Faculty of Medicine

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Author: search.filters.author.Efremov D

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    PREVALENCE OF AUTOANTIBODIES AGAINST THE PLATELET GLYCOPROTEIN COMPLEXES GP IIb/IIIa, GP Ib/IX AND GP Ia/IIa IN PATIENTS WITH CHRONIC LYMPHOCYTIC LEUKEMIA
    (Македонско лекарско друштво = Macedonian Medical Association, 2017)
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    Stojanovic A
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    Efremov D
    Chronic lymphocytic leukemia (CLL) is a malignant disorder characterized by the frequent occurrence of autoimmune hemolytic anemia (AIHA) and autoimmune idiopathic thrombocytopenic purpura (ITP). In this study we analyzed the presence of auto-Abs against the platelet GP complexes GP IIb/IIIa, GP Ib/IX and GP Ia/IIa in 55 consecutive CLL patients using a new antigen specific assay. All patients were simultaneously tested for anti-RBC auto-Abs with the direct antiglobulin test. Antiplatelet auto-Abs against one or more GP complexes was detected in 25 patients (45%). Anti-RBC auto-Abs were detected in 18 patients (33%), 6 of them (11%) had evidence of AIHA at the time the sample was taken. The obtained data show that platelet specific Abs develops frequently in patients with CLL, even more often than anti-RBC auto-Abs. The presence of platelet specific auto-Abs together with thrombocytopenia and normal Hb levels in 16% of patients indicated that ITP may be more common cause of thrombocytopenia in CLL than previously anticipated.
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    LOW FREQUENCY OF CLONAL B CELL EXPANSIONS IN PATIENTS WITH IDIOPATHIC THROMBOCYTOPENIC PURPURA
    (Македонско лекарско друштво = Macedonian Medical Association, 2021-01-01)
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    Efremov D
    Idiopathic thrombocytopenic purpura (ITP) is an autoimmune disorder characterized by an increased platelet destruction caused by autoantibodies directed against platelet membrane glycoproteins (GP), most commonly against GPIb/IX, GPIIb/IIIa and GPIa/IIa. In a few recent studies it has been reported that these antibodies frequently have a restricted light chain phenotype, supporting a clonal origin. In this study we wanted to explore the hypothesis of clonal B cell expansions in chronic ITP. We investigated 40 patients (28 women and 12 men) with chronic ITP for clonal B cell expansions using sensitive RT-PCR technique for analysing Ig-gene rearrangements. RNA was isolated from peripheral blood mononuclear cells separated on a Ficoll gradient. The RNA was converted into cDNA and then amplified using FW3 and IgM or IgG specific oligonucleotides to investigate the clonality of B-cells expressing the respective Ig isotype. The PCR fragments were analyzed on sequencing polyacrylamide gels or with an ABI prism 310 DNA analyser. We detected a monoclonal B cell population in only 1 patient and polyclonal rearrangement with one prominent band in 3 patients in the analysis of IgG heavy chain mRNA. The pattern of IgM heavy chain gene rearrangements was polyclonal in all cases. Our study indicates that clonal B-cell expansions are rare in patients with ITP. Most probably, the clonal B-cell expansion responsible for the production of autoantibodies in ITP, if present, is below the detection limit.