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Vitamin D poisoning (cholecalciferol)

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Synonym(s): Cholecalciferol (colecalciferol, vitamin D3) poisoning, calcipotriol (calcipotriene), calciferol (ergocalciferol, vitamin D2), calcitriol or tacalcitol


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 or 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 0.5 mg/kg in the dog, and calcipotriol may be toxic at 10 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.
  • 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.
  • Cholecalciferol (colecalciferol) supplements can vary hugely in dose from 10 µg (400 IU) to 1.25 mg (50,000 IU). Rodenticide baits are usually 0.075%. 
  • Vitamin D toxicosis is less frequently reported in cats but has occurred from ingestion of commercial pet food containing high concentrations of vitamin D and ingestion of rodenticides. 
  • In an experimental study, 8 of 10 cats given cholecalciferol 15,000 IU/kg/day died on days 3-31. Death occurred 1-2 days after the onset of clinical signs. The other two cats remained well. 
  • The risk of secondary exposure to cholecalciferol from ingestion of animals that have died from poisoning is low.  
  • Conversions:  
    • 1 mg = 41000 IU approximately 
    • 1 mcg = 41 IU approximately 
    • 1 IU = 0.025 mcg approximately 

Timecourse

  • Latency varies between toxicants.
  • Clinical signs generally become apparent within 12-36 hours with calciferol and cholecalciferol and from 6 hours with calcipotriol, calcitriol and tacalcitol. 

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.
  • Peterson M E, Fluegeman K (2013) Cholecalciferol. Topics Compan Anim Med 28, 24-37 PubMed.
  • Wehner A, Katzenberger J, Groth A, Dorsch R, Koelle P, Hartmann K, Weber K (2013) Vitamin D intoxication caused by ingestion of commercial cat food in three kittens. J Feline Med Surg 15 (8), 730-736 PubMed.
  • Hostutler R A, Chew D J, Jaeger J Q, Klein S, Henderson D, DiBartola S P (2005) Uses and effectiveness of pamidronate disodium for treatment of dogs and cats with hypercalcemia. J Vet Intern Med 19, 29-33 PubMed.
  • Sih T R, Morris J G, Hickman M A (2001) Chronic ingestion of high concentrations of cholecalciferol in cats. Am J Vet Res 62, (9), 1500-1506 PubMed
  • Morita T, Awakura T, Shimada A, Umemura T, Nagai T, Haruna A (1995) Vitamin D toxicosis in cats: Natural outbreak and Experimental study. J Vet Med Sci 57, (5), 831-837 PubMed.
  • Sato R, Yamagishi H, Naito Y, Murakami D, Oshima K, Takagi H, Fujita S, Saski J (1993) Feline vitamin D toxicosis caused by commercially available cat food. J Japan Vet Med Assoc 46, 577-581. 
  • El Bahri L (1990) Poisoning in dogs by vitamin D3-containing rodenticides. Comp Cont Educ Pract Vet 12 (10), 1414-1417 VetMedResource.
  • Thomas J B, Hood J C, Gaschk F (1990) Cholecalciferol rodenticide toxicity in a domestic cat. Aust Vet J 67, (7), 274-275 PubMed.
  • 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

  • Adams CA (2016) Cholecalciferol. In: Blackwell’s Five-Minute Veterinary Consult Clinical Companion Small Animal Toxicology, Wiley Blackwell, Ames, Iowa. pp 850-855. 
  • Rumbeiha W K (2013) Cholecalciferol. In: Small Animal Toxicology. 3rd edition. Editors M E Peterson and P A Talcott. Elsevier Inc., St Louis, MO. pp 489-498. 
  • Osweiler G D (1995) Toxicology. Philadelphia: Williams and Wilkins. ISBN: 0 6830 6664 1.

Organisation(s)

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