Session Information
Title: Systemic Lupus Erythematosus - Clinical Aspects I - Renal, Malignancy, Cardiovascular Disease
Session Type: Abstract Submissions (ACR)
Background/Purpose: Thrombosis is increased in SLE patients, with and without antiphospholipid antibodies. Aspirin and hydroxychloroquine are thought to have anti-platelet effects. We determined whether these drugs had an anti-platelet effect using formal platelet function studies in SLE patients.
Methods:
SLE patients about to start aspirin (81 mg #51) or hydroxychloroquine (400 mg #56) had platelet function tests before and at least 1 month after starting the medication. The changes were assessed statistically using paired t-tests for quantitative variables and McNemar’s test for binary variables.
Results:
Aspirin led to a very significant reduction in urine thromboxane, and a borderline reduction in ADP. SLE patients also appeared to be very sensitive to aspirin in terms of reduction in epinephrine. Hydroxychloroquine also led to a reduction in urine thromboxane.
|
Variable |
Mean change after treatment |
StdError |
P-value |
|
Aspirin Treatment |
|
|
|
|
Arachidonic Acid Aggregation |
-59.5200000 |
7.8713243 |
<0.0001 |
|
ADP Agonist |
-7.6938776 |
3.8310631 |
0.0503 |
|
Collagen ATP release (nm) |
-0.0225208 |
0.1725624 |
0.8967 |
|
Collagen Agonist |
-7.1020408 |
3.1146249 |
0.0271 |
|
Epinephrine Aggregation 10 μM |
-32.5714286 |
6.4571089 |
<0.0001 |
|
Aggregation ADP 10 μM |
1.9285714 |
5.3738364 |
0.7225 |
|
Thromboxane |
-1377.05 |
438.3165675 |
0.0049 |
|
Hydroxychloroquine Treatment |
|
|
|
|
Arachidonic Acid Aggregation |
3.9454545 |
5.3208451 |
0.4616 |
|
ADP Agonist |
-2.3454545 |
3.6381090 |
0.5219 |
|
Collagen ATP release (nm) |
0.0629091 |
0.1104904 |
0.5715 |
|
Collagen Agonist |
-1.4909091 |
3.3678888 |
0.6598 |
|
Epinephrine Aggregation 10 μM |
-1.7297297 |
3.9517831 |
0.6642 |
|
Aggregation ADP 10 μM |
-0.3947368 |
4.9373802 |
0.9367 |
|
Thromboxane |
-612.3913043 |
191.7715594 |
0.0042 |
We next dichotomized urine thromboxane to < 1500 and > 1500.
Table 2 Pre-post results based on various treatments.
|
Treatment |
Number (%) with low Thromboxane at both time points |
Number (%) with low at baseline and high at follow-up |
Number (%) with high at baseline and low at follow-up |
Number (%) with high Thromboxane at both time points |
P-value for difference in rates of High thromboxane pre vs. post1 |
|
Aspirin (all) |
4 (11%) |
2 (5%) |
22 (59%) |
9 (24%) |
<0.0001 |
|
Aspirin (no history of lupus anticoagulant) |
4 (14%) |
1 (4%) |
17 (61%) |
6 (21%) |
0.0002 |
|
Aspirin (history of lupus anticoagulant) |
0 (0%) |
1 (11%) |
5 (56%) |
3 (33%) |
0.21 |
|
Hydroxychloroquine |
11 (22%) |
1 (2%) |
7 (14%) |
31 (62% |
0.070 |
Conclusion: Aspirin led to a marked and significant change in urine thromboxane and epinephrine. Hydroxychloroquine also appeared to lead to a reduction in urine thromboxane. Because a major source of thromboxane is inflamed monocytes, this could represent an anti-inflammatory mechanism of hydroxychloroquine. Although not statistically significant (likely due to loss of power with only 9 patients with a history of the lupus anticoagulant), aspirin (81 mg) led to a reduction in urine thromboxane in the majority. About 25% of SLE patients appear to be aspirin resistent. Aspirin, in SLE patients at risk for, or who have had, arterial thrombosis, is a viable option.
Disclosure:
M. Petri,
None;
L. S. Magder,
None;
T. Kickler,
None.
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