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Vitamin D deficiency in adults

SNOMED: 34713006716 words•Updated 03/03/2026
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Exam Tips

  • In UK exams, remember: do not routinely test asymptomatic people; test 25(OH)D when symptoms or bone-disease treatment decisions make the result clinically actionable.
  • Learn thresholds precisely: <25 nmol/L deficiency risk, 25-50 nmol/L possible insufficiency, >50 nmol/L usually sufficient for bone health.
  • Classic osteomalacia vignette: diffuse bone pain + proximal weakness + raised ALP +/- low phosphate and secondary hyperparathyroidism.
  • State management in two phases: loading (confirmed deficiency) then long-term maintenance (especially in persistent risk groups).
  • Always mention safety: check for hypercalcaemia risk, interacting drugs (digoxin/thiazides), and caution in granulomatous disease/renal impairment.

Definition

Vitamin D deficiency in adults is a biochemical and clinical state in which circulating 25-hydroxyvitamin D is too low to maintain normal calcium-phosphate balance and optimal bone mineralization. In UK practice, deficiency is usually defined as serum 25(OH)D below 25 nmol/L, with 25-50 nmol/L often considered insufficient for some people, especially those with risk factors or bone disease.

Pathophysiology

Most vitamin D in the UK is generated in skin via UVB exposure (cholecalciferol, vitamin D3), with a smaller dietary contribution (D3 and ergocalciferol, D2). Vitamin D is hydroxylated in the liver to 25(OH)D, then in the kidney to active 1,25-dihydroxyvitamin D under parathyroid hormone regulation; low substrate availability and/or impaired liver-kidney activation lowers intestinal calcium and phosphate absorption. The resulting secondary hyperparathyroidism increases bone turnover and phosphate wasting, causing defective osteoid mineralization (osteomalacia), proximal myopathy, bone pain, falls risk, and fragility fracture susceptibility. Image reference: review a standard vitamin D metabolism pathway diagram (skin-liver-kidney axis) in a core medicine/endocrine textbook chapter on metabolic bone disease.

Risk Factors

  • Age >=65 years
  • Low sunlight exposure (housebound, institutionalized, extensive clothing cover, predominantly indoor lifestyle)
  • Darker skin pigmentation (for example African, African-Caribbean, South Asian ancestry in UK latitudes)
  • Winter season in UK (limited UVB at northern latitude)
  • Malabsorption states (coeliac disease, Crohn's disease, cystic fibrosis) or post-bariatric surgery
  • Obesity (BMI >30 kg/m2)
  • Severe liver disease or end-stage chronic kidney disease
  • Pregnancy or breastfeeding
  • Drug-related risk: enzyme-inducing antiepileptics (carbamazepine, phenytoin, phenobarbital), rifampicin, glucocorticoids, orlistat, colestyramine, some antiretroviral regimens

Clinical Features

Symptoms

  • Diffuse or focal bone pain (often lower back, pelvis, ribs, hips, legs)
  • Proximal muscle weakness (difficulty rising from chair or climbing stairs)
  • Chronic widespread musculoskeletal pain with fatigue
  • Falls, reduced mobility, impaired physical function
  • Fracture history (including fragility fractures)

Signs

  • Waddling gait
  • Proximal myopathy on examination
  • Bony tenderness (sternum, tibia, pelvis)
  • Features of osteomalacia in severe/prolonged deficiency
  • May be no signs in mild biochemical deficiency

Investigations

Serum 25-hydroxyvitamin D (25[OH]D):<25 nmol/L suggests deficiency; 25-50 nmol/L may be insufficient; >50 nmol/L generally adequate for most people
Bone profile (adjusted calcium, phosphate, ALP):Calcium low or low-normal, phosphate often low, ALP often raised in osteomalacia
Parathyroid hormone (PTH):Often raised (secondary hyperparathyroidism)
Renal function (U&E, eGFR):Assesses CKD-related impaired activation and guides dosing/monitoring
Liver function tests:May identify hepatic contributors to low vitamin D status
Targeted tests for cause (for example coeliac serology, malabsorption work-up):Performed when history suggests secondary causes or poor treatment response

Management

Lifestyle Modifications

  • Do not routinely test asymptomatic high-risk adults; offer maintenance supplementation advice
  • Encourage safe sunlight exposure in spring/summer while avoiding sunburn
  • Increase dietary vitamin D sources (oily fish, egg yolk, fortified foods) and adequate calcium intake
  • Address reversible causes: weight management, review interacting medicines, optimize malabsorption/chronic disease care

Pharmacological Treatment

Vitamin D replacement (loading for confirmed deficiency)

  • Colecalciferol oral loading regimens giving a total about 300,000 units over 6-10 weeks (for example 20,000 units capsules, frequency adjusted to reach total loading dose)
  • Ergocalciferol can be used when colecalciferol is unsuitable/unavailable

Use local formulary/BNF product strengths to construct regimen; check baseline calcium and consider repeat calcium after starting treatment, especially if symptomatic, renal impairment, granulomatous disease, or high-dose replacement.

Maintenance after repletion or for high-risk prevention

  • Colecalciferol 800-2000 units once daily (typical long-term range)
  • Higher maintenance doses (up to 4000 units/day) may be used in selected adults under supervision

Continue long term if risk factors persist; reinforce adherence, especially in winter and in people with low sun exposure.

Adjuncts and special situations

  • Calcium plus vitamin D combination products when dietary calcium is inadequate
  • Active vitamin D analogues (for example alfacalcidol/calcitriol) only for specialist indications such as advanced CKD, not routine nutritional deficiency

Contraindications/cautions: hypercalcaemia, metastatic calcification, severe renal stones history, primary hyperparathyroidism, sarcoidosis or other granulomatous disorders (higher hypercalcaemia risk). Important interactions include digoxin (arrhythmia risk with hypercalcaemia), thiazides (raise calcium), and drugs reducing vitamin D effect (antiepileptics, rifampicin, orlistat, colestyramine).

Complications

  • Osteomalacia
  • Secondary hyperparathyroidism
  • Reduced muscle strength and increased falls
  • Fragility fractures
  • Exacerbation of osteopenia/osteoporosis
  • Persistent pain and functional decline if untreated

Prognosis

With appropriate repletion and ongoing maintenance, most adults normalize vitamin D status and improve musculoskeletal symptoms/risk profile. Recurrence is common if risk factors remain (for example low sun exposure, malabsorption, obesity, interacting drugs), so long-term prevention is usually required.

Sources & References

💊BNF Drug References(7)

✅NICE Guidelines(1)

📖Textbook References(20)

  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1758)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 818)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1758)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1236)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 917)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 915, 916)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1176)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 194)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1237)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1806, 1807)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 194)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1304)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 914, 915)[context]
  • Guyton and Hall Textbook of Medical Physiology (John E. Hall, Michael E. Hall) (Z-Library).pdf(pp. 993)[context]
  • Guyton and Hall Textbook of Medical Physiology (John E. Hall, Michael E. Hall) (Z-Library).pdf(pp. 993, 994)[context]
  • Guyton and Hall Textbook of Medical Physiology (John E. Hall, Michael E. Hall) (Z-Library).pdf(pp. 320)[context]
  • Guyton and Hall Textbook of Medical Physiology (John E. Hall, Michael E. Hall) (Z-Library).pdf(pp. 994)[context]
  • Guyton and Hall Textbook of Medical Physiology (John E. Hall, Michael E. Hall) (Z-Library).pdf(pp. 993)[context]
  • Oxford Handbook of Clinical Diagnosis (Huw Llewelyn, Hock Aun Ang, Keir Lewis etc.) (Z-Library).pdf(pp. 576, 577)[context]
  • Oxford Handbook of Clinical Diagnosis (Huw Llewelyn, Hock Aun Ang, Keir Lewis etc.) (Z-Library).pdf(pp. 576, 577)[context]

Sources

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