Pakpoom Phoompoung1, Benoît Henry2, Georgina Daher-Reyes3, Hassan Sibai3, Shahid Husain4. 1. Transplant Infectious Diseases, Ajmera Transplant Centre; Faculty of Medicine Siriraj Hospital, Mahidol University, Bangkok, Thailand. 2. Transplant Infectious Diseases, Ajmera Transplant Centre. 3. Princess Margaret Cancer Centre, University Health Network, Toronto, Canada. 4. Transplant Infectious Diseases, Ajmera Transplant Centre. Electronic address: Shahid.husain@uhn.ca.
Abstract
BACKGROUND: The incidence and risk factors for invasive mold infections (IMI) in acute myeloid leukemia (AML) patients carrying FLT3 mutations have not been addressed. PATIENTS AND METHODS: This retrospective cohort included FLT3-mutated AML patients (2008-2018). Primary outcome was IMI incidence within 6 months after first induction or salvage therapy. RESULTS: We included 108 patients receiving fluconazole or micafungin prophylaxis. IMI incidence after induction and salvage therapy was 4.8% and 14.8%, respectively, and did not differ between patients receiving 3+7 regimen or 3+7 plus midostaurin (4.3% vs 4.5%). In a bivariate analysis, age (odds ratio, 1.11; P = .027) and FLT3 ITD mutation (odds ratio, 0.05; P = .023) were independently associated with IMI after induction chemotherapy. Gilteritinib was more frequently prescribed in patients with relapsed/refractory disease who developed IMI (50% vs 27.3%, P = .563). CONCLUSION: FLT3 ITD mutation may be a preventive factor for IMI. Neither midostaurin nor salvage gilteritinib significantly increased the risk of IMI in this population.
BACKGROUND: The incidence and risk factors for invasive mold infections (IMI) in acute myeloid leukemia (AML) patients carrying FLT3 mutations have not been addressed. PATIENTS AND METHODS: This retrospective cohort included FLT3-mutated AML patients (2008-2018). Primary outcome was IMI incidence within 6 months after first induction or salvage therapy. RESULTS: We included 108 patients receiving fluconazole or micafungin prophylaxis. IMI incidence after induction and salvage therapy was 4.8% and 14.8%, respectively, and did not differ between patients receiving 3+7 regimen or 3+7 plus midostaurin (4.3% vs 4.5%). In a bivariate analysis, age (odds ratio, 1.11; P = .027) and FLT3 ITD mutation (odds ratio, 0.05; P = .023) were independently associated with IMI after induction chemotherapy. Gilteritinib was more frequently prescribed in patients with relapsed/refractory disease who developed IMI (50% vs 27.3%, P = .563). CONCLUSION: FLT3 ITD mutation may be a preventive factor for IMI. Neither midostaurin nor salvage gilteritinib significantly increased the risk of IMI in this population.