The consequences of vitamin D (califerol) deficiency are low calcium and phosphate producing secondary hyperparathyroidism, a further reduction in phosphate levels and increased plasma levels of bone-derived alkaline phosphatase.

Clinically, this produces poor bone mineralisation - rickets in children, osteomalacia in adults:

• children with rickets classically present with bony abnormalities such as leg-bowing and knock-knees
  • may also be bony deformities of the chest, pelvis and skull, fractures in severe cases, delayed dentition, poor growth, and, rarely, bone pain
  • symptoms of hypocalcaemia, such as neuromuscular irritability (e.g. convulsions, tetany), cardiomyopathy or cardiac arrest may be the presenting feature - this is especially the case in very young infants
  • commonest cause of rickets is simple nutrient deficiency of vitamin D (from sunlight, diet or both)
• osteomalacia occurs if vitamin D deficiency occurs after closure of the epiphyses

Depending on the cause, there may be a rapid response to administration of small doses of calciferol.

Notes (2):

• in adults, lesser deficiency (insufficiency) is associated with various non-specific symptoms
• vitamin D deficiency and insufficiency are becoming more common in developed countries
  • in the UK, the prevalence of vitamin D deficiency in all adults is around 14.5%, and may be more than 30% in those over 65 years old, and as high as 94% in otherwise healthy south Asian adults
• in adults, extensive covering with clothing, failure to spend time outdoors or the use of anti-UVB sunscreens results in decreased skin synthesis of vitamin D and increases the likelihood of primary vitamin D deficiency, as does an inadequate diet
  • in adults over 65 years of age, an inadequate diet, reduced gut absorption and reduced mobility increase that risk, especially in those in residential care

Reference:

1. Drug and Therapeutics Bulletin 2006; 44 (2):12-16.
2. Drug and Therapeutics Bulletin 2006;44 (4);25-9.