1. Hospital based prospective longitudinal study of 231 patients of Antiphospholipid Syndrome and exploring the role of AntiAnnexin A5, Plasminogen Activator Inhibitor-1 (PAI-1) and platelet dysfunction in its pathogenesis. Departments of Medicine, Nephrology, Obstetrics and Gynaecology, Biochemistry and Immuno-pathology Division. Institute of Medical Sciences, Banaras Hindu University

2. INTRODUCTION Antiphospholipid syndrome (APS) was first described byGraham R. V. Hughes in 1983 as a clinical syndrome characterized by venous and arterial thrombosis, recurrent pregnancy loss, neurological disease and the presence of antiphospholipid antibodies (aPLs). Primary APS: When this syndrome occur without evidence ofanother identifiable autoimmune disorders. Secondary APS: When this syndrome occur in association with 3. The diagnosis of APS is confirmed in the presence of at least one clinical and one laboratory criterion (modified Sapporo criteria, 2006)Clinical Criteria1. Vascular thrombosis:one or more venous, arterial, or small vessel thrombotic events in any tissue or organ confirmed by imaging or histopathology .Thrombosis should be present without any significant evidence of inflammation in the vessel wall. (superficial vein thrombosis is not included in clinical criteria). 2. Pregnancy morbidity One or more unexplained deaths of a morphologically normal fetus at or beyond the 10th week of gestation. One or more premature births of a morphologically normal neonate before the 34th week of gestation because of eclampsia, severe preeclampsia, or placental insufficiency. Three or more consecutive spontaneous abortions before the 10th week of gestation (in the absence of parental chromosomal causes and maternal anatomic or hormonal abnormality). Miyakis S, Lockshin MD et al. 2006, J Thromb Haemo 4, 295-306 4. Laboratory Criteria1.aCL-Abs (IgG and/or IgM) present in serum or plasma on 2 or more occasions atleast 12 weeks apart (in medium or high titer, ie, >40 GPL [IgG phospholipid] or MPL [IgM phospholipid] units or >99th percentile, measured by a standardized enzyme-linked immunosorbent assay [ELISA])2.LA (lupus anticoagulant) present in plasma on 2 or more occasions at least 12 weeks apart (measured according to the guidelines of the International Society on Thrombosis and Haemostasis)3.Anti-b2GPI antibody (IgG and/or IgM) present in serum or plasma on 2 or more occasions at least 12 weeks apart (in titer >99th percentile, measured by a standardized ELISA). The diagnosis of APS cannot be confirmed if less than 12 weeks (or more than 5 years) separate the time of the positive aPL-Ab test and the time of the clinical manifestation. 5. Table : Clinical manifestations of APL Organs/Systems Manifestations Asymptomatic15-20% develop clinical events over timeVenous ThrombosisDVT, Budd-Chiari syndrome, Cortical vein/Sinus ThrombosisArterial ThrombosisTIA & stroke (thrombo-embolism also), PVD, CAD, Renal, IntestinalObstetricsRSFL- early & late foetal losses, IUGR, Pre-term labor (10wk %)27 +/4.336/8019 (22.05)11 13 (12.79) (15.11)33 (38.37)7 (10.93)77 45 (89.53) (52.32)Second 28.5 ary +/-6.9 APS (n=263/239 (34.61)9 4 (34.61) (15.38)5 (19.23)2 (7.69)23 14 (88.46) (53.84)Total (n=112)9/10328 20 (25.00) (17.85)17 (15.17)9 (8.03)100 59 (89.28) (52.67)27.75 +/-20 (17.85) 14. Estimation of Anti annexin A-V Antibody levels were measured by quantitativeenzyme-linked immunosorbent assay (ELISA), using the Zymutest kit 15. Results 16. p