Vitamin D deficiency

Which children should receive vitamin D supplementation?

Breast fed infants born of mothers with adequate vitamin D stores usually maintain adequate serum vitamin D levels for at least 2 months, but rickets may develop subsequently if these infants are not exposed to the sun or do not received supplementary vitamin D. The American Academy of Pediatrics recommends vitamin D supplementation of all breast fed infants in the amount of 400 IU/day, started soon after birth and given until the infant is taking more than 1000 mL/day of formula or vitamin-D fortified milk (for age >1 year).

What are radiographic findings of vitamin D deficiency?

Characteristic radiographic changes of the distal ulna and radius include widening; concave cupping; and frayed, poorly demarcated ends. The increased space seen between the distal ends of the radius and ulna and the metacarpal bones is the enlarged, nonossified metaphysis.

What is vitamin D?

Cholecalciferol (vitamin D3) is the mammalian form of vitamin D and is produced by ultraviolet irradiation of inactive precursors in the skin. Ergocalciferol (vitamin D2) is derived from plants. Vitamin D2 and D3 require further metabolism to become active. They are of equivalent potency. Clothing, lack of sunlight exposure, and skin pigmentation decrease generation of vitamin D in the epidermis and dermis.

What are external sources of vitamin D?

Fortified milk, cheese, liver; sunlight.

What medical problems may contribute to a vitamin D deficiency?

Malabsorption syndromes, cholestasis

What should serum levels be in vitamin D sufficiency?

Serum 25OHD levels recommended in certain high-risk populations. Serum concentrations of 25OHD: Vitamin D sufficiency- 20 to 100 ng/mL (50 to 250 nmol/L) Vitamin D insufficiency- 12 to 20 ng/mL (30 to 50 nmol/L) Vitamin D deficiency- <12 ng/mL (<30 nmol/L)

How does vitamin D deficiency present clinically?

The clinical manifestations of rickets are most common during the first 2 years of life and may become evident only after several months of a vitamin D-deficient diet. Craniotabes is caused by thinning of the outer table of the skull, which when compressed feels like a Ping-Pong ball to the touch. Enlargement of the costochrodral junction (rachitic rosary) and thickening of the wrists and ankles may be palpated. The anterior fontanelle is enlarged, and its closure may be delayed. In advanced rickets, scoliosis and exaggerated lordosis may be present. Bowlegs or knock-knees may be evident in older infants, and greenstick fractures may be observed in long bones.

How is vitamin D deficiency diagnosed?

The diagnosis of rickets is based on a history of poor vitamin D intake and little exposure to direct ultraviolet sunlight.

What is the pathophysiology of rickets?

The pathophysiology of rickets results from defective bone growth, especially at the epiphyseal cartilage matrix, which fails to mineralize. The uncalcified osteoid results in a wide, irregular, zone of poorly supported tissue, the rachitic metaphysis. This soft, rather than hardened, zone produces many of the skeletal deformities through compression and lateral bulging or flaring of the ends of the bones.

What are laboratory findings in vitamin D deficiency?

The serum calcium usually is normal but may be low; the serum phosphorus level usually is reduced, and serum alkaline phosphatase activity is elevated. When serum calcium levels decline to less than 7.5 mg/dL, tetany may occur. The best measure of vitamin D status is the level of 25-(OH)-D.

What are recommendations for vitamin D supplementation?

These doses are designed to maintain 25-hydroxyvitamin D (25OHD) levels >20 ng/mL (50 nmol/L) in most populations: All exclusively breastfed infants should receive 400 international units (10 micrograms) daily of vitamin D supplements, beginning within a few days after birth. Infants (born at term) - 400 international units (10 micrograms) daily. Infants who are exclusively breastfed require vitamin D supplements to achieve this target, as do some formula-fed infants. Use of supplements in exclusively breastfed neonates and infants may be avoided if maternal intake of vitamin D is 4000 to 6000 international units (100 to 150 micrograms) daily. Children 1 to 18 years of age - 600 international units (15 micrograms) daily.

What are the effects of excess vitamin D?

Toxic effects of excessive chronic vitamin D may include hypercalcemia, muscle weakness, polyuria, and nephrocalcinosis.

What is the metabolism of vitamin D?

Vitamin D (D2 and D3) is metabolized in the liver to calcidiol, or 25-hydroxyvitamin D (25-[OH]-D); this metabolite, which has little intrinsic activity, is transported by a plasma-binding globulin to the kidney, where it is converted to the most active metabolite calcitriol, or 1,25-dihydroxyvitamin D(1,25-[OH]2-D). The action of 1,25-(OH)2-D results in a decrease in the concentration of messenger RNA (mRNA) for collagen in bone and an increase in the concentration of mRNA for vitamin D-dependent calcium-binding protein in the intestine (directly mediating increased intestinal calcium transport). 1,25-(OH)2-D has direct feedback to the parathyroid gland and inhibits secretion of parathyroid hormone.

What are fat-soluble vitamins?

A, D, E, K

What is the purpose of vitamin D?

Maintain serum calcium, phosphorus levels.

What medications may contribute to a vitamin D deficiency?

Phenytoin, phenobarbital, mineral oil

What is the epidemiology of vitamin D deficiency?

Prevalence in the United States in the pediatric age range is approximately 15 percent. Vitamin D deficiency is common in infants who have dark skin pigmentation and those who are exclusively breastfed beyond three to six months of age Breastfed infants need to be exposed to sunlight for at least 30 minutes/week while wearing only a diaper in order to maintain 25OHD levels at >20 ng/mL.

What is the result of vitamin D deficiency?

Rickets: reduced bone mineralization.

What diets may contribute to a vitamin D deficiency?

Strict vegans Breast fed infants

What are clinical complications of vitamin D deficiency?

Vitamin D deficiency appears as rickets in children and as osteomalacia in postpubertal adolescents. Inadequate direct sun exposure and vitamin D intake are sufficient causes, but other factors, such as various drugs (phenobarbital, phenytoin) and malabsorption, may increase the risk of development of vitamin-deficiency rickets. Breast fed infants, especially those with dark-pigmented skin, are at risk for vitamin D deficiency.

Does vitamin D cross the placenta?

Vitamin D is transferred from the mother to the fetus across the placenta, and reduced vitamin D stores in the mother are associated with lower vitamin D levels in the infant. Vitamin D levels are particularly low in premature infants because they have less time to accumulate vitamin D from the mother through transplacental transfer.