Nicardipine in the treatment of Raynaud's phenomenon. Dissociation of platelet activation from vasopressin

Fredrick Wigley, Robert A Wise, R. Malamet, T. E. Scott

Research output: Contribution to journalArticle

Abstract

A new calcium channel blocker, nicardipine, was studied for treatment of Raynaud's phenomenon in a double-blind, placebo-controlled, crossover trial during the winter months. Clinical response was assessed by a patient-kept diary of symptoms and finger systolic pressure that was measured at room temperature and during cold challenge. In vivo platelet activation was determined by measuring plasma levels of the platelet-specific proteins, beta-thromboglobulin and platelet factor 4. When treatment with placebo was compared with treatment with nicardipine, no significant differences were found in the number of Raynaud's attacks per day, the severity of attacks, change in character in Raynaud's phenomenon, use of hands in winter months, patient assessment of medication or objective measurements of finger systolic pressure, and critical closing temperature. There was a reduction of plasma levels of beta-thromboglobulin and platelet factor 4 in the overall study group while taking nicardipine compared with that during the placebo period (mean change 5.0 ± 2.4 ng/ml, P = 0.054, and 1.4 ± 0.6 ng/ml, P <0.01, respectively). These results demonstrate that while nicardipine was not effective in reducing the episodes of Raynaud's phenomenon, it did inhibit in vivo platelet activation. These findings suggest that platelet activation is not the primary event in the pathogenesis of acute vasospasm in Raynaud's phenomenon, since reduction of platelet activation by the drug did not change the severity of vasospasm.

Original languageEnglish (US)
Pages (from-to)281-286
Number of pages6
JournalArthritis and Rheumatism
Volume30
Issue number3
StatePublished - 1987

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ASJC Scopus subject areas

  • Immunology
  • Rheumatology

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