Administration of vitamin K to newborn infants and childhood cancer.

OBJECTIVES: To investigate whether childhood cancer is associated with intramuscular administration of vitamin K to newborn infants. DESIGN: Routines for administration of vitamin K to infants born after normal deliveries during 1973-89 were obtained from maternity hospitals. Occurrence of cancer up to the end of 1991 was identified by comparing these records with the national cancer registry. Adherence to the routine method of administering vitamin K was checked with the medical records of a sample of 396 infants (196 who had developed childhood cancer and 200 controls). SETTING: All maternity hospitals in Sweden. SUBJECTS: 1,384,424 full term infants born after non-instrumental deliveries, 1,085,654 of whom were born in units where vitamin K was routinely given by intramuscular injection and 272,080 of whom were born where it was given orally. MAIN OUTCOME MEASURES: Odds ratios for cancer after intramuscular administration of vitamin K versus oral administration after stratification for year of birth. RESULTS: Adherence to routine method of administering vitamin K was 92% in the 235 cases where individual information could be found. The risk of cancer after intramuscular administration of vitamin K was not elevated compared with that after oral administration: odds ratios of 1.01 (95% confidence interval 0.88 to 1.17) for all childhood cancers and 0.90 (0.70 to 1.16) for childhood leukaemia. CONCLUSIONS: The alleged association between intramuscular vitamin K prophylaxis to newborn infants and childhood cancer could not be verified in the present study of full term infants born after non-instrumental delivery.

Four pairs of siblings with acute leukemia during 1966-1985 in the Nordic countries: indication of an elevated familial risk?

Four pairs of siblings with acute leukemia in the Nordic countries during 1966-1985 are reported. The national data indicate that the risk of leukemia is 5.9 times greater in siblings of children with leukemia.

Homozygous protein C deficiency in two siblings.

Homozygous protein C (PC) deficiency is reported in two siblings (girl and boy) who received their proper diagnoses at the ages of 7 4/12 and 1 3/12 years respectively. The girl had perinatal asphyxia without bleeding. At 1 year of age she developed purpura fulminans. Treatment with heparin and plasma was successful. At 7 4/12 years she developed tender, bluish nonnecrotic skin changes after an orthopedic operation. The PC level was 0.08 U/ml. The boy had had a large intraventricular hemorrhage neonatally and developed severe brain damage. At 1 3/12 years he manifested the same skin changes as his sister and was treated similarly. The PC level was 0.05 U/ml. Both children now receive warfarin continuously and are essentially free of symptoms. The cases represent homozygous phenotypes in a family with a recessive trait of PC deficiency without thrombotic disease. The cases also show that severe PC deficiency may be compatible with life beyond infancy without any specific therapy.

Combined deficiency of coagulation factors II, VII, IX, and X: a case of probable congenital origin.

Combined deficiency of coagulant activity of the vitamin K-dependent factors was found in a 14-year-old boy suffering from severe hemorrhages. Immunoassays revealed the presence of acarboxyprothrombin. The bleedings could be controlled, but the coagulation defects persisted during more than 2 years' follow-up and could not be corrected by oral or parenteral vitamin K. No intoxication or underlying disease was found. The abnormality was considered a congenital disorder of the carboxylation of prothrombin.

Variations of protease inhibitors in foetuses, newborn infants and in some neonatal disorders.

Low levels of protease inhibitors have been found on the 1st day of life in IRDS infants. 19 IRDS infants were studied together with foetuses and control term and preterm infants. Alpha1-antitrypsin, antichymotrypsin and alpha2-macroglobulin were measured with the electroimmuno assay. IRDS infants had significantly reduced concentration of alpha-antitrypsin and antichymotrypsin on the 1st day, the level increasing to normal on the 2nd day. In foetuses alpha1-antitrypsin was normal, antichymotrypsin 2% and alpha2-macroglobulin 1/3 of the normal adult level. The protease inhibitors are increased in infants born after premature rupture of foetal membranes. The part, if any, played by protease inhibitors is not entirely understood. The inhibitors may, theoretically, be of some importance in the dissolution of the hyaline membranes, protect against pulmonary vasoconstriction, protect pulmonary tissue against leucocyte and macrophage proteolytic enzymes and inhibit the release of or counteract vasoactive substances that might take part in the development of shock in IRDS babies.

Abnormal proteolysis in sick newborns.

87 newborn infants were studied on their first day of life for defects in the coagulation and fibrinolytic systems. The infants were divided into two diagnostic groups, one with IRDS, the other with mixed neonatal disorders. Factor V, fibrinogen and fibrin/fibrinogen degradation products (FDP) were abnormal more often than any of the other factors examined. The presence or absence of "multiple defects" appeared to depend on the severity of the illness and its ultimate course. Thus 28% of the surviving infants or 85% of those who died had "multiple defects". The pattern of abnormalities did not differ between the infants with IRDS and those with mixed disorders. The "multiple defects" are ascribed to the following mechanisms: (1) impaired synthesis due to vitamin K deficiency and/or liver damage, (2) abnormal proteolytic activity stimulated by tissue damage and causing (a) an activation of the coagulation process (b) activation of the fibrinolytic system, or (c) of both the coagulation and the fibrinolytic systems. Differentiation between these pathways to defective haemostasis are important when deciding upon therapeutic measures in addition to the basic treatment.

Cytarabine treatment of herpes simplex encephalitis in infants and small children. A report on three cases with a short review of the literature.

Three cytarabine-treated infants and children with herpes simplex encephalitis are presented. The effect of the treatment was excellent in 2 cases. One boy who had a CP syndrome died. It is assumed that the treatment with cytarabine should be started as early as possible with a dosage of 3 mg/kg body weight given intravenously once a day in a single injection for 5 days. No serious side effects have been noted. The advantage of cytarabine over idoxuridine, especially when treating small children and herpetic infections in the central nervous system, are emphasized.