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Inflammatory functional iron deficiency common in myelofibrosis, contributes to anaemia and impairs quality of life. From the Nordic MPN study Group

Authors :
Birgegard, Gunnar
Samuelsson, Jan
Ahlstrand, Erik
Ejerblad, Elisabeth
Enevold, Christian
Ghanima, Waleed
Hasselbalch, Hans
Nielsen, Claus H.
Knutsen, Havar
Pedersen, Ole B.
Sorensen, Anders
Andreasson, Bjorn
Birgegard, Gunnar
Samuelsson, Jan
Ahlstrand, Erik
Ejerblad, Elisabeth
Enevold, Christian
Ghanima, Waleed
Hasselbalch, Hans
Nielsen, Claus H.
Knutsen, Havar
Pedersen, Ole B.
Sorensen, Anders
Andreasson, Bjorn
Publication Year :
2019

Abstract

Objectives The study investigates the hypothesis that inflammation in myelofibrosis (MF) like in myeloma and lymphoma, may disturb iron distribution and contribute to anaemia. Methods A cross-sectional study of 80 MF and 23 ET patients was performed. Results About 35% of anaemic MF patients had functional iron deficiency (FID) with transferrin saturation amp;lt;20 and normal or elevated S-ferritin (amp;lt;500 mu g/L). In ET, FID was rare. In MF patients with FID, 70.6% were anaemic, vs 29.4% in patients without FID (P = 0.03). Hepcidin was significantly higher in MF patients with anaemia, including transfusion-dependent patients, 50.6 vs 24.4 mu g/L (P = 0.01). There was a significant negative correlation between Hb and inflammatory markers in all MF patients: IL-2, IL-6 and TNF-alpha, (P amp;lt; 0.01-0.03), LD (P = 0.004) and hepcidin (P = 0.03). These correlations were also seen in the subgroup of anaemic MF patients (Table ). Tsat correlated negatively with CRP (P amp;lt; 0.001). Symptom burden was heavier in MF patients with FID, and MPN-SAF quality of life scores correlated with IL-6 and CRP. Conclusions The inflammatory state of MF disturbs iron turnover, FID is common and contributes to anaemia development and impairment of QoL. Anaemic MF patients should be screened for FID.<br />Funding Agencies|Nordic Study Group for Myeloproliferative Neoplasms (NMPN)

Details

Database :
OAIster
Notes :
English
Publication Type :
Electronic Resource
Accession number :
edsoai.on1234602008
Document Type :
Electronic Resource
Full Text :
https://doi.org/10.1111.ejh.13198