Frequency of infections in 948 MPN patients: a prospective multicenter patient-reported pilot study
Autor
Crodel, Carl C.
Jentsch-Ullrich, Kathleen
Koschmieder, Steffen
Kämpfe, Dietrich
Griesshammer, Martin
Döhner, Konstanze
Jost, Philipp J.
Wolleschak, Denise
sfort, Susanne I
Stegelmann, Frank
Jilg, Stefanie
Hofmann, Verena
Auteri, Guiseppe
Rachow, Tobias
Ernst, Philipp
Brioli, Annamaria
Lilienfeld-Toal, Marie von
Hochhaus, Andreas
Palandri, Francesca
Heide, Florian H.
Institución
Resumen
Recently, several studies have reported on immunosuppression and infectious complications in patients with
myeloproliferative neoplasms (MPN) receiving Janus
kinase (JAK) inhibitor therapy (reviewed in [1]). These
datasets included analyses of large multicenter trials comparing JAK inhibitor therapy with best available therapy or
placebo control. Specific infections such as herpes virus
reactivation appear to be more prevalent in patients treated
with the JAK inhibitor ruxolitinib (RUX) and opportunistic
infections have been described also outside of clinical trials
[1]. However, it is not known to which extent the underlying malignancy (MPN) contributes to immunosuppression
and susceptibility to infection. Studies from a registry
provided early evidence that the risk of MPN patients to die
from infections may be increased when compared with
normal population controls [2] and this finding was most
recently underpinned by a large dataset of 8363 MPN
patients [3]. MPN patients were at higher risk for severe
bacterial and viral infections judged by hospital admissions
and deaths from infection. The question how the type of
pharmacologic treatment, the MPN subtype or the disease
stage may influence the risk for infectious complications
remains still unclear. Immunosuppressive effects of JAK
inhibitors are determined by their specificity [4], while other
cytoreductive agents such as hydroxycarbamide or interferons may also compromise the function of immune cells.
Finally, molecular and clinical heterogeneity of MPN, its
impact on cellular signaling, immune function and the
inflammatory phenotype may vary depending on the type of
driver mutation and disease burden