramadol. Although its exact mechanism is unknown, analgesic efficacy is thought to be due to mu-opioid agonist activity and the inhibition of norepinephrine reuptake.2Cases of life-threatening serotonin syndrome have been reported with the concurrent use of tapentadol and serotonergic drugs. Serotonergic drugs comprise selective serotonin reuptake inhibitors (SSRIs), serotonin and norepinephrine reuptake inhibitors (SNRIs), tricyclic antidepressants (TCAs), triptans, drugs that affect the serotonergic neurotransmitter system (eg, mirtazapine, trazodone, and tramadol), and drugs that impair metabolism of serotonin (including monoamine oxidase inhibitors [MAOIs]). Serotonin syndrome may occur within the recommended doses of these agents; It can include mental-status changes (eg, agitation, hallucinations, coma), autonomic instability (eg, tachycardia, labile blood pressure, hyperthermia), neuromuscular aberrations (eg, hyperreflexia, incoordination), and/or gastrointestinal symptoms (eg, nausea, vomiting, diarrhea) and can be fatal.2The authors note that caution is advised when tapentadol is co-administered with other drugs that may affect serotonergic neurotransmitter systems such as SSRIs, SNRIs, MAOIs, and triptans. If concomitant treatment of tapentadol with a drug affecting the serotonergic neurotransmitter system is clinically warranted, careful observation of the patient is advised, particularly during treatment initiation and dose increases.Case report submitted by: Lance E. Rhodes, PharmD, Director of Pharmacy, Garrett County Memorial Hospital, Oakland, Maryland, and David E. Cobb, PharmD Candidate, West Virginia University School of Pharmacy. 2013 Jul-Aug; 48(7): 542–549. Published online 2013 Jul 9. doi: 10.1310/hpj4870-542Etanercept-Induced Henoch-SchÖNlein Purpura
Copyright and License information DisclaimerCopyright notice Henoch-Schönlein purpura (HSP) is a type of vasculitis that causes bleeding in the capillaries in skin, joints, intestines, and kidneys. The main symptom is a purplish rash, typically on the lower legs and buttocks. HSP often causes abdominal pain and aching joints and, in some patients, kidney manifestations.A 61-year-old Caucasian male who had a history of ankylosing spondylitis (AS) with long-standing debilitating pain requiring significant opiate use, morning stiffness, and magnetic resonance evidence of active disease was treated with etanercept (Enbrel) 50 mg subcutaneously weekly. AS is a chronic inflammatory disease that primarily affects the axial skeleton. Extra-articular manifestations are less common but can typically involve the ascending aorta and aortic valve. AS is a disorder with an unclear etiology, however overexpression of tumor necrosis factor alpha is a feature.After 5 months of treatment with etanercept, the patient reported improved AS symptoms. Four weeks prior to presentation, the patient noted a nonblanching rash affecting the lower extremities without other systemic symptoms. A serum creatinine (Cr) was 1.1 mg/dL (reference range, 0.6-1.2 mg/dL), but urinalysis was not performed at that time. The patient was treated with prednisone 20 mg daily for leukocytoclastic vasculitis (LCV) secondary to a drug reaction by the dermatology service, and etanercept was discontinued. A skin biopsy confirmed LCV with IgA and C3 predominance.Four weeks later while still receiving prednisone 10 mg daily and colchicine without etanercept treatment, the patient presented to the hospital with worsening fatigue, new-onset peripheral synovitis, and petechiae involving both lower extremities up to his proximal thighs, lower abdomen, back, and hands. On exam, the patient was afebrile with normal vital signs. Extensive petechiae with coalescence and lower-extremity edema were present on dependent areas up to the lower abdomen and back. Lab data revealed a serum Cr 3.3 mg/dL that was elevated from 1.1 mg/dL 4 weeks prior. Complete blood count and liver function tests were within normal limits. Erythrocyte sedimentation rate was 69 mm/h (reference range, male < 17 mm/h) and C-reactive protein was 3.9 mg/dL (reference range, <10 mg/dL). Urinalysis showed proteinuria and microscopic red blood cells (31-60 per high-powered field). Serum IgA was 430 mg/dL (normal, 80-350 mg/dL), antinuclear antibody (ANA) 1:80, and antihistone antibody 6.3 U (normal ≤1 U).A clinical diagnosis of HSP induced by etanercept was suspected, and the patient was treated with intravenous pulse methylprednisone 1 g/day for 3 days followed by prednisone 1 mg/kg daily. A renal biopsy performed on day 3 revealed diffuse mesangial proliferative glomerulonephritis with segmental membranoproliferative features. Treatment was continued with high-dose corticosteroids with tapering of prednisone 10 mg every 2 weeks to prednisone 0.5 mg/kg followed by a slower taper. After 7 months, the patient showed resolution of small joint synovitis and skin rash with normalization of his serum Cr to 1.2 mg/dL. He continued to have residual lower extremity edema. There has not been a recurrence of HSP since discontinuation of etanercept.This case adds to the growing literature of TNF inhibitor (TNFi)–induced vasculitis and describes an uncommon case of TNFi-induced HSP in an AS patient. Although the development of HSP subsequent to TNFi use in patients with rheumatic diseases other than SA has been reported, there is a paucity of information in SA patients. The authors call for more study to identify the risk factors for the development of HSP in patients with AS. Renal function and urinalysis should be assessed in patients being treated with TNFi who develop new synovitis or skin rash. Rechallenging patients with the same TNFi should be avoided since HSP may recur.Rolle AS, Zimmerman B, Poon SH. Etanercept-induced Henoch-Schönlein purpura in a patient with ankylosing spondylitis. J Clin Rheum. 2013;19(2):90-93. 2013 Jul-Aug; 48(7): 542–549. Published online 2013 Jul 9. doi: 10.1310/hpj4870-542Vemurafenib-Associated Pancreatitis
Copyright and License information DisclaimerCopyright notice Vemurafenib (Zelboraf) is a BRAF kinase inhibitor indicated in metastatic melanoma patients with BRAF V600E mutation. Vemurafenib has not been associated with pancreatitis to date.A 49-year-old male with unresectable, stage IV melanoma was treated with first-line and investigational agents, but treatment was discontinued due to disease progression. The patient had a 4-month washout period since his last chemotherapy regimen, and it was determined that he was BRAF V600E mutation-positive. Treatment with vemurafenib was started at a dose of 960 mg orally twice daily. Two weeks after initiation, the patient presented to the emergency room with epigastric pain, elevated blood pressure, and a serum lipase of 1,544 units/L (reference range, <160 units/L). Common probable causes of pancreatitis were ruled out (gallstones, alcohol use, and infection), and the pancreatitis was attributed to vemurafenib therapy. The patient was also receiving lisinopril, metoprolol, opiates, prochlorperazine, senna, and docusate. Opiates and lisinopril can cause pancreatitis, but the patient’s symptoms dissipated upon discontinuation of vemurafenib. Therefore due to temporal considerations, these drugs were excluded as possible causes.Based on the severity of the patient’s condition and the survival advantage provided by vemurafenib, a rechallenge was attempted. Vemurafenib was initiated at a lower dose of 480 mg twice daily, however the patient developed pancreatitis after 2 doses. Vemurafenib was discontinued, and the patient had a complete resolution of symptoms. The authors point out that in light of the temporal relationship and rechallenge with vemurafenib, the Naranjo Scale yielded a score of 9 indicating a definite probability that the patient’s pancreatitis was caused by vemurafenib.Muluneh B, Buie LW, Collichio F. Vemurafenib-associated pancreatitis: case report. Pharmacotherapy. 2013;33(4):e43-e44. 相似文献19.
《Hospital pharmacy》2013,48(5):360-365
The purpose of this feature is to heighten awareness of specific adverse drug reactions (ADRs), discuss methods of prevention, and promote reporting of ADRs to the US Food and Drug Administration’s (FDA’s) MedWatch program (800-FDA-1088). If you have reported an interesting, preventable ADR to MedWatch, please consider sharing the account with our readers. Write to Dr. Mancano at ISMP, 200 Lakeside Drive, Suite 200, Horsham, PA 19044 (phone: 215-707-4936; e-mail: ude.elpmet@onacnamm). Your report will be published anonymously unless otherwise requested. This feature is provided by the Institute for Safe Medication Practices (ISMP) in cooperation with the FDA’s MedWatch program and Temple University School of Pharmacy. ISMP is an FDA MedWatch partner. 2013 May; 48(5): 360–365. Published online 2013 May 6. doi: 10.1310/hpj4805-360