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© 1992 British Society for Rheumatology

research-article

SERUM MASKS THE INHIBITION OF THROMBIN-INDUCED PROSTACYCLIN RELEASE PRODUCED BY ANTICARDIOLIPIN ANTIBODIES

N. LINDSEY, F. HENDERSON, R. MALIA*, M. GREAVES* and P. HUGHES*,

University Department of Medicine, Clinical Sciences Centre, Northern General Hospital Sheffield
*University Department of Haematology, Royal Hallamsh ire Hospital Sheffield

Correspondence to: Correspondence to Dr P. Hughes, University Department of Medicine, Clinical Sciences Centre, Northern General Hospital, Sheffield S5 7AU

The effect on thrombin-induced release of prostacyclin from human umbilical vein endothelial cells of preincubation with both serum and serum derived from platelet-poor plasma (PDS) from patients with systemic lupus erythematosus (SLE), systemic sclerosis, the antiphospholipid syndrome (APS) and normal controls was examined. Although no significant differences in thrombin-induced prostacyclin release were found in any of the patient groups, further analysis revealed that PDS from patients with SLE and APS that contained IgG anticardiolipin antibodies produced significant inhibition of prostacyclin release when compared with controls (P = 0.02). The effect was maximal with samples that contained both IgG and IgM anticardiolipin antibodies (P<0·01) and which had a significantly higher titre of IgG antibodies than samples which contained solely IgG antibodies (P<0·05). The absence of any corresponding inhibition of prostacyclin release by serum samples that contained anticardiolipin antibodies, possibly due to the release of masking stimulatory factors by platelets during coagulation, provides an explanation for the conflicting nature of previous reports.

KEY WORDS: Endothelium, Prostacyclin, Anticardiolipin antibodies, Systemic lupus erythematosis, Systemic sclerosis, Antiphospholipid syndrome


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