Vitamin D Metabolism
In response to reduced extracellular calcium, PTH increases the activity of the renal enzyme responsible for hydroxylation (1-alpha-hydroxylase) and, thus, activation of calcidiol to calcitriol. Activated vitamin D (1,25-dihydroxyvitamin D) increases intestinal calcium absorption and osteoclastic bone resorption. Under normal physiological conditions, calcitriol acts via a negative feedback loop to decrease PTH production.
Vitamin D deficiency
This is the most common nutritional deficiency worldwide. Vitamin D may be ingested from certain plant products (as ergocalciferol), with subsequent hepatic and renal hydroxylation, or as cholecalciferol from animal products such as fish and eggs or by endogenous synthesis in the skin when exposed to sunlight. Therefore, deficiency may arise due to reduced intake or intestinal absorption, reduced sun exposure, or decreased endogenous synthesis.
Persistent vitamin D deficiency may result in osteomalacia, with patients commonly presenting with percussion tenderness, bony pain and proximal muscle weakness, which may combine to cause a waddling gait. Such individuals are at an increased risk of fragility fractures. Resultant hypocalcaemia leads to a compensatory rise in PTH.
Management
Regular vitamin D supplementation of 600-800 IU per day is recommended to prevent deficiency in at-risk patients. National consensus guidelines recommend 50,000 IU vitamin D2 or vitamin D3 once weekly for 7 weeks, with those with malabsorption syndromes or other comorbidities utilising a higher dose regimen.
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