A challenging case: Primary hyperparathyroidism in a dog - Veterinary Medicine
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A challenging case: Primary hyperparathyroidism in a dog
Ultrasonographic examinations helped identify the source of this dog's persistent hypercalcemia.



Naturally occurring primary hyperparathyroidism is not common in dogs.1 It occurs when abnormal autonomously functioning parathyroid chief cells produce excessive PTH, most often because of a solitary adenoma.1 In one report of 72 dogs with primary hyperparathyroidism, benign adenomatous transformation of one parathyroid gland occurred in about 90% of cases, malignant transformation in 5%, and adenomatous hyperplasia in the remaining 5%.2 The condition typically affects older dogs and has no sex predilection, but Keeshonds are overrepresented and it was recently linked to a single gene with an autosomal dominant mode of inheritance.3

Clinical signs

When clinical signs develop in dogs with primary hyperparathyroidism, they tend to be mild, insidious, and nonspecific. The most common signs are polyuria, polydipsia, decreased appetite, weight loss, and lethargy. Other clinical signs frequently reported are related to cystic calculi or urinary tract infections.4

Commonly reported secondary signs related to hypercalcemia include anorexia, vomiting, and constipation. Pancreatitis is rarely observed. Mild or early disease may be nonsymptomatic and found unexpectedly on laboratory evaluation.


The hallmark for primary hyperparathyroidism is persistent progressive hypercalcemia. In dogs with confirmed primary hyperparathyroidism, 102 of 187 had an initial total calcium concentration of 12 to 14 mg/dl (3 to 3.5 mmol/L).4 Hypercalcemia in conjunction with an elevated PTH concentration and an undetectable PTHrP concentration is considered the gold standard for primary hyperparathyroidism diagnosis. However, about 75% of affected dogs have normal PTH concentrations,5 which are inappropriate in the face of hypercalcemia. In normal animals, a high calcium concentration should result in undetectable PTH concentrations.

Other consistent findings on serum chemistry profiles of affected dogs include low or low-normal phosphorus, blood urea nitrogen, and creatinine concentrations. The urine is typically hyposthenuric because calcium inhibits vasopressin's action on the renal tubules. In one study, 61 of 187 dogs with primary hyperparathyroidism had a history of urolithiasis, with a large proportion of dogs initially presenting because of urinary tract signs.4

Abdominal radiography and ultrasonography identified cystic calculi in 50 of 210 dogs with primary hyperparathyroidism examined in one study.1 Abdominal imaging as well as abdominal palpation and rectal examination are also important to evaluate the abdominal organs and lymph nodes for occult neoplasia or metastasis from an anal sac adenocarcinoma. Thoracic radiography is essential in the diagnostic evaluation of dogs with hypercalcemia to identify or rule out occult neoplasia.

If no other cause of hypercalcemia is identified, a cervical ultrasonographic examination should be performed to evaluate both thyroid glands and all four parathyroid glands. Although ultrasonography results are subjective in nature, one study demonstrated a significant size difference between neoplastic (adenocarcinoma and adenoma) and hyperplastic (primary hyperplasia and secondary [renal] hyperplasia) parathyroid tissue.2 In healthy dogs, the parathyroid glands are typically
< 3 mm in diameter, while parathyroid masses are usually > 4 mm in diameter.6 Many dogs with primary hyperparathyroidism have normal or low-normal PTH concentrations, which can make diagnosis difficult, but with abnormal parathyroid ultrasonography results, the diagnosis is more likely.

Although not commonly used in veterinary medicine, radionuclide scanning of the parathyroid glands is another method to diagnose primary hyperparathyroidism.


Treatment options for primary hyperparathyroidism include parathyroidectomy or alternative methods for ablating the affected parathyroid gland. Deciding which intervention to use should be based on lowering the risk of urolithiasis and urinary tract infections. The risk of renal failure secondary to hypercalcemia associated with primary hyperparathyroidism is reported to be low1 ; however, in a recent review of 29 dogs with primary hyperparathyroidism, renal failure was diagnosed in 24% either at presentation or up to six months after parathyroidectomy.7

Nonsurgical intervention. Nonsurgical interventions include percutaneous ultrasound-guided ethanol ablation and percutaneous ultrasound-guided radiofrequency heat ablation.8,9 Ethanol causes coagulation necrosis and vascular thrombosis within the parenchyma of the treated tissue.8 In one study, seven of eight dogs treated with ethanol (96%) injections achieved remission after the injection, with only one treatment being required in six of seven dogs and one dog requiring a second treatment to achieve complete remission.8

Percutaneous ultrasound-guided heat ablation has also been used in treating primary hyperparathyroidism in dogs.9 The main advantage of heat ablation over ethanol injection is the lowered potential to damage surrounding tissues. However, the overall outcome of one study showed that heat ablation and ethanol injection had similar remission rates.9

Surgery. Surgically removing the affected parathyroid gland, as was done in this case, is the gold standard of therapy. The most common postoperative complication is hypocalcemia because autonomous PTH production from the parathyroid tumor causes atrophy of the remaining parathyroid glands.

To help prevent hypocalcemia, maintain the total calcium concentration just below low-normal to allow the remaining parathyroid glands to regain normal PTH production. If total calcium and PTH concentrations are low after surgery, administer calcium and calcitriol to maintain calcium homeostasis until the autonomous function of the remaining parathyroid glands is restored.

Calcitriol is recommended to promote intestinal absorption of calcium, with a loading dose of 0.02 to 0.03 g/kg (20 to 30 ng/kg) daily orally for the initial three or four days and a maintenance dose of 0.005 to 0.015 g/kg (5 to 15 ng/kg) daily.10 Calcium supplementation can be provided by administering calcium gluconate, calcium lactate, calcium chloride, or calcium carbonate salts at 25 mg/kg orally every eight to 12 hours for four to six weeks after surgery.11

The risk of postoperative hypocalcemia correlates with the duration and severity of hypercalcemia before surgery and typically develops one to seven days after surgery.5 Because hypocalcemia can be life threatening, consider performing surgery early in the week to facilitate close monitoring of postoperative total calcium concentrations throughout the remainder of the week, unless round-the-clock care can be provided on weekends.


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