title: Serum erythropoietic inhibitors in patients with pure red cell aplasia.
abstract: Inhibitory mechanisms of erythropoiesis in 20 patients with pure red cell aplasia (PRCA) were investigated using the technique of in vitro hematopoiesis and an assay for human parvovirus. Complement-dependent serum inhibitors against late erythroid progenitors (CFU-E) were demonstrated in seven of 19 patients examined, and complement-dependent inhibitors against early erythroid progenitors (BFU-E) were demonstrated in three of these seven patients. Nonspecific and complement-independent inhibitors against CFU-E were thought to be associated with the etiology of PRCA in one patient. Human parvovirus-mediated erythropoietic suppression was demonstrated in a patient with complete remission of acute lymphoblastic leukemia complicated with marrow erythroid aplasia, whose serum showed a perfect inhibition against erythroid progenitor cells. T-cell-mediated erythroid suppression was not demonstrated in the patients examined. These findings reveal that erythroid aplasia is associated with complement-dependent serum erythropoietic inhibitor in some patients (36.8% in the present study) with PRCA, but it is difficult to identify the mechanism of erythroid aplasia in more than half of the patients with PRCA. In addition, our present study discovered the presence of parvovirus-mediated marrow pure red cell aplasia in one adult patient with acute lymphoblastic leukemia.
authors.affiliation: First Department of Internal Medicine, Niigata University, Japan.
authors.forename: M
authors.initials: M
authors.lastname: Takahashi
authors.forename: K
authors.initials: K
authors.lastname: Nikkuni
authors.forename: I
authors.initials: I
authors.lastname: Tanaka
authors.forename: T
authors.initials: T
authors.lastname: Furukawa
authors.forename: Y
authors.initials: Y
authors.lastname: Moriyama
authors.forename: A
authors.initials: A
authors.lastname: Shibata
authors.forename: S
authors.initials: S
authors.lastname: Satoh
authors.forename: Y
authors.initials: Y
authors.lastname: Kuwabara
authors.forename: Y
authors.initials: Y
authors.lastname: Maruyama
authors.forename: Y
authors.initials: Y
authors.lastname: Matsunaga
mesh_terms: D000328:Adult; D000368:Aged; D000956:Antigens, Viral / Q000097:blood; D001379:Azathioprine / Q000627:therapeutic use; D001798:Blood Proteins / Q000032:analysis*; D002648:Child; D003114:Colony-Forming Units Assay; D003165:Complement System Proteins / Q000502:physiology; D003520:Cyclophosphamide / Q000627:therapeutic use; D015672:Erythroid Precursor Cells / Q000473:pathology / Q000502:physiology; D004920:Erythropoiesis; D005260:Female; D006801:Humans; D007231:Infant, Newborn; D008297:Male; D008875:Middle Aged; D010321:Parvoviridae / Q000276:immunology / Q000502:physiology; D012010:Red-Cell Aplasia, Pure / Q000097:blood* / Q000188:drug therapy / Q000382:microbiology; D013256:Steroids / Q000627:therapeutic use; D013601:T-Lymphocytes / Q000502:physiology
chemical_list: D000956:Antigens, Viral; D001798:Blood Proteins; D013256:Steroids; C007627:erythropoiesis inhibiting factors; D003520:Cyclophosphamide; D003165:Complement System Proteins; D001379:Azathioprine