Evidence against Vitamin K Deficiency in Normal Neonates

1980 ◽  
Vol 44 (03) ◽  
pp. 159-160 ◽  
Author(s):  
R G Malia ◽  
F E Preston ◽  
V E Mitchell

SummaryUmbilical cord plasmas from 24 normal full-term neonates were studied. We confirmed the prolonged prothrombin time and low levels of Vitamin K dependent clotting factors previously described (1), but using a number of recently developed immunological and coagulation techniques we could find no evidence of vitamin K deficiency. We conclude that the decreased levels of vitamin K dependent clotting factors of normal neonates are the result of decreased synthesis by the immature liver and that it is questionable whether vitamin K prophylaxis is necessary for these infants.

PEDIATRICS ◽  
1970 ◽  
Vol 45 (5) ◽  
pp. 857-861
Author(s):  
Ordean L. Torstenson ◽  
G. Bennett Humphrey ◽  
J. Roger Edson ◽  
Warren J. Warwick

Three patients are discussed who presented with hemorrhagic diatheses who were subsequently diagnosed as having cystic fibrosis. Their prolonged prothrombin times and low levels of vitamin K-dependent clotting factors were due to vitamin K deficiency. In two patients we believe that the vitamin K deficiency was principally due to malabsorption caused by cystic fibrosis. In the third patient, malabsorption, diarrhea, antibiotic therapy, and low dietary intake all played a part in the development of vitamin K deficiency. Cystic fibrosis should be included in the differential diagnosis of patients under 1 year of age presenting with a bleeding tendency.


1968 ◽  
Vol 20 (01/02) ◽  
pp. 078-087 ◽  
Author(s):  
H. C Hemker ◽  
A. D Muller

SummaryPIVKA, the circulating anticoagulant protein found in vitamin K deficiency can, on kinetical grounds, be recognized as an analogue of factor X. The existence of analogues of other vitamin K-dependent clotting factors cannot be ruled out, but need not be assumed to explain the experimental results.


PEDIATRICS ◽  
1984 ◽  
Vol 73 (5) ◽  
pp. 712-716
Author(s):  
Nathaniel R. Payne ◽  
Duane K. Hasegawa

A 4-week-old, breast-fed female infant appeared healthy until signs and symptoms of CNS deterioration suddenly occurred. At presentation the infant was found to have a left-sided parietal intracerebral hematoma, markedly prolonged prothrombin time, and partial thromboplastin time, normal platelet count, and jaundice with a total and direct serum bilirubin level of 5.4 mg/dL and 2.6 mg/dL, respectively. Vitamin K1 and fresh frozen plasma returned the prothrombin time and partial thromboplastin time to normal values within 18 hours, suggesting that the infant had severe vitamin K deficiency complicated by intracerebral hemorrhage. Evaluation of the infant's direct hyperbilirubinemia led to the diagnosis of homozygous (pi-type ZZ [PiZZ]) α-1-antitrypsin deficiency. The clinical circumstances predisposing to vitamin K deficiency in newborns and infants are discussed. Based on our observations in this case, we suggest that cholestatic liver disease should be suspected when unexplained vitamin K deficiency occurs in early infancy. The role of vitamin K in hemostasis and the laboratory diagnosis of vitamin K deficiency are discussed as they apply to the evaluation of hemorrhage in newborns and infants.


2011 ◽  
Vol 7 (3) ◽  
pp. 295-299 ◽  
Author(s):  
Ashraf Shaker Zidan ◽  
Hesham Abdel-Hady

Object Although the incidence of vitamin K deficiency bleeding (VKDB) in neonates has dramatically decreased in the developed world since the adoption of routine vitamin K prophylaxis, in developing countries the incidence is still high. Intracranial hemorrhage (ICH) is the most dangerous complication. Early recognition and management are important to decrease the mortality rate and neurological sequelae. The authors conducted a prospective study between January 2008 and June 2010. They included all full-term neonates referred to the Department of Neurosurgery at Mansoura University Children's Hospital with ICH complicating VKDB and necessitating surgical evacuation. The objective was to evaluate the clinical presentation, diagnosis, hospital course, and outcome of ICH in full-term neonates with VKDB after surgical evacuation. Methods Thirty-two neonates with ICH due to VKDB were included. Diagnosis and classification of ICH were based on detailed history, physical examination, and the interpretation of CT or MR imaging studies. The diagnosis of VKDB was based on pretreatment coagulation studies (prothrombin time [PT] and partial thromboplastin time [PTT]), which are grossly abnormal, together with a normal platelet count and correction of coagulation results to normal after vitamin K administration. Results The mean age (± SD) at onset of symptoms was 20.4 ± 4.9 days. Two neonates (6.25%) had early VKDB, 7 (21.9%) had classic VKDB, and 23 (71.9%) had late VKDB. The most common neurological manifestations included focal seizures, disturbed consciousness level, and tense anterior fontanel. The most common general manifestations included pallor, respiratory distress, and bleeding from other sites. Radiological findings varied from acute subdural hemorrhage (SDH) in 18 cases (56.3%), intracerebral hemorrhage in 10 (31.3%), and acute SDH with underlying intracerebral hemorrhage, intraventricular hemorrhage, and/or subarachnoid hemorrhage in 4 (12.5%). Before administration of vitamin K, the PT was 72.1 ± 45.0 seconds and the PTT was 112.4 ± 57.6 seconds. Six to 12 hours after administration of vitamin K, the PT was 14.6 ± 1.6 seconds and the PTT was 34.4 ± 1.0 seconds. All patients underwent surgery for evacuation of the ICH after correction of PT, prothrombin activity, and international normalized ratio. Evacuation of the ICH was done by either free or osteoblastic bone flap. Six patients (18.8%) died, and the other 26 patients had variable degrees of morbidity during the follow-up period (3–24 months). Conclusions Vitamin K deficiency bleeding, especially the late-onset form, is an important cause of neonatal ICH. In the present study, the most frequent form of ICH in neonates was SDH. Focal seizures, disturbed consciousness level, tense anterior fontanel, unexplained anemia, and respiratory distress were the major presenting signs. Despite early surgical evacuation, these cases are associated with high mortality rate and neurological disabilities. Vitamin K prophylaxis at birth may reduce these severe complications.


Author(s):  
Sir Peter Gluckman ◽  
Mark Hanson ◽  
Chong Yap Seng ◽  
Anne Bardsley

Vitamin K is involved in blood clotting, and lack of this nutrient results in a hypocoagulable state, associated with a high risk of bleeding events. Deficiency is rare among adults, because vitamin K is widely available in foods. However, the placenta transmits vitamin K relatively poorly, leading to a general deficiency in full-term neonates, who are also particularly vulnerable to the effects of low vitamin K levels because of their immature clotting systems. Deficiency can lead to intracranial haemorrhage following birth trauma, or classic vitamin K deficiency bleeding. It is important to maintain adequate vitamin K status throughout pregnancy in order to avoid added risk to the neonate at birth and in the first few weeks of life. Supplementation of newborns by intramuscular injection should be universal.


2003 ◽  
Vol 22 (11) ◽  
pp. 617-621 ◽  
Author(s):  
C Payen ◽  
A Dachraoui ◽  
C Pulce ◽  
J Descotes

The association between paracetamol overdose and prolonged prothrombin time due to hepatic failure is well recognized. However, little is known of the possibility that paracetamol overdose can prolong the prothrombin time without overt hepatic failure. The few data from the literature suggest this is either due to a reduction in the functional levels of the vitamin K-dependent clotting factors by elevated doses of paracetamol, or a consequence of the administration of the antidote N-acetylcystein. The three reported cases provide further evidence that paracetamol overdose can be associated with a prolongation in the prothrombin time without overt hepatic failure. Even though the prothrombin time provides useful prognosis information, decisions regarding the management of these patients should not solely be based on this endpoint to avoid misinterpretation of the accuracy and the severity of liver failure.


1980 ◽  
Vol 43 (01) ◽  
pp. 016-019 ◽  
Author(s):  
M G Mazzucconi ◽  
R M Bertina ◽  
D Romoli ◽  
M Orlando ◽  
G Avvisati ◽  
...  

SummaryTwenty three patients belonging to 18 different pedigrees of Haemophilia B were studied with regard to ox-brain prothrombin time and its correlation to factor VII.Eleven among them were B-negative (no detectable factor IX antigen), five were B-reduced (factor IX antigen detectable but below the normal values) and seven were B-positive (normal levels of factor IX antigen).Ox-brain prothrombin time was found prolonged (≥ x̄ + 2.5 SD:99% confidence limits) in nine patients. Factor VII Activity (VII: C) was found reduced in 1/11 B-negative, in 2/5 B-reduced and in 4/7 B-positive patients. Factor VII Antigen (VII: Ag) was found normal in all but one patient.The ratio VII:C/VII:Ag was abnormal in eight patients independently from the variant of Haemophilia B. The underlying defect which causes the prolongation of Ox-brain prothrombin time due to factor VII: C mild deficiency is heterogeneous. Age, a mild Vitamin K deficiency, the presence of an inhibitor of Factor VII activation and other unknown causes, may be responsible for this pattern.


1993 ◽  
Vol 69 (04) ◽  
pp. 328-330
Author(s):  
D V Shah ◽  
J A Engelke ◽  
J W Suttie

SummaryBased on studies in intact animals, the presence of humoral factors, “coagulopoietins”, which regulate the synthesis of vitamin K-dependent plasma proteins has been proposed. These proposed factors are produced in response to vitamin K deficiency, coumarin treatment, or specific antibody depletion of vitamin K-dependent clotting factors. The production of pro-thrombin by rat hepatoma H4IIEC3 cells has now been shown to be dependent on the source of bovine serum in the media. Cells grown in serum from cows treated with dicoumarol produce about 20% more prothrombin in 24 h than those cells grown in control serum. The humoral factor causing this response is present early in the course of dicoumarol treatment, and the increase in prothrombin production is dependent on the amount of serum from a dicoumarol-treated cow in the media. Based on membrane filtration studies, the factor appears to be associated with the protein fraction of serum.


1968 ◽  
Vol 19 (03/04) ◽  
pp. 346-363 ◽  
Author(s):  
H. C Hemker ◽  
J. J Veltkamp ◽  
E. A Loeliger

SummaryApplication of enzyme kinetics to the results of thrombotest estimations in correlation with specific clotting factor estimations has led to the recognition of a protein moiety that occurs in plasma in vitamin K deficiency and acts as a competitive inhibitor of thrombin formation. A hypothesis is given by which the occurrence of this inhibitor is explained in terms of a biphasic synthesis of the vitamin K-dependent clotting factors.


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