Vitamin D poisoning (cholecalciferol)

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Sections available in full article Introduction, Presenting signs, Geographic incidence, Pathogenesis, Pathophysiology, Timecourse (incubation, duration), Diagnosis, Presenting problems, Client history, Clinical signs, Diagnostic investigation, Confirmation of diagnosis, Gross autopsy findings, Histopathology findings, Differential diagnosis, Treatment, Initial symptomatic treatment, Standard treatment, Monitoring, Subsequent management, Sequelae, Prognosis, Expected response to treatment, Reasons for treatment failure, Sources, Publications, Vetstream contributor(s),
Contributors Dr Rosalind Dalefield BVSc PhD DipABVT DipABT
Synonyms Cholecalciferol poisoning

Introduction

  • Rare.
  • Cause : poisoning with vitamin D3 rodenticide or ingestion of poisoned wild life. 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. Oversupplemetation with Vitamin D via the diet can also cause toxicosis, and suckling puppies are particularly susceptible if the dam is oversupplemented.
  • Signs : anorexia, vomiting.
  • Diagnosis : signs, hypercalcemia, polydipsia.
  • Treatment : detoxification, calcitonin, pamidronate, fluid diuresis, corticosteroids.
  • Prognosis : guarded to poor.

Diagnosis

Clinical signs

  • As listed previously.

Diagnosis

Differential diagnosis

  • Other causes of hypercalcemia Hypercalcemia: overview such as neoplasia (particularly lymphoma or anal sac apocrine gland adenocarcinoma), hyperparathyroidism, acute or chronic renal failure, pheochromocytoma, hypoadrenocorticoidism.
  • Other causes of polydipsia.

Sequelae

Prognosis

  • Generally guarded. Prognosis is good if treatment is intiated prior to onset of hypercalcemia and calcification of soft tissues, but animals are often presented too late.
  • Animals often deteriorate rapidly and may be dead within a few days.
  • Prognosis is grave if hematemesis is present.
  • If aggressive and prolonged (2-4 weeks) treament is given animals may survive.
  • Kidneys, lungs and/or heart may be permanently damaged by mineralization.

Expected response to treatment

  • Calcium levels should fall within hours of effective treatment.

Reasons for treatment failure

  • Animal is presented too late in the course of toxicosis.
  • Severe renal disease prior to treatment.

Sources

Publications

Refereed papers

  • Recent references from PubMed.
  • Durtnell R E (1999) Canine vitamin D Toxicosis. JSAP 40 (11), 550.
  • Gunther R, Felice L J, Nelson R K & Fransom A M (1988) Toxicity of vitamin D3 rodenticide to dogs. JAVMA 193 , 211-214.
  • Fan T M, Simpson K W, Trasti S & Birnbaum N (1998) Calcipotriol toxicity in a dog. JSAP 39 (12), 581-586.

Other sources of information

  • Rumbeiha W K (2006) Cholecalciferol. In: Small Animal Toxicology. 2nd edition. Editors M E Peterson and P A Talcott. Elsevier Inc., St Louis, MO. pp 629-642.
  • Bahri L E (1990) Poisoning in dogs by vitamin D3-containing rodenticides. Comp Cont Ed Pract Vet 12 , 1414-1417.

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