Placental Transfer of Vitamin K1 and Its Implications in Fetal Hemostasis

1988 ◽  
Vol 60 (01) ◽  
pp. 039-043 ◽  
Author(s):  
L Mandelbrot ◽  
M Guillaumont ◽  
M Leclercq ◽  
J J Lefrère ◽  
D Gozin ◽  
...  

SummaryVitamin K status was evaluated using coagulation studies and/ or vitamin IQ assays in a total of 53 normal fetuses and 47 neonates. Second trimester fetal blood samples were obtained for prenatal diagnosis under ultrasound guidance. Endogenous vitamin K1 concentrations (determined by high performance liquid chromatography) were substantially lower than maternal levels. The mean maternal-fetal gradient was 14-fold at mid trimester and 18-fold at birth. Despite low vitamin K levels, descarboxy prothrombin, detected by a staphylocoagulase assay, was elevated in only a single fetus and a single neonate.After maternal oral supplementation with vitamin K1, cord vitamin K1 levels were boosted 30-fold at mid trimester and 60 fold at term, demonstrating placental transfer. However, these levels were substantially lower than corresponding supplemented maternal levels. Despite elevated vitamin K1 concentrations, supplemented fetuses and neonates showed no increase in total or coagulant prothrombin activity. These results suggest that the low prothrombin levels found during intrauterine life are not due to vitamin K deficiency.

Nutrients ◽  
2020 ◽  
Vol 12 (3) ◽  
pp. 780
Author(s):  
Shunsuke Araki ◽  
Akira Shirahata

Vitamin K is essential for the synthesis of few coagulation factors. Infants can easily develop vitamin K deficiency owing to poor placental transfer, low vitamin K content in breast milk, and poor intestinal absorption due to immature gut flora and malabsorption. Vitamin K deficiency bleeding (VKDB) in infancy is classified according to the time of presentation: early (within 24 h), classic (within 1 week after birth), and late (between 2 week and 6 months of age). VKDB in infancy, particularly late-onset VKDB, can be life-threatening. Therefore, all infants, including newborn infants, should receive vitamin K prophylaxis. Exclusive breastfeeding and cholestasis are closely associated with this deficiency and result in late-onset VKDB. Intramuscular prophylactic injections reduce the incidence of early-onset, classic, and late-onset VKDB. However, the prophylaxis strategy has recently been inclined toward oral administration because it is easier, safer, and cheaper to administer than intramuscular injection. Several epidemiological studies have shown that vitamin K oral administration is effective in the prevention of VKDB in infancy; however, the success of oral prophylaxis depends on the protocol regimen and parent compliance. Further national surveillance and studies are warranted to reveal the optimal prophylaxis regimen in term and preterm infants.


1993 ◽  
Vol 16 (3) ◽  
pp. 301-305 ◽  
Author(s):  
E. A. M. Cornelissen ◽  
L. A. A. Kollée ◽  
T. G. P. J. van Lith ◽  
K. Motohara ◽  
L. A. H. Monnens

2017 ◽  
Vol 31 (5) ◽  
pp. 495-505 ◽  
Author(s):  
Yan-ni Mi ◽  
Na-na Ping ◽  
Bo Li ◽  
Xue Xiao ◽  
Yan-bing Zhu ◽  
...  

Nutrients ◽  
2020 ◽  
Vol 12 (9) ◽  
pp. 2513
Author(s):  
Signe Wikstrøm ◽  
Katrine Aagaard Lentz ◽  
Ditte Hansen ◽  
Lars Melholt Rasmussen ◽  
Jette Jakobsen ◽  
...  

Background: A low vitamin K status is common in patients on haemodialysis, and this is considered one of the reasons for the accelerated atherosclerosis in these patients. The vitamin is essential in activation of the protein Matrix Gla Protein (MGP), and the inactive form, dp-ucMGP, is used to measure vitamin K status. The purpose of this study was to investigate possible underlying causes of low vitamin K status, which could potentially be low intake, washout during dialysis or inhibited absorption capacity. Moreover, the aim was to investigate whether the biomarker dp-ucMGP is affected in these patients. Method: Vitamin K intake was assessed by a Food Frequency Questionnaire (FFQ) and absorption capacity by means of D-xylose testing. dp-ucMGP was measured in plasma before and after dialysis, and phylloquinine (vitamin K1) and dp-ucMGP were measured in the dialysate. Changes in dp-ucMGP were measured after 14 days of protein supplementation. Results: All patients had plasma dp-ucMGP above 750 pmol/L, and a low intake of vitamin K. The absorption capacity was normal. The difference in dp-ucMGP before and after dialysis was −1022 pmol/L (p < 0.001). Vitamin K1 was not present in the dialysate but dp-ucMGP was at a high concentration. The change in dp-ucMGP before and after protein supplementation was −165 pmol/L (p = 0.06). Conclusion: All patients had vitamin K deficiency. The reason for the low vitamin K status is not due to removal of vitamin K during dialysis or decreased absorption but is plausibly due to a low intake of vitamin K in food. dp-ucMGP is washed out during dialysis, but not affected by protein intake to a clinically relevant degree.


2017 ◽  
Vol 145 (5-6) ◽  
pp. 254-258 ◽  
Author(s):  
Jelena Martic ◽  
Katarina Pejic ◽  
Dobrila Veljkovic ◽  
Zorica Rakonjac ◽  
Milos Kuzmanovic ◽  
...  

Introduction/Objective. Vitamin K deficiency is common in newborn infants and without prophylaxis there is a risk of vitamin K deficiency bleeding (VKDB). The most frequent prophylactic approach is an intramuscular (IM) injection of vitamin K1 immediately after birth. Its efficiency to prevent late VKDB has been recently questioned by several reports. Based on our experience, we discuss the need for additional vitamin K1 supplementation after its IM administration at birth. Methods. We present a retrospective review of 12 infants, 11 with confirmed and one with probable late VKDB despite IM prophylaxis at birth, who were treated in the two largest tertiary care pediatric hospitals in Serbia during the last 15 years. Results. All the patients were exclusively breastfed. In 11 patients, daily weight gain was normal or increased, and one patient had failure to gain weight. Six infants were previously healthy, three infants received antibiotics prior to bleeding, and in two diarrhea and cholestasis, respectively, existed previously. An intracranial bleeding was documented in nine infants, four of whom died. Conclusion. Low content of phytomenadione in human milk could occasionally be attributed to late VKDB despite postnatal IM injection of vitamin K1 in otherwise healthy, exclusively breastfed infants. This might be aggravated by transient disturbance of vitamin K turnover due to antibiotic use, acute diarrhea, or transient cholestasis. We suggest that an additional vitamin K1 supplementation after postnatal IM prophylaxis could be justified in exclusively breastfed infants.


PEDIATRICS ◽  
1969 ◽  
Vol 44 (5) ◽  
pp. 745-749
Author(s):  
Herbert I. Goldman ◽  
Peter Amadio

Sixty infants, 1 to 18 months of age, with diarrhea, were treated with a skimmed milk diet and succinylfathiazole. Thirty received supplemental vitamin K1 and had oral vitamin K intakes, expressed as K1 activity, of 16.1 to 36.3 µg/kg/day. Hypoprothrombinemia was not observed. Thirty did not receive supplementation and had intakes, similarly expressed, of 9.2 to 29.5 µg/kg/day. A single episode of hypoprothrombinemia was recorded on an intake of 9.8 µg/kg/day. In a group of 15 infants with clinical bleeding episodes due to vitamin K deficiency, the oral vitamin K intakes, expressed as K1 activity, were 0.0 to 8.4 µg/kg/day. These data suggest that, in infants who have diarrhea and/or are receiving antimicrobials, there exists a risk of vitamin K deficiency if the dietary intake contains less than the approximate equivalent of 10 µg/kg/day of vitamin K1 activity.


1987 ◽  
Author(s):  
R V Kries ◽  
M J Shearer ◽  
P T McCarthy ◽  
M Haug ◽  
C Harzer

Fatal vitamin K deficiency haemorrhage has been observed in breast fed babies. Though the incidence of vitamin K deficiency haemorrhage seems to be low in exclusively breastfed babies in Germany, subclinical vitamin K deficiency is by far more common as demonstrated in recent studies. Vitamin K concentrations in human milk are lower than in cow's milk and infant formula, however, nothing is known about the factors determinating the vitamin K1 concentrations in human milk. Vitamin K1 concentrations in human milk were studied during the first five weeks of lactation with respect to a) stage of lactation, b) interindividual differences, c) relationship of vitamin K1 to other lipids, and d) influence of oral supplements of vitamin K1 given to the mother. Milk samples from 9 mothers were collected on day 1,3,5,22,29 and 36 of lactation using standarized techniques.a) Vitamin K1 concentrations in colostral milk, day 1-5 (median 1,8 ng/ml) were significanctly higher than in mature milk, day 22-36 (median 1,1 ng/ml) (Wilcoxon U-Test p< 0,01). These changes during the course of lactation must be considered for estimation of the vitamin K supply in breastfed babies.b) Vitamin K concentrations both for colostral and mature milk were found to vary widely: colostral milk 0,6-4,4 ng/ml, mature milk 0,4 - 2,8 ng/ml.c) For colostral milk regression analyses revealed good correlations of vitamin K1 to cholesterol but none to total lipid and phospholipids, whereas no correlation to either lipid was observed for mature milk. Cholesterol appears to have a role in vitamin K1 secretion into colostral milk.d) Vitamin K1 concentrations of maternal milk were influenced by oral supplements given to the mother. Even with a dose of 100 μ vitamin K1 (similar to the dose which may be ingested with a meal) a twofold increase of the vitamin K1. content of breast milk was observed. These data suggest that mutritional factors may influence the vitamin concentration in human milk. Vitamin K supplements for breastfeeding mothers on vitamin K1 poor diets could improve the vitamin K supply of these babies.


Author(s):  
Dina Simes ◽  
Carla Viegas ◽  
Nuna Araújo ◽  
Catarina Marreiros

Abstract Vitamin K has been recognized as a key factor for the synthesis of blood clotting factors in the liver, and is currently known to be involved in a wide range of biological processes and is associated with many pathological conditions.The most well-known function of vitamin K is as a cofactor for the &gamma;-glutamyl carboxylase (GGCX) enzyme responsible for the post-translational modification of vitamin K-dependent proteins (VKDPs) through the conversion of specific glutamic acid (Glu) into calcium binding &gamma;-carboxyglutamic acid (Gla) residues. Vitamin K deficiency has been linked to several pathological conditions such as cardiovascular diseases (CVD), chronic kidney disease (CKD), osteoarthritis (OA) , rheumatoid arthritis (RA), osteoporosis, cancer, dementia, certain skin pathologies, functional decline, and disability.&nbsp; A new concept on the involvement of vitamin K in inflammation is growing. In fact, novel roles have been disclosed for vitamin K independent of its activity as a cofactor for GGCX, such as an antioxidant, anti-inflammatory, promoter of cognition, inhibition of tumor progression, and transcriptional regulator of osteoblastic genes. A growing number of studies has raised an increasing interest on the use of vitamin K as a health promoting supplement.&nbsp; Aging societies represent a major economic challenge for health care systems, and diet supplements promoting healthy aging and improving the prognosis of age-related diseases, are required to be implemented in clinical practice.This work thoroughly reviews available data regarding differences between vitamin K1 and K2, contextualized with clinical aspects of vitamin K deficiency, including their sources, functions, target activity, and involvement in age-related diseases. Processes for the chemical and biological production of vitamin K1 and K2 will be briefly addressed. Additionally, novel sources with potential biotechnological application, and new formulations to improve vitamin K absorption and bioavailability are presented.


1987 ◽  
Author(s):  
J J Lefrère ◽  
D Gozin ◽  
J P Soulier ◽  
P Mavier ◽  
L Bettan ◽  
...  

An elevation of des-gamma-carboxyprothrombin (DCP) has been observed in about 70 % of cases of hepatocellular carcinoma (HCC). Howewer, an increased DCP is not specific of HCC. Oral anticoagulant therapy increases the DCP level by preventing the gamma-carboxylation of prothrombin : thereafter an increased DCP can not be used as an HCC marker before three weeks have elapsed after stopping anti vitamin K therapy. Furthermore, since vitamin K is necessary for the gamma-carboxylation of vitamin K dependent factors, a vitamin K deficiency increases the DCP level long before the modification of the prothrombin time. It is thus imperative to eliminate an underlying vitamin K deficiency before attributing an increased DCP to a HCC. We used a method of DCP assay using staphylocoagulase. We studied the effect of an intravenous injection of 20 mg of vitamin K1 on DCP level in 7 patients with histologically proven HCC and in 10 patients with various disorders (5 alcoholic cirrhosis, 1 chronic hepatitis, 4 pancreatic cancer). All these 17 patients had increased DCP before vitamin K injection. In a second sampling obtained 15 days or more after injection, only the 7 patients with HCC kept increased DCP level. In patients of both categories in whom we obtained intermediary samplings, we observed that the DCP level decreased In all cases. The normalisation of the DCP level was lasting only in those patients without HCC, confirming the hypothesis of an underlying vitamin K deficiency ; this decrease was very transitory in those patients with HCC, suggesting that the elevated DCP came from a yet unexplained (but not linked to a vitamin K deficiency) mechanism. We may conclude that an increased DCP level 15 days after vitamin K injection may constitute a specific marker of HCC.


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