Vascular dementia among patients with ITP (immune thrombocytopenic purpura) and risk factors

Y. S. Ahn, L. L. Horstman, W. Jy, J. J. Jimenez, Y. Cui, M. A. Escobar, B. Bowen

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Abstract

Some ITP antibodies impair platelet (Pit) aggregation to increase bleeding while others may induce platelet activation to promote thrombosis. We reported increased platelet microparticles (PMP), markers of platelet activation, in ITP and that some patients (pts) with higher PMP suffered recurrent TIA and progressive dementia, and MRI showed ischémie small vessel disease (J Lab Clin Med 119:334, 1992). We now report clinical, laboratory and radiologie characteristics of 20 chronic ITP pts with this syndrome, and factors promoting progression to more advanced dementia. Clinical findings: All 20 pts (14 women , 8 men , mean age 56.8) had chronic ITP treated with steroids; 7 had splenectomy. ITP was severe in 13 (Pit <20K), milder in 7 (Pit 20K, <80K), and in 10 the Pit count fluctuated. All 20 rarely manifested bleeding, even in severe thrombocytopenia. CNS dysfunction was initially subtle, commonly dizzy or weak spells, forgetfulness, followed by sporadic imbalance, numbness/ tingling, blurred/ double vision, slurred speech, mild confusion, seizure. Progression to dementia: In 11 pts, cognitive dysfunction progressed fast in 5 yr (Group I); 8 progressed to advanced dementia, requiring custodial care. All 7 splenectomized pts were in Group I. In the other 9 (Group II), it progressed more slowly or was stable. In Group I, the ITP was severe, often with surges of Pit counts to normal or above. In Group II, ITP was milder and stable. In both groups, Pit counts increased significantly, or ITP went into remission, when CNS dysfunction was evident; this increase was more marked in Group 1 than II (p<0.01). Laboratory: Platelet activation was detected by increased CD62p and PMP. Marked elevation of platelet-associated IgM was frequent in Group I. Anticardiolipin antibodies (IgG or IgM) was positive in <lβ. Radiologie. Brain MRI showed periventricular white matter lesions in 85%, hyperintense white matter lesions in subcortical (75%) or cortical (50%) areas, indicating ischémie small vessel diseases. Large infarcts (15%), cortical atrophy (35%), were less frequent. Summary: Subsets of ITP pts are at higher risk of thrombosis than bleeding. Patients asymptomatic from severe thrombocytopenias, with Pit activation, appear more prone to thrombosis, especially if poteniated by unacccustomed rise in Pit count by splenectomy or other measures. Thrombotic complication in ITP has been underestimated. We noted acute MI in young ITP pts with few risks and clean coronary arteries (Clin Ap Thr Hem 3:46,97). The possibility of long-term thrombotic complications in later life should be weighed in the treatment. Therapy should not be aimed solely at increasing Pit count but individualized based on clinical manifestation and assessment of risk of both bleeding and thrombosis.

Original languageEnglish (US)
Pages (from-to)250a
JournalBlood
Volume96
Issue number11 PART I
StatePublished - Dec 1 2000

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ASJC Scopus subject areas

  • Biochemistry
  • Immunology
  • Hematology
  • Cell Biology

Cite this

Ahn, Y. S., Horstman, L. L., Jy, W., Jimenez, J. J., Cui, Y., Escobar, M. A., & Bowen, B. (2000). Vascular dementia among patients with ITP (immune thrombocytopenic purpura) and risk factors. Blood, 96(11 PART I), 250a.