Felis ISSN 2398-2950

Vitamin D poisoning (cholecalciferol)

Synonym(s): Cholecalciferol poisoning, calciferol poisoning, calcipotriol poisoning

Contributor(s): Rosalind Dalefield

Introduction

  • Cause: poisoning with vitamin D3 rodenticide or ingestion of poisoned wildlife. Ingestion of human medications containing vitamin D, which are prescribed for a variety of conditions including hypoparathyroidism, osteomalacia, osteoporosis, renal failure, psoriasis, and to prevent recurrence of cancer.
  • Signs: anorexia, vomiting, polydipsia, polyuria, fetid diarrhea.
  • Diagnosis: signs, hypercalcemia.
  • Treatment: detoxification, calcitonin, pamidronate, fluid diuresis, corticosteroids.
  • Prognosis: guarded to poor.

Pathogenesis

Pathophysiology

  • Excess vitamin D   →   hypercalcemia   →   clinical signs.
  • Toxicity data for cats are lacking, but they are believed to be more sensitive to poisoning than dogs. (Cholecalciferol may be toxic at a dose as low as 2 µg/kg in the dog, and calcipotriol may be toxic at 50 µg/kg in the dog.)
  • Vitamin D3   →   25(OH)D3 in liver   →   1,25(OH)2D3 (calcitriol) and 24R,25(OH)2D3 in kidney.
  • Calcitriol is the principal active metabolite.
  • The parent compound and metabolites cause:
    • Calcium uptake from intestine.
    • Calcium resorption from renal tubules.
    • Resorption of calcium from bone.
  • Hypercalcemia Hypercalcemia: overview   →    calcium deposition in soft tissues, including kidney   →    renal failure.
  • Animals with pre-existing renal failure or hyparathyroidism have increased susceptibility.
    • Hypercalcemia can also lead to conduction dysfunction in the heart. 
    • Metastatic calcification in soft tissues.
    • Cellular degeneration and necrosis.
  • Cholecalciferol is rapidly absorbed from the GI tract and transported to the liver by vitamin D binding protein.
  • Hepatic metabolism to the principal circulating metabolite, 25-hydroxycholecalciferol (25(OH)D3) is very rapid.
  • Within 24 hours of ingestion, serum 25(OH)D3increases 15-20 times above the normal level of 3-4 µmol/l.
  • 25(OH)D3 is further metabolized to calcitriol (1,25-dihydroxycholecalciferol, 1,25(H)2D3) in the kidney.
  • Serum 1,25(OH)2D3increases to approximately 3x normal, peaking at 48-96 hours after ingestion, but returns to normal levels within 7 days.

Timecourse

  • Latency varies between toxicants.
  • Clinical signs generally become apparent 36-48 hours after ingestion of cholecalciferol.
  • Clinical signs develop 8-24 hours after ingestion of 25(OH)D3, 1,25(H)2D3or their analogues..

Diagnosis

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Treatment

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Outcomes

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Further Reading

Publications

Refereed papers

  • Recent references from PubMed and VetMedResource.
  • El Bahri L (1990) Poisoning in dogs by vitamin D3-containing rodenticides. Comp Cont Educ Pract Vet 12 (10), 1414-1417 VetMedResource.
  • Moore F M, Kudish M, Richter K et al (1988) Hypercalcaemia associated with rodenticide poisoning in three cats. JAVMA 193 (9), 1099-1100 PubMed.

Other sources of information

  • Rumbeiha W (2006) Cholecalciferol. In: Small Animal Toxicology. Eds: M E Peterson and P A Talcott. Philadelphia: W B Saunders. ISBN: 0 7216 7826 2.
  • Rumbeiha W (2001) Cholecalciferol. In: Small Animal Toxicology. 2nd edn. Eds: M E Peterson and P A Talcott. Elsevier Inc, St Louis. ISBN: 0 7216 0639 3.
  • Osweiler G D (1995) Toxicology. Philadelphia: Williams and Wilkins. ISBN: 0 6830 6664 1.

Organisation(s)


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