Antiplatelet glycoprotein autoantibodies in patients with autoimmune diseases with and without thrombocytopenia

Abstract

The presence and specificity of antiplatelet autoantibodies in 32 patients with primary and 18 patients with secondary autoimmune thrombocytopenic purpura (AITP), as well as 11 non-thrombocytopenic patients with systemic autoimmune diseases, were studied. By means of the direct and indirect monoclonal antibody immobilization of platelet antigen (MAIPA) assay, antiplatelet autoantibodies were detected using monoclonal antibodies specific for platelet glycoproteins (GPs) Ib, IIb/IIIa, Ia/IIa, and IV. Serum antiplatelet autoantibodies were found in 18 of 32 primary AITP patients (56%), 6 of 18 secondary AITP patients (33%), and 5 of 11 nonthrombocytopenic patients (45%). Platelet-associated autoantibodies were detected in five of eight patients with primary (62%) and in four of eight patients with secondary AITP (50%) and in two of four patients without thrombocytopenia (50%). Multiple antibody reactivity, mainly against GPs IIb/IIIa and Ib and, in a few patients, against Ia/IIa, was found. Using MAIPA, platelet xylene eluates from 20 patients were also studied. Antiplatelet elutable autoantibodies were related to thrombocytopenia; autoantibodies against membrane GPs Ib and IIb/IIIa were demonstrable in 84 and 63% of eluates from patients with primary and secondary AITP, respectively, but not in eluates from nonthrombocytopenic patients. The presence of antiplatelet antibodies thus appears to be a common feature of many autoimmune diseases apart from the thrombocytopenia, but the (primary or secondary) etiology of the immune thrombocytopenia cannot be differentiated on the grounds of their specificity.

Age-Related Prevalence of Platelet-Associated Immunoglobulins G in Nonthrombocytopenic Patients with Autoimmune Thyroid Disease and Autoimmune Polyglandular Syndrome

“…In this respect, it has been reported that, in 8 patients with thrombocytopenia, paIgG disappeared following successful treatment of H. pylori infection [23]. These findings further support the hypothesis that, in patients with AITD, the presence of paIgG may represent a ‘danger flag’ for the presence of APS rather than of AITP, according to what has been reported in studies dealing with platelet disorders [8, 11, 15, 16, 17]. …”

“…Also the presence of platelet-specific antibodies, recognizing glycoproteins Ib and IIb/IIIa, better characterizes the presence of AITP [15]which may be also under the influence of several abnormal lymphocyte-mediated mechanisms [16]. The presence of paIgG in these patients may only represent a frequent but not an obligatory event [15, 16, 17]. In our study, where nonthrombocytopenic patients were examined, the presence of circulating immunocomplexes, which usually coexist with platelet-specific antibodies [17, 18], more likely accounts for the high prevalence of paIgG.…”

“…The presence of paIgG in these patients may only represent a frequent but not an obligatory event [15, 16, 17]. In our study, where nonthrombocytopenic patients were examined, the presence of circulating immunocomplexes, which usually coexist with platelet-specific antibodies [17, 18], more likely accounts for the high prevalence of paIgG. Their presence has been characterized in several autoimmune diseases with or without thrombocytopenia [17, 18]and may represent a further immune sign in type 3 APS [7].…”

Autoantibody Level Modification in Adult Patients with Idiopathic Thrombocytopenic Purpura following Intravenous Immunoglobulin Treatment

“…Thus, the immunomodulatory effect of IVIg that inhibits T-and B-cell formation, with the consequent inhibition of pathologic Ab secretion [11], provides an explanation for Ab level decrease. Furthermore, ITP is one of the diseases in which Abs can be inhibited by IVIg in vitro, by binding of anti-idiotypes to the respective Abs (additional examples include myasthenia gravis, systemic lupus erythematosus and the antiphospholipid syndrome [13]). In vitro, Berchtold et al [7] have shown concentrationdependent inhibition of Abs from 8 patients with ITP by IVIg.…”

Autoimmune Thrombocytopenia

“…Also using direct platelet eluates, Bettaieb et al (1992) demonstrated GP IIbIIIa-specific PA-IgG in patients with human immunodeficiency virus. Direct MAIPA was positive in 5 of 8 patients with ITP, as well as in 4 of 8 patients with disease-related thrombocytopenia, such as SLE, and also in 2 of 4 patients with systemic autoimmune disease without thrombocytopenia (Cordiano et al, 1996). Brighton et al (1996) …”