Patient Education
Introduction:
Vitamin D is essential for intestinal calcium absorption and plays a central role in maintaining calcium homeostasis and skeletal integrity.1 It is well-established that prolonged and severe vitamin D deficiency leads to rickets in children and osteomalacia in adults. More marginal vitamin D deficiency is likely to be a significant contributing factor to osteoporosis risk.2 Extensive research suggests that vitamin D deficiency in children is common and represents a global health problem.3
Mechanism of Action of vitamin D:
Vitamin D is a fat-soluble steroid that is essential for maintaining normal calcium metabolism.3 Vitamin D is a fat-soluble vitamin that is synthesized in human skin after exposure to ultraviolet radiation.4 Vitamin D is also present in certain foods and is stable in normal cooking procedures.3 The vitamin D3 diffuses into the circulation and is transported protein-bound to the liver where it is hydroxylated to 25(OH)D3 (calcidiol). In the kidney, 25(OH)D undergoes a further hydroxylation at the first carbon, catalyzed by 1, hydroxylase, to form 1,25(OH)2D3 (calcitriol), which is the biologically most active form of vitamin D.2 In addition, 1,25(OH)2D3 has many biologic effects that are non-calcaemic in nature. In addition, many organs including the gut, brain, heart, pancreas, skin, kidneys, and immune system have receptors for 1,25(OH) vitamin D and can synthesize this hormone from vitamin D.3 Vitamin D is involved in the production of defensins and cathelicidin - antimicrobial peptides that provide a natural defense against potential microbiological pathogens. Vitamin D supplementation increases cathelicidin production. Low vitamin D levels are associated with an increased incidence of respiratory tract infections and tuberculosis.10
Vitamin D deficiency:
Rickets is a disorder of mineralization of the bone matrix (osteoid) in growing bone, involving both the growth plate (epiphysis) and newly formed cortical and trabecular bone.2 The definition of rickets is "an interruption in the development and mineralization of the growth plate of bone, with radiographic abnormalities"5. It is commonly seen in infants. Clinical and laboratory manifestations include muscle weakness, tetany, bowing deformity of the long bones, beading of ribs, wrist widening, double malleoli, decreased bone density, and abnormal biochemistry (low serum calcium, phosphorus, vitamin D, and high alkaline phosphatase, PTH).2 People with prolonged vitamin D deficiency tend to have chronic elevations in serum parathyroid hormone (PTH), known as secondary hyperparathyroidism, which may have consequences for bone health.2
Merely having insufficiency/deficiency of vitamin D levels in the blood does not constitute rickets.6. Thus it is possible to get vitamin D deficiency in children even without radiological signs of rickets. Even mild vitamin D insufficiency can have detrimental effects on bone mineral acquisition and bone remodeling7. It is possible that a more marginal deficiency of vitamin D during early life may contribute to osteoporosis risk as well as potentially to the development of various other chronic diseases such as cardiovascular disease, hypertension, diabetes, cancer which are frequent in Western societies.2
Serum levels of Vitamin D3:
Serum or plasma 25(OH)D3 is the most commonly used and appropriate biochemical marker of vitamin D status.2 Although 1,25(OH)2D3 represents the active form of the vitamin, due to tight regulation of its production as well as a relatively short half-life (4-6 h), it is not a good indicator of vitamin D status.2 There is a lack of consensus on levels of 25(OH)D that define different stages of vitamin D status.2 It is clearly recognized that serum/plasma 25(OH)D3 levels below 12.5 nmol/l can result in bone diseases, such as rickets in infants and osteomalacia in adults.2 There is also evidence that circulating 25(OH)D3 levels below 20-25 nmol/l may result in rickets and osteomalacia in the longer term.2 Mild vitamin D deficiency (also referred to as vitamin D insufficiency) is characterized by serum 25(OH)D3 levels between 25-50 nmol/l, which may be associated with serum PTH elevations up to 15% and with normal to high bone turnover.2
Causes of Vitamin D Deficiency:
Dietary intakes of vitamin D are less than the recommended level in many children. In addition, low exposure to the sun may contribute to vitamin D deficiency. It is recommended that approximately 30 min of skin exposure (without sunscreen) of the arms and face to sunlight can provide all the daily vitamin D needs of the body.9
Treatment and Prevention of Vitamin D deficiency and insufficiency:
In India, where there is no fortification of food with vitamin D, supplementation remains an important alternative for improving the vitamin D status of individuals.8 Children may need a supplement containing at least 200 IU vitamin D. In the absence of adequate sun exposure, children and adults need 800-1000 IU of vitamin D/day.9
1. Parfitt A M, Gallagher J C, Heaney R P. et al Vitamin D and bone health in the elderly. Am J Clin Nutr 1982. 361014-1031.
2. Cashman KD. Vitamin D in childhood and adolescence. Postgrad Med J. 2007; 83: 230-235.
3. Staud R. Vitamin D: More than Just Affecting Calcium and Bone. Current Rheumatology Reports 2005, 7:356-364.
4. DeLuca HF, Zierold C: Mechanisms and functions of vitamin D. Nutr Rev 1998, 56:S4-10.
5. Dorland's illustrated medical dictionary, 30th edn (2003) Definition of rickets. Saunders, Philadelphia, p 1633.
6. Slovis TL, Chapman S. Evaluating the data concerning vitamin D insufficiency/deficiency and child abuse. Pediatric Radiology. 2008.
7. Fares JE, Choucair M, Nabulsi M, Salamoun M, Shahine CH, El-Hajj Fuleihan G. Effect of gender, puberty, and vitamin D status on biochemical markers of bone remodeling. Bone 2003; 33: 242-247.
8. Marwaha RK, Tandon N, Agarwal N, Puri S, Agarwal R, Singh S, Mani K. Impact of two regimens of vitamin D supplementation on calcium - vitamin D - PTH axis of schoolgirls of Delhi. Indian Pediatr. 2010; 47:761-769.
9. Holick MF. Vitamin D deficiency. N Engl J Med 2007; 357: 266-281.
10. Bartley J. Vitamin D, innate immunity and upper respiratory tract infection. Laryngol Otol. 2010; 124:465-469.