Studies of granulocyte kinetics in normal and granulocytopenic subjects.
Granulopoiesis was studied simultaneously by three methods in normal subjects and in subjects with neutropenia of various aetiologies: in vitro labelling of autologous and homologous granulocytes for the study of peripheral kinetics, in vivo labelling with DF32P (di-isopropyl-flourophosphate 32P) or 75Se-selenomethionine, and bone marrow autoradiography after in vitro labelling with 3H-thymidine for the study of bone marrow granulopoiesis. Three main mechanisms of neutropenia can be distinguished: a) peripheral hyperdestruction, corpuscular or extra-corpuscular, and false leukopenias (change in the distribution of peripheral granulocytes from the circulating to the marginal granulocyte pool; b) quantitative bone marrow insufficiency without qualitative abnormality; c) qualitative abnormality in bone marrow granulopoiesis with cell death in either the maturation stage or the proliferative stage. There is no exact correlation between clinical and kinetic classifications, but most cases of post-infection chronic neutropenias and idiopathic neutropenias fall into the first two categories, and most cases of benzol intoxication and bone marrow insufficiency due to X-irradiation fall into the last category. Some of these last patients developed an acute myeloblastic leukaemia in the two following years and can be considered as preleukaemic states.
D000380:Agranulocytosis / Q000209:etiology / Q000503:physiopathology*; D001853:Bone Marrow / Q000187:drug effects / Q000378:metabolism / Q000528:radiation effects; D001854:Bone Marrow Cells; D005258:Felty Syndrome / Q000150:complications; D006098:Granulocytes / Q000473:pathology; D006410:Hematopoiesis; D006801:Humans; D007700:Kinetics; D009503:Neutropenia / Q000209:etiology / Q000503:physiopathology; D011832:Radiation Injuries; D013163:Splenomegaly / Q000150:complications; D014376:Tuberculosis / Q000150:complications; D014965:X-Rays