RELATIVE ERYTHROID HYPERPLASIA IN THE BONE-MARROW AT DIAGNOSIS OF APLASTIC-ANEMIA - A PREDICTIVE MARKER FOR A FAVORABLE RESPONSE TO CYCLOSPORINE THERAPY
S. Nakao et al., RELATIVE ERYTHROID HYPERPLASIA IN THE BONE-MARROW AT DIAGNOSIS OF APLASTIC-ANEMIA - A PREDICTIVE MARKER FOR A FAVORABLE RESPONSE TO CYCLOSPORINE THERAPY, British Journal of Haematology, 92(2), 1996, pp. 318-323
Predicting the treatment response of aplastic anaemia (AA) is essentia
l when considering cyclosporine (CyA) therapy among several treatment
options, because it requires at least 2 months to determine whether th
e therapy is beneficial to a patient with AA. To identify the characte
ristics of patients with AA who are likely to respond to CyA therapy w
e retrospectively reviewed the clinical records and bone marrow smears
of patients treated with CBA. Among 30 patients who received the ther
apy for at least 3 months within 1 year after diagnosis of AA. and who
had not been exposed to antilymphocyte or antithymocyte globulin, 16
(53%) responded with disease remission. CyA-responsive patients had a
significantly higher ratio of erythroblasts to granulocytes (E/G ratio
) in the bone marrow at the time of diagnosis as compared with patient
s refractory to therapy (P = 0.004). Multivariate analysis revealed th
at a high E/G ratio (> 0.6) was significantly associated with a good r
esponse to CyA (P = 0.03): 15 (83%) of the 18 patients with an E/G rat
io > 0.6 responded, but only one (8%) of the 12 with an E/G ratio less
than or equal to 0.6 did. Although the presence of subclinical paroxy
smal nocturnal haemoglobinuria was suspected from the relative erythro
blastosis observed in the bone marrow of these patients, flow cytometr
ic analysis of neutrophils in the peripheral blood failed to reveal ne
utrophils deficient for glycosyl-phosphatidylinositol (GPI) anchored m
embrane proteins in all but one case. Identification of the presence o
f relative erythroid hyperplasia in the bone marrow when AA is diagnos
ed may help to predict a favourable response to CyA therapy, and there
fore facilitate the selection of optimal therapy for AA.