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PubMed1991

Seasonal incidence of subclinical vitamin K deficiency during early newborn period.

Eleven-Sixty six healthy, non-vitamin K treated and exclusively breast-fed 5-day-old newborns were screened with PIVKA-II and Hepaplastin test for subclinical vitamin K deficiency for two years. PIVKA-II values in 96 babies (8.2%) ranged from 1 to 8 micrograms/ml. These babies were divided into two groups: 83 (86.5%) had relatively low values ranging from 1 to 2 micrograms/ml, and 13 (13.5%) had higher values ranging from 2 to 8 micrograms/ml. Eleven babies in the latter group (84.6%) had a seasonal deviation in incidence in the summer and early fall (p less than 0.05). This seasonal variation in severe subclinical vitamin K deficiency during the early newborn period corresponds with the results of an epidemical survey of idiopathic late onset hemorrhagic disease in newborns in Japan, suggesting similar causative factors in both of these hemorrhagic diseases.

Biomarkers↗
PubMed1999

Effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin or 2,2',4,4',5,5'-hexachlorobiphenyl on vitamin K-dependent blood coagulation in male and female WAG/Rij-rats.

Newborns are susceptible to hemorrhages (hemorrhagic disease of the newborn or HDN) due to vitamin K deficiency. Induction of cytochrome P450 in the fetal liver by maternal anticonvulsant therapy such as phenobarbital or phenytoin is considered to be a major cause. An observed increase in late hemorrhagic disease (LHD) in breast fed neonates gave rise to the hypothesis that PCBs and dioxins, P450-inducing contaminants present in human milk, might effect vitamin K-dependent blood coagulation. This hypothesis was studied in rats. Administration of a single oral dose of 0.003, 0.03, 0.3, 3 or 30 nmol 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) per kg bodyweight or 0.75, 4, 20, 100 or 500 micromol 2,2',4,4',5,5'-hexachlorobiphenyl/kg bw (HxCB) to female and male rats resulted in dose-related reductions of the vitamin K-dependent coagulation factor VII. The highest factor VII reduction in female rats was 44%, observed after TCDD exposure. The Lowest Observed Adverse Effect Level (LOAEL) of TCDD on female factor VII levels was 0.3 nmol/kg bw (96 ng/kg). There was a significant inverse correlation between Factor VII levels and induction of hepatic ethoxyresorufin O-deethylating (EROD) activity, reflecting CYP1A1, and total P450 content. HxCB had no effect on female coagulation factors. In contrast, in male rats only exposure to HxCB, which induces mainly CYP2B1 and 2B2, decreased both coagulation factors dramatically up to 88%. The LOAEL of HxCB on factor VII in male rats was 100 micromol/kg bw (36 mg/kg). In general, effects on coagulation factors in male rats exceeded those in females. In addition, sex-dependent differences of TCDD and HxCB were observed on the hepatic vitamin K cycle enzyme activities in female and male rats. Vitamin K-dependent (gamma-glutamyl carboxylase activity was mainly induced in female rats; 2.3-fold in the highest dose group of TCDD. In male rats only vitamin K 2,3-epoxide reductase (KO-reductase) activity was induced 1.7-fold by the highest dose of HxCB. KO-reductase activity in female rats was also increased by TCDD, however, less pronounced than the carboxylase activity. Concluding, the hepatic vitamin K cycle still functions and is not blocked by TCDD or HxCB, thus explaining the observed reduction in factor VII. Finally, the possible role of P450 in vitamin K deficiency is discussed. Based on these results it is suggested to investigate the possible role of PCBs and dioxin-like compounds in LHD in more detail.

Animals↗
PubMed1962

The propagation of the virus of epizootic hemorrhagic disease of deer in newborn mice and HeLa cells.

The New Jersey strain of EHD virus has been propagated in newborn Swiss mice by the intracerebral route and is regularly lethal beyond the first serial mouse passage. A complement-fixing antigen prepared from the brains of infected mice reacts positively with the sera of deer recovered from infection with either the New Jersey or South Dakota strain of virus, but not with the serum of normal deer. The mouse-passaged virus induced an inapparent infection in an experimental deer. The virus can also be grown serially in HeLa cell culture and induces a characteristic cytopathic effect. It is neutralizable in such cultures to high titer by the sera of deer recovered from EHD (New Jersey strain) and to lower titer by the serum of a deer recovered from EHD (South Dakota strain). Normal deer serum does not neutralize the virus in tissue culture. The HeLa cell-passaged virus induced typical lethal EHD in an experimental deer and virus could be recovered from most of the tissues of this animal in HeLa cell culture. An unexplained prozone of inhibition of cytopathogenicity at low dilutions was observed in cultures of some of the organs. The fact that EHD virus exhibited a limited sensitivity to sodium desoxycholate suggests that it may belong in the arbor virus group.

Animals↗
PubMed1994

The vitamin K controversy.

Discussion about the efficacy and safety of vitamin K prophylaxis has recently restarted. In this review, new developments in diagnosis of vitamin K deficiency (including vitamin K plasma levels and protein induced by vitamin K absence [PIVKA]-II detection) and therapy of early, classic, and late hemorrhagic disease of the newborn are highlighted. Special attention is brought to the efficacy of preventing early and late hemorrhagic disease. The recently described association between intramuscular vitamin K administration and cancer is debated. The very high plasma levels, the intramuscular injection itself, or the adjuvants in the solution might all be responsible. These factors are all absent in oral administration. Therefore, we recommend repeated oral administration for preventing classic and late hemorrhagic disease of the newborn. Additionally, we recommend maternal supplementation of vitamin K for preventing early hemorrhagic disease of the newborn, especially when the mother is using medications that interfere with vitamin K metabolism.

Administration, Oral↗
PubMedDate not supplied

[Intra-cranial hemorrhage in infants due to vitamin K deficiency - report of 2 cases]

OBJECTIVE: Drive attention to the late form of the hemorrhagic disease of the newborn, secondary to vitamin K deficiency, as a cause of intracranial hemorrhage in young infants.METHODS: The authors describe and analyze two cases of late hemorrhagic disease of the newborn, secondary to vitamin K deficiency, producing intracranially hemorrhage during the second month of age. The most important publications on this subject are reviewed.RESULTS: Both infants had not received prophylaxis with vitamin K at birth. They were both being fed exclusively on breast milk. They developed intracranial hemorrhage, and the clotting defect was rapidly corrected with intramuscular vitamin K. At 3 and 4 years of age, one of them has showed normal psychomotor development, and the other has showed moderate developmental delay with microcephaly.CONCLUSION: Late hemorrhagic disease of the newborn must be considered in young infants, between 2 and 12 weeks of age, with intracranial hemorrhage, especially those fed exclusively on breast milk who did not receive vitamin K at birth. It may produce neurodevelopmental delay. The clotting defect is rapidly corrected with intramuscular vitamin K. This condition is preventable. The prophylaxis is recommended with 1 mg of intramuscular vitamin K to all newborns, at birth, even without risk factors.

Journal Article↗
PubMedDate not supplied

[Late hemorragic disease of the newborn: case report]

OBJECTIVE: In this study the authors review this subject, and call attention for the late hemorrhagic disease of the newborn, due to the severity and higher risk of mortality and neurological sequelae.METHODS: In this article, four cases of children, age raging from 12 to 21 days, with late hemorrhagic disease associated with vitamin K deficiency were reported. RESULTS: All newborns had multiple hemorrhagic manifestations of the disease. The systems more affected were digestive tract, urinary system, umbilical cord, respiratory system and nervous system.CONCLUSION: Three forms of hemorrhagic disease of newborn have been related with vitamin K deficiency. However, late vitamin K deficiency bleeding is not common and may not be diagnosed by pediatrician. This form of disease can be prevented by vitamin K prophylaxis administration after birth.

Journal Article↗