Thrombophilia and thrombosis in systemic lupus erythematosus: a case-control study.
نویسندگان
چکیده
METHODS AND RESULTS Forty eight consecutive patients with SLE were included (39 women, 9 men), 15 with and 33 without past thrombosis (Th and NTh group, respectively). Twenty thrombotic events were identified: 17 deep venous and 1 arterial thrombosis, 2 osteonecrosis. Both groups had comparable clinical, biological, therapeutic data, and mean (SD) SLE disease activity index (SLEDAI) (5 (4.6) v 5.3 (4.8)). Patients were examined at least one month after thrombosis (>3 months in 11 out of 15). The following parameters were determined: protein C, total and free protein S (in 43 patients because five had antivitamin K treatment), antithrombin, activated protein C resistance (APCR), the R506Q mutation of the factor V gene and the G20210A allele of the prothrombin gene, lupus anticoagulant (LAC) (activated partial thromboplastin time, tissue thromboplastin inhibition test, and platelet neutralisation procedure), IgG anticardiolipin antibodies (aCL), IgG and IgM anti-β2-glycoprotein I (anti-β2GPI) antibodies, IgG and IgM antiprothrombin antibodies. Homocysteinaemia (fasting and after oral methionine load (100 mg/kg)) was measured in 38 patients (9 Th, 29 NTh patients). Table 1 gives the main results. LAC and aCL >30 GPL units were associated with thrombosis, unlike anti-cofactor antibodies. Anti-β2GPI was detected only in positive LAC subjects. Free protein S levels were negatively correlated with the SLEDAI (r=−0.33, p=0.025), and anti-DNA levels (r=−0.31, p=0.04), but not with C reactive protein or ESR. Antiphospholipid/cofactor antibodies were present in 6/8 patients with low free protein S and in 12/35 patients with normal free protein S (p=0.05). One of the two patients with APCR was negative for factor V Leiden. G20210A prothrombin gene mutation was present in one NTh patient. Homocysteinaemia was highly correlated with creatininaemia (r=0.64, p<0.0001), but not with current or cumulative steroid dose (p=0.08). The patient with arterial thrombosis had neither antiphospholipid/cofactor antibodies nor thrombophilic factor.
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عنوان ژورنال:
- Annals of the rheumatic diseases
دوره 62 10 شماره
صفحات -
تاریخ انتشار 2003