Surgery STAT: An overview of primary hyperparathyroidism in dogs
Differential diagnoses for hypercalcemia
In addition to PHP, hypercalcemia could be caused by malignancy (e.g., lymphosarcoma, apocrine gland adenocarcinoma of the anal sac, thymoma), Addison's disease, vitamin D toxicosis, renal disease or skeletal lesions. Or the finding could be a spurious laboratory error. Hypercalcemia of malignancy, Addison's disease and renal failure seem to be the most common causes of hypercalcemia in dogs.Recent studies, however, have shown that up to one-third of dogs with PHP may be asymptomatic, and their calcium concentrations may be only mildly increased. Therefore, PHP may actually be more common among middle-aged and older dogs than previously thought.
Most dogs have four parathyroid glands, though the actual number of glands can vary. The parathyroid glands are located either external to the thyroid capsule or within the capsule. Parathyroid glands may be ectopic (i.e., located in an abnormal position because of their development). The thymus develops alongside the internal parathyroid glands, and islets of parathyroid tissue may break off and continue descending into the mediastinum with the thymus, resulting in additional and ectopic parathyroid glands. Parathyroid glands normally are small, ranging in size from 2 to 4 mm; they may be difficult to detect or can easily be mistaken for a thyroid cyst or nodule.
The parathyroid glands generate, store and secrete parathyroid hormone (PTH). PTH is made autonomously and stored within the gland's cells. PTH is secreted in response to decreased extracellular calcium concentrations. Special calcium-sensing receptors reside within the chief cells of the parathyroid glands that send signals to either increase or decrease PTH synthesis and release. PTH acts directly on the kidneys to increase calcium reabsorption, phosphorus excretion and biosynthesis of calcitriol. Calcitriol and PTH act synergistically to increase calcium and phosphate release from bones. Calcitriol also will increase calcium reabsorption in the intestines.
A dog with primary hyperparathyroidism may have signs classified as the following:
Urinary signs seem to be the most common, with up to 50 percent of patients having urinary tract infections or bladder stones. Renal insufficiency or failure may be correlated with the total calcium concentration and prolonged hypercalcemia.
In dogs with PHP, hypercalcemia may be noted incidentally on routine geriatric blood work. Since the true incidence of PHP can be underestimated, it's a good idea to evaluate any dog with a slightly increased calcium concentration. A standard workup for such dogs includes a full physical examination with thorough lymph node evaluation and a rectal examination to assess the anal sacs. If a full serum chemistry profile, complete blood count, and urinalysis have not already been performed, these tests should be ordered and the results assessed.
Next, evaluate the ionized calcium concentration, as this is the most accurate way of assessing a patient's true calcium status. Laboratory orders for PTH and PTH-related protein tests usually can be submitted at the same time to help keep costs down and prevent the owner from having to bring the patient back to the hospital several times.
Given the high incidence of urinary tract infections, a urine culture also should be considered as dictated by the clinical signs; ordering an abdominal radiograph to assess for bladder stones would be prudent.
Finally, a three-view thoracic radiographic examination can be useful to assess cardiothoracic structures. And ultrasonography can detect the parathyroid nodule preoperatively, but this is user-dependant because of the small size of the parathyroid glands.