Clinical importance of antibodies against platelet activating factor in antiphospholipid syndrome manifestations.
BACKGROUND
We assessed whether antibodies against platelet activating factor (PAF) are related to the presence of antiphospholipid syndrome (APS) clinical manifestations, in particular thrombosis, in patients with connective tissue diseases.


METHODS
Anti-PAF, anticardiolipin (aCL), antibeta2 glycoprotein I (antibeta2GPI) and antiphosphatidylcholine (anti-PC) antibodies were determined in 52 patients with APS, 29 patients with systemic lupus erythematosus (SLE) aCL but without APS, 30 patients with SLE without aCL, and 30 patients with scleroderma. A new enzyme-linked immunosorbent assay (ELISA) was developed for determining anti-PAF antibodies in a bovine serum-free fashion.


RESULTS
The ELISA showed high specificity. Homologous inhibition experiments showed 60-70% inhibition. Anti-PAF antibodies were found in 18/52 APS patients, 10/29 SLE/aCL+ patients, 9/30 SLE/aCL- patients and 3/30 scleroderma patients. Anti-PAF antibodies were significantly associated with anti-PC antibodies (odds ratio [OR] 12. 7, P < 0.01), and there was a modest association with immunoglobulin G (IgG) aCL (OR 3.1, P > 0.10), but not with IgM aCL or antibeta2GPI. Three SLE/aCL+ patients and five SLE/aCL- patients had clinical manifestations characteristic of APS. All these patients had anti-PAF antibodies, while none had high titres of aCL or antibeta2GPI antibodies and only one had anti-PC antibodies. Among the combined APS and SLE groups, the presence of anti-PAF antibodies was significantly associated with clinical manifestations which are characteristic of APS (OR 2.6, P = 0.02). The effect was independent of IgG aCL and antibeta2GPI antibodies.


CONCLUSIONS
Anti-PAF antibodies are common in APS and SLE and comprise an independent factor for the development of thrombosis. Several patients experiencing thromboses have anti-PAF antibodies without other antiphospholipid specificities.
Tektonidou
M G
MG
National University of Athens, Greece.
Petrovas
C A
CA
Ioannidis
J P
JP
Vlachoyiannopoulos
P G
PG
Moutsopoulos
H M
HM
D000328:Adult; D000368:Aged; D017153:Antibodies, Anticardiolipin / Q000097:blood*; D000918:Antibody Specificity; D016736:Antiphospholipid Syndrome / Q000453:epidemiology / Q000276:immunology*; D004797:Enzyme-Linked Immunosorbent Assay / Q000379:methods; D005260:Female; D006023:Glycoproteins / Q000276:immunology; D006801:Humans; D007074:Immunoglobulin G / Q000097:blood; D007075:Immunoglobulin M / Q000097:blood; D008297:Male; D008875:Middle Aged; D016017:Odds Ratio; D010713:Phosphatidylcholines / Q000276:immunology; D010972:Platelet Activating Factor / Q000276:immunology*; D012595:Scleroderma, Systemic / Q000453:epidemiology / Q000276:immunology; D016036:Seroepidemiologic Studies; D013927:Thrombosis / Q000453:epidemiology / Q000276:immunology; D053482:beta 2-Glycoprotein I
D017153:Antibodies, Anticardiolipin; D006023:Glycoproteins; D007074:Immunoglobulin G; D007075:Immunoglobulin M; D010713:Phosphatidylcholines; D010972:Platelet Activating Factor; D053482:beta 2-Glycoprotein I