Intracranial arterial anomalies can coexist with cervicofacial hemangioma. Aneurysmal and occlusive changes are potentially progressive and can result in cerebral infarction. A causative association between occlusive cerebrovascular disease and pharmacologic treatment has not been excluded.
Abstract. The After reduction of disulfide bonds, the PIl" antigenicity was not observed, and IgG bound nonspecifically to a protein band with an apparent molecular weight of 45,000. We have also identified anti-platelet antibodies in patients with idiopathic thrombocytopenic purpura and determined their antigenic specificity. Antibodies which bind to a 100,000-mol wt protein were found in nine of thirteen patients with chronic disease. The antigens in three of these cases were studied in detail by using both reduced and nonreduced control and Glanzmann's This paper was presented in abstract form in 1982. Blood. 60(5)Suppl. 1:1848.
Summary. Platelet-associated and plasma autoantibodies against platelet glycoproteins (GP) have been demonstrated in patients with autoimmune thrombocytopenia (AITP) using various methods. Eight laboratories in seven countries participated in this international study to evaluate the interlaboratory agreement using glycoprotein-specific immunoassays for these autoantibodies. The participating laboratories received blind samples of frozen washed platelets and plasma from 22 normal donors and 22 AITP patients. Platelet-associated and plasma autoantibodies against GPIIb-IIIa and GPIb-IX were measured by MAIPA, immunobead assay or modified antigen capture assay. Of the control samples, 96 . 0% and 97 . 2% of all results for platelet-associated and plasma autoantibodies to GPIIb-IIIa/ GPIb-IX, respectively, were negative. The mean variation coefficient of the control samples of platelet-associated and plasma autoantibodies was 89·5% (range 11·1-272·9%) and 46·5% (range 21·0-78·0%), respectively. In 20/22 patient samples, platelet-associated autoantibodies to either glycoprotein were noted by at least two laboratories. The mean degree of agreement in these samples was 74·0%. There was a significant correlation in the individual antibody measurements between all laboratories (Kendall coefficient of concordance 0·60 and 0·38, P < 0·001; Spearman rank order test, range of correlation coefficient 52·3-94·0% and 42·2-85·0%, P < 0·05, for anti-GPIIbIIIa and anti-GPIb-IX, respectively). In contrast, plasma autoantibodies to either glycoprotein were noted by at least two laboratories in only 13/22 patient samples. Moreover, the degree of agreement was poor (50·1%) and a significant correlation was noted between only six pairs of laboratories. We conclude that methods used in this study yield good interlaboratory agreement in measuring platelet-associated autoantibodies against GPIIb-IIIa and GPIb-IX. In contrast, poor agreement was found in detecting plasma autoantibodies to the same glycoproteins.
Varicella zoster infection in children can be complicated by acute idiopathic thrombocytopenic purpura (ITP). To determine the etiologic mechanism of this thrombocytopenia, we studied three children with clinically diagnosed varicella infection. Immunoblot analysis of these patients' anti-platelet antibodies identified a unique band at 85 kD. Characterization of this protein revealed that it was platelet surface glycoprotein V (GPV) because it was not affected by a disulfide bond reduction but was cleaved by thrombin. Bernard-Soulier syndrome (BSS) platelets deficient in GPIb-IX and GPV did not react with the sera from our varicella-infected study patients. There was no apparent cross-reactivity between anti-varicella antibody and patients' anti-GPV Ig. We report here the first cases of GPV as the target antigen in autoimmune thrombocytopenia.
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