Diagnosing and treating primary hypoparathyroidism in dogs and cats - Veterinary Medicine
Medicine Center
DVM Veterinary Medicine Featuring Information from:


Diagnosing and treating primary hypoparathyroidism in dogs and cats
The diagnosis is fairly straightforward, and, regardless of the cause, treatment is aimed at relieving the clinical signs related to hypocalcemia. With early detection and proper care, the prognosis for patients with hypoparathyroidism is good.


Expense is the major disadvantage of this drug.11 Additionally, calcitriol is available in only two tablet sizes (0.25 and 0.5 μg).2 To make small dosage adjustments, a liquid formulation is helpful.1,2 The loading dosage of calcitriol is 20 to 40 ng/kg/day orally divided for two to four days, followed by a maintenance dosage of 5 to 20 ng/kg/day divided every 12 hours.1,2 Some authors recommend up to 30 to 60 ng/kg/day.10 The dose may be divided to maximize its priming effects on the intestinal epithelial cells to transport calcium.2 Parenteral formulations of calcitriol are available when the oral formulations are ineffective or not well-tolerated.1

Oral calcium salt supplementation

The final component of long-term treatment of primary hypoparathyroidism at home is the administration of an oral calcium salt supplement (carbonate, lactate, gluconate, and chloride), given concurrently with the vitamin D analogue.1,3,10 In the immediate post-tetany period, high quantities of calcium in the gut increase calcium absorption independent of the presence of a vitamin D analogue.2,3 Later oral calcium supplementation also provides the necessary calcium on which vitamin D analogues function.1-3 The dosage for oral elemental calcium in dogs is 1 to 4 g/day (in cats 0.5 to 1 g/day),1,3 or more specifically 25 to 50 mg/kg or 100 to 500 mg/kg,2,10 divided three to four times daily. Commercially made pet foods contain sufficient calcium for animals with normal calcitriol concentrations.1-3 Therefore, oral calcium supplementation can be slowly reduced over two to four months once the vitamin D analogue administered has stabilized the serum calcium concentration.1-3 If hyperphosphatemia persists, oral calcium supplementation may be continued as a phosphate binder.2

Several calcium supplements are available that can be used during long-term management of primary hypoparathyroidism. In people, calcium carbonate is the treatment of choice because it has a relatively high calcium concentration (40%), which requires administration of fewer pills; it is widely available as over-the-counter antacids; it is inexpensive; and it does not cause gastric irritation.1-3 One disadvantage of calcium carbonate is that it may cause an alkalemia, which may aggravate hypocalcemia.1,3 Despite this, calcium carbonate is used frequently in veterinary medicine. Calcium gluconate (10% available calcium) and lactate (13%) contain less elemental calcium than calcium carbonate, so more tablets must be administered to achieve the same effect.1-3 Calcium chloride tablets contain more elemental calcium (27%) but are irritating to the gastric mucosa and should be given with food.1-3

Other therapeutic options used in human medicine

Oral vitamin D and calcium supplementation does not completely address the lack of PTH because hypercalciuria will persist.2,16 People with long-term management of hypoparathyroidism may develop nephrocalcinosis, urolithiasis, and decreased renal function.2 It has not been established that these complications occur in animals, but this appears possible.2 In people with hypoparathyroidism, thiazides are administered to reduce hypercalciuria and may decrease the necessary dose of vitamin D analogue through increased renal retention of calcium.2,16 It is not known if thiazide diuretics would have a similar effect in dogs or cats.2

In people, daily subcutaneous administration of PTH can be effective in maintaining serum calcium concentrations.2 Canine and human PTH are fairly homologous, and an immune response may not be mounted by dogs receiving human PTH.2 However, human PTH is expensive and not readily available, and eventual formation of anti-PTH antibodies is a foreseeable complication.1,9,14


Click here