Infection and Drug Resistance
Eculizumab-Induced Acute Heart Failure Decompensation in a Patient with Clinically Suspected Complement-Mediated Thrombotic Microangiopathy: A Case Report
By Huang J, Ni T, Liu H and 7 others.
Abstract
Jiayang Huang,1,* Tongtian Ni,2,* Hong Liu,3 Yi Yao,2 Mengjiao Li,2 Bing Zhao,2 Ke Zhang,1 Wangsheng Li,1 Enqiang Mao,2 Yihui Wang,2 Juan He11Department of Pharmacy, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, 200025, People’s Republic of China; 2Department of Emergency, The Second Hospital of Shanxi Medical University, Taiyuan, Shanxi, 030001, People’s Republic of China; 3Department of Emergency Medicine, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, 200025, People’s Republic of China*These authors contributed equally to this workCorrespondence: Yihui Wang; Juan He, Email wangyihui581@163.com; hejuanwin@126.comAbstract: Eculizumab is a highly effective and generally safe therapy for atypical hemolytic uremic syndrome (aHUS), a rare subtype of thrombotic microangiopathy (TMA). This report presents a case of recurrent episodes of acute decompensated heart failure temporally related to its administration, a possible adverse effect that is exceedingly rare and poorly documented in the literature. A 45-year-old woman presented with altered mental status and received a clinical diagnosis of complement-mediated thrombotic microangiopathy based on the presence of thrombotic microangiopathy and marked complement activation. Within hours of the first and subsequent eculizumab infusions, she developed recurrent episodes of acute decompensated heart failure, evidenced by respiratory distress, tachycardia, soaring pro-BNP levels, and echocardiographic confirmation of left ventricular dysfunction. These episodes consistently impeded weaning from mechanical ventilation. The temporal association was reinforced when withholding eculizumab was associated with symptom resolution, while a subsequent reduced-dose challenge promptly reinduced cardiac decompensation. This case raises the possibility that eculizumab may trigger acute decompensated heart failure in susceptible patients. It alerts clinicians to monitor for this potentially life-threatening complication and underscores a significant therapeutic dilemma when first-line therapy is associated with severe adverse effects. Further investigation is needed to understand the mechanism and identify at-risk patients.Keywords: atypical hemolytic uremic syndrome, eculizumab, adverse drug reaction, heart failure, case report




