A circulating level of 25-hydroxyvitamin D > 50nmol/l indicates a normal level. 30 – 50 nmol/L suggests vitamin D insufficiency. < 30nmol/L suggests vitamin D deficiency.
Prolonged or chronic deficiency of 25(OH)D levels lead to low calcium and phosphate absorption, resulting in hypocalcaemia. As a result, PTH concentrations rise leading to secondary hyperparathyroidism. This prompts the accelerated bone loss process, resulting in osteomalacia in adults and rickets in children.
The main causes of vitamin D deficiency are inadequate dietary intake and insufficient sunlight exposure. Other causes are due to:
- Malabsorption – bariatric surgery or post gastrectomy, chronic pancreatic disease, cystic fibrosis, Crohns disease, coeliac disease, biliary disease – PBC, strictures.
- Chronic kidney disease causing defective synthesis of 1,25-dihydroxyvitamin synthesis.
- Liver dysfunction impairing the production of 25-hydroxyvitamin D.
- Drug related : anticonvulsants, HAART, rifampicin.
- End organ resistance to vitamin D metabolites (hereditary vitamin D resistant rickets).
- Patients with a history of extensive burns due to inefficient vitamin D synthesis in the skin.
At risk groups of vitamin D deficiency:
- People confined indoors – often older patients residing in nursing homes, those needing prolonged hospital stays, housebound, institutionalised groups.
- Over 65 year olds.
- Increased skin pigmentation.
- Malabsorption – coeliac disease, post gastrectomy, cystic fibrosis, IBD.
- Pregnant and breast feeding women.
- Inadequate daily sun exposure due dermatological conditions adversely affected by sunlight requiring additional SPF applications or full barrier clothing to protect the skin, or for individuals who cover their skin for cultural reasons.
