Anti-phospholipid syndrome in seven leprosy patients with thrombotic events on corticosteroid and/or thalidomide regimen: insights on genetic and laboratory profiles

Abstract INTRODUCTION Corticosteroids and/or thalidomides have been associated with thromboembolism events (TBE) in multibacillary (MB) leprosy. This report aimed to determine genetic and laboratory profiles associated with leprosy and TBE. METHODS Antiphospholipid antibodies (aPL), coagulation-related exams, prothrombin and Leiden's factor V mutations, and ß2-glycoprotein-I (ß2GPI) Val247Leu polymorphism were assessed. RESULTS Six out of seven patients with leprosy were treated with prednisone and/or thalidomide during TBE and presented at least one positive aPL. All patients presented ß2GPI polymorphism, and one showed prothrombin mutation. CONCLUSIONS Corticosteroid or thalidomide adverse effects and aPL and ß2GPI polymorphisms may cause TBE in patients with MB leprosy.

Placental histomorphology in unexplained foetal loss with thrombophilia.

BACKGROUND & OBJECTIVES: Acquired and genetic thrombotic conditions, both organ and non organ specific, are associated with increased foetal wastage. This study was carried out to examine the placenta from women with abnormal pregnancies and a history of unexplained foetal loss, and to associate with maternal thrombophilia status. METHODS: Placentas from eight women with history of unexplained foetal loss were analyzed for histopathological characteristics. All the women were simultaneously screened for the common acquired and genetic thrombophilia markers i.e., lupus anticoagulants ( LA), IgG / IgM antibodies for anticardiolipin (ACA), beta2 glycoprotein 1 (beta2GPI) and annexin V, protein C (PC), protein S (PS), antithrombin III (AT III), factor V Leiden ( FVL) mutation, prothrombin (PT) gene G20210A, methylene tetrahydrofolate reductase (MTHFR) C 677T, endothelial protein C receptor (EPCR) 23 bp insertion and plasminogen activator inhibitor ( PAI-1 4G/5G) polymorphisms RESULTS: Six of eight women were positive for one or more thrombophilia markers. The placenta in all the cases except one, showed the characteristic features of infarct fibrin deposition and calcification. Among two women who were negative for thrombophilia, one showed clear evidence of thrombus in the placental sections while the other did not show any characteristic infarcts in the placental sections. INTERPRETATION & CONCLUSION: Our findings showed that the histopathological examination of the placentas confirmed thrombophilia as the aetiological cause of thrombosis in 6 of the 8 women. The presence of thrombus in a negative thrombophilia woman suggests yet unidentified thrombophilia markers or probably non-haemostatic factors causing thrombosis.

Study of antibodies to B2-glycoprotein I, protein C and protein S as markers of arterial and venous thrombosis in patients with systemic lupus erythematosus

In order to clarify the association between antibodies to phospholipidbinding plasma protein particularly; B2-glycoprotein I, protein C and protein S and thrombotic complications in systemic lupus erythematosus patients [SLE], 42 patients with SLE were selected and 10 healthy subjects were also included as a control group, their age and sex matched with our patients. The Anti phospholipid antibodies [APL Abs] were measured by an Enzyme Linked Immunosorbant Assay [ELISA] system. The thrombotic events were determined by venography, arteriography, dopler ultrasound, computed tomography [CT] and magnetic resonant image [MIR]. Our result showed that all types of IgG APL Abs were detected in SLE patients [30% for anti-B2-Glycoprotein I, 21% for anti-protein C and 28% for anti-protein S], thrombotic events were detected in 12 of SLE patients [7 arterial and 5 venous]. The prevalence of LA and aCL were significantly higher in SLE patients with thrombosis than in those without thrombosis [P < 0.01], but there was non significant change between the prevalence of LA and aCL in patients with arterial and venous thrombosis [P> 0.05]. Concentration and prevalence of anti-B2-GPI was significantly higher in patients with arterial thrombosis than in those with venous thrombosis [P< 0.01]. The concentration and prevalence of anti-protein C and anti-protein S Abs were significantly higher in patients with venous thrombosis than in those with arterial thrombosis [P < 0.01]. There was non significant change in disease activity score between SLE patients with and without thrombotic events. There was significant correlation between the concentration of anti-B2-GPI Abs and aCL [r = 6.86, P < 0.01] and significant correlation between the concentration of Anti-protein C and Anti-protein S Abs [r = 0.66, P < 0.01]. We concluded that, anti-B2-GPI Abs, anti-protein C and anti-protein S Abs may play a differential role in thrombotic complications where anti-B2-GPI Abs may be associated primarily with arterial thrombosis and anti-protein C and/or anti-protein S Abs may be associated primarily with venous thrombosis