Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002871 (anemia)
 52,094 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The in vitro effect of recombinant human GM-CSF (rHuGM-CSF) was tested on bone marrow-derived multilineage (CFU-GEMM) as well as megakaryocytic (CFU-Mk), erythroid (BFU-E), and granulocyte-macrophage (CFU-GM) progenitors in a group (n = 16) of patients with myelodysplastic syndromes (MDS). Hematopoietic progenitor cell growth was markedly impaired in MDS patients as compared to normal controls (p less than 0.05, at least). Recombinant HuGM-CSF supported the growth of CFU-GEMM, CFU-Mk, and BFU-E at lower, equivalent, or slightly higher frequencies that those found in cultures plated with medium conditioned by peripheral blood leukocytes (PHA-LCM), but it was invariably ineffective in improving growth values. Recombinant HuGM-CSF supported the growth of granulocyte-macrophage colonies in 15 of 16 cases. The overall incidence (mean +/- SEM) of CFU-GM in cultures containing rHuGM-CSF (5 ng/ml) was significantly higher than the one found in cultures stimulated with PHA-LCM (40 +/- 15 vs. 17 +/- 7, p less than 0.05). Upon culture with rHuGM-CSF (5 ng/ml), in 5 of 15 patients de novo colony formation was observed (8 +/- 4) and in 4 of 15 patients CFU-GM growth (129 +/- 33) fell within normal range. Doses of rHuGM-CSF higher than 5 ng/ml did not result in a further increase of MDS-derived colony formation. It is concluded that rHuGM-CSF (a) does not improve the growth of CFU-GEMM, CFU-Mk, and BFU-E; (b) may completely restore the growth of CFU-GM in a subgroup of MDS patients; (c) while ineffective in improving anemia and thrombocytopenia, its in vivo in MDS may correct leukopenia through an effect at the level of granulocyte-macrophage progenitor cell compartment, at least in a subset of highly responsive patients.
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PMID:Growth of human hematopoietic colonies from patients with myelodysplastic syndromes in response to recombinant human granulocyte-macrophage colony-stimulating factor. 265 96

Successful kidney transplantation is followed by the anemia correction due to re-establishment of normal erythropoietin secretion. The possible role of growth factors and cytokines regulating hematopoiesis in this anemia correction are not completely understood. The aim of this study was to investigate the role of erythropoietin and other stimulators in the regulation of erythropoiesis after kidney transplantation. Thirty-six kidney graft recipients with stable graft function for more than 12 months were studied. According to the hemoglobin levels they were divided into: group 1 (12 patients) with normal graft function (sCr = 145.2 +/- 15.8 micromol/l) and normal hemoglobin (12.7+/-0.3 g/dl), group 2 (11 patients) with normal graft function (sCr = 135 +/- 6.5 miromol/l) and posttransplant erythrocytosis (Hb = 18.1 +/- 0.2 g/dl) and group 3 (13 patients) with chronic graft failure (sCr = 223.7 +/- 28.9 micromol/l, range 181-294) and anemia (Hb = 9.0 +/- 0.8 g/dl). Early erythroid progenitors (BFU-E) from peripheral blood, serum immunoreactive Epo and burst promoting activity (BPA) in PHA-LCM prepared from patients' peripheral blood mononuclear cells were measured in all studied patients. The expected Epo for Hb was found normal in patients with normal graft function, 10 times higher in patients with PTE and low in patients with anemia. BPA in PHA-LCM prepared from PTE was increased in 4/6 patients, normal in 4/6 anemic patients, but it was decreased in 5 patients with normal Hb. The mean values were 20.8 +/- 6.3 in PTE group and 16.2 +/- 6.8 in anemic group, and 4.1 +/- 1.8 (at the level of normal controls) in group 1. The number of BFU-E derived colonies was low in most patients with normal hemoglobin and anemia, and increased in most patients with PTE. Spontaneous BFU-E colonies i.e. without Epo added to the cultures were found in 7 of 12 patients with PTE. The mean values of BFU-E showed significant differences between patients with PTE (17.43 +/- 7.3), and patients with normal hemoglobin and anemia (4.39 +/- 1.2 vs. 6.5 +/- 1.1). The results presented suggest that inappropriate Epo secretion depends on the graft function and is the primarily important regulator that caused PTE or anemia after kidney transplantation. Synergistic action of BPA with Epo as well as increased sensitivity of early erythroid precursors to these stimulators could explained sustained erythropoiesis in PTE patients. The high BPA levels in anemic transplant patients with moderate chronic graft failure could be beneficial if rHuEpo treatment is applied in this patient group.
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PMID:Erythropoiesis after kidney transplantation: the role of erythropoietin, burst promoting activity and early erythroid progenitor cells. 1131 88

Chronic viral infections of animals associated with immune complex disease resemble a number of human disorders. At present, on the basis of showing (a) virus, host antiviral antibody, and C3 deposited in a granular pattern along the glomerular capillary wall and in the mesangia and (b) virus-host Ig (presumably antiviral antibody) complexes in the circulation, immune complex disease occurs in chronic murine infections with LCM, LDV, MSV, and ADM. In addition, granular deposits in the glomeruli in Coxsachie B, polyoma, other leukemic viral infections in mice, equine anemia, and hog cholera suggest that immune complex disease also occurs in these infections. In transplacental LCM infections maternal antiviral antibody transferred in utero or via milk induces very early and severe immune complex disease. The severity of immune complex nephritis in mice neonatally or transplacentally infected with LCM virus is directly proportional to the amount of Ig elutable from the kidney and to the proportion of this Ig which reacts with the infecting virus.
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PMID:Immune complex disease in chronic viral infections. 1986 77