Calceferol injection
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calciferol injection uses dose pharmacology
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Here is a complete overview of Calciferol Injection drawn from authoritative pharmacology textbooks and clinical references:
Calciferol Injection
What Is Calciferol?
"Calciferol" is a broad term for Vitamin D compounds. In the injectable context it refers primarily to:
- Ergocalciferol (Vitamin D2) - plant-derived, available orally and as injection
- Cholecalciferol (Vitamin D3) - animal/skin-derived, available for oral and IM injection
Both require hepatic 25-hydroxylation and then renal 1-alpha-hydroxylation to form the fully active metabolite calcitriol (1,25-dihydroxycholecalciferol), which is itself available as a separate injectable preparation.
- Goodman & Gilman's Pharmacological Basis of Therapeutics, p. 1079
Pharmacokinetics (ADME)
| Parameter | Detail |
|---|---|
| Absorption | Absorbed from the small intestine; bile is essential for adequate GI absorption |
| Distribution | Circulates bound to vitamin D-binding protein; stored in fat depots for prolonged periods |
| Half-life | Disappears from plasma with a t½ of 20-30 hours, but adipose depot storage can last weeks to months |
| Metabolism | Liver → 25-hydroxyvitamin D (storage form); Kidney → 1,25-(OH)₂D (active calcitriol) |
| Excretion | Primarily via bile/feces |
Injectable (IM/IV) forms bypass the GI absorption requirement, making them especially useful in malabsorption states.
- Goodman & Gilman's, p. 1078
Indications (Therapeutic Uses)
- Nutritional Rickets - prophylaxis and cure in infants and children
- Osteomalacia - including drug-induced (anti-epileptics) and malabsorption-related
- Metabolic Rickets / CKD-MBD (chronic kidney disease-mineral bone disorder)
- Hypoparathyroidism - maintaining plasma calcium (often with calcium supplements)
- Vitamin D-resistant Rickets (Type II / Familial Hypophosphatemia)
- Osteoporosis - prevention and adjunct treatment
- Malabsorption states - GI disease, biliary disease, post-bariatric surgery (where oral absorption is unreliable)
- Obesity (BMI >30) - higher doses often required due to sequestration in adipose tissue
- Goodman & Gilman's, pp. 1078-1079; Goldman-Cecil Medicine
Dosing
| Indication | Dose |
|---|---|
| Nutritional rickets (treatment) | 1,000 IU/day (basic); 3,000-4,000 IU/day for rapid healing |
| Severe deficiency (25-OH vitamin D <20 ng/mL) | Ergocalciferol 50,000 units weekly x 8 weeks |
| Hypoparathyroidism | 50,000-200,000 USP units/day + calcium lactate 4 g six times/day |
| Familial hypophosphatemia / Vit D-resistant rickets | 50,000-200,000 units/day (with phosphate supplements) |
| Stoss therapy (single IM dose) | 100,000-300,000 IU IM - establishes a depot, useful in malabsorption |
| Maintenance (>50 years) | 800-1,000 IU/day (with calcium) |
The injectable (IM depot) dose of 100,000-300,000 IU is used when compliance with oral therapy is poor or absorption is unreliable. One study found 100,000 IU cholecalciferol IM is safe and effective for correcting deficiency in the elderly.
Available Vitamin D Analogues (Injectable & Oral)
| Drug | Form | Notes |
|---|---|---|
| Ergocalciferol (Calciferol, D2) | Oral, IM | Requires hepatic + renal activation; indicated for hypoparathyroidism, familial hypophosphatemia |
| Cholecalciferol (D3) | Oral, IM | Natural form; depot IM injection available |
| Calcitriol (1,25-dihydroxyvitamin D3) | Oral, IV | Fully active; no renal activation required; used in CKD/dialysis |
| Alfacalcidol (1α-OHD3) | Oral | Pre-activated at 1α; requires only hepatic hydroxylation |
| Doxercalciferol | Oral, IV | Prodrug; hepatic activation only; used for secondary hyperparathyroidism |
| Paricalcitol | IV, oral | Synthetic calcitriol analogue; suppresses PTH with less hypercalcemia |
- Goodman & Gilman's, p. 1079
Adverse Effects and Toxicity
The primary toxicity is hypervitaminosis D, leading to:
- Hypercalcemia (most common) - with or without hyperphosphatemia
- Hypercalciuria - kidney stones, nephrocalcinosis
- Soft tissue/vascular calcification
- Renal impairment (can be severe and irreversible if prolonged)
- GI symptoms - nausea, vomiting, constipation, anorexia
Management of toxicity:
- Immediate withdrawal of vitamin D
- Low-calcium diet
- Glucocorticoids (reduce intestinal calcium absorption)
- Vigorous IV fluid support (forced saline diuresis)
- Loop diuretics (furosemide) to enhance calciuresis
Plasma calcium typically normalizes, and soft tissue calcium is slowly mobilized. Recovery of renal function occurs unless severe damage has occurred.
- Goodman & Gilman's, p. 1078
Special Considerations
- Malabsorption states (Crohn's, celiac, biliary disease, post-bariatric surgery): oral absorption unreliable → IM injection preferred
- CKD: impaired renal 1α-hydroxylation → calcitriol or alfacalcidol preferred over ergocalciferol/cholecalciferol
- Anti-epileptic drug users: accelerated catabolism of vitamin D metabolites → increased requirements
- Narrow therapeutic window in D-resistant rickets: monitor closely to avoid toxicity
- Pregnancy: adequate vitamin D is essential; third trimester fetal calcium accumulation >85% occurs in this period - premature infants especially at risk
Monitoring
- Serum 25-OH vitamin D (storage/status marker)
- Serum calcium and phosphate
- Serum PTH (in CKD-MBD and hypoparathyroidism)
- Urinary calcium (to detect hypercalciuria before symptomatic hypercalcemia)
- Renal function (creatinine, BUN)
Sources: Goodman & Gilman's The Pharmacological Basis of Therapeutics (pp. 1078-1079); Goldman-Cecil Medicine; Washington Manual of Medical Therapeutics; RxList - Calciferol; Medscape Dosing Reference
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