Vitamin D deficiency in children- How to manage it?

Vitamin D deficiency is highly prevalent in the Indian subcontinent. According to an estimate, it is as high as 50-90 % and is attributed to low dietary calcium along with skin colour and changing lifestyle. Abu Shady et al. have suggested that low sun exposure, obesity, and low level of maternal education were significant determinants of Vitamin D insufficiency.

Deficiency of Vitamin D leads to Rickets in children. It is a disease of growing bone caused by unmineralized matrix at the growth plates in children only before fusion of the epiphyses.

Vitamin D deficiency most frequently occurs in infancy because of a combination of poor intake and inadequate cutaneous synthesis. Transplacental transport of vitamin D, mostly 25-D, typically provides enough vitamin D for the 1st 2 mo of life unless there is severe maternal vitamin D deficiency. Infants who receive formula receive adequate vitamin D, even without cutaneous synthesis. Because of the low vitamin D content of breast milk, breastfed infants rely on cutaneous synthesis or vitamin supplements. Cutaneous synthesis can be limited because of the ineffectiveness of the winter sun in stimulating vitamin D synthesis; avoidance of sunlight because of concerns about cancer, neighbourhood safety, or cultural practices; and decreased cutaneous synthesis because of increased skin pigmentation. Vitamin D deficiency can also be secondary to unconventional dietary practices, such as vegan diets that use unfortified soy milk or rice milk.

There are several factors which may contribute to Vitamin D deficiency and are as follows-

Maternal Factors

• Dark skin pigmentation


• Full body clothing cover


• High latitude during winter/spring season


• Other causes of restricted sun (UVB) exposure, e.g., predominant indoor living, disability, pollution, cloud cover


• Low–vitamin D diet

• Low-calcium diet

• Poverty, malnutrition, special diets

Infant/Childhood Factors

• Neonatal vitamin D deficiency secondary to maternal deficiency/vitamin D deficiency
  
  
  
  • Lack of infant supplementation with vitamin D
  
  
  • Prolonged breastfeeding without appropriate complementary feeding from 6 mo
  
  
  • High latitude during winter/spring season
  
  
  • Dark skin pigmentation and/or restricted sun (UVB) exposure, e.g., predominant indoor living, disability, pollution, cloud cover
  
  
  • Low–vitamin D diet
  
  
  
  


• Low-calcium diet
  
  
  
  • Poverty, malnutrition, special diet.
  
  
  
  

The diagnosis of rickets is based on the presence of classic radiographic abnormalities. It is supported by physical examination findings, history, and laboratory results consistent with a specific etiology.

Laboratory findings include increased levels of ALP, PTH, and 1,25-D. Calcium levels may be normal or low, although symptomatic hypocalcemia is uncommon. There is decreased urinary excretion of calcium, and serum phosphorus levels may be low as a result of renal wasting of phosphate from secondary hyperparathyroidism. In some children, there is coexisting nutritional vitamin D deficiency, with low 25-D levels.

The treatment of vitamin D deficiency is very important and a multipronged approach has to be adopted. Children with nutritional vitamin D deficiency should receive vitamin D and adequate nutritional intake of calcium and phosphorus. There are 2 strategies for administration of vitamin D. With stoss therapy, vitamin D (300,000-600,000 IU) is administered orally (preferred) or intramuscularly as 2-4 doses over 1 day (vitamin D ₃is preferred to D ₂ because of longer half-life of D ₃ ). Since the doses are observed, stoss therapy is ideal in patients in whom adherence to therapy is questionable. The alternative strategy is daily vitamin D with a minimum dose of 2,000 IU/day for a minimum of 3 mo. Either strategy should be followed by daily vitamin D intake of 400 IU/day if <1 yr old or 600 IU/day if >1 yr old. It is important to ensure that children receive adequate dietary calcium (minimum of 500 mg/day) and phosphorus; this dietary intake is usually provided by milk, formula, and other dairy products, although calcium supplements may be needed in some patients.

Children who have symptomatic hypocalcemia might need intravenous (IV) calcium acutely, followed by oral calcium supplements, which typically can be tapered over 2-6 wk in children who receive adequate dietary calcium. Transient use of IV or oral 1,25-D ( calcitriol ) is often helpful in reversing hypocalcemia in the acute phase by providing active vitamin D during the delay as supplemental vitamin D is converted to active vitamin D. Calcitriol doses are typically 0.05 µg/kg/day. IV calcium is initially given as an acute bolus for symptomatic hypocalcemia (20 mg/kg calcium chloride or 100 mg/kg calcium gluconate). Some patients require a continuous IV calcium drip, titrated to maintain the desired serum calcium level. These patients should transition to enteral calcium, and most infants require approximately 1,000 mg of elemental calcium.

Nutritional supplementation

Foods that provide vitamin D include:

• Fatty fish, like tuna, mackerel, and salmon.


• Foods fortified with vitamin D, like some dairy products, orange juice, soy milk, and cereals.


• Beef Liver.


• Cheese.


• Egg yolks.

Preventive Measures

• Sun exposure (UVB content of sunlight depends on latitude and season)


• Vitamin D supplementation


• Strategic fortification of the habitual food supply


• Normal calcium intake

Dr Gunjan Makkar is a columnist with medical dialogues and specialises in paediatric updates.