The Journal of antimicrobial chemotherapy · 2025
Clinical characteristics and risk factors of tigecycline-induced acute pancreatitis in kidney transplant recipients: a retrospective study.
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Feng Lijuan, Hong Yuanyuan, Fan Jiawang, Yang Chunlan, Huang Yan, Xu Yuanbao, Liao Guiyi, Su Yong
Аннотация
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.
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.