scholarly journals Vitamin K deficiency under enteral feeding: real or imagined threat

2021 ◽  
Vol 4 (4) ◽  
pp. 01-04
Author(s):  
Jochanan E. Naschitz ◽  
Natalia Zaigraykin ◽  
Elena Zlotover ◽  
Faisal Neime

Patients receiving enteral feeding may develop vitamin K deficiency if the nutrition formula does not meet their daily vitamin K requirement. Vitamin K is essential for clotting factors II, VII, IX and X to be released in their functional form. Under vitamin K deficiency a coagulopathy may develop which is marked by prolongation of the prothrombin time (PT). There might be a need, unrecognized to-day, for monitoring the PT in patients receiving enteral feeding to unmask a latent coagulopathy. We assessed the prevalence of a prolonged PT in patients receiving enteral feeding for 3 months of more with one or a combination of the enteral formulas Osmolite®, Jevity®, Easymilk®. Twenty-three residents in long-term hospital care received solely enteral feeding for an average of 37 months, SD 21 months. The median daily vitamin K supplied by enteral feeding was 96.8 mcg (average 103.3 mcg, SD 28.8); this does not satisfy the 150 mcg of vitamin K required by the Food and Drug Administration. In 21 patients the PT-INR was 1-1.2 (normal). The PT was prolonged in two patients. In one of the latter, prolongation of PT-INR was not confirmed two days later. In the second case, the patient having repeatedly a PT-INR 1.4 (and a normal APTT), administration of vitamin K did not correct the PT. In conclusion, long-term vitamin K-deficient nutrition did not affect the vitamin K-dependent coagulation. This data may argue against the supposed need to monitor the PT in patients receiving long-term enteral nutrition.

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.


2018 ◽  
Vol 45 (2) ◽  
pp. 461-465 ◽  
Author(s):  
Genichiro Sotodate ◽  
Atsushi Matsumoto ◽  
Yu Konishi ◽  
Yukiko Toya ◽  
Mikiya Endo ◽  
...  

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.


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.


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.


2015 ◽  
Vol 2015 ◽  
pp. 1-3 ◽  
Author(s):  
Andrew S. Lane ◽  
Jennifer L. Stallworth ◽  
Kacey Y. Eichelberger ◽  
Kenneth F. Trofatter

A 21-year-old primigravida had a pregnancy complicated by hyperemesis gravidarum (HG) beginning at 7-week gestation. Despite medical therapy, she lost 18% of her prepregnancy weight. Early ultrasound at 14 weeks demonstrated a flattened facial profile with nasal hypoplasia (Binder phenotype) consistent with vitamin K deficiency from HG. She had a percutaneous endoscopic gastrojejunostomy tube placed for enteral feeding at 15-week gestation. At repeated anatomy ultrasound at 21-week gestation, delivery, and postnatal pediatric genetics exam, nasal hypoplasia was consistent with vitamin K deficiency embryopathy from HG. Nausea and vomiting of pregnancy is a common condition. HG, the most severe form, has many maternal and fetal effects. Evaluation of vitamin K status could potentially prevent this rare and disfiguring embryopathy.


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 γ-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 γ-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.  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.  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.


Sign in / Sign up

Export Citation Format

Share Document