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Clinical characteristics and risk factors of tigecycline-induced acute pancreatitis in kidney transplant recipients: a retrospective study

替加环素 医学 内科学 急性胰腺炎 胰腺炎 肾移植 回顾性队列研究 重症监护医学 肾移植 移植 器官移植 抗生素 生物 微生物学
作者
Lijuan Feng,Yuanyuan Hong,Jintu Fan,Chunlan Yang,Yan Huang,Yongming Xu,Guiyi Liao,Yong Su
出处
期刊:Journal of Antimicrobial Chemotherapy [Oxford University Press]
卷期号:80 (7): 1980-1987 被引量:1
标识
DOI:10.1093/jac/dkaf159
摘要

Abstract Objective Acute pancreatitis (AP) is a severe but insufficiently recognized adverse effect of tigecycline in kidney transplant (KT) recipients. This study aimed to identify the clinical characteristics and risk factors associated with tigecycline-induced AP in this population. Methods A single-center retrospective study was conducted in KT recipients treated with tigecycline. The clinical characteristics of patients who developed AP were analyzed, and risk factors for tigecycline-induced AP were assessed using univariate analysis and multivariate logistic regression. Results 80 KT recipients were enrolled, of whom nine developed AP (incidence: 11.25%), and four died. The mean time from tigecycline administration to AP onset was 7.00 days, to symptomatic relief after discontinuation was 4.87 days, and to normalisation of pancreatic enzymes after discontinuation was 8.75 days. The analysis revealed that tacrolimus trough concentration (C0 Tac) and post-transplant acute kidney injury (AKI) were independent risk factors for tigecycline-induced AP in KT recipients. Logistic regression analysis produced a combined predictive expression: Ycombined = AKI + 0.064C0 Tac−2.789. Receiver operating characteristic curve analysis determined that the C0 Tac cut-off was 13.9 ng/mL. The area under the curve for C0 Tac and combined predictor were 0.802 and 0.853, respectively. Conclusion The incidence of AP following tigecycline treatment was significantly higher in KT recipients than in non-transplant patients. Post-transplant AKI and elevated C0 Tac concentrations were identified as independent risk factors for the development of AP. Close monitoring of renal function and ensuring therapeutic monitoring of C0 Tac levels may help prevent AP.
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