Sulfasalazine and its metabolites inhibit platelet function in patients with inflammatory arthritis

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• 作者：Paul A. MacMullan ; Anne M. Madigan ; Nevin Paul ; Aaron J. Peace…
• 关键词：Cardiovascular disease ; DMARDs ; Inflammation ; Platelet function ; Sulfasalazine
• 刊名：Clinical Rheumatology
• 出版年：2016
• 出版时间：February 2016
• 年：2016
• 卷：35
• 期：2
• 页码：447-455
• 全文大小：491 KB
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• 作者单位：Paul A. MacMullan (4)
  Anne M. Madigan (1)
  Nevin Paul (2)
  Aaron J. Peace (2)
  Ahmed Alagha (3)
  Kevin B. Nolan (3)
  Geraldine M. McCarthy (1)
  Dermot Kenny (2)
  
  4. Division of Rheumatology, University of Calgary, Calgary, Canada
  1. Rheumatology Department, Mater Hospital, Dublin, Ireland
  2. Department of Molecular and Cellular Therapeutics, Royal College of Surgeons in Ireland, 123 St Stephen’s Green, Dublin 2, Ireland
  3. Department of Biochemistry, RCSI, Dublin, Ireland
  
• 刊物类别：Medicine
• 刊物主题：Medicine & Public Health
  Rheumatology
  
• 出版者：Springer London
• ISSN：1434-9949

文摘

The purpose of this study is to assess the effect of sulfasalazine and its metabolites on platelet function in patients with inflammatory arthritis (IA). One hundred thirty-five consecutive patients with an established diagnosis of IA were screened. Those with a history of cardiovascular disease (CVD), taking anti-platelet agents or non-steroidal anti-inflammatory drugs (NSAIDs) were excluded. A total of 32 patients were investigated, 15 taking sulfasalazine and 17 taking other disease-modifying anti-rheumatic drugs (DMARDs) and no sulfasalazine. These two cohorts were compared to 15 patients with stable CVD on long-term aspirin. The effect of sulfasalazine and its metabolites on arachidonic acid (AA)-induced platelet aggregation was also tested in vitro in samples from healthy donors (n = 18). Demographics, CVD risk factors and disease activity indices were similar in the sulfasalazine and other DMARD groups. AA-induced platelet aggregation was significantly inhibited in the sulfasalazine group (9 ± 7 %) and comparable to that in the aspirin group (10 ± 6 %). In contrast, there was no effect on AA-induced platelet aggregation in the other DMARDs group (77 ± 12 %) (p < 0.001). Furthermore, sulfasalazine therapy had no effect on platelet aggregation in response to multiple other agonists. Sulfasalazine and its metabolites (5-aminosalicylic acid and sulfapyridine) exerted an additive and dose-dependent inhibitory effect on AA-induced platelet aggregation in vitro (p < 0.001). The inhibition of AA-induced platelet aggregation by sulfasalazine is comparable to that achieved by aspirin and is dependent on both sulfasalazine and its metabolites. This represents a potential mechanism that may contribute to the known cardioprotective effect of sulfasalazine in patients with IA. Keywords Cardiovascular disease DMARDs Inflammation Platelet function Sulfasalazine