학술논문

New hematologic populations at risk of invasive aspergillosis: focus on new targeted, biological, and cellular therapies.
Document Type
Academic Journal
Author
Girmenia C; Dipartimento di Ematologia, Oncologia, e Dermatologia, Azienda Policlinico Umberto I, Sapienza University of Rome, Rome, Italy.
Source
Publisher: F1000 Research Ltd Country of Publication: England NLM ID: 101594320 Publication Model: eCollection Cited Medium: Internet ISSN: 2046-1402 (Electronic) Linking ISSN: 20461402 NLM ISO Abbreviation: F1000Res Subsets: MEDLINE
Subject
Language
English
Abstract
The introduction of new targeted, biological, and cellular therapies in patients with hematologic malignancies has improved the outcomes of patients but in parallel has changed the frequency and epidemiology of infections, including invasive aspergillosis (IA). In this article, recent literature on the epidemiology and clinical findings of IA in patients who have lymphoproliferative and myeloproliferative diseases and are undergoing novel targeted treatment with kinase inhibitors, agents targeting cell surface antigens, chimeric antigen receptor-modified T cells, and antibodies to immune checkpoint molecules is reviewed and the clinical impact of IA on the overall management of the underlying disease is discussed. Overall, IA represents a variable and uncommon complication in these populations, but given the increasing eligibility criteria of these novel treatments (particularly in patients with relapsed or refractory hematologic malignancies) and the prolonged periods of therapy, a considerable number of unusual cases of Aspergillus infections can be expected in clinical practice.
Competing Interests: No competing interests were disclosed.Competing interests: Russell E Lewis and Corrado Girmenia have collaborated together on ECIL-6 Guideline articles in the last three years.Competing interests: Marcio Nucci and Corrado Girmenia have collaborated together on ECIL-6 Guideline articles in the last three years.No competing interests were disclosed.