Vitamin K deficiency
|Vitamin K deficiency|
|Classification and external resources|
Vitamin K1 Deficiency
Vitamin K1-deficiency may occur by disturbed intestinal uptake (such as would occur in a bile duct obstruction), by therapeutic or accidental intake of a vitamin K1-antagonist such as warfarin, or, very rarely, by nutritional vitamin K1 deficiency. As a result, Gla-residues are inadequately formed and the Gla-proteins are insufficiently active.
Symptoms include ecchymosis, petechiae, hematomas, oozing of blood at surgical or puncture sites, stomach pains; risk of massive uncontrolled bleeding; cartilage calcification; and severe malformation of developing bone or deposition of insoluble calcium salts in the walls of arteries.
In infants, it can cause some birth defects such as underdeveloped face, nose, bones, and fingers.
Vitamin K is activated in the liver by epoxide reductase. Activated vitamin K is then used to gamma carboxylate (and thus activate) certain enzymes involved in coagulation: Factors II, VII, IX, X, and proteins C and S. Inability to activate the clotting cascade via these factors leads to the bleeding symptoms mentioned above.
Notably, when one examines the lab values in Vitamin K deficiency [see below] the PT is elevated, but the PTT is normal or only mildly elevated. This may seem counterintuitive given that the deficiency leads to decreased activity in factors of both the intrinsic pathway (F-IX) which is monitored by PTT, as well as the extrinsic pathway (F-VII) which is monitored by PT. However, Factor VII has the shortest half-life of all the factors carboxylated by vitamin K; so therefore, when deficient, it is the PT that rises first, since the activated Factor VII is the first to "disappear." In later stages of deficiency, the other factors (which have longer half lives) are able to "catch up," and the PTT becomes elevated as well.
|Condition||Prothrombin time||Partial thromboplastin time||Bleeding time||Platelet count|
|Vitamin K deficiency or warfarin||Prolonged||Normal or mildly prolonged||Unaffected||Unaffected|
|Disseminated intravascular coagulation||Prolonged||Prolonged||Prolonged||Decreased|
|Von Willebrand disease||Unaffected||Prolonged or unaffected||Prolonged||Unaffected|
|Liver failure, early||Prolonged||Unaffected||Unaffected||Unaffected|
|Liver failure, end-stage||Prolonged||Prolonged||Prolonged||Decreased|
|Factor V deficiency||Prolonged||Prolonged||Unaffected||Unaffected|
|Factor X deficiency as seen in amyloid purpura||Prolonged||Prolonged||Unaffected||Unaffected|
|Bernard-Soulier syndrome||Unaffected||Unaffected||Prolonged||Decreased or unaffected|
|Factor XII deficiency||Unaffected||Prolonged||Unaffected||Unaffected|
Vitamin K2 Deficiency
According to a study published in the October 14, 2008 edition of PLoS Medicine, Vitamin K1 (5 mg of K1/day) does not protect against age-related decreasing bone density, but may protect against fractures and cancers, in postmenopausal women taking calcium and vitamin D supplements.
The prevalence of vitamin K deficiency varies by geographic region.
For infants in the United States, vitamin K1 deficiency without bleeding may occur in as many as 50% of infants younger than 5 days old. Therefore, the Committee on Nutrition of the American Academy of Pediatrics recommends that 0.5 to 1.0 mg Vitamin K1 be administered to all newborns shortly after birth.
Postmenopausal and elderly women in Thailand have high risk of Vitamin K2 deficiency, compared with the normal value of young, reproductive females. Current dosage recommendations for Vitamin K may be too low.
The deposition of calcium in soft tissues, including arterial walls, is quite common, especially in those suffering from atherosclerosis, suggesting that Vitamin K deficiency is more common than previously thought.
- Vitamin K Deficiency eMedicine. Author: Pankaj Patel, MD. Coauthor(s): Mageda Mikhail, MD, Assistant Professor. Updated: Dec 18, 2008
- Vitamin K Does Not Prevent Bone Density Loss, but May Prevent Fractures and Cancers Newswise, Retrieved on October 13, 2008.
- Angela M. Cheung et al. (2008), Vitamin K Supplementation in Postmenopausal Women with Osteopenia (ECKO Trial): A Randomized Controlled Trial
- Geleijnse JM, Vermeer C, Grobbee DE, et al. (2004). "Dietary intake of menaquinone is associated with a reduced risk of coronary heart disease: the Rotterdam Study". J. Nutr. 134 (11): 3100–5. PMID 15514282.
- Erkkilä AT, Booth SL (2008). "Vitamin K intake and atherosclerosis". Curr. Opin. Lipidol. 19 (1): 39–42. doi:10.1097/MOL.0b013e3282f1c57f. PMID 18196985.
- Wallin R, Schurgers L, Wajih N (2008). "Effects of the blood coagulation vitamin K as an inhibitor of arterial calcification". Thromb. Res. 122 (3): 411–7. doi:10.1016/j.thromres.2007.12.005. PMC 2529147. PMID 18234293.
- American Academy of Pediatrics Committee on Fetus and Newborn (July 2003). "Controversies concerning vitamin K and the newborn. American Academy of Pediatrics Committee on Fetus and Newborn". Pediatrics 112 (1 Pt 1): 191–2. doi:10.1542/peds.112.1.191. PMID 12837888.
- Bunyaratavej N (2007). "[Experience of vitamin K2 in Thailand]". Clin Calcium (in Japanese) 17 (11): 1752–60. PMID 17982197.
- Adams J, Pepping J (2005). "Vitamin K in the treatment and prevention of osteoporosis and arterial calcification". Am J Health Syst Pharm 62 (15): 1574–81. doi:10.2146/ajhp040357. PMID 16030366.
- Berkner KL, Runge KW (2004). "The physiology of vitamin K nutriture and vitamin K-dependent protein function in atherosclerosis". J. Thromb. Haemost. 2 (12): 2118–32. doi:10.1111/j.1538-7836.2004.00968.x. PMID 15613016.
- Cees Vermeer, Vitamin K: the effect on health beyond coagulation - an overview. "Food and Nutrition Research", 2012 full text