Death of Twins After Intravenous Varicella Zoster Immunoglobulin
Death of Twins After Intravenous Varicella Zoster Immunoglobulin
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静脉注射水痘带状疱疹免疫球蛋白后双胞胎死亡
DOI：
10.1345/aph.1e311
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发表时间：
2005
期刊：
影响因子：
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通讯作者：
J. Puliyel
中科院分区：
文献类型：
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作者：
V. Bhambhani;Nirmal Kumar;J. Puliyel
致编辑：呋喃妥因于1953年被引入用于治疗泌尿生殖道常见的革兰氏阳性和革兰氏阴性病原体。与呋喃妥因相关的血液学反应被认为是罕见的。1，2我们描述了一个与呋喃妥因短期疗程相关的粒细胞缺乏症病例。病例报告。一位74岁的白色男性在长期护理主诉右下腹疼痛和尿潴留。检查时的生命体征为BP 118/62 mm Hg，脉搏93次/分，呼吸率24次/分，体温37.7 ℃。尿培养及药敏试验报告为甲氧西林敏感金黄色葡萄球菌。患者未出现肾功能不全，肌酐清除率估计为64 mL/min。患者被诊断为尿路感染，并接受呋喃妥因100 mg每日4次治疗。2个月前的基线血细胞计数显示总白色血细胞（WBC）计数为5.7 × 103/mm3，粒细胞计数为4.2 × 103/mm3。呋喃妥因治疗第5天，总WBC和粒细胞计数分别降至1.9 × 103/mm3和0.5 × 103/mm3（图1）。对患者进行检查时，未显示低血压或过敏反应体征。治疗5天后停用呋喃妥因，改用头孢呋辛。呋喃妥因停药后2天，总WBC和粒细胞计数分别增加至2.5 × 103/mm3和1.1 × 103/mm3（图1）。20天后，总WBC和粒细胞计数继续改善。Naranjo概率量表显示粒细胞缺乏症和呋喃妥因之间可能存在关系。根据全球药物不良反应数据，约0.0004%的呋喃妥因治疗导致血液学反应。1在对921例患者的评价中，20例患者出现呋喃妥因相关的血液恶液质。这些患者均未表现出与呋喃妥因相关的肾功能不全。20例病例中有2例导致与呋喃妥因相关的致命性粒细胞缺乏症，但第二种药物是一个促成因素（磺胺甲嘧啶、磺胺丙氧嘧啶、左美丙嗪）。2另一例呋喃妥因引起的致命性粒细胞缺乏症涉及一名14岁黑人女性，患有系统性红斑狼疮和肾衰竭。4在一例病例中，在短期呋喃妥因150 mg/天治疗后，发生复发性粒细胞缺乏症。5这位62岁的女性再次接受治疗，3天内发生粒细胞缺乏症。患者在呋喃妥因停药后痊愈。在比较这些病例时，粒细胞缺乏症的发生似乎与肾功能无关，但肌酐清除率<60 mL/min将是一个风险因素。2，5由于我们的患者疗程短且肾功能充足，呋喃妥因诱导的粒细胞缺乏症可能有利于免疫反应，而不是作为发病机制的毒性作用。然而，蓄积仍可能在粒细胞缺乏症的发生中发挥作用。2，4，5大多数研究报告呋喃妥因作为尿路感染的治疗选择;它耐受性良好，不良反应的风险相对较低。根据文献，粒细胞缺乏症很少发生，但仍需考虑为可能的不良反应。1，2监测总WBC、粒细胞计数和肾功能可预防呋喃妥因治疗患者的粒细胞缺乏症。
TO THE EDITOR: Nitrofurantoin was introduced in 1953 for treatment of gram-positive and gram-negative pathogens common to the genitourinary tract. Hematologic reactions associated with nitrofurantoin are considered rare.1,2 We describe a case of agranulocytosis associated with a short course of nitrofurantoin. Case Report. A 74-year-old white man in long-term care complained of right lower-quadrant pain and urinary retention. Vital signs upon examination were BP 118/62 mm Hg, pulse 93 beats/min, respiratory rate 24 breaths/min, and temperature 37.7 ̊C. Urine culture and sensitivity test reported methicillin-sensitive Staphylococcus aureus. The patient did not exhibit renal insufficiency, with estimated creatinine clearance 64 mL/min. The patient was diagnosed with a urinary tract infection and treated with nitrofurantoin 100 mg 4 times a day. Baseline blood cell count 2 months earlier had shown a total white blood cell (WBC) count of 5.7 × 103/mm3 and granulocyte count of 4.2 × 103/mm3. On the fifth day of nitrofurantoin therapy, total WBC and granulocyte counts decreased to 1.9 × 103/mm3 and 0.5 × 103/mm3, respectively (Figure 1). No signs of hypotension or allergic reaction were illustrated upon examination of the patient. Nitrofurantoin was discontinued after 5 days of therapy and replaced with cefuroxime. Two days following discontinuation of nitrofurantoin, the total WBC and granulocyte counts increased to 2.5 × 103/mm3 and 1.1 × 103/mm3, respectively (Figure 1). Twenty days later, the total WBC and granulocyte counts continued to improve. The Naranjo probability scale showed a probable relationship between agranulocytosis and nitrofurantoin.3 Discussion. According to worldwide adverse drug reaction data, approximately 0.0004% of nitrofurantoin treatments have resulted in hematologic reactions.1 In an evaluation of 921 patients, 20 patients presented with blood dyscrasias associated with nitrofurantoin. None of those patients demonstrated renal insufficiency associated with nitrofurantoin. Two of the 20 cases resulted in fatal agranulocytosis associated with nitrofurantoin, but a second drug was a contributing factor (sulfamerazine, sulfaproxyline, levomepromazin).2 Another case of fatal nitrofurantoin-induced agranulocytosis involved a 14-year-old black female with systemic lupus erythematosus and renal failure.4 In one case, recurrent agranulocytosis occurred after a short course of nitrofurantoin 150 mg/day.5 The 62-year-old woman was rechallenged, and agranulocytosis developed within 3 days. The patient recovered after discontinuation of nitrofurantoin. In comparing these cases, agranulocytosis seemed to occur independently of renal function, but creatinine clearance <60 mL/min would be a risk factor.2,5 Due to our patient’s short course of therapy and adequate renal function, agranulocytosis induced by nitrofurantoin may favor an immunologic reaction rather than a toxic effect as the pathogenetic mechanism. However, accumulation may still play a role in the development of agranulocytosis.2,4,5 Most studies report nitrofurantoin as a treatment option for urinary tract infections; it is well tolerated and has a relatively low risk of adverse effects. According to the literature, agranulocytosis rarely occurs, but still needs to be considered as a possible adverse effect.1,2 Monitoring the total WBC, granulocyte count, and renal function may prevent agranulocytosis in patients treated with nitrofurantoin.