Anticardiolipin, anticentromere and anti-Scl-70 antibodies in patients with systemic sclerosis and severe digital ischaemia.
OBJECTIVE
Following observation of weakly positive anticardiolipin (aCL) antibodies in four of eight patients with systemic sclerosis (SSc) and severe digital ischaemia requiring amputation, the association between the presence of these and other antibodies and severe peripheral ischaemia in patients with SSc was examined.


METHODS
ACL antibodies (IgG and IgM), anticentromere and anti-Scl-70 antibodies were measured in a further 60 patients with SSc over a one year period. Thirty one of the 68 patients in whom aCL antibodies were assayed had 'severe ischaemia', having suffered digital ischaemia severe enough to warrant amputation (13 patients), surgical debridement or admission for intravenous vasodilator therapy.


RESULTS
There was no difference in aCL positivity between those with severe ischaemia and those without, nor between those who had amputations and those who had not. Three of the 31 patients (10%) with severe ischaemia had IgG and eight (26%) IgM aCL antibodies in weak to moderate titre compared to 10 (27%) and 6 (16%) respectively of the remaining patients (p = 0.06 for IgG and p = 0.25 for IgM, Fisher's exact test). Seventeen of the 31 patients (55%) with severe ischaemia were anticentromere antibody positive compared with nine of 37 (24%) without ischaemia (p = 0.01). Six patients with severe ischaemia had anti-Scl-70 antibodies compared with two of the 37 without ischaemia (p = 0.08).


CONCLUSIONS
The findings do not support an association between aCL antibodies and severe ischaemia in SSc, but confirm the previously reported association between anticentromere antibodies and severe peripheral ischaemia. Although anti-Scl-70 antibodies were present only in a small number of patients, there was also a tendency for these to be associated with severe ischaemia, suggesting that patients with either anticentromere or anti-Scl-70 antibodies should be considered at risk of digital loss.
Herrick
A L
AL
Rheumatic Diseases Centre, University of Manchester, Hope Hospital, Salford, United Kingdom.
Heaney
M
M
Hollis
S
S
Jayson
M I
MI
D000328:Adult; D000368:Aged; D017153:Antibodies, Anticardiolipin / Q000097:blood*; D000974:Antibodies, Antinuclear / Q000097:blood; D001323:Autoantibodies / Q000097:blood*; D002503:Centromere / Q000276:immunology*; D004264:DNA Topoisomerases, Type I; D005260:Female; D005385:Fingers / Q000098:blood supply*; D006801:Humans; D007511:Ischemia / Q000209:etiology / Q000276:immunology*; D008297:Male; D008875:Middle Aged; D009687:Nuclear Proteins / Q000276:immunology; D012595:Scleroderma, Systemic / Q000150:complications / Q000276:immunology*
D017153:Antibodies, Anticardiolipin; D000974:Antibodies, Antinuclear; D001323:Autoantibodies; D009687:Nuclear Proteins; C048100:Scl 70 antigen, human; D004264:DNA Topoisomerases, Type I