Vitamin K deficiency

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Vitamin K deficiency
Classification and external resources
Specialty endocrinology
ICD-10 E56.1
ICD-9-CM 269.0
DiseasesDB 13962
eMedicine med/2385
Patient UK Vitamin K deficiency
MeSH D014813

Vitamin K deficiency or hypovitaminosis K is a form of avitaminosis[citation needed] resulting from insufficient vitamin K1 or vitamin K2 or both.[1]

Signs and symptoms[edit]

Symptoms include bruising,[2] petechiae,[2] hematomas,[2] 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.[2]

Vitamin K is changed to its active form in the liver by the enzyme 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 protein C and protein S. Inability to activate the clotting cascade via these factors leads to the bleeding symptoms mentioned above.[citation needed]

Notably, when one examines the lab values in Vitamin K deficiency [see below] the prothrombin time is elevated, but the partial thromboplastin time is normal or only mildly prolonged. 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; 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.

Cause[edit]

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.[citation needed]

Diagnosis[edit]

Treatment[edit]

Vitamin K2 Deficiency[edit]

Menaquinone (vitamin K2), but not phylloquinone (vitamin K1), intake is associated with reduced risk of CHD mortality, all-cause mortality and severe aortic calcification.[3][4][5]

Epidemiology[edit]

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, with the classic hemorrhagic disease occurring in 0.25-1.7% of infants.[2] 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.[6]

Postmenopausal and elderly women in Thailand have high risk of Vitamin K2 deficiency, compared with the normal value of young, reproductive females.[7] Current dosage recommendations for Vitamin K may be too low.[8] 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.[9]

Because colonic bacteria synthesize a significant portion of the Vitamin K required for human needs, individuals with disruptions to or insufficient amounts of these bacteria can be at risk for Vitamin K deficiency. Newborns, as mentioned above, fit into this category, as their colons are frequently not adequately colonized in the first five to seven days of life. (Consumption of the mother's milk can undo this temporary problem.) Another at-risk population comprises those individuals on any sort of long-term antibiotic therapy, as this can diminish the population of normal gut flora.[citation needed]

See also[edit]

References[edit]

  1. ^ "Vitamin K Deficiency: Background, Physiology, Complications and Prognosis". 
  2. ^ a b c d e Vitamin K Deficiency eMedicine. Author: Pankaj Patel, MD. Coauthor(s): Mageda Mikhail, MD, Assistant Professor. Updated: Feb 13, 2014
  3. ^ 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. 
  4. ^ Erkkilä AT, Booth SL (2008). "Vitamin K intake and atherosclerosis". Curr. Opin. Lipidol. 19 (1): 39–42. doi:10.1097/MOL.0b013e3282f1c57f. PMID 18196985. 
  5. ^ 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 2529147free to read. PMID 18234293. 
  6. ^ 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. 
  7. ^ Bunyaratavej N (2007). "[Experience of vitamin K2 in Thailand]". Clin Calcium (in Japanese). 17 (11): 1752–60. PMID 17982197. 
  8. ^ 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. 
  9. ^ 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. 

Further reading[edit]