(Stroke. 2000;31:2437.)
© 2000 American Heart Association, Inc.
Original Contributions |
From the Department of Paediatrics (G.G.), University of Magdeburg, Magdeburg; the Departments of Clinical Chemistry and Laboratory Medicine and of Arteriosclerosis Research (R.J.), and the Department of Paediatrics (R.S., A.K., U.N.-G.), University of Münster, Münster; the Department of Paediatrics (R.S.), University of Halle an der Saale, Halle an der Saale; the Department of Paediatrics (K.K.), University of Munich, Munich; and the Department of Paediatrics (C.H.), University of Frankfurt, Frankfurt, Germany.
Correspondence to Ulrike Nowak-Göttl, MD, Department of Paediatrics, Westfälische Wilhelms-University, Albert-Schweitzer-Strasse 33, D-48149 Münster, Germany. E-mail leagottl{at}uni-muenster.de
Background and PurposeThe present multicenter case-control study was prospectively designed to assess the extent to which single and combined clotting factor abnormalities influence the onset of symptomatic ischemic stroke in full-term neonates.
MethodsLipoprotein (Lp)(a); the factor V (FV) G1691A mutation; the prothrombin (PT) G20210A variant; the methylenetetrahydrofolate reductase (MTHFR) T677T genotype; antithrombin; protein C; protein S; and anticardiolipin antibodies (ACAs) were investigated in 91 consecutively recruited neonatal stroke patients and 182 age- and sex-matched healthy controls.
ResultsSixty-two of 91 stroke patients (68.1%) had at least 1 prothrombotic risk factor compared with 44 control subjects (24.2%) (odds ratio [OR]/95% confidence interval [CI], 6.70/3.84 to 11.67). An increased Lp(a) level (>30 mg/dL) was found in 20 patients and 10 controls (OR/95% CI, 4.84/2.16 to 10.86); FV G1691A was present in 17 patients and 10 controls (OR/95% CI, 3.95/1.72 to 9.0); the PT G20210A variant was detected in 4 patients and 4 controls (OR/95% CI, 2.04/0.49 to 8.3); the MTHFR TT677 genotype was found in 15 patients and 20 controls (OR/95% CI, 1.59/0.77 to 3.29); and protein C type I deficiency was found in 6 neonates. Neither antithrombin deficiency nor protein S deficiency was found in the neonatal patients studied. Acquired IgG ACAs were found in 3 cases. Additional triggering factors, ie, asphyxia, septicemia, maternal diabetes, and perinatally acquired renal venous thrombosis, were reported in 54.0% of patients.
ConclusionsBesides acquired triggering factors, the data presented here suggest that genetic prothrombotic risk factors play a role in symptomatic neonatal stroke.
Key Words: factor V lipoproteins neonate prothrombin risk factors stroke
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