1CHOLECALCIFEROL (VITAMIN D3) TOXICITY IN ANIMALSChavhan S G3, Brar R S1, Banga H S1and N D Singh21. Professor’s, Departme...
2 The plant species like golden oat grass (Trisetum flavescens), Cestrum diurnum andSolanum nigricans are reported to hav...
3Clinical Signs: Diarrhoea, subnormal body temperature and progressive wasting. Anorexia, dullness, rigidity of limbs an...
4 Pamidronate: Dogs: 1.3-2 mg/kg, slow IV in 0.9% sodium chloride solution over a periodof 2-4 hours. It may be repeated ...
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Cholecalciferol (Vitamin D3) Toxicity in Animals

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Cholecalciferol (Vitamin D3) Toxicity in Animals

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Cholecalciferol (Vitamin D3) Toxicity in Animals

  1. 1. 1CHOLECALCIFEROL (VITAMIN D3) TOXICITY IN ANIMALSChavhan S G3, Brar R S1, Banga H S1and N D Singh21. Professor’s, Department of Veterinary Pathology, College of Veterinary Science, GADVASU, Ludhiana, Punjab-141004.2. Assistant Professor, Dept. of Vety. Pathology, College of Veterinary Science, GADVASU, Ludhiana, Punjab-141004.3. Corresponding Author: Dr. Sambhaji G. Chavhan, Assistant Professor, Department of Veterinary Pathology, VeterinaryCollege, KVAFSU, Bidar, Karnataka-585401.Email: drsam24183@gmail.com, Website: www.vetclinpath.inVitamins are organic compounds needed in small amounts for the normal growth andactivity of the body. Most of the vitamins cannot be synthesized by the body but are naturallyfound in foods obtained from the plants and animals. Vitamins are either water-soluble or fat-soluble and water-soluble vitamins are excreted rapidly than fat soluble vitamins.Vitamin D is not a single compound but different compounds are reported to have avitamin D activity (Smith, 1982). Among them vitamin D3 (cholecalciferol) and vitamin D2(ergocalciferol) are important. Vitamin D3 was found to be approximately ten times moretoxic than vitamin D2 (Chen and Bosmann, 1964; Hunt et al., 1972). The vitamin D3 toxicityreported to cause generalized calcification mainly of soft tissues (Long, 1984).Nowadays use of vitamin D3 (cholecalciferol) in commercial pet, livestock and infantfeed supplements, multivitamin preparations and as a rodenticide increased risk of toxicity.Various plant species reported to have a high concentration of vitamin D analogue have beenreported as a source of vitamin D3 toxicity in livestock. The most common source of vitaminD3 toxicity in dogs and cats is accidental ingestion of rodenticide baits containingcholecalciferol (Rumbeiha, 2006). So, in present article we summarized various aspects ofvitamin D3 toxicity in detail.Sources of Toxicity: Vitamin D3 nowadays also used as rodenticide. The rodenticide preparations are availablein different formulations like granules, flakes, tablets, baits containing 0.075%cholecalciferol. The most common source of vitamin D3 toxicity in dogs and cats isaccidental ingestion of rodenticide baits containing cholecalciferol (Rumbeiha, 2006). Vitamin D3 is widely used as feed supplement in commercial livestock, pet and infantfeeds. The presence of excessive amount of vitamin D3 in commercial feed supplementsreported causing toxicity especially in pets, swine and human infants (Stevenson et al.,1976; Long, 1984; Morita et al., 1995; Roberson et al., 2000).
  2. 2. 2 The plant species like golden oat grass (Trisetum flavescens), Cestrum diurnum andSolanum nigricans are reported to have a high concentration of vitamin D3 analogue. Thegrazing of livestock on pastures containing these plant species have been reported tocause a disorder called enzootic calcinosis or Manchester wasting disease (Beasly, 1999). Accidental ingestion of human medications containing vitamin D analogues used fortreatment of number of diseases like hypophosphatemic disorders, hypoparathyroidism,osteomalacia, osteoporosis and renal failure (Beasly, 1999).Toxicity: Based upon clinical reports, toxicoses have occurred in dogs from the ingestion ofcholecalciferol at 0.5 - 3 mg/kg body weight. Administration of 10 - 20 mg/kg to dogs ofcholecalciferol-based rodenticide resulted in death in 4 dogs. Younger animals appear at higher risk to the development of toxicosis. Acute oral LD50 in dogs of technical material in oil has been reported to be 85 mg/kg.This has lead to an underestimate of the actual hazard of the rodenticide products for thisspecies. Relay toxicosis: not reported in experimental studies. 40 IU vitamin D = 1 mcg. Thus, 1 IU of vitamin D3 = 0.025 mcg of cholecalciferol.Mechanism of Action: Physiologically vitamin D and its metabolites maintain normal calcium levels in blood byincreasing intestinal absorption of calcium, stimulating bone resorption and decreasingrenal excretion of calcium. In high doses, Vitamin D2 and D3 accelerate these mechanisms many a times leading tomarked hypercalcemia as result of which calcium salts are deposited in soft tissues suchas kidneys, blood vessels, heart and lungs. Thus, soft tissues tend to become calcifiedwhile a bone tends to be rarified. The mineralization of vital organs viz. kidneys, heart and lungs cause structural damagethat leads to decreased functional capacity of these tissues and organs. The loss offunction contributes to the development of ongoing end stage clinical signs as well aslong term signs in animals that survive. The cause of death reported in vitamin D3 toxicityincludes cardiac and renal failure (Beasly, 1999; Morrow, 2001; Sandhu and Brar, 2009).
  3. 3. 3Clinical Signs: Diarrhoea, subnormal body temperature and progressive wasting. Anorexia, dullness, rigidity of limbs and difficulty in movement. Affected animals cannot walk properly/ shows tumbling movements and even cannotopen mouth. Ruffled body coat, severe progressive emaciation, dehydration and weakness. Difficulty in respiration, exhibited snoring sound during respiration, shivering andepistaxis. Before death, nervous signs like aimless running, rolling and epileptic seizures can beseen (Chavhan et al., 2011).Clinicopathological findings: Increased plasma levels of calcium (hypercalcemia), phosphorus and Blood UreaNitrogen (BUN). The gross postmortem findings include white chalky deposits ofcalcium on epicardial surface of heart and serosal surface of intestine. The stomach andintestines may reveal bloody ingesta in the lumen with marked hemorrhages on mucosa.The pin point white chalky deposits of calcium can be observed on capsules of bothkidneys. Histopathologically, the mineralization of various visceral organs (viz. heart,lungs, kidneys, aorta etc.) can be observed (Chavhan et al., 2011).Diagnosis: History of ingestion of rodenticide or in case of grazing livestock, the pasture should bechecked for presence of calcinogenic plants. Clinical signs, elevated level of calcium, phosphorus and BUN. In dead animals, diagnosis can be done from gross postmortem and histopathologicalfindings (calcification/mineralization of various visceral organs).Treatment: No specific antidote available for cholecalciferol toxicity. Treatment of Vitamin D3toxicosis is aimed primarily at lowering the elevated serum calcium levels. The followingdrugs can be used to lower the calcium level. Corticosteroids (cortisone and prednisone): Dogs & cats: 1-2 mg/kg, orally orintramuscular, once daily. Salmon calcitonin: Dogs & cats: 4-6 IU/kg, 2-3 times daily.
  4. 4. 4 Pamidronate: Dogs: 1.3-2 mg/kg, slow IV in 0.9% sodium chloride solution over a periodof 2-4 hours. It may be repeated at 96 hours. Fluid therapy along with diuretics (frusemide) helps to reduce hypercalcemia. Emesis orgastric lavage, administration of activated charcoal and osmotic cathartic helps to removeunabsorbed toxicant.Prognosis: Prognosis of vitamin D based rodenticide toxicosis is guarded, if the clinicalsigns are severe or advanced.REFERENCES1. Beasley V R. 1999. Veterinary Toxicology. International Veterinary Information Service(www.ivis.org), Ithaca, New York, USA.2. Chavhan SG, Brar RS, Banga HS, Sandhu HS, Sodhi S, Gadhave PD, Kothule VR andKammon AM. 2011. Clinicopathological Studies on Vitamin D3 Toxicity and TherapeuticEvaluation of Aloe vera in Rats. Toxicology International 18(1): 35-43.3. Chen PS and Bosman HB. 1965. Comparision of the hypercalcemic action of vitamins D2and D3 in chicks and the effect on tetracycline fixation by bone. J. Nutr. 87: 148-154.4. Hunt RD, Garcia FG and Walsh RJ. 1972. A comparison of the toxicity of ergocalciferoland cholecalciferol in Rhesus monkeys (Macaca mulatta). J. Nutr. 102: 975-986.5. Long GG. 1984. Acute toxicosis in swine associated with excessive dietary intake ofvitamin D. JAVMA 184: 164-170.6. Morita T, Awakura T, Shimada A, Umemura T, Nagai T and Haruna A. 1995. Vitamin Dtoxicosis in cats: Natural outbreak and experimental study. J. Vet. Med. Sci. 57: 831-837.7. Morrow C. 2001. Cholecalciferol poisoning. Vet. Med. 12: 905-911.8. Roberson RJ, Swecker WS and Hullender LL. 2000. Hypercalcemia andhypervitaminosis D in two lambs. JAVMA 216: 1115-1118.9. Rumbeiha W K. 2006. Specific toxicants: cholecalciferol. In: Peterson M E and Talcott PA (ed). Small Animal Toxicology. 2ndEdn. Saunders Elsevier, Missouri, USA.pp:629-642.10. Sandhu HS and Brar RS. 2009. Pesticides: Organic Rodenticides (Vitamin DCompounds). In: Textbook of Veterinary Toxicology. 2ndEdn. Kalyani Publishers,Ludhiana, India. pp: 244-246.11. Smith SE. 1982. Vitamins. In: Swenson MJ. (ed). Duke’s Physiology of DomesticAnimals. Comstock Publishing Associate, Cornell University Press, USA. pp:380-382.12. Stevenson RG, Palmer NC and Finley GG. 1976. Hypervitaminosis D in rabbits. Can.Vet. Jour. 17: 54-57.*********************************************************

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