ACQUIRED DEFICIENCY OF ANTITHROMBIN IN ASSOCIATION WITH A HYPERCOAGULABLE STATE AND IMPAIRED FUNCTION OF LIVER AND OR KIDNEY IN PREECLAMPSIA/

To determine whether decreases in plasma antithrombin (AT) level, as s een in non-gestational acquired AT deficiency, result from a hypercoag ulable state and/or liver/kidney damage, AT activity was measured in 2 4 uncomplicated and 30 preeclamptic women. The fifth percentile of AT levels in the normal pregnancies was used as a cut-off value to subdiv ide the preeclamptic patients into two groups. Markers of activated co agulation, i.e. levels of thrombin-antithrombin complex (TAT), fibrin D-dimer, soluble fibrin, von Willebrand factor (vWF) and platelet coun ts, were determined. Indicators of hepatic or renal function, i.e. con centrations of alanine aminotransferase (ALT), aspartate aminotransfer ase (AST), creatinine, urinary albumin (U-albumin) and serum albumin ( S-albumin), were assayed. AT levels were lower in those with preeclamp sia than in the normal pregnancy group (P < 0.01). In the group with A T levels less than the cut-off point, levels of fibrin D-dimer (P ( 0. 05), soluble fibrin (P < 0.05), vWF (P < 0.05), ALT (P < 0.05), AST (P < 0.05), creatinine (P < 0.01) and U-albumin (P < 0.01) were increase d, whereas platelet counts (P < 0.05) and S-albumin (P < 0.05) were de creased. All patients with ALT levels > 0.46 mu kat/l, AST > 0.58 mu k at/l, S-albumin <23 g/l and/or U-albumin >4.9 g/24 h had AT levels les s than or equal to cut off. AT levels correlated with vWF (r(s) = -0.7 3, P < 0.01) and creatinine (r(s) = -0.70, P < 0.01). It is suggested that in preeclampsia, acquired AT deficiency is secondary to a hyperco agulable state, end/or associated with impaired hepatic and/or renal f unction.