老年人药品不良反应分析

目的：了解老年人服用药物出现的不良反应。方法：采用回顾性的调查方法,对首都医科大学宣武医院2005—2008年所收集的933份老年人用药不良反应进行数据分析。结果：在统计的这933份不良反应报表中,男性406例,女性527例,平均年龄71.73岁;涉及药物245种,主要为中成药269例（28.83%）,其次为抗感染及抗病毒药227例（24.33%）;不良反应的主要表现是皮肤及其附件损害,其次是中枢神经系统症状;用药途径主要为静脉滴注和口服。结论：重视和加强老年人用药不良反应的监测工作,以保证用药的安全性。     

老年人药品不良反应分析

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。     

药品不良反应监测质量评估指标体系的建立

目的：为药品不良反应监测质量评价提供科学的参考依据。方法：采用专家法和层次分析法（AHP法）确定评估指标及权重。结果：从监测机构、监测人员、监测制度和监测报告四个维度确定各评估指标并计算出对应的权重系数,初步构建药品不良反应监测质量评估指标体系。结论：构建出药品不良反应监测质量评估指标体系。     

老年人用药风险管理原则和措施

目的 探讨老年人用药风险的原因,并提出风险管理原则和措施。方法 从药动学特点、药效学特点、多重用药、用药依从性4个方面分析老年人用药风险高的原因,并阐述老年用药风险管理原则。结果 根据老年人用药风险管理原则,建立老年多学科工作团队,进行老年综合评估管理实践,探索建立老年人用药风险的主动管理措施。结论 基于老年人用药原则,积极探索主动用药风险管理措施是目前改善老年人多重用药问题的有效方法。     

331例抗感染药致老年人药品不良反应分析

目的：了解抗感染药致老年人药品不良反应（ADR）的情况,分析其相关因素。方法：回顾性调查分析我院2004年1月～2009年12月收集上报的ADR报告中,抗感染药致老年人ADR的特点和规律。结果：抗感染药致老年人ADR共331例,占上报ADR例数的9．87％。涉及抗感染药为14类55个品种,喹诺酮类药物引起的ADR占首位,其中以左氧氟沙星为主;给药途径主要为静脉给药;以皮肤及附件的损害最常见。结论：抗感染药致老年ADR与抗感染药的种类、给药途径、给药剂量等多种因素相关,临床上给老年人使用抗感染药时应注意合理用药,以减少或避免老年人ADR的发生。     

药品不良反应监测浅析

据世界卫生组织统计,世界每年死亡病例中约有5%系药物不良反应所致.据测算我国因药物不良反应每年死亡人数约达20万左右.现将有关药物不良反应监测内容浅析如下.     

309例老年人严重药品不良反应报告分析

目的统计分析湖南省2007年老年人严重药品不良反应发生的特点及规律。方法对湖南省2007年报告的老年人严重药品不良反应数据进行回顾性统计分析。结果在报告的309份老年人严重药品不良反应报告表中,严重药品不良反应的发生主要与抗感染药物、中药制剂、静脉给药方式、联合用药以及年龄有关。严重药品不良反应的主要临床表现为过敏性休克、心脏毒性以及肝肾毒性。结论加强老年人严重药品不良反应监测工作,促进临床合理用药。     

400例老年人严重药品不良反应病例分析

目的分析造成老年人严重药品不良反应的风险因素,为制定老年人高风险用药目录及其风险管理的评价指标提供参考。方法采用回顾性的研究方法,对北京市药品不良反应监测中心2009年1月～2011年6月收集到的老年人严重药品不良反应报告进行综合分析。结果老年人严重药品不良反应涉及的药品以抗感染药物、抗肿瘤药物、中药制剂、中枢神经系统用药和循环系统用药居前5位;给药途径以静脉滴注为最多,其次为口服用药;不良反应累及系统-器官以皮肤及其附件损害为最多、其次为全身性损害和肝胆系统损害。结论老年人严重药品不良反应分析可以为老年人用药风险与管理的评估指标提供参考,但哪些药品对老年人具有较高风险还有待进一步研究。     

关于药品不良反应与药品不良反应监测的若干问题探讨

随着国家的发展,人们对自身的生活水平要求逐渐提高,但是,在日常生活中,经常会出现药品不良反应使人们的身体健康与生命安全造成不良影响,不仅对医院造成名誉的影响,还会使国家的发展受到影响。所以,医院相关人员应该对药品不良反应进行有效的分析,研究药品问题出现的原因,改善监测工作,对药品的质量加以保证,避免出现不必要的问题。本文根据对药品不良反应监测问题的分析,提出几点解决问题的措施,以供相关工作人员参考。     

抗肿瘤药物的严重不良反应与防治

目的：介绍临床常用抗肿瘤药物的严重不良反应与防治对策。方法：通过对药品说明书相关内容作汇总分析．并结合临床实践进行阐述。结果与结论：抗肿瘤药物相对于其他类药物具有不良反应发生较多且对机体影响较大的特点．应积极采取有效的防治措施,避免或减轻不良反应对患者造成的损害．这对于提高肿瘤患者的治疗效果和生活质量有重要临床意义。     

新型冠状病毒肺炎治疗中的药物不良反应与防治

围绕《新型冠状病毒感染的肺炎诊疗方案（试行第六版）》中的治疗试用药物,包括抗病毒药物、糖皮质激素和中药,从各药的作用机制、药物相互作用、药物不良反应等方面,综述新型冠状病毒肺炎（COVID-19）治疗中可能出现的不良反应及防治策略,为临床治疗方案的合理选择提供参考。     

线粒体DNA相关的药物不良反应及其防治

线粒体是细胞中能量储存和供给的场所,也是动物细胞核外唯一含有遗传效应物质的细胞器。线粒体DNA自身的结构特点使其容易受到损伤,其独立的复制表达系统往往可成为外源物质攻击的靶点。很多药物的不良反应均与mtDNA损伤有关。以抗逆转录病毒药物、抗肿瘤药物和抗生素为例,综述线粒体DNA相关药物不良反应及其相关机制,并对防治方法进行了探讨。     

莫西沙星的严重不良反应及其防范

目的:提示临床高度关注莫西沙星的不良反应。方法:检索我院不良反应监测系统,对其中莫西沙星产生的3例严重不良反应报告进行分析。结果:3例莫西沙星严重不良反应中,暴发性肝衰竭1例,经抢救无效死亡;过敏性休克2例,经抢救未产生严重后果。结论:临床应重视莫西沙星严重不良反应的危害性。     

分子靶向抗肿瘤药物的不良反应及其处理对策

目前已有多种分子靶向抗肿瘤药物在我国上市,靶向治疗药物以其显著的疗效和良好的耐受性在临床上得到了广泛的应用,很多恶性肿瘤患者已从中获益。早期快速诊断并采取有效干预措施是改善肿瘤患者预后的重要手段,对改善患者生活质量和提高靶向治疗效果也尤为重要。本文对近年来分子靶向抗肿瘤药物的相关文献进行分析归纳,从皮肤系统、消化系统、循环系统、血液系统等多方面对分子靶向药物的不良反应及其处理对策进行了综述,旨在为国内,临床医药人员的实际工作提供参考借鉴,以期制定良好的治疗方案并减少药物的不良反应。     

抗高血压药物的不良反应及预防策略

目的探讨不同类型抗高血压药物的不良反应,为临床预防提供依据。方法采用回顾性调查法,对医院收治800例高血压患者应用抗高血压药物的不良反应进行统计和分析。结果男性和女性的抗高血压药物的不良反应率,60岁以上分别为52．80％和53．87％,60岁以下分别为47．29％和46．35％,差异有显著性（P〈0．05）;联合用药的不良反应率为48．81％,低于单用药物的54．87％（P〈0．05）;不良反应症状为咳嗽（4．45％）、低血压（3．67％）、头痛（3．36％）、眩晕（3．21％）和其他（2．20％）。结论采用个体化治疗原则和药物联合应用,能降低抗高血压药物的不良反应。     

新型抗癫痫药物的严重不良反应及其防范

目的：综合5种新型抗癫痫药物在国外文献中报道的严重不良反应（Serious adverse reactions,SARs）,提出相应的防范措施。方法：检索1990～2009年MEDLINE／PUBMED数据库中有关新型抗癫痫药物不良反应的文献,从中筛选出5种新型抗癫痫药物SARs的英文文献共132篇,将其SARs的临床表现、发生率、机制、危险因素、预防措施进行总结和分析。结果：加巴喷丁（GBP）可引起行为异常、认知障碍、诱发肌阵挛发作;拉莫三嗪（LTG）可引起严重皮疹、肝肾功能衰竭、弥散血管内凝血、致畸;左乙拉西坦（LEV）可引起抑郁、行为异常、自杀倾向;托吡酯（TPM）可引起抑郁、认知障碍、急性闭角性青光眼、肾结石;奥卡西平（OXC）可引起低钠血症、血管神经性水肿、加重肌阵挛发作等。若能个体化选用抗癫痫新药,并采取合理的预防措施,可以避免或降低用药风险。结论：已在我国上市的新型抗癫痫药物均有SARs,这些不良反应导致了患者的生活质量下降,甚至危及生命,因此,临床医师在选用药物、监护治疗时必须熟悉与警惕这些新药的SARs,制定防范措施。     

ISMP Adverse Drug Reactions

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.

• Hosp Pharm. 2013 Feb; 48(2): 100–103.
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• Aspirin/Clopidogrel-Induced Spontaneous Liver Hematoma

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.

• Hosp Pharm. 2013 Feb; 48(2): 100–103.
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• Adenosine-Induced Severe Bronchospasm in a Patient Without Pulmonary Disease

2013 Feb; 48(2): 100–103. Published online 2013 Feb 1. doi: 10.1310/hpj4802-100

Adenosine-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.

• Hosp Pharm. 2013 Feb; 48(2): 100–103.
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• Paclitaxel-Induced Acral Erythema

2013 Feb; 48(2): 100–103. Published online 2013 Feb 1. doi: 10.1310/hpj4802-100

Paclitaxel-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.

• Hosp Pharm. 2013 Feb; 48(2): 100–103.
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• Acute Laryngeal Dystonia Associated with Aripiprazole

2013 Feb; 48(2): 100–103. Published online 2013 Feb 1. doi: 10.1310/hpj4802-100

Acute 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.

• Hosp Pharm. 2013 Feb; 48(2): 100–103.
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• Incidence of Thrombocytopenia During Heparin Prophylaxis

2013 Feb; 48(2): 100–103. Published online 2013 Feb 1. doi: 10.1310/hpj4802-100

Incidence 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.

• Hosp Pharm. 2013 Feb; 48(2): 100–103.
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• Oral Fluoroquinolones and the Risk of Retinal Detachment

2013 Feb; 48(2): 100–103. Published online 2013 Feb 1. doi: 10.1310/hpj4802-100

Oral 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.

• Hosp Pharm. 2013 Feb; 48(2): 100–103.
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• Prenatal Exposure to Antidepressants: How Safe are They?

2013 Feb; 48(2): 100–103. Published online 2013 Feb 1. doi: 10.1310/hpj4802-100

Prenatal 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.

• Hosp Pharm. 2013 Feb; 48(2): 100–103.
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• Proton Pump Inhibitors: The Good, The Bad, and The Unwanted

2013 Feb; 48(2): 100–103. Published online 2013 Feb 1. doi: 10.1310/hpj4802-100

Proton 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.