A Comparative Study of Platelet Reactivity in Arthritis*

Abstract

We utilized a standardized in vitro method which employs transmission electron microscopy to monitor the degree of surface activation (cytoplasmic spreading) and amount of aggregation displayed by platelet populations from 314 patients with one of five distinct rheumatic diseases and from 72 normal subjects. The percentage of patients in each group whose platelet populations were hyperactive was as follows: polymyalgia rheumatica, 75 percent; scleroderma, 65 percent; primary gout, 61 percent; rheumatoid arthritis, 57 percent; and degenerative joint disease, 40 percent. Pair-wise contrasts performed after an analysis of variance suggest the following differences and similarities: (1) the mean differential platelet count of the normal subjects differed from that in each disease state; (2) the platelet responsivity in patients with degenerative joint disease most closely resembled that in normal subjects; (3) the platelet response in polymyalgia rheumatica plus temporal arteritis was the most abnormal; and (4) platelet response in scleroderma, rheumatoid arthritis, and gout closely resembled each other. The increased platelet response in vitro may reflect the in vivo presence of disease-related "risk factors" (hyperuricemia, immune complexes, and atherosclerosis). Those patients with "triggered" platelet populations may be appropriate candidates for antiplatelet therapy.

The Inflammatory Role of Platelets: Translational Insights from Experimental Studies of Autoimmune Disorders

“…Further, platelet aggregates and platelet or PMP adherent to leukocytes have been detected in both blood and synovial fluids of RA patients [58,64,65,66,67,68,69,70]. In vitro, it was shown that platelets are hyper-responsive to further activation, potentially reflecting the in vivo priming of platelets during disease [71,72]. …”

Platelet function in rheumatoid arthritis: arthritic and cardiovascular implications

“…Examples are rheumatoid seropositivity, antibodies against beta-2-microglobulin and circulating immune complexes (another link between autoimmune reactions and prothrombotic state in RA) [53,56,57]. Interestingly, increased in vitro platelet sensitivity to agonists and autoimmune factors has also been found in other rheumatic diseases (e.g., polymyalgia rheumatica, systemic sclerosis, gout), where common mechanisms of immune complex formation and accelerated atherogenesis can be inhibited by anti-platelets [58].…”

Critical Determinants of Cardiovascular Risk in Rheumatoid Arthritis

“…For that matter, several studies have shown elevated markers of thrombin generation and fibrin turnover, previously associated with augmented thrombotic coronary risk, in RA patients with active disease [81][82][83][84]. Moreover, findings of enhanced platelet reactivity and activation have been consistently reported, which evidently relates to and even predicts future adverse cardiovascular events [85][86][87][88][89].…”