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

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 (CV...

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Bibliographic Details
Published in:Clinical rheumatology 2016-02, Vol.35 (2), p.447-455
Main Authors: MacMullan, Paul A., Madigan, Anne M., Paul, Nevin, Peace, Aaron J., Alagha, Ahmed, Nolan, Kevin B., McCarthy, Geraldine M., Kenny, Dermot
Format: Article
Language:English
Subjects:
Adult
Antirheumatic Agents - metabolism
Antirheumatic Agents - pharmacology
Antirheumatic Agents - therapeutic use
Arthritis, Rheumatoid - drug therapy
Blood Platelets - drug effects
Cohort Studies
Female
Humans
Male
Medicine
Medicine & Public Health
Middle Aged
Original Article
Platelet Function Tests
Rheumatology
Spondylarthropathies - drug therapy
Sulfasalazine - metabolism
Sulfasalazine - pharmacology
Sulfasalazine - therapeutic use
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Summary: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  
ISSN:0770-3198
1434-9949
DOI:10.1007/s10067-014-2769-x