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Myeloperoxidase‐deficient polymorphonuclear leucocytes (VI): Relation to cytogenetic abnormalities in primary myelodysplastic syndromes
Author(s) -
BendixHansen Knud,
Kerndrup Gitte,
Pedersen Bent
Publication year - 1986
Publication title -
scandinavian journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.904
H-Index - 84
eISSN - 1600-0609
pISSN - 0036-553X
DOI - 10.1111/j.1600-0609.1986.tb02641.x
Subject(s) - myeloperoxidase , myelodysplastic syndromes , cytogenetics , immunology , medicine , incidence (geometry) , pathology , chromosome , biology , bone marrow , genetics , inflammation , gene , physics , optics
Relations between cytogenetic status, FAB‐classification and an abnormal subpopulation of myeloperoxydase (MPO)‐deficient polymorphonuclears (PMN) in 45 patients with myelodysplastic syndrome (MDS) are reported. Clonal abnormalities were demonstrated in 85% of the patients, with a lower incidence in the RA+ group (refractory anaemia with ring sideroblasts) compared to the others (p = 0.004). In 12 patients a spontaneous progression in cytogenetic aberrations occurred and in 7 of these (60%) a simultaneous progression in FAB‐subtype was seen. The appearance of MPO‐deficient PMNs was observed in 6 of these patients (55%). A progression in FAB‐subtype was noted in further 4 patients and 2 additional patients developed MPO‐deficient PMNs. Only one sufficient cytogenetic investigation was available in these patients. Thus 100% of the fully studied patients showed progression in cytogenetic abnormalities when a progression in FAB‐subtype or a development of MPO‐deficient PMNs was seen. 3 (49%) of the 8 patients developing MPO‐deficient PMNs too showed a progression in FAB‐subtype. Although no significant correlation to specific categories of structural aberrations or abnormalities in specific chromosome pairs could be demonstrated, clonal cytogenetic aberrations seem to be involved when the disease progresses and when MPO‐deficient PMN develop.