ABSTRACT. Purpose. Elevated lipoprotein (a) [LP (a)] concentrations are independent risk factors of coronary heart disease or stroke in young adults. To clarify its role in childhood thromboembolism, Lp (a) was measured in 72 children with thromboembolism.Methods. In addition to Lp (a), defects of the protein C anticoagulant system, antithrombin, and antiphospholipid antibodies were investigated in children with arterial (n ؍ 36) or venous (n ؍ 36) thrombosis.Results. Enhanced Lp (a) >50 mg/dL was diagnosed in 8 out of 36 children with arterial and 5 out of 36 patients with venous thrombosis. Of the 72 children, 25 showed the factor V Leiden mutation, 10 showed protein C deficiency, 2 showed antithrombin deficiency, and 4 showed primary antiphospholipid syndrome. Three children with increased Lp (a) were heterozygous for the factor V Leiden mutation, and 1 girl showed additional protein C deficiency.Conclusions. Lipoprotein (a) [Lp (a)] is a cholesterol-rich plasma lipoprotein with a lipid composition similar to that of low-density lipoproteins (LDL). The protein composition is different from that of LDL, consisting of two major proteins, apolipoprotein (apo) B and apo (a). 1,2Lp (a) levels vary from person to person but are genetically determined as a dominant trait, minimally affected by race, age, and sex.3,4 Numerous groups agree in their findings that individuals with increased concentrations of Lp (a) have a higher risk of premature coronary heart disease, 5-7 unrelated to the remaining lipoproteins. In addition, the risk of stroke 3,8 -12 as well as for restenosis after coronary artery bypass surgery 13,14 correlates highly with increased Lp (a) concentrations. Little is known, however, about the relation between increased Lp (a) concentrations and childhood thrombosis at various sites. We used a commercially available enzyme-linked immunosorbent assay to measure Lp (a) in a population of children with arterial or venous thrombosis. METHODSSeventy-two infants and children aged from birth to 18 years consecutively recruited between 1992 and 1996 and primarily treated for arterial (n ϭ 36) or venous (n ϭ 36) thrombosis were enrolled in this study. In the majority of cases arterial thrombosis occurred in the central nervous system. Sixteen of 36 infants developed embolic stroke or multiple thrombosis in the neonatal period (attributable to the uncertainty in differentiating between embolic and local stroke in the majority of cases investigated, all children with initial symptoms of stroke were categorized in the arterial group). In addition, 11 children Ͼ1 year of age suffered an ischemic embolic, local, or lacunar stroke. Left intracardial thrombus formation was diagnosed in 4 of 36 patients, the femoral artery was occluded in two children and aortic thrombosis was found in two infants. Venous thromboses were found in the femoral vein (n ϭ 10), renal veins (n ϭ 8), superior caval vein (n ϭ 6), central nervous system (n ϭ 7), and portal vein (n ϭ 5), respectively. In the majority of cases, underlying di...
66 children with ALL, who were admitted to the University Children's Hospital at Münster for treatment according to the BFM protocol 79/81, presented initially with the following abnormal hemostatic parameters: Prolongation of bleeding time (89%), thrombocytopenia (83%), pathological prothrombin time (69%), increased FDP (32%, reduced F XIII (33%), abnormal short PTT (34%). There was a significant discrepancy between immunologically and functionally measured fibrinogen, which is only partially explained by the presence of FDP. Patients with T-cell leukemia (n = 11) had significantly higher WBC, longer prothrombin times, and lower fibrinogen levels than patients with Non-T/non-B ALL. The initial coagulation parameters did not discriminate the 6 patients who presented life threatening bleeding episodes. The two patients with high blast count (350 000 and 548 000/mm3) and T-ALL had intracranial bleeding before therapy started; in one of them vascular infiltration of blast cells was demonstrated at autopsy. Two other patients had bacterial infections, which in one case led to local bleeding into the lungs and in the other case to DIC. Two further children presented intracranial bleeding episodes which could be associated with asparaginase therapy. 5 of the 6 patients with life threatening episodes had a platelet count of more than 35 000/mm3.
Recommendations for vitamin K supplementation were recently changed to 3 x 1 mg orally in healthy term neonates and 0.2 mg parenterally in prematures and high-risk neonates. Prothrombin times (PT) at reduced vitamin K doses (120 patients, 170 samples) during the first 6 weeks of life were below 40% in 6 patients only; all low PTs were unrelated to vitamin K. In the remaining patients, median PT was 100%; 79% of patients had values above 70%. PT was related to birthweight, gestational age and age. There was no decrease over the observation period. Following reduced oral and parenteral vitamin K regimens PTs were well within published reference values for neonates given larger amounts of vitamin K.
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