Biomedical subjects
Publications and source records attributed to W Muntean.
A five-month-old infant with Reye's syndrome developed disseminated intravascular coagulation, which was successfully controlled by heparin. A fatal outcome could not, however, be averted. The pathogenetic role of disseminated intravascular coagulation in Reye's syndrome is discussed.
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Factor VIII activity and factor VIII associated antigen were determined in healthy term newborns. On the first day of life factor VIII activity was higher than in adults. The activity reached the adult level at about the tenth day. The factor VIII associated antigen was found higher than the activity and did not decrease in the first ten days. Studies of the factor VIII associated antigen of newborns by the two-dimensional immunoelectrophoresis showed the same pattern as compared to adults.
Intracranial hemorrhage is a rare, lifethreatening complication of immun-allergic thrombocytopenia (ITP). A 4 8 1/2 year old boy, who developed intracranial hemorrhage while receiving long term steroid treatment for ITP, was successfully managed by emergency splenectomy. Possible treatment for this condition is discussed.
Coagulation studies from capillary blood, consisting of the determination of fibrinogen, factors II and V and proactivator-plasminogen, were done in 104 newborns. In healthy newborns fibrinogen and factor V was found near the adult level, while factor II and proactivator-plasminogen showed a severe deficit. None of the coagulation factors was dependent of gestational age. Fibrinogen was significantly lower in the group of children with perinatal asphyxia. In ill newborns there was a significant correlation between fibrinogen and factor II and fibrinogen and factor V as was between factors II and V. No correlation could be demonstrated between proactivator-plasminogen and any of the other coagulation factors.
An infant, aged seven months, developed toxic shock with acute renal failure as a sequel to the development of hypertonic dehydration. The anuric phase persisted despite treatment of the dehydration and diuretic infusions. The coagulation tests showed signs of disseminated intravascular coagulation and so the child was given fibrinolytic therapy for 36 hours following initial heparinization. Excretion of urine recommenced 8 hours after the initiation of fibrinolytic therapy. Peritoneal dialysis was carried out in parallel with the fibrinolytic treatment without haemorrhagic complications. It was possible to terminate dialysis on the fourth day already and renal function subsequently recovered completely.
Methods are described for the determination of the thromboplastin time, the thrombin time, for fibrinogen and factor II, V and X from capillary blood. These methods are easy to perform and comparison of the results from venous and capillary blood showed a very good correlation. The described methods seem suitable for routine coagulation tests in pediatrics.
Healthy newborns have a very low risk of thrombosis. It has been suggested that this is partly due to the anticoagulant effect of alpha-2-macroglobulin (a2-M). This broad-spectrum protease binding glycoprotein is physiologically elevated in newborns over adult values and has been shown to complex generated alpha-thrombin. In our present study, we point out that a2-M also acts as a procoagulant by inhibiting activated protein C (APC). In all experiments performed in cord and adult plasma the anticoagulant action of APC was diminished in a dose-dependent manner when a2-M levels were successively elevated, reflected in increased thrombin potential (TP), and enhanced at low a2-M levels, reflected in decreased TP.
BACKGROUND: Childhood obesity may be associated with thyroid dysfunction. Both obesity and hypothyroidism are related to increased risk of coronary heart disease (CHD) in adults through high levels of serum lipids and/or hemostatic abnormalities. OBJECTIVE: To investigate a possible relationship between thyroid function and hemostatic markers for CHD in obese children and adolescents. STUDY DESIGN: Thirty-nine obese children and adolescents were investigated for thyroid function and markers for CHD after overnight fast. Thyroid hormones were measured by radioimmunoassay. Factor VII coagulant activity (VIIc) and factor VIII coagulant activity (VIIIc) were determined using one stage clotting assays; fibrinogen was measured according to the method of Clauss; von Willebrand factor antigen (vWF-Ag), tissue type plasminogen activator antigen (tPA-Ag), and plasminogen activator inhibitor-1 antigen (PAI-1-Ag) were determined by ELISA. RESULTS: We found a significant inverse correlation between fT4 and factor VIIc (r = -0.33, p = 0.03) and fibrinogen (r = -0.35, p = 0.02), which remained significant after adjustment for body fat mass. Factor VIIIc (r = -0.26, p = 0.066) and vWF-Ag (r = -0.28, p = 0.053) tended to be correlated negatively to fT4. fT4 did not correlate with tPA-Ag and PAI-1-Ag. fT3 was inversely related to factor VIIc (r = -0.3, p = 0.039), which was not independent of body fat mass, and showed a less impressive negative correlation with fibrinogen (r = -0.27, p = 0.058). fT3 did not correlate with vWF-Ag, tPA-Ag, or PAI-1-Ag. There was no relationship between TSH and the determined hemostatic markers. CONCLUSION: Our study demonstrates a close relationship between thyroid function and hemostatic markers for CHD in obese children and adolescents and suggests that thyroid dysfunction is associated with an unfavorable hemostatic state even in pediatric patients.
A 17-year-old girl known to suffer from essential thrombocytosis (ET) was admitted with severe abdominal pain that was due to sonographically verified portal and hepatic vein thrombosis. ET is a well-documented disease and portal vein thrombosis has often been reported in adults but not in children and adolescents suffering from ET. Coincidence of ET, urinary tract infection, oral contraception, and cessation of acetylsalicylic acid therapy might be responsible for the early manifestation of portal and hepatic vein thrombosis in our patient.
Vitamin K is required for the synthesis of active forms of some coagulation factors. Bleeding due to low levels of the vitamin K dependent coagulation factors (classic hemorrhagic disease of the newborn) is most frequently seen in newborns with a low intake of breast milk, who are not fed supplemental formula, since transplacental transfer of vitamin K seems to be small and breast milk is relatively deficient in vitamin K. Severe bleeding due to vitamin K deficiency is also observed in 4-12 weeks old infants. The reason for the deficiency in otherwise healthy infants of this age is unclear. Classic hemorrhagic disease of the newborn is not existent in infants given vitamin K intramuscularly at birth. Also, the late manifestation of vitamin K deficiency has been observed virtually exclusively in infants, who had not been given vitamin K parenterally at birth. Since most newborns will be breast fed and supplemental formula feeding will not be required in most healthy full term newborns, all newborns should be given a dose of vitamin K intramuscularly immediately after birth. Whether it is safe to administer vitamin K to the mother or orally to the child requires further investigation.
Inherited thrombophilia has been suggested as a cause of Legg-Calvé-Perthes disease in up to 75% of patients. This prevalence seems high compared to the prevalence of inherited thrombophilia in other thrombotic disorders (average, 30%). Therefore, we investigated 44 patients with Legg-Calvé-Perthes disease for antithrombin-III, protein-C, and protein-S deficiency and activated protein C (APC) resistance. Three (6.8%) of our patients were positive for APC resistance, and one patient (2.2%) showed deficiency of protein-C activity. Our results suggest that inherited thrombophilia is not associated with avascular necrosis of the femoral head (Legg-Calvé-Perthes disease).