Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002874 (aplastic anemia)
 5,905 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The short-term effect of a domestically produced equine antithymocyte globulin (ATG) was analyzed in 6 patients with acquired severe aplastic anemia (AA). All patients received 5 doses of ATG every other day in a 60-min intravenous infusion. Five peripheral blood immunoregulatory mononuclear cell (MNC) subsets, defined by monoclonal antibodies, were enumerated before and 24 h after each application of ATG. Following the first dose of ATG there was a significant and transient reduction in the absolute number of helper T lymphocytes. There was no statistically significant difference pre-ATG to post-ATG in the absolute number of MNC expressing activation antigen Tac (interleukin-2 receptor). However, Tac+ cells, which were significantly increased before ATG therapy, decreased to nearly normal levels after the fourth dose of ATG. A significant and sustained increment in the absolute number of monocytes (CD14+ cells) occurred following the third dose of ATG. The absolute numbers of MNC, suppressor T lymphocytes and cells bearing HLA-DR antigen remain without significant change along ATG treatment. These results suggest that: (a) Tac+ cells are probably involved in the pathogenesis of AA; (b) the target of ATG may be a Tac+ cell, and (c) ATG may stimulate monopoiesis.
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PMID:Changes in peripheral blood mononuclear cell subpopulations during antithymocyte globulin therapy for severe aplastic anemia. 250 90

Twenty-two patients with adult onset aplastic anaemia were analysed before and after therapy with anti-thymocyte globulin (ATG). Lymphocyte phenotype, lymphokine levels or production, and haematopoietic progenitor cell number were measured 3 months after therapy; clinical response was determined 1 year post-therapy. By flow cytometry there was a significant reduction in both the proportion and absolute number of peripheral blood lymphocytes expressing activation antigen Tac (IL-2 receptor) and in the proportion of HLA-DR+ lymphocytes. For T cells bearing HLA-DR, there were proportional decreases in both activated helper and suppressor cells. There was no statistically significant difference pre-ATG to post-ATG in the absolute numbers of total, helper and suppressor lymphocytes. In all 10 haematologic responders the number of Tac bearing lymphocytes after ATG therapy was in the normal range, but half of 12 non-responding patients continued to have abnormally elevated numbers of Tac+ T cells. The proportion of Tac+ cells were not related to transfusion history. Gamma-interferon levels in serum by radioimmunoassay were elevated in almost half the aplastic patients; post-ATG, gamma-interferon was detectable in only three patients. Haematologic response to ATG therapy was associated with increased numbers of haematopoietic progenitors post-treatment, but pre-treatment values were not predictive of a response. These results are consistent with a pathogenic role for activated T-cells and their lymphokine products and suggest that the target of ATG therapy may be a Tac+ lymphocyte.
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PMID:Lymphocyte phenotype and lymphokines following anti-thymocyte globulin therapy in patients with aplastic anaemia. 311 88

Activation-associated antigens such as CD11b, CD14 and CD64 of neutrophils have been reported. Although CD48 is an activation antigen of lymphocytes and monocytes, whether it is an activation antigen of neutrophils has not previously been examined. Herein, using FACS analysis, we examined the expression of surface CD48 on neutrophils activated in vivo by G-CSF administered for the treatment of idiopathic aplastic anemia. CD48 expression was increased 24 h after the initial G-CSF infusion and peaked within 1 week. Within a few days after discontinuation of G-CSF administration, it returned to the pretreatment level. This indicates that CD48 is an activation antigen of neutrophils.
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PMID:Increased expression of CD48 on neutrophils activated in childhood patients with aplastic anemia. 753 99