Symptomatic ischemic stroke in full-term neonates - Role of acquired and genetic prothrombotic risk factors

Background and Purpose-The present multicenter case-control study was prosp ectively designed to assess the extent to which single and combined clottin g factor abnormalities influence the onset of symptomatic ischemic stroke i n full-term neonates, Methods-Lipoprotein (Lp)(a); the factor V (FV) G1691A mutation; the prothro mbin (PT) G20210A variant; the methylenetetrahydrofolate reductase (MTHFR) T677T genotype; antithrombin; protein C, protein S; and anticardiolipin ant ibodies (ACAs) were investigated in 91 consecutively recruited neonatal str oke patients and 182 age- and sex-matched healthy controls. Results-Sixty-two of 91 stroke patients (68.1%) had at least 1 prothromboti c 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 t o 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 deficienc y nor protein S deficiency was found in the neonatal patients studied. Acqu ired IgG ACAs were found in 3 cases. Additional triggering factors, ie, asp hyxia, septicemia, maternal diabetes, and perinatally acquired renal venous thrombosis, were reported in 54.0% of patients. Conclusions-Besides acquired triggering factors, the data presented here su ggest that genetic prothrombotic risk factors play a role in symptomatic ne onatal stroke.