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Query: UMLS:C0002874 (aplastic anemia)
 5,905 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A short-term methylcellulose technique was used to study the proliferation of marrow-derived stromal, erythroid and myeloid colonies from normal controls and from patients with aplastic anaemia. There was a significant reduction in all colony types in patients with aplastic anaemia when compared with normal controls. In 4 patients who achieved remission following treatment with ATG + oxymetholone or with oxymetholone alone there was a return to normal range of stromal colonies and also of CFU-E. There was no change in the numbers of BFU-E's and only a slight increase in the numbers of CFU-C's.
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PMID:Human marrow stromal cells in short-term semi-solid bone marrow culture in aplastic anaemia. 397 67

The activity capable of promoting the growth of human erythroid burst-forming cells (BFU-E) in culture was measured in the sera from 39 patients with aplastic anemia (AA) and compared with similar activity in patients with various other hematologic disorders and 31 normal subjects. Burst-promoting activity (BPA) was determined by its ability to support erythroid burst growth from adherent cell-depleted normal human marrow cells. The results were expressed as the percentage of burst growth supported by test serum compared with cultures established in the presence of 20% test serum and 2.5% phytohemagglutinin-stimulated lymphocyte conditioned medium. The mean BPA level in normal serum was 18.5% (1.5 +/- SEM) and was not significantly different from BPA levels in patients with various forms of nonhypoplastic anemia or polycythemia (10.2% +/- 1.2%). In contrast, 15 of the 39 patients with AA had elevated BPA levels, ranging from 40.0% to 106.0%. These elevated levels did not correlate with serum erythropoietin or hematocrit values, white blood cell count, platelet count, time from diagnosis, or the presence or numbers of BFU-E in circulation. The BPA was shown not to be T cell growth factor (interleukin-2), and the effect was not blocked by the addition of cyclosporine to culture, consistent with a direct effect of this activity on BFU-E. When the 39 patients with AA were treated with antithymocyte globulin, 20 obtained a complete or partial remission. BPA levels determined from sera obtained before treatment did not correlate with response or duration of survival but did correlate with granulocyte-macrophage colony-stimulating activity (GM-CSA).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hematopoietic growth factors in human serum. erythroid burst-promoting activity in normal subjects and in patients with severe aplastic anemia. 404 96

Colony forming unit (CFU) assays were developed for feline granulocyte-macrophage (CFUGM), early erythroid (day 2 CFUE), and late erythroid (day 7 CFUE) colonies in methylcellulose medium. Feline CFUGM and both day 2 and day 7 CFUE were enhanced by feline macrophage conditioned medium and late CFUE often were intimately associated with macrophages. Kittens were inoculated with the Kawakami-Theilen (KT) strain of feline leukemia virus (FeLV) and sequential changes in marrow CFU determined. Erythroid aplasia, characterized by progressive non-regenerative anemia, lymphopenia, and a profound decrease in early and late CFUE but not CFUGM was induced by 3 to 5 weeks after FeLV-KT inoculation. The susceptibility of kittens to FeVL-induced erythroid aplasia was strongly age-related; neonatal kittens were most sensitive and substantial natural resistance developed by 4 weeks of age. The results demonstrate that FeLV-KT infection induced a rapid and selective suppression of erythroid progenitor cells and represents a suitable model of experimentally-induced acquired erythroid aplasia.
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PMID:Feline leukemia virus-induced erythroid aplasia: in vitro hemopoietic culture studies. 627

A case of idiopathic severe aplastic anemia with spontaneous complete remission is described. Hematologic parameters normalized spontaneously 94 days after onset. However, the ability of the patient's bone marrow cells to form granulocytic-macrophagic colony-forming units (CFU-GM) or erythroid burst-forming units (BFU-E) was depressed until the 288th day, in spite of the normalization of blood counts. Incubation of the patient's bone marrow cells with antilymphocytic globulin prior to the culture experiment normalized the number of CFU-GM and BFU-E in correlated studies. Coculture of a target marrow with several concentrations of the patient's lymphocytes or serum resulted in a complete inhibition of CFU-GM. BFU-E growth was inhibited by the patient's lymphocytes, but not by serum, which rather showed burst-promoting activity. The inhibitory effect on target bone marrow persisted for 288 days, when it disappeared concomitantly with the restoration of spontaneous CFU-GM and BFU-E growth.
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PMID:Lack of in vitro colony formation in a patient with severe aplastic anemia after spontaneous autologous hematologic reconstitution. 640 69

Immunotherapy, consisting of lymphocyte depletion or plasmapheresis in combination with cyclophosphamide and prednisone, was employed in three patients with refractory pure red cell aplasia and six patients with aplastic anemia of various etiologies. All three patients with pure red cell aplasia responded to plasmapheresis. One patient with atypical aplastic anemia showed partial recovery following lymphocyte depletion; the other five patients showed no evidence of a clinical response. The effect of patients' sera or bone marrow on formation of myeloid or erythroid colonies by bone marrow from normal individuals was determined in vitro. A decline in serum inhibition of erythroid colony formation was observed in the patients with pure red cell aplasia following treatment. Any changes in serum inhibition were less marked or unrelated to treatment outcome in the patients with aplastic anemia, although the single patient who responded to lymphocyte depletion exhibited reversal of coculture bone marrow inhibition. Our experience suggests that in vitro assay methods may not adequately predict the response of patients with aplastic anemia to this form of immunotherapy, and furthermore clinical improvement was too sporadic for this treatment to be recommended. Plasmapheresis may be a useful adjunct in patients with pure red cell aplasia, but remissions may not be dramatic or sustained.
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PMID:A trial of immunotherapy in aplastic anemia and pure red cell aplasia. 644 16

Two in vitro tests were applied to 54 consecutive patients with severe aplastic anemia who were treated in Seattle with antithymocyte globulin. In the first test, peripheral blood mononuclear cells were collected from each patient before antithymocyte globulin therapy and then treated with a panel of monoclonal antibodies and complement. The treated peripheral blood mononuclear cells were assayed for erythroid burst-forming units (BFU-E). This test was designed to determine whether removing various subpopulations of peripheral blood mononuclear cells would increase the number of detectable BFU-E. In the second test, peripheral blood was collected within 48 hr after completion of antithymocyte globulin therapy, and cells were immediately assayed for BFU-E without any further treatment. Data from both tests were analyzed to determine whether the in vitro results correlated with patient response to therapy. Binary logistic regression analyses indicate that a modest correlation (p = 0.04) exists between test 1 in vitro results and patient response to therapy. However, the strength of this association appears to decrease as the interval between diagnosis and treatment increases. In contrast, test 2 had a very significant correlation (p = 0.001) with response to therapy among patients diagnosed more than 1 mo prior to treatment, whereas such an association was not apparent among patients treated within 1 mo of diagnosis.
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PMID:Correlation of two in vitro tests with clinical response to immunosuppressive therapy in 54 patients with severe aplastic anemia. 669 39

In an attempt to predict the clinical response to androgens, the effects of added fluoxymesterone (FMT) on the in vitro growth of marrow erythroid progenitors (CFU-E) were examined in 15 patients with aplastic anemia and 6 control subjects with normal marrow morphology. In the control group, the addition of FMT enhanced the growth of CFU-E in vitro, the maximum absolute increase being dependent on the basal number of CFU-E. In 10 out of the 11 aplastic anemia patients who responded to androgens in vivo. FMT enhanced the growth of CFU-E in vitro. In this group, there was a positive correlation between the basal number of CFU-E and the maximum absolute increase of CFU-E induced by FMT. In patients who did not respond to androgens in vivo, all except one showed no increase in the growth of CFU-E in vitro by the addition of FMT. Furthermore, in four out of seven patients examined prior to androgen therapy, the addition of FMT enhanced the in vitro growth of CFU-E. Androgen therapy in vivo resulted in marked hematological improvements in all of these four patients. Two out of the remaining three patients in whom FMT did not enhance the in vitro growh of CFU-E failed to respond in androgen therapy. These results indicate that an in vitro CFU-E culture system to the presence of FMT may be helpful in predicting the response to androgens in vivo in patients with aplastic anemia.
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PMID:Correlation between in vitro and in vivo response to androgens in patients with aplastic anemia. 673 87

In a study of 16 patients with aplastic anaemia, an attempt has been made to relate ferrokinetic data to haematological measurements and clinical course. There was a positive relationship of cellularity on trephine biopsy with plasma iron clearance and erythrocyte iron turnover, but not with red cell utilisation. Bone marrow aspirate provided less reliable information on erythropoietic function than did trephine biopsy. There was good correlation between all the ferrokinetic parameters and reticulocyte count, but not between reticulocyte count and marrow cellularity, even by trephine. Patients whose ferrokinetic studies indicate a less severe erythroid depression (i.e., plasma clearance T 1/2 less than 200 min and red cell utilisation greater than 35%) are more likely to survive without transplantation than those with more abnormal ferrokinetic results, but such studies alone are of only limited value in clinical management of the individual patient.
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PMID:Ferrokinetic studies and prognosis in aplastic anaemia. 678 93

A 6-year-old girl with severe aplastic anaemia improved promptly after treatment with anti-human lymphocyte globulin (ALG). Blood T lymphocytes were proved to have a suppressive effect on erythroid colony formation. ALG was administered intravenously at a dose of 15 mg/kg/d for 5 d. By the 14th d she showed a prompt increase in the reticulocyte count. Within the next 2 weeks slight increase of the platelet count was observed while the neutrophil count remained unchanged. The suppressive effect of T cells on erythroid colony formation weakened when the reticulocyte count exceeded 100 X 10(9)/l. About 4 months after administration of ALG, a decreased reticulocyte count was observed along with frequent nasal bleeding. Again the T cells exhibited a suppressive effect on erythroid colony formation. The results of serial co-culture studies revealed a close correlation between the T-cell suppressive effect on erythroid colony formation and reticulocyte response. The findings suggest an immune-mediated mechanism for the haematopoietic disorder in this patient.
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PMID:Severe aplastic anaemia treated with anti-lymphocyte globulin. The relationship between clinical course and erythroid colony suppression by T cells. 698 5

We studied the role of ABH antigens in determining graft outcome in 104 patients who received HLA-identical bone marrow transplants for aplastic anaemia and acute leukaemia. ABH compatibility had no significant effect on incidence of graft rejection or graft-versus-host disease. Fifteen recipients ahd pre-transplant antibodies against donor ABH antigens. In 14, large volume plasma exchange and transfusion of donor-type erythrocytes was successful in reducing the antibody titre to low or undetectable levels. In one patient, plasma exchange was unsuccessful and red cells were removed from the marrow inoculum by unit gravity sedimentation. This approach prevented transfusion reaction, and permitted engraftment of all haematopoietic cell lines despite persistently elevated antibody titres. Parallel in vitro studies revealed that antibodies to ABH antigens failed to inhibit the growth of progenitor cells committed to both granulocyte-macrophage (CFU-C) and erythroid (BFU-E) development. These findings indicate that ABH-antigens are not clinically important transplantation antigens and suggest that ABH antigens are not operationally present on hematopoietic stem cells.
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PMID:ABH antigens and bone marrow transplantation. 699 Sep 58


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