Dietary-Related Skeletal Changes in a Shetland Sheepdog Puppy

McMillan, Chantal; Griffon, Dominique J.; Marks, Steven L.; Mauldin, Glenna E.

doi:10.5326/0420057

Cited by 17 publications

(19 citation statements)

References 9 publications

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“…10 The diet that precipitated skeletal changes in the dog of this report was deficient in calcium, phosphorus, and vitamin D (although some calcium carbonate has since been added to the premix 36 ). In the previous report, 10 the puppy' s bone mineral density prior to initiating a diet change was only moderately decreased (80% of the value expected in clinically normal puppies of the same age).…”

Section: Discussionmentioning

confidence: 83%

“…[10][11][12] Although the diet mixture fed to the dog of this report was not analyzed for vitamin D content, the specific diet components (muesli-vegetable premix and ground beef) are not adequate sources of 1,25-hydroxyvitamin D 3 , 4 nor was the muesli-vegetable premix supplemented with vitamin D by the manufacturer. However, radiography revealed severe curvature of the scapulae, which is a common vitamin D deficiencyinduced deformity in dogs and sheep.…”

Section: Discussionmentioning

confidence: 97%

“…[16][17][18][19] Briefly, low blood calcium concentration is detected by calcium-sensing receptors in the chief cells of the parathyroid gland. 10,12,15,21,22 In addition to deficiencies or excesses of any 1 constituent, a secondary pathologic change can develop because of feedback mechanisms, altered calcium-to-phosphorus ratio, or metabolic deficiencies. 15,16 This active form of vitamin D activates calcium-binding proteins (calbindins) along with calcium channels and pumps, thereby enhancing enterocyte absorption of calcium and phosphorus from duodenal and colonic sites.…”

Section: Discussionmentioning

confidence: 99%

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Diffuse osteopenia and myelopathy in a puppy fed a diet composed of an organic premix and raw ground beef

Taylor¹,

Geiger²,

Saker³

et al. 2009

javma

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In the dog of this report, vitamin D-dependent rickets type I and suspected nutritional secondary hyperparathyroidism developed following intake of a nutritionally incomplete and unbalanced diet. The raw meat-based, home-prepared diet fed to the dog was not feed-trial tested for any life stage by the Association of American Feed Control Officials, and its gross nutrient imbalance induced severe metabolic, orthopedic, and neurologic abnormalities. Inadvertent malnutrition can be avoided through proper diet assessment and by matching nutrient profiles with patients' nutritional needs.

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Section: Discussionmentioning

confidence: 83%

Section: Discussionmentioning

confidence: 97%

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Diffuse osteopenia and myelopathy in a puppy fed a diet composed of an organic premix and raw ground beef

Taylor¹,

Geiger²,

Saker³

et al. 2009

javma

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show abstract

“…141 Ten weeks later, the dog presented with varus deformities of the forelimbs, failure to grow, and prominent metaphyses, and radiographically, it had widened physes. 141 The renal failure diet had low protein and phosphate levels, which were inadequate for growth. Replacement of the diet with one specific for growing puppies led to resolution of clinical signs.…”

Section: Dogsmentioning

confidence: 99%

“…Replacement of the diet with one specific for growing puppies led to resolution of clinical signs. 141 In a recent report, VDDR I and suspected nutritional secondary hyperparathyroidism were diagnosed in an 8-month-old Shetland Sheepdog with diffuse osteopenia and myelopathy fed an organic premix and raw ground beef. 195 The term vitamin D-dependent rickets type I was used incorrectly in this case, given that this form of rickets is associated with a genetic defect in the activity of renal 1a-hydroxylase, rather than with a deficient diet.…”

Section: Dogsmentioning

confidence: 99%

Vitamin D Metabolism and Rickets in Domestic Animals

2010

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Rickets and osteomalacia are increasing in prevalence in people because of cultural practices, breast-feeding, decreased sun exposure, and increased sunscreen usage. Several hereditary forms of rickets owing to either renal phosphate wasting or defects in vitamin D metabolism are also reported in people. Rickets is well recognized in domestic animals, but published reports are not always supported by microscopic findings, and diagnoses based on clinical signs and radiology are unreliable. Most cases in domestic animals are caused by dietary deficiency of either vitamin D or phosphorus, but occasional inherited forms are reported in pigs, sheep, cats, and dogs. There is variation between species in susceptibility to dietary vitamin D and phosphorus deficiency and in the ability to manufacture vitamin D in their skin. A number of mouse models have been discovered or created to study human skeletal diseases and skeletal homeostasis. With the discovery that vitamin D is involved in not only calcium and phosphorus homeostasis but also in the immune system and cancer, there is great potential for new and existing animal models to generate valuable information about vitamin D and its many functions. This review presents an overview of vitamin D metabolism and rickets in domestic and laboratory animals and makes comparisons where appropriate with the disease in humans. Keywords bone, rickets, vitamin D, phosphorus, genetic diseasesRickets is a classic metabolic bone disease of humans and animals, first described in the first and second centuries. 158,165 With the discovery that vitamin D could prevent rickets, the prevalence of this disease in developed countries plummeted; however, it still occurs. In fact, the prevalence of rickets and vitamin D insufficiency is increasing in people of all ages in the developed world, due in part to decreased sunlight exposure and widespread sunscreen usage. 88 The disease is well recognized in animals, but published reports are uncommon and sometimes confusing.The pathogenesis of rickets involves impaired mineralization of physeal and epiphyseal cartilage during endochondral ossification and of newly formed osteoid. Most cases in domestic animals are caused by dietary deficiency of either vitamin D or phosphorus, but occasional inherited forms are reported. 109,200 Osteomalacia is caused by a failure of newly formed osteoid to mineralize, but it occurs in adults after closure of growth plates. 109In this article, we review vitamin D metabolism and rickets, with reference to the disease in domestic animals but presenting comparison with the disease in humans where appropriate. Biology of Vitamin D Activation of Vitamin DVitamin D is available from two sources: isomerization of 7-dehydrocholesterol (7-DHC) in the skin to vitamin D 3 following exposure to ultraviolet light or from ingestion of vitamin D 2 or D 3 in the diet. Only a few foods, including cod liver oil and fatty fish such as salmon and sardines, naturally contain high concentrations of vitamin D 3 .49 Vitamin D 2 i...

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Long‐Term Management of Food Hypersensitivity in the Dog

Cave

2013

Veterinary Allergy

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Dietary-Related Skeletal Changes in a Shetland Sheepdog Puppy

Cited by 17 publications

References 9 publications

Diffuse osteopenia and myelopathy in a puppy fed a diet composed of an organic premix and raw ground beef

Diffuse osteopenia and myelopathy in a puppy fed a diet composed of an organic premix and raw ground beef

Vitamin D Metabolism and Rickets in Domestic Animals

Long‐Term Management of Food Hypersensitivity in the Dog

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