Biomedical subjects

R Yelenosky

Publications and source records attributed to R Yelenosky.

12 recordsLinked to original sources

PubMed1978

Antibody against megakaryocytes in idiopathic thrombocytopenic purpura.

Purified human IgG from both serum and the culture of human splenic cells was radiolabeled with 125I. Incubation of radiolabeled IgG from patients with idiopathic thrombocytopenic purpura (ITP) with normal homologous platelets or bone marrow cells resulted in significant (P less than .001) binding when compared with control IgG. Radioautographs showed that the radioactivity was associated with the platelets or megakaryocytes. The antiplatelet antibody in ITP has specificity for antigens associated with both platelets and megakaryocytes and suggests that thrombopolesis may also be affected in this disease.

Animals↗

PubMed1977

Platelet-derived acid phosphatase isoenzyme in the serum in thrombocythemia.

Acid phosphatase is present in platelets and is released during the clotting process. In thrombocythemic conditions, this may increase serum enzymatic activity. An illustrative case in which the determination of plasma enzymatic activity suggested a platelet origin of elevated serum levels, confirmed by isoenzyme fractionation on disk polyacrylamide gel electrophoresis is presented. It is concluded that in the presence of thrombocytosis a plasma sample is preferable to a serum sample for determination of acid phosphatase activity.

Acid Phosphatase↗

PubMed1977

Immune neutropenia.

A patient with hyperthyroidism and severe neutropenia had a clinical course and family history that suggested an immune cause. Neutrophil-binding IgG was demonstrated in serum using the Fab-anti Fab assay. The antineutrophil factor bound specifically to either homologous or autologous neutrophils and could be adsorbed by the target neutrophils. The quantity of IgG required to saturate the neutrophil-binding sites (175 000 molecules per neutrophil) and the serum concentration (1.3 mug/ml) were determined. It was estimated that at the time that blood and marrow neutrophils were markedly reduced, serum contained sufficient neutrophil-binding IgG to saturate the binding sites of 1.2 times the total blood neutrophil pool.

Agranulocytosis↗

PubMed1976

The effect of corticosteroids on human IgG synthesis.

The effect of prolonged, high-dose corticosteroid therapy on total IgG synthesis rates by human bone marrow and splenic leukocytes was studied in patients with immune thrombocytopenia. Marrow IgG production rates begin to decrease 3 weeks after beginning therapy and reach levels approximately one-fourth of pre-treatment rates after 6 weeks. No effect of corticosteroids on splenic IgG production rates could be shown. Marrow IgG synthesis rates in these patients were on the average from 3 to 10 times greater than corresponding splenic production rates and, in addition, appeared to correlate with serum IgG levels. These data suggest that the marrow is an important contributor to the total body IgG pool; and since corticosteroids appear to suppress marrow IgG production, this may be one reason for their therapeutic usefulness in antibody-mediated diseases.

Antibody Formation↗

PubMed1975

Thrombocytopenia associated with gold therapy. Observations on the mechanism of platelet destruction.

Severe thrombocytopenia developed in a patient with rheumatoid arthritis during gold therapy. Increased numbers of marrow megakaryocytes, shortened 51Cr-labeled platelet survival and platelet phagocytosis by splenic macrophages indicated that thrombocytopenia was due to excessive platelet destruction. Aurothiomalate disodium antigenicity was demonstrated by increased lymphocyte blastogenesis, and accentuation of blood and splenic leukocyte migration in the presence of the gold salt. In vitro splenic immunoglobulin G (IgG) production was markedly increased, and a significant portion of the culture-produced IgG attached specifically to homologous platelets and platelet membranes. Serum antiplatelet antibodies could not be demonstrated, nor could it be shown that gold enhanced the binding of splenic-synthesized IgG to platelets. The data indicate an immunologic mechanism for gold-associated thrombocytopenia and permit speculation as to possible ways in which unidentified antigens may be involved in the pathogenesis in idiopathic thrombocytopenic purpura.

Antigens↗

PubMed1974