Anti-corpus luteum antibody and menstrual irregularity in patients with systemic lupus erythematosus and Hashimoto's thyroiditis.

The aim of the present study was to verify the presence of anti-corpus luteum antibodies (anti-CoL) in systemic lupus erythematosus (SLE) and Hashimoto's thyroiditis (HT) patients, as well as establish its possible correlation with menstrual and/or hormonal disturbances in both populations and with SLE activity. Forty-six patients with SLE, 31 with HT, four with both SLE and HT, and 36 healthy women were studied. Out of these, seven (15.2%) patients with SLE, three (9.7%) with HT, three (75%) with both pathologies, and none of the healthy controls tested positive for anti-CoL. The presence of anti-CoL was not significantly correlated to menstrual disturbance (P = 0.083), changes in the level of follicle stimulating hormone (P = 1.0), luteinizing hormone (P = 0.284), estradiol (P = 0.316), prolactin (P = 1.0) or SLE activity measured by SLEDAI (P = 0.756) in SLE patients. There were not enough patients testing positive for anti-luteal antibodies among those with HT or both HT and SLE (three from each group) for a statistical analysis. In conclusion, we found no association between anti-CoL and menstrual or hormonal disturbance in patients with SLE. Also anti-CoL was not specific for SLE, and was not found to be a marker of ovarian failure in SLE.

Complement-fixing activity of anticardiolipin antibodies in patients with and without thrombosis.

We have analysed in vitro the complement-fixing activity of anticardiolipin antibodies (C-fix aCL) from patients with persistent and moderate/high titres IgG aCL antibodies: 21 with thrombosis and 11 without thrombosis. Titre and C-fix ability of aCL were measured by ELISA. APS and non-APS patients were similar with regard to mean levels of IgG aCL (46 +/- 24 versus 51 +/- 30 GPL, P = 0.7), frequency of IgM aCL (P = 0.7) and a comparable predominance of IgG2 aCL reactivity on ELISA (95% versus 100%, respectively, P = 1.0). Remarkably, a high frequency of C-fix aCL (71% versus 92%, P = 0.35) was observed in both groups. Similarly, no difference was observed in the mean level of C-fix aCL in APS and non-APS patients (7 +/- 6 versus 9 +/- 8 SDunits, P = 0.3). Analysis of 10 primary and 11 secondary APS also revealed a comparable IgG aCL mean titre (57 +/- 29 versus 37 +/- 11, P = 0.06), frequency of IgM aCL (P = 0.6) and of C-fix aCL (70% versus 73%, P = 0.99). Among APS patients six had exclusive arterial events and seven exclusive venous events. The IgG aCL mean titre (36 +/- 10 versus 36 +/- 11 GPL, P = 0.9) and the frequency of IgM aCL antibodies (P = 0.56) in these subgroups of patients were comparable. There was a trend of higher frequency of C-fix aCL in patients with exclusive venous events (100%) compared to 50% of those with exclusive arterial events (p = 0.07). Importantly, C-fix aCL titre was higher in the former group compared to the later one (8 +/- 5 SDunits versus 2 +/- 2 SDunits, P = 0.016). Our data support the notion of a high frequency of C-fix aCL in APS. Although it does not discriminate those patients without thrombotic events with persistent moderate/high levels of aCL, this property seems to be more relevant in venous events and may provide the basis for further understanding the distinct pathogenic mechanisms underlying arterial and venous occlusive disorders of APS.