section name header

Basics ⬇

Outline

BASICS

Overview!!navigator!!

  • PHPT is caused by excessive and autonomous secretion of PTH by hyperplastic or neoplastic parathyroid chief cells. Excessive PTH secretion originates from parathyroid hyperplasia, adenoma, or adenocarcinoma. This results in hypercalcemia (due to increased renal calcium reabsorption and excessive bone resorption), hypophosphatemia (due to decreased renal phosphorus reabsorption), and excessive bone loss
  • Systems affected—endocrine and musculoskeletal

Signalment!!navigator!!

  • Any sex or breed
  • Reported in aged equids

Signs!!navigator!!

  • Intermittent weakness
  • Weight loss
  • Anorexia
  • Enlargement of facial bones
  • Shifting lameness
  • Difficult mastication

Causes and Risk Factors!!navigator!!

Excessive, uncontrolled secretion of PTH by chief cells of 1 or more parathyroid glands.

Diagnosis ⬆ ⬇

Outline

DIAGNOSIS

Differential Diagnosis!!navigator!!

  • Fibrous osteodystrophy may result from NSHPT in horses fed diets with excessive phosphorus, phytates, or oxalates, or low in calcium. However, depending on the cause, (phosphorus vs. oxalates), hypocalcemia (or normocalcemia) with variable phosphorus concentrations is consistent with NSHPT
  • HHM from tumors (e.g. lymphoma, carcinomas) secreting PTHrP can lead to hypercalcemia and hypophosphatemia. PTHrP binds the PTH receptor. PTH is low and PTHrP high with HHM
  • Other causes of hypercalcemia—chronic renal failure and hypervitaminosis D
  • Normal serum blood urea nitrogen, creatinine concentration, and urine specific gravity rule out chronic renal failure
  • Ingestion of oxalate-containing plants and vitamin D toxicosis can be eliminated based on history. In addition, vitamin D toxicosis is characterized by hyperphosphatemia

CBC/Biochemistry/Urinalysis!!navigator!!

  • Hypercalcemia, hypophosphatemia, and hyperphosphaturia are characteristic
  • Hyperchloremic metabolic acidosis has been associated

Other Laboratory Tests!!navigator!!

  • Fractional excretion of phosphorus (reference range 0.0–0.5%) is increased
  • PTH (increased) and PTHrP (normal)

Imaging!!navigator!!

  • Decreased bone density of appendicular and axial bones, which becomes evident when >30% of bone mass is lost. Skull radiography may reveal radiolucency, fibrous proliferation of facial bones, and loss of the lamina dura surrounding premolars and molars
  • Endoscopic examination may reveal narrowing of the nasal passages
  • Nuclear scintigraphy using technetium (99mTc) sestamibi and ultrasonography may help identify adenomas

Other Diagnostic Procedures!!navigator!!

Horses have 2 pairs of parathyroid glands—the cranial pair is adjacent to the cranial pole of the thyroid gland and the caudal pair has variable location along the trachea to the thoracic inlet. Biopsy is indicated in any mass in these locations in a horse with signs of PHPT.

Pathologic Findings!!navigator!!

  • Parathyroid gland chief cell hyperplasia, adenoma, or adenocarcinoma
  • Equine parathyroid glands may be difficult to distinguish from surrounding tissues
  • With parathyroid neoplasia, atrophy of the nonaffected parathyroid tissue is expected
  • Single or multiple glands may be affected

Treatment ⬆ ⬇

TREATMENT

  • Surgical removal of the affected parathyroid gland and medical treatment for hypercalcemia
  • Hypocalcemia may develop after removal of affected parathyroid gland
  • Reduce calcium intake in animals with hypercalcemia
  • Long-term follow-up is recommended as adenomas may develop in other parathyroid glands, based on other species
  • IV fluid therapy may promote calcium excretion

Medications ⬆ ⬇

MEDICATIONS

Drug(s) of Choice

  • Diuretics and corticosteroids may promote calcium excretion
  • Vitamin D analogs may be considered to suppress parathyroid gland function. Drugs that reduce osteoclast activity/bone resorption (e.g. bisphosphonates) should be considered

Follow-up ⬆ ⬇

FOLLOW-UP

  • Monitor electrolytes, acid–base status, bone density, and PTH concentrations
  • Possible complications—difficulty chewing because of loosening teeth and lameness secondary to osteopenia

Miscellaneous ⬆ ⬇

Outline

MISCELLANEOUS

Abbreviations!!navigator!!

  • HHM = humoral hypercalcemia of malignancy
  • NSHPT = nutritional secondary hyperparathyroidism
  • PHPT = primary hyperparathyroidism
  • PTH = parathyroid hormone
  • PTHrP = PTH-related protein

Suggested Reading ⬆ ⬇

Frank N, Hawkins JF, Couëtil LL, Raymond JT. Primary hyperparathyroidism with osteodystrophia fibrosa of the facial bones in a pony. J Am Vet Med Assoc 1998;212:84–86.

Tomlinson JE, Johnson AL, Ross MW, et al. Successful detection and removal of a functional parathyroid adenoma in a pony using technetium Tc-99 m sestamibi scintigraphy. J Vet Intern Med 2014;28:687–692.

Toribio RE. Disorders of calcium and phosphate metabolism in horses. Vet Clin North Am Equine Pract 2011;27:129–147.

Wong D, Sponseller B, Miles K, et al. Failure of technetium Tc99m sestamibi scanning to detect abnormal parathyroid tissue in a horse and a mule with primary hyperparathyroidism. J Vet Intern Med 2004;18:589–593.

Author(s) ⬆

Author: Ramiro Toribio

Consulting Editors: Michel Levy and Heidi Banse

Acknowledgment: The author and editors acknowledge the prior contribution of Laurent Couëtil.