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Peer-reviewed veterinary case report

Primary hyperparathyroidism caused by a functional parathyroid adenoma in a horse.

Journal:
Journal of the American Veterinary Medical Association
Year:
1998
Authors:
Peauroi, J R et al.
Affiliation:
Veterinary Medical Teaching Hospital · United States
Species:
horse

Plain-English summary

A 14-year-old Arabian gelding was losing weight and had stopped eating for three weeks. Tests showed that he had high levels of calcium in his blood, while his phosphorus levels were normal or low. Further examination after he passed away revealed a growth in his parathyroid gland, leading to a diagnosis of primary hyperparathyroidism, which is a condition where the parathyroid gland produces too much hormone. This case highlights that primary hyperparathyroidism should be considered as a possible cause of high calcium levels in horses when other common causes have been ruled out. Unfortunately, the treatment options for this condition were not detailed in the study, so we don't know how effective they were.

Abstract

A 14-year-old Arabian gelding had weight loss and anorexia of 3 weeks' duration. Results of repeated laboratory tests revealed persistent hypercalcemia and serum phosphorus concentration that was within or less than the reference range. Parathyroid hormone concentration was high. Histologic examination of specimens obtained at necropsy revealed parathyroid adenoma. A diagnosis of primary hyperparathyroidism attributable to a functional parathyroid adenoma was made. Abnormalities in calcium and phosphorus concentrations were similar to those seen with primary hyperparathyroidism in dogs, in which this syndrome is best described. Primary hyperparathyroidism should be considered to be a potential cause of hypercalcemia in horses in which other more common causes of hypercalcemia, such as humoral hypercalcemia of malignancy, nutritional secondary hyperparathyroidism, chronic renal failure, vitamin D toxicosis, and bony or granulomatous disease, are ruled out.

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Original publication: https://pubmed.ncbi.nlm.nih.gov/9638193/