title: Acquired deficiency of antithrombin in association with a hypercoagulable state and impaired function of liver and/or kidney in preeclampsia.
abstract: To determine whether decreases in plasma antithrombin (AT) level, as seen in non-gestational acquired AT deficiency, result from a hypercoagulable state and/or liver/kidney damage, AT activity was measured in 24 uncomplicated and 30 preeclamptic women. The fifth percentile of AT levels in the normal pregnancies was used as a cut-off value to subdivide the preeclamptic patients into two groups. Markers of activated coagulation, i.e, levels of thrombin-antithrombin complex (TAT), fibrin D-dimer, soluble fibrin, von Willebrand factor (vWF) and platelet counts, were determined. Indicators of hepatic or renal function, i.e. concentrations of alanine aminotransferase (ALT), aspartate aminotransferase (AST), creatinine, urinary albumin (U-albumin) and serum albumin (S-albumin), were assayed. AT levels were lower in those with preeclampsia than in the normal pregnancy group (P < 0.01). In the group with AT 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 increased, whereas platelet counts (P < 0.05) and S-albumin (P < 0.05) were decreased. All patients with ALT levels > 0.46 mu kat/1, AST > 0.58 mu kat/1, S-albumin < 23 g/1 and/or U-albumin > 4.9 g/24 h had AT levels < or = cut off. AT levels correlated with vWF (rs = - 0.73, P < 0.01) and creatinine (Rs = -0.70, P < 0.01). It is suggested that in preeclampsia, acquired AT deficiency is secondary to a hypercoagulable state, and/or associated with impaired hepatic and/or renal function.
authors.affiliation: Department of Laboratory Medicine/Blood Coagulation Research, Karolinska Hospital, Karolinska Institute, Stockholm, Sweden.
authors.forename: S
authors.initials: S
authors.lastname: He
authors.forename: K
authors.initials: K
authors.lastname: Bremme
authors.forename: M
authors.initials: M
authors.lastname: Blombäck
mesh_terms: D000410:Alanine Transaminase / Q000097:blood; D000419:Albuminuria / Q000378:metabolism; D000990:Antithrombin III / Q000032:analysis; D020152:Antithrombin III Deficiency; D001219:Aspartate Aminotransferases / Q000097:blood; D003404:Creatinine / Q000097:blood; D005260:Female; D005337:Fibrin / Q000032:analysis; D006801:Humans; D007668:Kidney / Q000503:physiopathology*; D008099:Liver / Q000503:physiopathology*; D010447:Peptide Hydrolases / Q000032:analysis; D011225:Pre-Eclampsia / Q000503:physiopathology*; D011247:Pregnancy; D011250:Pregnancy Complications, Hematologic / Q000503:physiopathology*; D012709:Serum Albumin / Q000032:analysis; D014841:von Willebrand Factor / Q000032:analysis
chemical_list: D012709:Serum Albumin; C046193:antithrombin III-protease complex; D014841:von Willebrand Factor; D000990:Antithrombin III; D005337:Fibrin; D003404:Creatinine; D001219:Aspartate Aminotransferases; D000410:Alanine Transaminase; D010447:Peptide Hydrolases