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Prepublished online as a Blood First Edition Paper on April 17, 2002; DOI 10.1182/blood-2002-01-0136.
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Blood, 15 July 2002, Vol. 100, No. 2, pp. 474-482
HEMATOPOIESIS
Anemia of chronic disease in rheumatoid arthritis is associated
with increased apoptosis of bone marrow erythroid cells: improvement
following anti-tumor necrosis factor- antibody therapy
Helen A. Papadaki,
Heraklis
D. Kritikos,
Vasilis Valatas,
Dimitrios T. Boumpas, and
George D. Eliopoulos
From the Departments of Hematology and Rheumatology,
Clinical Immunology and Allergiology of the University of Crete School
of Medicine, Heraklion, Crete, Greece.
Circumstantial evidence has implicated tumor necrosis factor  (TNF-) in the pathogenesis of anemia of chronic disease (ACD) in
rheumatoid arthritis (RA). We investigated the role of TNF- in
erythropoiesis of patients with active RA (n = 40) and the effect of
anti-TNF- antibody administration (cA2). Patients with RA had lower
numbers of CD34+/CD71+ and
CD36 /glycophorin A+ (glycoA+)
bone marrow (BM) cells and increased proportions of apoptotic cells
within the CD34+/CD71+ and
CD36+/glycoA+ cell compartments, compared to
healthy controls (n = 24). Erythroid burst-forming units (BFU-Es)
obtained by BM mononuclear or purified CD34+ cells were
significantly lower in RA patients compared to controls. These
abnormalities were more pronounced among patients with ACD. Increased
TNF- levels in patient long-term BM culture supernatants inversely
correlated with BFU-Es and hemoglobin levels and positively with the
percentage of apoptotic CD34+/CD71+ and
CD36+/glycoA+ cells. Following cA2 therapy, a
normalization was documented in the number of
CD34+/CD71+ and
CD36/glycoA+ cells, the number of
BFU-Es, and the proportion of apoptotic CD34+/CD71+ and
CD36+/glycoA+ cells, which was associated with
a significant increase in hemoglobin levels compared to baseline.
Recovery from anemia was more prominent in patients with ACD. The
exogenous addition of an anti-TNF- antibody in the cultures
increased BFU-E number in patients prior to cA2 treatment but not after
treatment, further substantiating the inhibitory role of TNF- on
patients' erythropoiesis. We conclude that TNF--mediated apoptotic
depletion of BM erythroid cells may account for ACD in RA and that cA2
administration may ameliorate ACD in these patients by down-regulating
the apoptotic mechanisms involved in erythropoiesis.
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