Anticardiolipin antibodies in autoimmune thrombocytopenic purpura

Harris, E. N.; Gharavi, Azzudin E.; Hegde, U. M.; Derue, G.; Morgan, S. H.; Englert, H.; Chan, J; Asherson, Ronald A.; Hughes, G. R. V.

doi:10.1111/j.1365-2141.1985.tb02989.x

Cited by 223 publications

(87 citation statements)

References 6 publications

(1 reference statement)

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“…In this study, we investigated the frequency of APAs in patients with ITP, and we found that more than one third of these patients (37.8%) had APAs at the time of diagnosis, a finding consistent with other reports. 4,5 Although many researchers have suggested that APA positivity is not correlated with the development of APS in patients with ITP, 5,7 there are case reports on the development of APS in patients who initially presented with ITP. 14 In this study, we found that 14 of 31 patients (45.1%) who were persistently positive for APAs developed APS in the follow-up period.…”

Section: Discussionmentioning

confidence: 99%

“…Some investigators suggest that antibodies other than APA, mainly those against GPIIb-IIIa and other membrane GPs, cause thrombocytopenia in patients with APS. 2,3 Although Harris et al 4 found anticardiolipin antibodies (ACAs) in 30% of ITP patients at the time of diagnosis, many researchers have questioned the clinical significance of this observation. Elevated levels of APAs are common in ITP and often do not change significantly with immunosuppressive therapy.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Antiphospholipid antibodies and antiphospholipid syndrome in patients presenting with immune thrombocytopenic purpura: a prospective cohort study

Diz‐Küçükkaya

Hacıhanefioğlu

Yenerel

et al. 2001

Blood

199

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The pathogenetic role and the clinical importance of the presence of antiphospholipid antibodies (APAs) in patients with immune thrombocytopenic purpura (ITP) are not clear. In this study, the prevalence and clinical significance of APAs were investigated in patients with ITP. Eighty-two newly diagnosed ITP patients were prospectively studied. They were evaluated for the presence of lupus anticoagulant (LA) and immunoglobulin G/M anticardiolipin antibodies (ACAs). Thirtyone patients (37.8%) were APA positive at diagnosis. No statistically significant differences were found between the APA-positive and APA-negative groups regarding gender, initial platelet counts, or response to methylprednisolone therapy. After 5 years of followup, cumulative thrombosis-free survival of APA-positive (n ‫؍‬ 31) and APA-negative (n ‫؍‬ 51) ITP patients was 39% and 97.7%, respectively. A significant difference was found between these groups by log-rank test (P ‫؍‬ .0004). In addition, LA was an important risk marker for the development of thrombosis in ITP patients.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Antiphospholipid antibodies and antiphospholipid syndrome in patients presenting with immune thrombocytopenic purpura: a prospective cohort study

Diz‐Küçükkaya

Hacıhanefioğlu

Yenerel

et al. 2001

Blood

199

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“…Thrombocytopenia in SLE is strongly associated with aPL (1,(20)(21)(22)(23). The IgG isotype of aPL has been detected in 72% of SLE patients with thrombocytopenia.…”

Section: Thrombocytopenia and Hemolytic Anemiamentioning

confidence: 99%

Origin and pathogenesis of antiphospholipid antibodies

Celli

Gharavi

1998

Braz J Med Biol Res

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Antiphospholipid antibodies (aPL) are a heterogeneous group of antibodies that are detected in the serum of patients with a variety of conditions, including autoimmune (systemic lupus erythematosus), infectious (syphilis, AIDS) and lymphoproliferative disorders (paraproteinemia, myeloma, lymphocytic leukemias). Thrombosis, thrombocytopenia, recurrent fetal loss and other clinical complications are currently associated with a subgroup of aPL designating the antiphospholipid syndrome. In contrast, aPL from patients with infectious disorders are not associated with any clinical manifestation. These findings led to increased interest in the origin and pathogenesis of aPL. Here we present the clinical features of the antiphospholipid syndrome and review the origin of aPL, the characteristics of experimentally induced aPL and their historical background. Within this context, we discuss the most probable pathogenic mechanisms induced by these antibodies.

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“…However, platelet activation should be a pre-requisite for APLA-platelet binding because it leads to the exposure of negatively charged phospholipids on the platelet surface. 10 Nojima et al 11 showed that plasma containing both anticardiolipin and LA increased platelet activation in the presence of low concentrations of ADP, suggesting that these antibodies promote platelet activation, thus contributing to the pathogenesis of arterial thrombosis and thrombocytopenia. Jy et al 9 found that platelet activation predisposes to thrombosis in the presence of chronic EC activation in subjects positive for APLA.…”

Section: 3mentioning

confidence: 99%