Clinical Exposures: An incidental finding of primary hyperparathyroidism in a dog - Veterinary Medicine
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Clinical Exposures: An incidental finding of primary hyperparathyroidism in a dog

VETERINARY MEDICINE


Discussion

Primary hyperparathyroidism is an infrequent cause of hypercalcemia in dogs. A single parathyroid gland adenoma is found in most cases (90%), but diffuse parathyroid hyperplasia (5%) and parathyroid gland adenocarcinoma (5%) have been reported.1,2 Dogs typically have four parathyroid glands: two internal and two external. In one study, adenomas were found to involve the internal and external parathyroid glands with equal frequency,3 but this is in contrast to another study that reported a predominance of adenomas affecting the external parathyroid glands.4 Surgical removal of the affected gland is the preferred definitive treatment for primary hyperparathyroidism.

Primary hyperparathyroidism is typically diagnosed in older dogs (mean age of 10.5 years) and has no reported gender predisposition.1,2 Keeshonds may be predisposed to developing primary hyperparathyroidism.1,2 The clinical signs of primary hyperparathyroidism (e.g. polyuria, polydipsia, lethargy, anorexia, weakness) are attributed to hypercalcemia and are typically mild and nonspecific.1-3,5 In most cases, the hypercalcemia is incidentally discovered on a routine serum chemistry profile.

PTH, calcitriol (1,25-dihydroxycholecalciferol), and calcitonin are the main regulators of calcium homeostasis. Hypocalcemia is the main stimulus for PTH synthesis and secretion by the chief cells of the parathyroid gland. Elevated PTH concentrations directly promote calcium resorption from bone, increase calcium reabsorption from renal tubules, and indirectly increase calcium absorption from the intestines (through activation of calcitriol synthesis by the proximal tubules of the kidneys). Hypercalcemia inhibits PTH synthesis, increases PTH degradation, and decreases PTH secretion.1,2,5 Primary hyperparathyroidism results from a defect in normal calcium homeostasis resulting in excessive and inappropriate (relative to the serum calcium concentration) PTH production by the parathyroid glands.1-3

The first step in diagnosing primary hyperparathyroidism is to confirm hypercalcemia by repeating the total serum calcium or ionized calcium measurement on a fasting nonhemolyzed sample.1,2,4 Measuring the ionized calcium concentration is preferred over a total serum calcium concentration, since it is the biologically active form of calcium. A total serum calcium concentration measurement includes the ionized (50%), protein-bound (40%), and complexed (10%) fractions. Once hypercalcemia is confirmed, a thorough list of differential diagnoses and a diagnostic plan should be formulated and followed, as described elsewhere.1,5

Additional findings supportive of primary hyperparathyroidism include elevated serum alkaline phosphatase activity, a decreased serum phosphorus concentration, and calcium-based nephroliths.1 Serum phosphorus concentrations are typically low or low-normal in dogs with primary hyperparathyroidism, because elevated PTH concentrations promote urinary phosphorus excretion by inhibiting proximal renal tubular reabsorption. The low or low-normal phosphorus concentrations typically found in primary hyperparathyroidism are thought to be somewhat protective against soft tissue mineralization, since a low phosphorus value decreases the calcium and phosphorus product to less than 60 to 70, which is typically required for dystrophic mineralization.1,5,6 Elevations in serum alkaline phosphatase activities (mainly the bone isoenzyme) reflect the increased osteoblastic activity caused by the increased PTH concentrations. Primary hyperparathyroidism is then confirmed by evaluating intact PTH, ionized calcium, and PTH-related protein concentrations. PTH-related protein is structurally and functionally related to PTH and is important in the pathogenesis of humoral hypercalcemia of malignancy.1,5 With primary hyperparathyroidism, an inappropriately high PTH concentration is found in conjunction with an elevated ionized calcium concentration since hypercalcemia should normally suppress PTH secretion.1-3 Finding an undetectable PTH-related protein concentration further solidifies a diagnosis of primary hyperparathyroidism, because it rules out humoral hypercalcemia of malignancy.1,2,5,6

The preoperative management of hyperparathyroidism includes diuresis with 0.9% saline solution to achieve extracellular fluid volume expansion and promote calciuresis. Saline solution is the most appropriate fluid for volume expansion and calciuresis in hypercalcemic patients since it is completely devoid of calcium and also has a slightly higher sodium concentration, thereby promoting calciuresis better then calcium-containing balanced electrolyte solutions. If 0.9% sodium chloride is not available, other balanced electrolyte solutions can be effective in lowering the serum calcium concentration.1,6 Furosemide, calcitonin (calcitonin-salmon), bisphosphonates, and sodium bicarbonate can also be used to manage hypercalcemia.1-3,6 Additional therapy was not indicated in this dog because the total serum calcium concentration had decreased to 13 mg/dl before surgery with saline diuresis alone. Preoperative calcitriol administration is recommended in patients with total serum calcium concentrations greater than 14 mg/dl or with chronic hypercalcemia, to circumvent a hypocalcemic crisis in the postoperative period.2 Although unproven, we suspected that this dog's hypercalcemia was chronic, since calcium-based cystic calculi had been surgically removed three years before and large radiopaque nephroliths were visible on abdominal radiographs. Unfortunately, serum calcium concentrations were not measured at the time of the dog's cystotomy to confirm our suspicion.

Calcium supplementation is also indicated in the postoperative period to prevent hypocalcemia. The goal of therapy is to maintain the serum calcium concentration at the lower end of the normal range, thereby not suppressing endogenous PTH production from the remaining atrophied parathyroid glands. Hypocalcemia typically develops within the first week after surgery and coincides with the decrease in PTH concentration after surgical removal of the autogenously PTH-producing mass.1,2 The remaining parathyroid glands are typically atrophied because of the chronic negative feedback associated with hypercalcemia. These atrophied parathyroid glands are unable to synthesize and secrete enough PTH to maintain normocalcemia in the postoperative period. This postoperative hypocalcemia is usually transient, and most patients can be weaned off the calcitriol and calcium supplementation within three or four months of surgery.1,2

The prognosis for patients with primary hyperparathyroidism is greatly affected by the secondary changes resulting from the hypercalcemia, especially renal failure. Dogs with moderate to severe azotemia typically have a worse prognosis than dogs with minimal or reversible renal disease. After surgery, some dogs require lifelong medical management of their renal failure.1-3

The photographs and information for this case were provided by Robert J. Vasilopulos, DVM, MS, Department of Small Animal Internal Medicine, College of Veterinary Medicine, Mississippi State University, Mississippi State, MS 39762-6100.

REFERENCES

1. Rosol, T. et al.: Disorders of calcium: Hypercalcemia and hypocalcemia. Fluid Therapy in Small Animal Practice (S.P. DiBartola, ed.). W.B. Saunders, Philadelphia, Pa., 2000; pp 163-174.

2. Feldman, E.C.: Disorders of the parathyroid glands. Textbook of Veterinary Internal Medicine, 5th Ed. (S.J. Ettinger; E.C. Feldman, eds.). W.B. Saunders, Philadelphia, Pa., 2000; pp 1379-1399.

3. Berger, B.; Feldman, E.C.: Primary hyperparathyroidism in dogs: 21 cases (1976-1986). JAVMA 191 (3):350-356; 1987.

4. Wisner, E.R. et al.: High-resolution parathyroid sonography. Vet. Radiol. Ultrasound 38 (6):462-466; 1997.

5. Vasilopulos, R.J.; Mackin, A.J.: Humoral hypercalcemia of malignancy: Pathophysiology and clinical signs. Compend. Cont. Ed. 25:122-128; 2003.

6. Vasilopulos, R.J.; Mackin, A.J.: Humoral hypercalcemia of malignancy: Diagnosis and treatment. Compend. Cont. Ed. 25:129-136; 2003.


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