Synopsis
Recognise defective adult bone mineralisation, distinguish nutritional vitamin-D deficiency from renal or phosphate-wasting causes, interpret the calcium-phosphate-parathyroid pattern, and replace missing substrate safely while treating the underlying disorder.
- Osteomalacia is failure to mineralise newly formed adult osteoid; suspect it with diffuse bone tenderness, proximal weakness, waddling gait, insufficiency fractures or Looser pseudofractures.
- The common nutritional pattern is low 25-hydroxyvitamin D, raised ALP, raised PTH and low phosphate; adjusted calcium may be low or preserved by secondary hyperparathyroidism.
- Request adjusted calcium, phosphate, ALP, PTH, vitamin D, magnesium, renal and liver profiles first, then distinguish substrate deficiency, CKD and phosphate wasting.
Key red flags
Perioral tingling, carpopedal spasm, seizure, laryngospasm or arrhythmia with low calcium requires monitored emergency replacement rather than an outpatient vitamin-D course.
Investigation priorities
Identify the biochemical mineralisation pattern and kidney, liver or magnesium contributions before replacement.
Management branches
Diffuse pain, proximal weakness, low-trauma fracture or unexpectedly low density raises a mineralisation concern.
- Obtain mineral, renal, liver, magnesium, PTH and vitamin-D tests before high-dose replacement when clinical stability permits.
- Identify urgent hypocalcaemia, critical phosphate depletion or fracture, then separate common vitamin-D deficiency from CKD and isolated renal phosphate wasting.
Key medicines
Colecalciferol loadingGive a total near 300,000 units orally over six to ten weeks; a common regimen is 50,000 units once weekly for six weeks, followed immediately by maintenance.
Colecalciferol maintenanceUse 800–2,000 units orally once daily after loading while risk persists; higher maintenance in malabsorption or selected obesity needs clinical and biochemical supervision.