Parainfluenza virus infections after hematopoietic stem cell transplantation: risk factors, response to antiviral therapy, and effect on transplant outcome

Citation
Wg. Nichols et al., Parainfluenza virus infections after hematopoietic stem cell transplantation: risk factors, response to antiviral therapy, and effect on transplant outcome, BLOOD, 98(3), 2001, pp. 573-578
Citations number
14
Categorie Soggetti
Hematology,"Cardiovascular & Hematology Research
Journal title
BLOOD
ISSN journal
00064971 → ACNP
Volume
98
Issue
3
Year of publication
2001
Pages
573 - 578
Database
ISI
SICI code
0006-4971(20010801)98:3<573:PVIAHS>2.0.ZU;2-8
Abstract
Parainfluenza virus (PIV) infections may be significant causes of morbidity and mortality in patients undergoing stem cell transplantation, but data r egarding their impact on transplant-related mortality is limited. This stud y sought to determine the risk factors of PIV acquisition and progression t o lower respiratory tract infection, their Impact on transplant-related mor tality, and the effectiveness of antiviral therapy. A total of 3577 recipie nts of hematopoietic stem cell transplantation (HSCT) between 1990 and 1999 were studied. PIV infections occurred in 253 patients (7.1%); 78% of these infections were community acquired. Multivariable analysis identified the receipt of an unrelated transplant as the only risk factor for PIV acquisit ion; the dose of corticosteroids at the time of PIV infection acquisition w as the primary factor associated with the development of PIV-3 pneumonia, b oth among allogeneic and autologous HSCT recipients. Both PIV-3 upper respi ratory infection and pneumonia were associated with overall mortality. Pulm onary copathogens were isolated from 29 patients (53%) with pneumonia. Mort ality was highly influenced by the presence of copathogens and the need for mechanical ventilation. Aerosolized ribavirin with or without intravenous immunoglobulin did not appear to alter mortality from PIV-3 pneumonia, nor did such therapy decrease the duration of viral shedding from the nasophary nx among patients with pneumonia. Corticosteroid administration thus drives the development of PIV pneumonia in a dose-dependent fashion, even among a utologous HSCT recipients. Both upper and lower tract PIV infections are pr edictors of mortality after HSCT. Currently available antiviral therapy app ears to be inadequate in reducing viral shedding or mortality once pneumoni a is established.