W13.333 Expression of LRP1 by human osteoblast-like cells: A mechanism for the delivery of dietary vitamin K to bone

2004 ◽  
Vol 5 (1) ◽  
pp. 77
Author(s):  
A NIEMEIER
2004 ◽  
Vol 5 (1) ◽  
pp. 77
Author(s):  
A. Niemeier ◽  
M. Kassem ◽  
U. Beisiegel ◽  
W. Ruether ◽  
J. Heeren

1997 ◽  
Vol 77 (03) ◽  
pp. 504-509 ◽  
Author(s):  
Sarah L Booth ◽  
Jacqueline M Charnley ◽  
James A Sadowski ◽  
Edward Saltzman ◽  
Edwin G Bovill ◽  
...  

SummaryCase reports cited in Medline or Biological Abstracts (1966-1996) were reviewed to evaluate the impact of vitamin K1 dietary intake on the stability of anticoagulant control in patients using coumarin derivatives. Reported nutrient-drug interactions cannot always be explained by the vitamin K1 content of the food items. However, metabolic data indicate that a consistent dietary intake of vitamin K is important to attain a daily equilibrium in vitamin K status. We report a diet that provides a stable intake of vitamin K1, equivalent to the current U.S. Recommended Dietary Allowance, using food composition data derived from high-performance liquid chromatography. Inconsistencies in the published literature indicate that prospective clinical studies should be undertaken to clarify the putative dietary vitamin K1-coumarin interaction. The dietary guidelines reported here may be used in such studies.


2019 ◽  
Vol 25 (19) ◽  
pp. 2149-2157 ◽  
Author(s):  
Massimo Lamperti ◽  
Andrey Khozenko ◽  
Arun Kumar

There is an increased use of oral anticoagulants for the prevention of venous and arterial thrombosis. Vitamin-K antagonists have been used for decades as the main oral anticoagulants but they have the draback a complex therapeutic management, slow onset of action and by a different oral intake caused by dietary vitamin K intake. New non-vitamin K antagonist oral anticoagulants (NOACs) have been developed to overcome the limitations of warfarin. Their management is easier as it requires a fixed daily dose without coagulation monitoring. Although their therapeutic profile is safe, proper attention should be paid in case of unexpected need for the reversal of their coagulation effect and in case a patient needs to have a scheduled surgery. For non-acute cardiac surgery, discontinuation of NOACs should start at least 48 hours prior surgery. Intracranial bleedings associated with NOACs are less dangerous comparing to those warfarin-induced. NOACs need to be stopped ≥24 hours in case of elective surgery for low bleeding-risk procedures and ≥48 hours for high bleeding-risk surgery in patients with normal renal function and 72 hours in case of reduced CrCl < 80. The therapy with NOACs should be resumed from 48 to 72 hours after the procedure depending on the perceived bleeding, type of surgery and thrombotic risks. There are some available NOAC reversal agents acting within 5 to 20 minutes. In case of lack of reversal agent, adequate diuresis, renal replacement therapy and activated charcoal in case of recent ingestion should be considered.


2004 ◽  
Vol 124 (3) ◽  
pp. 348-354 ◽  
Author(s):  
T. Khan ◽  
H. Wynne ◽  
P. Wood ◽  
A. Torrance ◽  
C. Hankey ◽  
...  

PEDIATRICS ◽  
1970 ◽  
Vol 45 (5) ◽  
pp. 892-892
Author(s):  
Herbert I. Goldman

Dr. Goldman commented as follows: The letter of Drs. Burgio and Vaccaro presents additional evidence that dietary vitamin K deficiency may occur during the course of diarrhea and/or the use of antimicrobials. We are continuing to study this matter in an attempt to define the vitamin K requirement under these circumstances.


2008 ◽  
Vol 22 (S1) ◽  
Author(s):  
Nancy Presse ◽  
Bryna Shatenstein ◽  
Marie‐Jeanne Kergoat ◽  
Guylaine Ferland

BMJ Open ◽  
2020 ◽  
Vol 10 (5) ◽  
pp. e035953
Author(s):  
Teresa R Haugsgjerd ◽  
Grace M Egeland ◽  
Ottar K Nygård ◽  
Kathrine J Vinknes ◽  
Gerhard Sulo ◽  
...  

ObjectiveThe role of vitamin K in the regulation of vascular calcification is established. However, the association of dietary vitamins K1 and K2 with risk of coronary heart disease (CHD) is inconclusive.DesignProspective cohort study.SettingWe followed participants in the community-based Hordaland Health Study from 1997 - 1999 through 2009 to evaluate associations between intake of vitamin K and incident (new onset) CHD. Baseline diet was assessed by a past-year food frequency questionnaire. Energy-adjusted residuals of vitamin K1 and vitamin K2 intakes were categorised into quartiles.Participants2987 Norwegian men and women, age 46–49 years.MethodsInformation on incident CHD events was obtained from the nationwide Cardiovascular Disease in Norway (CVDNOR) Project. Multivariable Cox regression estimated HRs and 95% CIs with test for linear trends across quartiles. Analyses were adjusted for age, sex, total energy intake, physical activity, smoking and education. A third model further adjusted K1 intake for energy-adjusted fibre and folate, while K2 intake was adjusted for energy-adjusted saturated fatty acids and calcium.ResultsDuring a median follow-up time of 11 years, we documented 112 incident CHD cases. In the adjusted analyses, there was no association between intake of vitamin K1 and CHD (HRQ4vsQ1 = 0.92 (95% CI 0.54 to 1.57), p for trend 0.64), while there was a lower risk of CHD associated with higher intake of energy-adjusted vitamin K2 (HRQ4vsQ1 = 0.52 (0.29 to 0.94), p for trend 0.03). Further adjustment for potential dietary confounders did not materially change the association for K1, while the association for K2 was slightly attenuated (HRQ4vsQ1 = 0.58 (0.28 to 1.19)).ConclusionsA higher intake of vitamin K2 was associated with lower risk of CHD, while there was no association between intake of vitamin K1 and CHD.Trial registration numberNCT03013725


Nutrients ◽  
2020 ◽  
Vol 12 (6) ◽  
pp. 1772
Author(s):  
Renata Mozrzymas ◽  
Dariusz Walkowiak ◽  
Sławomira Drzymała-Czyż ◽  
Patrycja Krzyżanowska-Jankowska ◽  
Monika Duś-Żuchowska ◽  
...  

This is the first study to evaluate vitamin K status in relation to dietary intake and phenylalanine dietary compliance in patients with phenylketonuria (PKU). The dietary and PKU formula intake of vitamin K was calculated in 34 PKU patients, with vitamin K status determined by the measurement of prothrombin induced by vitamin K absence (PIVKA-II). Blood phenylalanine concentrations in the preceding 12 months were considered. There were significantly more phenylalanine results exceeding 6 mg/dL in patients with normal PIVKA-II concentrations than in those with abnormal PIVKA-II levels (p = 0.035). Similarly, a higher total intake of vitamin K and dietary vitamin intake expressed as μg/day (p = 0.033 for both) and %RDA (p = 0.0002 and p = 0.003, respectively) was observed in patients with normal PIVKA-II levels. Abnormal PIVKA-II concentrations were associated with a lower OR (0.1607; 95%CI: 0.0273–0.9445, p = 0.043) of having a median phenylalanine concentration higher than 6 mg/dL. In conclusion, vitamin K deficiency is not uncommon in phenylketonuria and may also occur in patients with adequate vitamin K intake. PKU patients with better dietary compliance have a higher risk of vitamin K deficiency. The present findings highlight the need for further studies to re-evaluate dietary recommendations regarding vitamin K intake, both concerning formula-based and dietary consumption of natural products.


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