Abstract

The cause of the thrombotic tendency in patients having the lupus anticoagulant (LA) is unknown. Since inhibition of prostacyclin production by endothelial cells (EC) may be a pathogenetic factor, the effect of sera from normal subjects (NS, n=9), SLE (systemic lupus erythematosus) + LA (n=9) and SLE-LA (n=13) on the production of PGI2 by cultured human EC was studied.Confluent 1° cultures of human umbilical vein EC were incubated with 1, 5, 10 and 20% sera from the above for 24 hours. After stimulation with thecalcium ionophore A23187, 6-keto-PGF1α(the stable metabolite of PGI2) in the supernatant was measured by radioimmunoassay.A dose dependent inhibition of 6-keto-PGF1α was observed with all the sera but only the 10 and 20% sera from patients with SLE-LA produced a significantly greater inhibition than control sera. The mean production of 6-keto-PGFia (ng/104 cells) was 2.278 (NS), 2.6594 (SLE-LA) and 2.1418 (SLE + LA)after incubation with 1% sera for 24 hours. This decreased to 1.3647, 0.6517 and 0.942 respectively following incubation with 20% sera. This represented a 44% (NS), 71% (SLE-LA) and 62% (SLE + LA) inhibition of 6-keto-PGF1α production compared to serum free media.The non-significant reduction in prostacyclin production by sera from patients with SLE and the lupus anticoagulant suggests that other factors are responsible for the thrombotic tendency in these patients.

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