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Levofloxacin induced Stevens-Johnson syndrome/ toxic epidermal necrolysis overlap syndrome: case reports

机译:左氧氟沙星诱发史蒂文斯-约翰逊综合征/中毒性表皮坏死溶解重叠综合征:病例报告

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Fluoroquinolones are widely used because of their broadspectrum of activity. Their benefit-risk profile needscareful evaluation as they can induce T cell-dependentreactions including Stevens-Johnson syndrome (SJS) andtoxic epidermal necrolysis (TEN). Here we present tworare cases of SJS/TEN overlap syndrome and SJS causedby levofloxacin. Case 1. A 70-year-old woman with ahistory of chronic obstructive pulmonary disease wastreated with levofloxacin for acute bronchitis. After takingmedications for 10 days she complained of generalizedskin eruptions and mucosal erosions. On the day ofadmission in the burn intensive care department 28% ofher body surface was covered by rash, blistering and epidermalpeeling; 65% of body surface presented dusky redskin. Levofloxacin was stopped and our patient was treatedwith topical solution to keep the wounds moist, fluidreplacement, well balanced nutrition, systemic corticosteroidsand intravenous immune globulin (IVIG). Wealso administrated teicoplanin because of S. aureusinfection of central i.v. catheter confirmed by a positiveculture. She was subsequently treated with meropenembecause of a Klebsiella pneumoniae urinary tract infection.The main laboratory findings were: anemia, leukocytosisand increased CRP levels. The diagnosis wasperformed on the basis of clinical and histological features.Gradually her symptoms improved and the epidermalpeeling also subsided. Case 2. A 72-year-oldwoman was referred to our department with multipleskin lesions involving more than 50 % of the total bodysurface area occurred after 2 weeks of starting levofloxacintreatment for pneumonia. She developed high feverand had the appearance of a severe burn patient.Laboratory analysis showed anaemia, leukocytosis,hypoalbuminaemia and elevated procalcitonin and CRP.The levofloxacin treatment was stopped immediately andreplaced with teicoplanin and meropenem. Subsequentlybecause of A. baumanii complex infection of the centrali.v. catheter she was treated also with colistin. Our managementincluded IVIG treatment, intravenous glucocorticoids,proper fluid balance, attention to nutritionalstatus and pain relief. The skin lesions healed within3 weeks and the patient left our department in good generalcondition.ConclusionsEven if there are little published data on levofloxacinTEN/SJS, this fluoroquinolone can be implicated inthese delayed ADR requiring early diagnosis and carefulmonitoring.
机译:氟喹诺酮类化合物因其广谱的活性而被广泛使用。他们的利益-风险特征需要仔细评估,因为它们可以诱导T细胞依赖性反应,包括史蒂文斯-约翰逊综合征(SJS)和毒性表皮坏死症(TEN)。在这里,我们介绍了由左氧氟沙星引起的SJS / TEN重叠综合征和SJS的两种罕见情况。病例1.一位患有慢性阻塞性肺病史的70岁妇女接受了左氧氟沙星治疗急性支气管炎。服药10天后,她主诉皮肤普遍性爆发和粘膜侵蚀。烧伤重症监护室入院当天,其28%的身体表面被皮疹,水疱和表皮剥离覆盖; 65%的体表呈现暗红色。停用左氧氟沙星,并为该患者提供局部溶液治疗,以保持伤口湿润,补液,营养均衡,全身性皮质类固醇和静脉免疫球蛋白(IVIG)。由于金黄色葡萄球菌感染中枢静脉,我们还给予替考拉宁治疗。导管经阳性培养证实。随后她因肺炎克雷伯菌尿路感染接受了美罗培南的治疗。主要实验室检查结果为:贫血,白细胞增多和CRP水平升高。根据临床和组织学特征进行诊断。症状逐渐改善,表皮剥离也逐渐消失。案例2.一名72岁的女性被转介到我科,在开始左氧氟沙星治疗肺炎2周后发生多处皮肤病变,占总表面积的50%以上。她发高烧并有重度烧伤患者的外观。实验室分析显示贫血,白细胞增多,低白蛋白血症和降钙素原和CRP升高。左氧氟沙星治疗立即停止并用替考拉宁和美罗培南代替。随后由于鲍曼不动杆菌复杂的中央感染。导管,她也接受了大肠杆菌素治疗。我们的管理包括IVIG治疗,静脉注射糖皮质激素,适当的体液平衡,注意营养状况和缓解疼痛。结论:即使左氧氟沙星TEN / SJS的公开数据很少,该氟喹诺酮也可能与这些延迟的ADR有关,需要早期诊断和仔细监测。

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