ANTIMITOCHONDRIAL ANTIBODIES TYPE-5 ARE M ARKERS OF THE ANTIPHOSPHOLIPID SYNDROME

In order to investigate the clinical value of anti-mitochondria antibo dies type 5 (anti-M5), we carried out a retrospective study on 48 pati ents With these antibodies. Seventeen of these 48 patients (35%) satis fied at least 4 criteria of the revised American Rheumatism Associatio n classification of SLE. Twenty-nine (61 %) had at least one clinical manifestation of anti-phospholipid syndrome; thirteen had symptoms con sistent with primary anti-phospholipid syndrome; five had isolated rec urrent thrombosis; five had Evans' syndrome; four had auto-immune haem olytic anaemia; two had immunologic thrombocytopenia. Two of tile 48 p atients had no clinical manifestations, but only anti-M5 and a false l aboratory test for syphilis (FBTS). Our data confirm that patients wit h anti-M5 have a high prevalence of: 1) thrombosis (42% had three or m ore deep thromboses) and fetal loss (21%); 2) auto-immune cytopenia wi th idiopathic thrombocytopenic purpura (29%) and autoimmune haemolytic anaemia (54%); 3) laboratory nor markers of anti-phospholipid syndrom e (lupus anticoagulant (71%), FBTS (95%) and anticardiolipin antibodie s (aCL) (71%)). For 32 patients with anti-M5, anti-beta 2 glycoprotein I antibodies were also tested; 12 (38%) were positive, all of whom ha d IgG aCL, ie none had anti-beta 2GPI antibodies without aCL. There wa s no association between the presence of anti-beta 2GPI antibodies and recurrent thrombosis among patients with anti-M5. All these findings suggest that anti-M5 is another marker of the antiphospholipid syndrom e. Even though the prevalence of anti-M5 is low, especially in SLE, it was the only marker of the the anti-phospholipid syndrome in two pati ents; this appears to justify routine screening for these antibodies.