Vitamin D is a hormone in steroid form rather than a vitamin. The main source of vitamin D is cutaneous synthesis after exposure to solar ultraviolet B radiation (wavelength, 290-310 nm). Cutaneous vitamin D production is influenced by age, skin pigmentation, latitude, and season of the year. Uptake of Vitamin D with only natural products can not meet the recommended daily requirements. Human milk contains 10-60 IU/L of Vitamin D which is far from daily requirement.

Rickets are usually seen among infants between ages of 6 months and 3 years old age who are not exposed to sunlight, and breastfed without appropriate vitamin D supplementation in winter season. The classic effect of 1.25-dihydroxyvitamin D is on active calcium transport in the intestinal cell. Vitamin D deficiency in infant and children adversely affects calcium metabolism resulting in Rickets, hypocalcemic convulsions, bowing of weight-bearing bones, muscle weakness, hypoplasia of tooth, general ill health, and poor growth. The skull is frequently soft and enlarged with delayed closure of the fontanels.

Vitamin D also plays a role in the pathogenesis of auto-immune disease, hypertension, diabetes mellitus, and congestive heart failure and also regulates specific cell differentiation and proliferation.

The incidence of vitamin D deficiency in our population is 1.6-19%. Treatment for Rickets may be administered gradually over several months or in a single day's dose (stoss therapy) with vitamin D. Stoss therapy may be advantageous when compliance with therapy and/or follow up is a problem. However, such high doses of vitamin D can lead to hypercalcemia. Rickets is due to a deficiency in vitamin D, and can be prevented by exposure to sunlight or by dietary supplements of vitamin D. It is recommended that adequate intake of vitamin D to prevent Rickets in infants is 400 IU per day in first year and preferably for three years.

Keywords: Rickets, Vitamin D, hypophosphataemic Rickets, hereditary Rickets