Use of pamidronate to reverse vitamin D3-induced toxicosis in dogs

Wilson K. Rumbeiha From the Departments of Veterinary Pathology (Rumbeiha, Fitzgerald, Chiapuzio), Small Animal Clinical Sciences (Kruger), Large Animal Clinical Sciences (Nachreiner, Kaneene), and Pharmacology and Toxicology (Braselton), College of Veterinary Medicine, Michigan State University, East Lansing, MI 48824.

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John M. Kruger From the Departments of Veterinary Pathology (Rumbeiha, Fitzgerald, Chiapuzio), Small Animal Clinical Sciences (Kruger), Large Animal Clinical Sciences (Nachreiner, Kaneene), and Pharmacology and Toxicology (Braselton), College of Veterinary Medicine, Michigan State University, East Lansing, MI 48824.

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Scott F. Fitzgerald From the Departments of Veterinary Pathology (Rumbeiha, Fitzgerald, Chiapuzio), Small Animal Clinical Sciences (Kruger), Large Animal Clinical Sciences (Nachreiner, Kaneene), and Pharmacology and Toxicology (Braselton), College of Veterinary Medicine, Michigan State University, East Lansing, MI 48824.

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Raymond F. Nachreiner From the Departments of Veterinary Pathology (Rumbeiha, Fitzgerald, Chiapuzio), Small Animal Clinical Sciences (Kruger), Large Animal Clinical Sciences (Nachreiner, Kaneene), and Pharmacology and Toxicology (Braselton), College of Veterinary Medicine, Michigan State University, East Lansing, MI 48824.

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John B. Kaneene From the Departments of Veterinary Pathology (Rumbeiha, Fitzgerald, Chiapuzio), Small Animal Clinical Sciences (Kruger), Large Animal Clinical Sciences (Nachreiner, Kaneene), and Pharmacology and Toxicology (Braselton), College of Veterinary Medicine, Michigan State University, East Lansing, MI 48824.

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W. Emmett Braselton From the Departments of Veterinary Pathology (Rumbeiha, Fitzgerald, Chiapuzio), Small Animal Clinical Sciences (Kruger), Large Animal Clinical Sciences (Nachreiner, Kaneene), and Pharmacology and Toxicology (Braselton), College of Veterinary Medicine, Michigan State University, East Lansing, MI 48824.

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Crystal L. Chiapuzio From the Departments of Veterinary Pathology (Rumbeiha, Fitzgerald, Chiapuzio), Small Animal Clinical Sciences (Kruger), Large Animal Clinical Sciences (Nachreiner, Kaneene), and Pharmacology and Toxicology (Braselton), College of Veterinary Medicine, Michigan State University, East Lansing, MI 48824.

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Abstract

Objectives

To determine whether pamidronate di-sodium can reduce vitamin D3-induced hypercalcemia in dogs and whether combination treatment with calcitonin is more effective than treatment with pamidronate alone.

Animals

20 clinically normal male Beagles.

Procedure

All dogs were given 8 mg of cholecalciferol (CCF)/kg of body weight once orally, then were assigned randomly to 4 groups of 5 dogs each. Dogs were given 0.9% NaCl solution IV (group 1), calcitonin SC and 0.9% NaCl solution IV (group 2), pamidronate and 0.9% NaCl solution IV (group 3), or a combination of all 3 agents (group 4). Dogs were observed for 28 days, and serial blood and urine samples were collected for determination of serum biochemical, electrolyte, and 25(OH)D3 values, CBC, and urine mineral excretion. Samples of kidney, stomach, lung, aorta, liver, duodenum, and brain were evaluated by light microscopy and quantitative mineral analysis.

Results

Two dogs in group 1 were euthanatized 4 days after CCF administration because of severe clinical signs of disease. Dogs in group 3 lost less weight and had significantly lower serum phosphorus, total and ionized calcium, and urinary zinc concentrations, compared with dogs in group 1. On day 4, serum urea nitrogen concentration was significantly lower in dogs of groups 3 and 4, compared with dogs in group 1. Mild to moderate mineralization of kidneys and stomach were observed in the 2 group-1 dogs euthanatized on day 4.

Conclusions

Pamidronate administration effectively prevents CCF-induced hypercalcemia and mineralization of soft tissues.

Clinical Relevance

Pamidronate is a potentially useful antidote against CCF toxicosis in dogs. (Am J Vet Res 1999;60:1092-1097)

Abstract

Objectives

To determine whether pamidronate di-sodium can reduce vitamin D3-induced hypercalcemia in dogs and whether combination treatment with calcitonin is more effective than treatment with pamidronate alone.

Animals

20 clinically normal male Beagles.

Procedure

All dogs were given 8 mg of cholecalciferol (CCF)/kg of body weight once orally, then were assigned randomly to 4 groups of 5 dogs each. Dogs were given 0.9% NaCl solution IV (group 1), calcitonin SC and 0.9% NaCl solution IV (group 2), pamidronate and 0.9% NaCl solution IV (group 3), or a combination of all 3 agents (group 4). Dogs were observed for 28 days, and serial blood and urine samples were collected for determination of serum biochemical, electrolyte, and 25(OH)D3 values, CBC, and urine mineral excretion. Samples of kidney, stomach, lung, aorta, liver, duodenum, and brain were evaluated by light microscopy and quantitative mineral analysis.

Results

Two dogs in group 1 were euthanatized 4 days after CCF administration because of severe clinical signs of disease. Dogs in group 3 lost less weight and had significantly lower serum phosphorus, total and ionized calcium, and urinary zinc concentrations, compared with dogs in group 1. On day 4, serum urea nitrogen concentration was significantly lower in dogs of groups 3 and 4, compared with dogs in group 1. Mild to moderate mineralization of kidneys and stomach were observed in the 2 group-1 dogs euthanatized on day 4.

Conclusions

Pamidronate administration effectively prevents CCF-induced hypercalcemia and mineralization of soft tissues.

Clinical Relevance

Pamidronate is a potentially useful antidote against CCF toxicosis in dogs. (Am J Vet Res 1999;60:1092-1097)

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