{'fraction_non_alphanumeric': 0.042458100558659215, 'fraction_numerical': 0.016201117318435754, 'mean_word_length': 5.175862068965517, 'pattern_counts': {'":': 0, '<': 2, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Platelet Reactivity and Disease Activity in Subjects with Psoriatic Arthritis

Objective. Platelet aggregation plays a major role in vascular mortality. Individuals with psoriatic arthritis (PsA) are highly predisposed to vascular mortality. We evaluated the correlation between disease activity and platelet aggregation in individuals with PsA. Methods. Individuals with PsA receiving tumor necrosis factor-α (TNF-α) blockers (n = 114) and healthy controls (n = 114) matched for age, sex, and cardiovascular risk factors were tested for light transmission aggregometry. None was receiving antiinflammatory drugs. Platelet aggregation (max-A%) was defined as maximal light transmittance achieved within 5 min after the addition of 0.1 or 0.2 mM arachidonic acid or 0.4 μM adenosine diphosphate. A value of ≥ 50% irreversible light transmittance (LT-50%) following platelet stimulation was used to define platelet hyperreactivity. Minimal disease activity (MDA) was evaluated in subjects with PsA. Results. Regardless of the agent used, individuals with PsA showed a higher max-A% and achieved LT-50% more often than controls. Among individuals with PsA, those achieving MDA exhibited a max-A% similar to that of controls, both being significantly lower (p < 0.001) than max-A% of subjects with active disease. Subjects with active disease showed platelet hyperreactivity (LT-50%) more often than those achieving MDA (p < 0.001). For increasing quartiles of max-A%, C-reactive protein levels increased and prevalence of MDA decreased. Conclusion. Compared with those achieving MDA, subjects with active PsA disease had abnormally high platelet reactivity. Whether this is relevant for the cardiovascular risk profile of subjects with PsA receiving TNF-α blockers requires further evaluation.