Benign familial hyperphosphatasemia in Siberian Huskies

D. F. Lawler From the Departments of Pet Nutrition Research (Lawler, Herndon, Fischer) and Data Services (Keltner), Ralston Purina Co, Checkerboard Square, St Louis, MO 63164; Department of Clinical Pathology, College of Veterinary Medicine, University of Illinois, Urbana, IL 61801 (Hoffman); Animal Diagnostic Laboratory, College of Veterinary Medicine, Michigan State University, East Lansing, Ml 48824 (Nachreiner); and Department of Small Animal Clinical Sciences, College of Veterinary Medicine, University of Minnesota, St Paul, MN 55108 (Hegstad).

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D. G. Keltner From the Departments of Pet Nutrition Research (Lawler, Herndon, Fischer) and Data Services (Keltner), Ralston Purina Co, Checkerboard Square, St Louis, MO 63164; Department of Clinical Pathology, College of Veterinary Medicine, University of Illinois, Urbana, IL 61801 (Hoffman); Animal Diagnostic Laboratory, College of Veterinary Medicine, Michigan State University, East Lansing, Ml 48824 (Nachreiner); and Department of Small Animal Clinical Sciences, College of Veterinary Medicine, University of Minnesota, St Paul, MN 55108 (Hegstad).

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W. E. Hoffman From the Departments of Pet Nutrition Research (Lawler, Herndon, Fischer) and Data Services (Keltner), Ralston Purina Co, Checkerboard Square, St Louis, MO 63164; Department of Clinical Pathology, College of Veterinary Medicine, University of Illinois, Urbana, IL 61801 (Hoffman); Animal Diagnostic Laboratory, College of Veterinary Medicine, Michigan State University, East Lansing, Ml 48824 (Nachreiner); and Department of Small Animal Clinical Sciences, College of Veterinary Medicine, University of Minnesota, St Paul, MN 55108 (Hegstad).

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R. F. Nachreiner From the Departments of Pet Nutrition Research (Lawler, Herndon, Fischer) and Data Services (Keltner), Ralston Purina Co, Checkerboard Square, St Louis, MO 63164; Department of Clinical Pathology, College of Veterinary Medicine, University of Illinois, Urbana, IL 61801 (Hoffman); Animal Diagnostic Laboratory, College of Veterinary Medicine, Michigan State University, East Lansing, Ml 48824 (Nachreiner); and Department of Small Animal Clinical Sciences, College of Veterinary Medicine, University of Minnesota, St Paul, MN 55108 (Hegstad).

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R. L. Hegstad From the Departments of Pet Nutrition Research (Lawler, Herndon, Fischer) and Data Services (Keltner), Ralston Purina Co, Checkerboard Square, St Louis, MO 63164; Department of Clinical Pathology, College of Veterinary Medicine, University of Illinois, Urbana, IL 61801 (Hoffman); Animal Diagnostic Laboratory, College of Veterinary Medicine, Michigan State University, East Lansing, Ml 48824 (Nachreiner); and Department of Small Animal Clinical Sciences, College of Veterinary Medicine, University of Minnesota, St Paul, MN 55108 (Hegstad).

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P. A. Herndon From the Departments of Pet Nutrition Research (Lawler, Herndon, Fischer) and Data Services (Keltner), Ralston Purina Co, Checkerboard Square, St Louis, MO 63164; Department of Clinical Pathology, College of Veterinary Medicine, University of Illinois, Urbana, IL 61801 (Hoffman); Animal Diagnostic Laboratory, College of Veterinary Medicine, Michigan State University, East Lansing, Ml 48824 (Nachreiner); and Department of Small Animal Clinical Sciences, College of Veterinary Medicine, University of Minnesota, St Paul, MN 55108 (Hegstad).

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B. J. Fischer From the Departments of Pet Nutrition Research (Lawler, Herndon, Fischer) and Data Services (Keltner), Ralston Purina Co, Checkerboard Square, St Louis, MO 63164; Department of Clinical Pathology, College of Veterinary Medicine, University of Illinois, Urbana, IL 61801 (Hoffman); Animal Diagnostic Laboratory, College of Veterinary Medicine, Michigan State University, East Lansing, Ml 48824 (Nachreiner); and Department of Small Animal Clinical Sciences, College of Veterinary Medicine, University of Minnesota, St Paul, MN 55108 (Hegstad).

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Abstract

Objective

To evaluate benign familial hyperphosphatasemia involving serum alkaline phosphatase (SAP) in pups.

Design

Pups with markedly increased SAP activity were evaluated and compared with unaffected siblings, and with other unaffected Siberian Husky pups from the same colony.

Animals

8 related litters of Siberian Husky pups (n = 56).

Procedure

At ages 11 and 16 weeks, pups were given physical examinations and blood was obtained for hematologic and serum biochemical analyses (including electrolytes and isoenzymes of alkaline phosphatase), ionized calcium concentration, and serum parathyroid hormone concentration. Diet, growth and health performance, skeletal radiographs, and genealogical data also were evaluated.

Results

Of 42 pups tested, 17 had markedly high total SAP values. Mean total SAP activity of affected pups at ages 11 and 16 weeks was over 5 times greater than mean total SAP activity of unaffected siblings and other unaffected Siberian Husky pups of the same age (P <0.001). Clinical, radiologic, and biochemical evaluation of the subjects revealed no other abnormal findings. The source of the increased SAP activity was characterized in 5 affected pups as bone isoenzyme. The mode of inheritance could not be deduced from the data, but the trait clearly is familial and autosomal.

Conclusion

The condition described in the family of Siberian Huskies bears similarity to human benign, persistent, familial hyperphosphatasemia.

Clinical Relevance

Benign familial hyperphosphatasemia should be considered in the differential diagnosis of markedly increased SAP activity in young dogs. (Am J Vet Res 1996; 57:612–617)

Abstract

Objective

To evaluate benign familial hyperphosphatasemia involving serum alkaline phosphatase (SAP) in pups.

Design

Pups with markedly increased SAP activity were evaluated and compared with unaffected siblings, and with other unaffected Siberian Husky pups from the same colony.

Animals

8 related litters of Siberian Husky pups (n = 56).

Procedure

At ages 11 and 16 weeks, pups were given physical examinations and blood was obtained for hematologic and serum biochemical analyses (including electrolytes and isoenzymes of alkaline phosphatase), ionized calcium concentration, and serum parathyroid hormone concentration. Diet, growth and health performance, skeletal radiographs, and genealogical data also were evaluated.

Results

Of 42 pups tested, 17 had markedly high total SAP values. Mean total SAP activity of affected pups at ages 11 and 16 weeks was over 5 times greater than mean total SAP activity of unaffected siblings and other unaffected Siberian Husky pups of the same age (P <0.001). Clinical, radiologic, and biochemical evaluation of the subjects revealed no other abnormal findings. The source of the increased SAP activity was characterized in 5 affected pups as bone isoenzyme. The mode of inheritance could not be deduced from the data, but the trait clearly is familial and autosomal.

Conclusion

The condition described in the family of Siberian Huskies bears similarity to human benign, persistent, familial hyperphosphatasemia.

Clinical Relevance

Benign familial hyperphosphatasemia should be considered in the differential diagnosis of markedly increased SAP activity in young dogs. (Am J Vet Res 1996; 57:612–617)

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