Patients with SLE and Arterial Thrombosis May Benefit from Treatment with Aspirin

SAN DIEGO, CA—Aspirin is a viable option in patients with systemic lupus erythematosus (SLE) at risk for—or who have had—arterial thrombosis, a study presented at the 2013 ACR/ARHP Annual Meeting concluded.

Patients with SLE are known to have an increased risk of thrombosis, both those with and without antiphospholipid antibodies. To determine whether aspirin or hydroxychloroquine have antiplatelet effects, Michelle Petri, MD, MPH, Director of the Lupus Center at the Johns Hopkins University School of Medicine, Baltimore, MD, and colleagues conducted formal platelet function studies in patients about to start aspirin (81mg; n=51) or hydroxychloroquine (400mg; n=56).

Platelet function tests were performed before and at least 1 month after initiation of the respective medications. Changes were assessed using paired t-tests for quantitative variables and McNemar's test for binary variables.

They examined aspirin treatment in all patients, aspirin use in patients both with and without a history of lupus anticoagulant, and hydroxychloroquine in patients. For each set of patients, they noted those who had low levels of thromboxane at both pre/post time points, those with low levels at baseline and high levels at follow-up; high levels at baseline and low levels at follow-up; and high levels at both time points.

When urine thromboxane was dichotomized to <1500 and >1500 and pre/post results compared based on the various treatments, the investigators found that “aspirin led to a very significant reduction in urine thromboxane (P=0.0049), and a borderline reduction in adenosine diphosphate (ADP; P=0.0503).” Patients with SLE “also appeared to be very sensitive to aspirin in terms of reduction in epinephrine (P<0.0001).”

Patients who received aspirin had reductions in arachidonic acid aggregation (P<0.0001) and collagen agonist (P=0.0271), but not in collagen adenosine triphosphate release (P=0.8967) or aggregation ADP (P=0.7225).

Hydroxychloroquine treatment was found to lead to a significant reduction in urine thromboxane (P=0.0042), but none of the other variables studied. “Because a major source of thromboxane is inflamed monocytes, this could represent an anti-inflammatory mechanism of hydroxychloroquine,” Dr. Petri noted.

Researchers concluded that aspirin (81mg) led to a reduction in urine thromboxane in the majority and it is a viable option for SLE patients at risk  or have a history of arterial thrombosis.
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