Vitamin K deficiency diseases

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Vitamin K deficiency can occur in any age group. Vitamin K deficiency in infants causes hemorrhagic disease of newborn. Vitamin K (VK) is necessary for the function of clotting factors.
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The vitamin K-related factors are required for binding of calcium and formation of bone proteins. Its deficiency can cause osteoporosis. Vitamin K deficiency can promote calcification of arteries and other soft tissues.

There are three major forms of vitamin K. Phylloquinone (K1) is present in our diet. Phylloquinone is fat-soluble and is found in nature in a variety of green plants and leaves. Several plant sources of food are rich in phylloquinone. Vitamin K2 are menaquinones with nine subtypes. The subtypes, MK-4, MK-7, MK-8 and MK-9 are nutritionally the most important. Vitamin K2 deficiency can increase the risk for bone fractures, osteoporosis disease and vascular calcification. Vitamin K2 is synthesized by the intestinal bacteria and is also present in fermented food such as cheese, curd and the traditional Japanese dish "natto". Vitamin K3, K4 and K5 are synthetic products.

Vitamin K deficiency causes

In neonates the causes of insufficiency and related disease are, low stores of vitamin K, low transmission across the placenta, low availability in breast milk and near sterile gut.
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In adults the causes include, malnutrition, malabsorption, fat malabsorption, prolonged illness, frequent use of antibiotics, prolonged parenteral nutrition, malabsorption diseases, coumarin anticoagulants, biliary diseases, alcoholism and certain anticonvulsants.

Vitamin K deficiency symptoms

The symptoms of VK inadequacy in the body include, oral, nasal, cutaneous, gastrointestinal, intrathoracic bleeding and lack of blood coagulation. Easy bruisability, petechiae, hematomas, oozing of blood at surgical or puncture sites is common. Developing bones may deform and there may be bone loss. Vascular, soft tissue and cartilage calcification is another sign. Prenatal insufficiency may cause birth defects such as underdeveloped face, nose, bones and fingers.

Vitamin K deficiency diseases

The deficiency of phylloquinone and menaquinones causes several adverse effects. As VK controls the formation of several coagulation factors, the insufficiency of serum VK can cause Vitamin K deficiency-related bleeding (VKDB) disease. The matrix γ-carboxy-glutamyl (Gla) protein is activated by VK and its inadequacy in the serum causes osteoporosis disease and fragile bones.

Vitamin K deficiency-related bleeding (VKDB)

Vitamin K deficiency causes hemorrhagic disease in neonates with symptoms such as oral, nasal, cutaneous, gastrointestinal, intrathoracic and umbilical bleeding. In severe cases intracranial bleeding may occur. Nearly 50% of the newborn may have subclinical VK inadequacy. There is an impaired production of coagulation factors II, VII, IX, X, protein C and protein S by the liver due VK insufficiency. Hemorrhagic disease of the newborn leading to devastating consequences can occur when prophylactic vitamin K is not administered.

Worldwide efforts to control VKDB

American Academy of Pediatrics recommends the prophylactic use of VK for newborn since 1961. They recommend a single, intramuscular dose of 0.5 to 1 mg for all neonates. Its prophylactic use is also recommended by the American College of Obstetricians and Gynecologists. The Canadian Paediatric Society and the Committee on Child and Adolescent Health, College of Family Physicians of Canada, recommend a single intramuscular dose of 0.5 mg-1.0 mg to all neonates within the first 6 hours after birth. To combat the deficiency related bleeding disease, UK National Health System, recommended that babies weighing less than 2.5 kg should be administered 400 μg/kga and those weighing more than 2.5 kg, 1 mg of vitamin K. Italian Society of Neonatology also recommends VKDB preventive intramuscular VK administration at birth.

Vascular calcification diseases

Blood vessel calcification occurs when calcium accumulates in the tunica intima and/or tunica media layers of the blood vessel wall. In cardiovascular diseases, calcification of the tunica intima and tunica media layers of the coronary arteries is a major controllable cause of mortality and morbidity. Matrix Gla protein (MGP) is member of a family of Gla-containing proteins. Matrix Gla-protein (MGP) is vitamin K-dependent and is not related to blood coagulation. MGP is a strong inhibitor of calcification of arterial vessel wall and cartilage.

Schurgers LJ et al. reported that the MGP inhibitory mechanism involves "inhibition of bone morphogenetic protein 2 and 4 (BMP-2 and -4), suppression of osteochondrogenic transdifferentiation of vascular smooth muscle cells and direct inhibition of calcium-crystal growth; in all cases MGP requires vitamin K-dependent γ-carboxylation." Overexpression of MGP reduces both intimal and medial calcification of arteries with atherosclerotic plaques. The calcification of tunica intima is a great risk for plaque rupture.

Osteoporosis and fractures

Vitamin K is a coenzyme for glutamate carboxylase. Glutamate carboxylase mediates the conversion of glutamate to gamma-carboxyglutamate (Gla). Matrix Gla protein (MGP) along with another vitamin K-dependent protein, osteocalcin, participate in the organisation of bone tissue. Menaquinone insufficiency in the serum results in a decreased level of active osteocalcin and MGP which are essential for the maintenance of bone strength and lowering risk for osteoporosis disease. The gamma-carboxylation of the Gla proteins is essential for attracting and incorporating Ca2+ ions into hydroxyapatite crystals.

Bügel S. et al. in the study 'Vitamin K and bone health in adult humans' reported that "vitamin K insufficiency is associated with low bone mineral density (BMD) and increased fractures. Vitamin K supplementation, on the other hand, has been shown to improve the bone turnover profile and decrease the level of circulating undercarboxylated osteocalcin." The dietary recommendations are based on the requirement of the blood coagulation and related diseases. In relation to bone health, the requirement of vitamin K may be much higher.

Vitamin K deficiency treatment

The treatment of VK deficiency diseases is by taking food rich in phylloquinone and menaquinone. If the need arise oral and injectable supplements are administered. People taking anticoagulants such as warfarin should be careful about the amount of dietary or supplementary VK they take. Phylloquinone is contraindicated during warfarin therapy as it can counteract the action of warfarin and reverse its drug activity.

Vitamin K food sources

Phylloquinone (K1) is present in vegetable oils like olive, canola, cottonseed, safflower and soybean oils. Leafy, green vegetables are also good sources of phylloquinone. Green peas, beans, spinach, oats and whole grains are good food sources. Menaquinone (K2) is present in fermented foods like cheese and curd.
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References:
1.Hubbard D, Tobias JD. Intracerebral hemorrhage due to hemorrhagic disease of the newborn and failure to administer vitamin K at birth. South Med J. 2006 Nov;99(11):1216-20.
2.http://www.cdc.gov/ncbddd/vitamink/facts.html
3.Giuseppe Lippi, Massimo Franchini. Vitamin K in neonates: facts and myths. Blood Transfus. 2011 Jan; 9(1): 4–9.
4.Bügel S. Vitamin K and bone health in adult humans. Vitam Horm. 2008;78:393-416.
5.Pearson DA. Bone health and osteoporosis: the role of vitamin K and potential antagonism by anticoagulants. Nutr Clin Pract. 2007 Oct;22(5):517-44.
6.Schurgers LJ, Joosen IA, Laufer EM, Chatrou ML, Herfs M, Winkens MH, Westenfeld R, Veulemans V, Krueger T, Shanahan CM, Jahnen-Dechent W, Biessen E, Narula J, Vermeer C, Hofstra L, Reutelingsperger CP. Vitamin K-antagonists accelerate atherosclerotic calcification and induce a vulnerable plaque phenotype. PLoS One. 2012; 7(8): e43229.
7.Shea MK, Holden RM. Vitamin K status and vascular calcification: evidence from observational and clinical studies. Adv Nutr. 2012 Mar 1;3(2):158-65.
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Current topic on nutrition: Vitamin K deficiency diseases.