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

Blood cell development is regulated by a variety of hematopoietic growth factors that mediate the growth, maturation, and activation of hematopoietic cell elements. Several of these factors have been isolated and are now being produced by means of recombinant DNA techniques in quantities sufficient for study and clinical use. Three factors in particular have recently received considerable attention in the clinical arena: recombinant human granulocyte colony-stimulating factor (G-CSF), granulocyte macrophage colony-stimulating factor (GM-CSF), and erythropoietin (EPO). Although both may prove to be clinically useful, G-CSF and GM-CSF have distinct and different biological characteristics. The regulatory action of G-CSF is apparently lineage-specific for the proliferation and maturation of neutrophil granulocytes. GM-CSF is less restricted in its actions, affecting all granulocytes, especially eosinophil granulocytes. It also stimulates the proliferation and activation of monocyte-macrophages and induces these cells to produce a number of cytokines. EPO mediates the growth of erythroid progenitors into mature erythrocytes. The CSFs and EPO have many potential clinical applications, including enhancing myeloid effector cell production and function, rendering malignant cells more susceptible to killing by cycle-specific agents, and correcting the anemia of end-stage renal disease.
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PMID:Introduction and overview of hematopoietic growth factors. 265 99

A case of AML accompanied by HTLV-I associated myelopathy (HAM) is reported. A 37-year-old woman was admitted to our hospital in April 1985 because of severe anemia, general malaise and fever. On admission, anemia, thrombocytopenia and leukocytosis consisting of 32% myeloblasts and 6% promyelocytes were noted. A bone marrow study revealed marked myeloid hyperplasia, and a diagnosis of acute myelogenous leukemia (M2) was made. In order to improve the patient's severe anemia and thrombocytopenia, a large amount of blood transfusion was applied at once. Thereafter BHAC-DMP therapy was commenced resulting in complete remission 3 months after initiating chemotherapy. Hematological improvement has continued (as of May 1988). In June 1986 the patient showed a gait disturbance of slowly progressive course. Neurological examination revealed hyperactive knee and ankle jerks with a positive Babinski's sign, and foot clonus were also noted bilaterally. Sphincter impairment was detected. A CSF sample contained slight pleocytosis with some abnormal lymphocytes similar to those found in adult T cell leukemia. Antibodies to HTLV-I were found in the CSF and serum by EIA method. According to these findings we diagnosed the patient's illness as HAM, referring to the new clinical entity named by Osame. This patient had undergone a blood transfusion 14 months before the onset of this myelopathy, therefore the transmission of exogenous antigens through blood transfusion may be the cause of HAM. Corticosteroid pulse treatment was administered and striking improvements countering gait disturbance resulted in this patient.
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PMID:[Acute myelogenous leukemia accompanied by HTLV-I associated myelopathy (HAM) caused by blood transfusion]. 274 79

Administration of 3'-azido-3'-deoxythymidine (AZT) to patients with acquired immunodeficiency syndrome (AIDS) causes significant anemia and neutropenia. The bone marrow cytotoxicity of AZT has been attributed to deoxyribonucleotide pool perturbations that might result in impaired DNA synthesis in normal bone marrow elements. We examined the effect of human recombinant granulocyte-macrophage colony-stimulating factor (rGM-CSF) on AZT-mediated biochemical perturbations and in vitro growth inhibition of normal bone marrow myeloid progenitor cells. Exposure of nonadherent, bone marrow mononuclear cells (BMMC) to 100 ng/ml of rGM-CSF for 6 h resulted in approximately twofold increments in the mean intracellular deoxycytidine triphosphate (dCTP) and thymidine triphosphate (dTTP) levels. Administration of 10 microM AZT alone to BMMC for 6 h markedly reduced dCTP and dTTP levels and generated significant levels of AZT triphosphate (AZT-TP). Coadministration of rGM-CSF (100 ng/ml) along with AZT (10 microM) partly restored dCTP and dTTP levels and significantly reduced AZT-TP levels. Furthermore, simultaneous exposure of BMMC for 4 h to 100 ng/ml of rGM-CSF reduced the mean DNA incorporation of [3H]AZT (10 microM) from 27.2 to 19.1 pmol/micrograms of DNA. Additionally, the inhibitory effects of AZT (10 microM) on granulocyte-macrophage colony-forming unit (CFU-GM) colony growth were significantly reduced in the presence of 100 ng/ml of rGM-CSF. These in vitro studies suggest that rGM-CSF partly corrects AZT-mediated biochemical perturbations as well as reduces the cytotoxicity of AZT in normal human bone marrow myeloid progenitor cells.
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PMID:The effect of recombinant human granulocyte-macrophage colony-stimulating factor (rGM-CSF) on 3'-azido-3'-deoxythymidine (AZT)-mediated biochemical and cytotoxic effects on normal human myeloid progenitor cells. 278 47

A case of pseudotumor cerebri associated with iron deficiency anemia due to colon cancer is reported in a 37-year-old woman. Her initial symptoms were vomiting and severe headache. On physical examination, no lymph nodes and abdominal mass were palpable but marked anemia was noted in her skin and conjunctiva . Neurological examination revealed papilledema in her both eyes and stiff neck. There was no abnormal findings on CT scan on admission. Spinal puncture revealed CSF pressure as high as 620 mmH2O with normal cells, protein, sugar and chloride levels. Hematological examination revealed iron deficiency anemia and thrombocytosis. Angiography at third day revealed no sinus occlusion, but retention of contrast media was seen on the cortical vein of parietal lobe and right transverse sinus. Brain scintigram at sixth day revealed mild accumulation in left parietal lobe, so small venous infarction was suggested. There were two circumscribed stenotic lesions of right ascending colon in the barium enema, and right hemicolectomy was achieved. The pathological diagnosis was adenocarcinoma. The symptoms of pseudotumor cerebri was completely disappeared soon after the surgery together with resolution of anemia. She lives with no deficits now 1 year 3 months after surgery. In conclusion much attention is necessary to a patient of pseudotumor cerebri with iron deficiency anemia for the presence of cancer, because not only this central nervous system lesion is reversible and curable but also the cancer itself may be curable by surgery.
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PMID:[A case of pseudotumor cerebri associated with colon cancer]. 280 39

A new kind of myeloproliferative disorder (L-8313) has been discovered. It was transplantable into syngeneic mice with spleen cells. The mice showed hepato-splenomegaly with a marked leukocytosis and anemia 3 weeks after transplantation of L-8313 cells. The number of GM-CFU and CFU-S per spleen increased to more than 40 times normal. The results of chromosomal and PGK analysis demonstrated that these increased stem cells were of host origin. Both the culture medium of the spleen cells and the serum from L-8313 bearing mice showed high levels of IL-3, BPA and CSF. Consequently, hematopoietic cells of the host mice underwent remarkable proliferation in response to these stimulating factors when L-8313 cells were transplanted. We also have been successful in establishing an in-vitro cell line and have maintained it for over one year. The phenotype of L-8313 cells was Thy 1.2 positive. Some L-8313 cells showed a positive acid phosphatase reaction but the cytochemical character of myeloid lineage was not observed. Therefore, L-8313 is considered to be a T-cell derived hematopoietic regulatory cell neoplasm with the ability to produce several hematopoietic stimulating factors.
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PMID:Myeloproliferative disorder due to abnormal production of hematopoietic stimulators. 288 2

The inhibitory effect by hairy cell conditioned medium (HCCM) on the growth of granulocyte and erythrocyte colony forming cells was studied in vitro. The percent inhibition of CFU-C formation by HCCM from four hairy cell leukemia (HCL) patients ranged from 36% to 76%, while no inhibition was observed with conditioned medium (CM) obtained from three B-cell chronic lymphocytic leukemia (B-CLL) patients nor from two normal controls. HCCM inhibited specially the growth of rG-CSF responding stem cells. The hairy cell-derived colony inhibitory factor from HCCM was nondialyzable, fairly stable to heat treatment, and trypsin sensitive. Its maximal inhibitory activity against granulopoiesis was observed in the fractions of 5,000 to 6,000 daltons. Moreover HCCM inhibited CFU-E colony formation but not BFU-E. These results indicate that hairy cells produce a factor that inhibits granulopoiesis and erythropoiesis in vitro. This factor may play a role in neutropenia and anemia observed in HCL.
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PMID:Inhibition against CFU-C and CFU-E colony formation by soluble factor(s) derived from hairy cells. 292 Feb 12

A 23-year-old male who had suffered recurrent relapses of acute myelocytic leukemia was treated with a protocol including neocarzinostatin (NCS) and complete remission was obtained. At the age of 11 years, he had complained of general fatigue and anemia, and was diagnosed as having AML because of the presence of leukemic cell infiltration in the bone marrow as well as peripheral blood. Auer bodies and a positive reaction to peroxidase were found. The last episode of relapse occurred at the age of 15 years, when he achieved complete remission following a trial protocol which included NCS. NCS seemed to be effective after it had been used intravenously for a short time. The patient has maintained complete remission for the past 7 years and has had no consolidation therapy in the last 3 years. For the last 18 months, he has been working in a market as a clerk 8 hours a day. NCS with a rapid infusion time seems to have effects on leukemic cells when it used with proteolytic enzyme. Neither skull radiation nor testicular biopsy were attempted. Results of CSF examination were within normal limits, but EEG and CT scan revealed the probability of early-stage leukoencephalopathy, although no significant clinical signs were observed. He had suffered an asthmatic attack before the onset of AML, but no further attack occurred until several months ago. In order to establish any relationship between these two diseases, further detailed analysis will be necessary.
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PMID:[A case of complete remission following recurrent relapses 12 years after onset of acute myelocytic leukemia. Response to protocol including neocarzinostatin]. 296 38

The antileukemic activity of murine recombinant granulocyte-macrophage colony-stimulating factor (rGM-CSF) and a combination of rGM-CSF and recombinant interleukin-3 (rIL-3) was examined by using a murine model of spontaneous B-cell leukemia (BCL1) in BALB/c mice. All untreated mice inoculated with 2 x 10(2) BCL1 cells developed leukemia within 4 weeks, with extreme lymphocytosis and a massive increase in both spleen weight and cell number while the number of myeloid progenitors (CFU-C) per spleen was decreased. In contrast, rGM-CSF-or rGM-CSF- and rIL-3-treated recipients did not show any evidence of leukemia or splenomegaly at 4 weeks and showed a significant increase in CFU-C per spleen. Hematologic parameters in the peripheral blood of untreated mice showed anemia and thrombocytopenia. Significant elevations in these parameters were recorded in mice treated with either protocol of CSF. Treatment of recipient mice with either rGM-CSF or rGM-CSF and rIL-3 prolonged their median survival from 6 weeks in untreated controls (range, 5 to 9 weeks) up to the time they were killed at 105 days. Adoptive transfer of spleen cells obtained from mice treated with rGM-CSF, mice treated with a combination of rGM-CSF and rIL-3, and untreated controls, into normal secondary recipients indicated improved survival in recipients inoculated with rGM-CSF. These data indicate that CSFs may inhibit in vivo expansion of leukemic cells of lymphoid origin.
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PMID:Therapeutic potential of recombinant granulocyte-macrophage colony-stimulating factor and interleukin-3 in murine B-cell leukemia. 304 86

A case of septic aneurysms complicated with simultaneous subdural and intracerebral hematoma is presented. A 13-year-old girl had been operated on for endocardial cushion defect when she was 5 years old, and residual mitral regurgitation was followed up. She suddenly complained of headache, vomited and lost consciousness. She was brought to the Tokyo Women's Medical College Hospital by an ambulance. On arrival, she was semicomatose. Her left pupil was mydriatic and did not react to light. Right hemiparesis was noted. Systolic murmur was audible in the apical region of the heart. Laboratory data showed a mild anemia and a white cell count of 23,000. CT scan showed a subdural hematoma in the left frontotemporoparietal region and a small subcortical hematoma in the left occipital lobe. An emergency operation was carried out for the subdural hematoma. When the dura was opened, about 10 ml bloody CSF flowed out. A hematoma weighing about 50 g was removed. A bleeding point or an aneurysm could not be discovered on the dura, arachnoid membrane or surface of the brain at the operation. On the 15th day after the operation, when the fever was decreased, cerebral angiography was done. The left vertebral angiogram showed an aneurysm on a peripheral branch of the calcarine artery, which was considered the origin of the subcortical hematoma in the left occipital lobe. The left carotid angiogram showed no aneurysm. On the seventh day after that study, the aneurysm did not appear by left vertebral angiography. She was discharged with no neurological deficit. One month later, she was admitted again with a high fever.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of septic aneurysm complicated with simultaneous subdural and intracerebral hematoma]. 384 Nov 93


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