Impact of invasive aspergillosis occurring during first induction therapy on outcome of acute myeloid leukaemia (SEIFEM-12B study).


Journal

Mycoses
ISSN: 1439-0507
Titre abrégé: Mycoses
Pays: Germany
ID NLM: 8805008

Informations de publication

Date de publication:
Oct 2020
Historique:
received: 03 06 2020
revised: 15 07 2020
accepted: 16 07 2020
pubmed: 23 7 2020
medline: 2 6 2021
entrez: 23 7 2020
Statut: ppublish

Résumé

Acute myeloid leukaemia (AML) patients are at high risk of invasive aspergillosis (IA) after first induction chemotherapy (CHT). Although IA risk factors have been identified, few data are available on impact of IA, occurring during induction phase, on overall AML outcome. The end point of this multicentre, case-control, study was to evaluate whether IA, occurring after first induction CHT, can affect treatment schedule and patient's outcome. We identified 40 AML patients (cases) who developed IA during first induction phase, 31 probable (77.5%) and 9 proven (22.5%). These cases were matched with a control group (80 AML) without IA, balanced according to age, type of CHT, AML characteristics and cytogenetic-molecular risk factors. The overall response rate to induction CHT was the same in the 2 groups. In the 40 cases with IA, the overall response rate to antifungal treatment was favourable (80%) but it was significantly affected by the achievement of leukaemia complete remission (CR) with induction CHT. In fact, in cases with AML responsive to induction CHT, responses of IA to antifungal therapy were 96% compared to 21% in cases of AML not responsive to induction treatment (P < .0001). The adherence to the schedule and full doses of CHT were reported in 35% of cases (14/40) and in 76% of controls (61/80) (P = .0001; OR 6.7; 95% CI 2.7-16.6). After first induction CHT, a significant higher number of cases (15/40; 37.5%) compared to controls (9/80; 11%) could not receive additional cycles of CHT (P = .0011, OR 4.8; 95% CI 1.9-12.3). The IA-related mortality was 22.5%. The median OS of cases was significantly worse than OS of controls with a difference of 12.3 months (12.1 vs 24.4 months, P = .04). However, the occurrence of IA during first induction phase did not have a significant impact on the OS of cases who achieved a CR of AML with induction CHT which are able to proceed, despite the IA, with their therapeutic program, achieving the same OS as the control group with AML in CR (P = ns). These data show that IA during first induction CHT can delay the subsequent therapeutic program and has a significant impact on OS, specifically in AML patients who did not achieved a CR of AML with the first course of CHT.

Sections du résumé

BACKGROUND BACKGROUND
Acute myeloid leukaemia (AML) patients are at high risk of invasive aspergillosis (IA) after first induction chemotherapy (CHT). Although IA risk factors have been identified, few data are available on impact of IA, occurring during induction phase, on overall AML outcome.
PATIENTS AND RESULTS RESULTS
The end point of this multicentre, case-control, study was to evaluate whether IA, occurring after first induction CHT, can affect treatment schedule and patient's outcome. We identified 40 AML patients (cases) who developed IA during first induction phase, 31 probable (77.5%) and 9 proven (22.5%). These cases were matched with a control group (80 AML) without IA, balanced according to age, type of CHT, AML characteristics and cytogenetic-molecular risk factors. The overall response rate to induction CHT was the same in the 2 groups. In the 40 cases with IA, the overall response rate to antifungal treatment was favourable (80%) but it was significantly affected by the achievement of leukaemia complete remission (CR) with induction CHT. In fact, in cases with AML responsive to induction CHT, responses of IA to antifungal therapy were 96% compared to 21% in cases of AML not responsive to induction treatment (P < .0001). The adherence to the schedule and full doses of CHT were reported in 35% of cases (14/40) and in 76% of controls (61/80) (P = .0001; OR 6.7; 95% CI 2.7-16.6). After first induction CHT, a significant higher number of cases (15/40; 37.5%) compared to controls (9/80; 11%) could not receive additional cycles of CHT (P = .0011, OR 4.8; 95% CI 1.9-12.3). The IA-related mortality was 22.5%. The median OS of cases was significantly worse than OS of controls with a difference of 12.3 months (12.1 vs 24.4 months, P = .04). However, the occurrence of IA during first induction phase did not have a significant impact on the OS of cases who achieved a CR of AML with induction CHT which are able to proceed, despite the IA, with their therapeutic program, achieving the same OS as the control group with AML in CR (P = ns).
CONCLUSIONS CONCLUSIONS
These data show that IA during first induction CHT can delay the subsequent therapeutic program and has a significant impact on OS, specifically in AML patients who did not achieved a CR of AML with the first course of CHT.

Identifiants

pubmed: 32697010
doi: 10.1111/myc.13147
doi:

Substances chimiques

Antifungal Agents 0

Types de publication

Journal Article Multicenter Study

Langues

eng

Sous-ensembles de citation

IM

Pagination

1094-1100

Informations de copyright

© 2020 Blackwell Verlag GmbH.

Références

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Auteurs

Anna Candoni (A)

Clinica Ematologica, Azienda Sanitaria-Universitaria Friuli Centrale (ASUFC), Udine, Italy.

Francesca Farina (F)

IRCCS Ospedale San Raffaele, Milano, Italy.

Katia Perruccio (K)

Oncoematologia Pediatrica, Ospedale SM Misericordia, Perugia, Italy.

Roberta Di Blasi (R)

Istituto di Ematologia, Fondazione Policlinico Universitario A. Gemelli-IRCCS-Università Cattolica del Sacro Cuore, Roma, Italy.

Marianna Criscuolo (M)

Istituto di Ematologia, Fondazione Policlinico Universitario A. Gemelli-IRCCS-Università Cattolica del Sacro Cuore, Roma, Italy.

Chiara Cattaneo (C)

Divisione di Ematologia, ASST-Spedali Civili di Brescia, Brescia, Italy.

Mario Delia (M)

Sezione di Ematologia, Dipartimento dell'Emergenza e dei Trapianti d'Organo-Università di Bari, Bari, Italy.

Maria Elena Zannier (ME)

Clinica Ematologica, Azienda Sanitaria-Universitaria Friuli Centrale (ASUFC), Udine, Italy.

Giulia Dragonetti (G)

Istituto di Ematologia, Fondazione Policlinico Universitario A. Gemelli-IRCCS-Università Cattolica del Sacro Cuore, Roma, Italy.

Rosa Fanci (R)

Unità Funzionale di Ematologia, Azienda Ospedaliero-Universitaria Careggi e Università di Firenze, Florence, Italy.

Bruno Martino (B)

UOC Ematologia, Ospedale Bianchi Melacrino Morelli, Reggio Calabria, Italy.

Maria Ilaria Del Principe (MI)

Cattedra di Ematologia, Dipartimento di Biomedicina e Prevenzione, Università degli Studi di Roma 'Tor Vergata', Roma, Italy.

Luana Fianchi (L)

Istituto di Ematologia, Fondazione Policlinico Universitario A. Gemelli-IRCCS-Università Cattolica del Sacro Cuore, Roma, Italy.

Nicola Vianelli (N)

Istituto di Ematologia, Dipartimento di Onco-Ematologia, Policlinico S. Orsola-Malpighi Università di Bologna, Bologna, Italy.

Anna Chierichini (A)

UOC Ematologia Azienda Ospedaliera S. Giovanni Addolorata, Roma, Italy.

Mariagrazia Garzia (M)

UOC Ematologia, Ospedale San Camillo, Roma, Italy.

Giuseppe Petruzzellis (G)

Clinica Ematologica, Azienda Sanitaria-Universitaria Friuli Centrale (ASUFC), Udine, Italy.

Gianpaolo Nadali (G)

UOC di Ematologia, Azienda Ospedaliera Universitaria Integrata di Verona, Verona, Italy.

Luisa Verga (L)

Clinica Ematologica, Ospedale San Gerardo, ASST Monza, Università Milano Bicocca, Milano, Italy.

Alessandro Busca (A)

Dipartimento di Oncologia, Ematologia, A.O.U. Città della Salute e della Scienza di Torino, SSD Trapianto allogenico di Cellule Staminali, Torino, Italy.

Livio Pagano (L)

Istituto di Ematologia, Fondazione Policlinico Universitario A. Gemelli-IRCCS-Università Cattolica del Sacro Cuore, Roma, Italy.

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