Vitamin D Deficiency, VDD


## Basic Introduction

  • VDD is also known as hypovitaminosis D
  • It is the most common nutritional deficiency worldwide in both children and adults affecting >40% of the adult population >50 years of age in US and Europed.
  • It is now considered a pandemic disease globally

## Causes of VDD

  • Inadequate exposure to sunlight
  • Intestinal malabsorption e.g. in celiac sprue, short bowel syndrome and cystic fibrosis
  • Chronic liver disease
  • Chronic kidney disease
  • Hypocalcaemia of hypothyroidism
  • Hypophosphatemia
  • Antiepileptics such as phenytoin and phenobarbitone (that promote vitamin D metabolism)
  • Inadequate nutritional quantities (especially in infants where Vitamin D in breast milk can sometimes be inadequate)

## Physiological function of Vitamin D

  • Maintenance of calcium and phosphorus homeostasis by supporting calcium absorption in the intestine and skeleton mineralization
  • Regulation of the immune response
  • Supporting of the process of cell differentiation
  • It plays some roles in the secretion and metabolism of hormones, e.g. parathyroid hormone and insulin

## Sources of Vitamin D

  • 80-90% of Vitamin D (mainly cholecalciferol or Vitamin D3) is derived from exposure to the sun's ultraviolet B rays (where the precursor molecule, 7-dehydrocholesterol, is converted to D3) and only 10-20% is nutritionally derived from:


_Animal fat and oils


## Metabolism of vitamin D

  • Vitamin D3 (cholecalciferol) and Vitamin D2 (ergocalciferol) are the natural forms of Vitamin D
  • They are transported to the liver where they are converted to calcifediol (25-hydroxycholecalciferol)
  • Calcifediol is then transported to the kidneys and converted to calcitriol (1, 25-dihydroxycholecalciferol), which is thought to be the most active form of Vitamin D.

## Statistics

  • VDD is more common in higher latitude due to less days of exposure to the sun shine.
  • The overall prevalence rate of VDD in USA has been reported as 41.6%, with the highest rate being seen in blacks (82.1%), followed by Hispanics (69.2%)f
  • The prevalence of VDD in exclusively breastfed infants at the Aga Khan University Hospital, Nairobi, Kenya, has been reported to be 24%e

_It is often asymptomatic

## Rickets in children

  • Bowing of the legs
  • Curved tibia, fibula, femur, radius, ulna and humerus
  • Protruding forehead
  • Large forehead
  • Pigeon chest
  • Depressed ribs
  • Enlarged epiphysis at wrist
  • Kyphosis (excessive outward curvature of the spine that causes hunching of the back)
  • Protruding abdomen

## Osteomalacia (inadequate mineralization of the bones) in adults

  • Bending of bones
  • Compressed vertebrae
  • Inability to walk and "waddling" gait
  • Diffuse joint and bone pain
  • Diminished stature
  • Pathological fracture of bones
  • Flattening of pelvic
  • Hypocalcemia
  • Muscle weakness
  • Soft bones

## Osteoporosis (sometimes)

## Other symptoms

  • Muscle aches
  • Muscle weakness
  • Fasciculation
  • Neonatal tetany
  • Clinical review
  • Measurement of plasma levels of calcidiol (25-hydroxyvitamin D or 25-OH-D); Normal Range 75–250 nmol/L in adults. In infants and young children, the value < 27.5nmol/l suggests VDDc.
  • Combination of testing of the serum levels of 25-OH-D and parathyroid hormone is so far the best indicator of VDDc
  • An elevated serum concentration of alkaline phosphatase can also be an indicator of VDD (though not a specific test) c
  • X-ray of the bones
  • Multiple myeloma
  • Primary hyperparathyroidism
  • Fibromyalgia
  • Idiopathic infantile hypercalcemia
  • Blount's syndrome
  • Hypophosphatasia
  • Paget's disease
  • Chronic fatigue syndrome
  • Nutritional counseling
  • Sun shine exposure (but balance with the risk of skin cancers as a result of over-exposure)
  • Fortification of food with Vitamin D supplement
  • Promotion of administration of vitamin D from birth to 6 months: Oral drops Vitamin D 400 IU OD x 6/12 (from birth).
  • Patients with renal disorders are likely to require vitamin D supplementation

1. Holick MF (2007). "Vitamin D Deficiency". New England Journal of Medicine. 357 (3): 266–81. doi:10.1056/NEJMra070553. PMID 17634462.

2. Food and Nutrition Board, Institute of Medicine. Dietary reference intakes for calcium, phosphorus, magnesium, vitamin D, and fluoride. Washington, DC, National Academy Press, 1999.

3. Allen, L. H., De Benoist, B., Dary, O., Hurrell, R., & World Health Organization. (2006). Guidelines on food fortification with micronutrients.

4. Holick, M. F., & Chen, T. C. (2008). Vitamin D deficiency: a worldwide problem with health consequences. The American journal of clinical nutrition, 87(4), 1080S-1086S.

5. Said, N. A. (2015). Prevalence of vitamin D deficiency in exclusively breastfed infants at the Aga Khan University Hospital, Nairobi (Unpublished master's dissertation). Aga Khan University, East Africa.

6. Forrest, K. Y., & Stuhldreher, W. L. (2011). Prevalence and correlates of vitamin D deficiency in US adults. Nutrition research, 31(1), 48-54.


## Sunshine exposure for 5 to 30 minutes

## Vitamin D therapy:

  • For VDD: 400 I.U OD
  • For VDD caused by intestinal malabsorption or chronic liver disease: 40,000 I.U daily
  • For hypocalcemia of hypoparathyroidism: Up to 100,000 I.U daily

## Correction of calcium and phosphate deficiencies

## Management of the underlying condition

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