Primary hypoparathyroidism in dogs and cats: Physiology, clinical signs, and initial diagnostic tests - Veterinary Medicine
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Primary hypoparathyroidism in dogs and cats: Physiology, clinical signs, and initial diagnostic tests
To understand this rare condition, you must be familiar with the physiology of calcium regulation. The net effect of a low PTH concentration is hypocalcemia, and the severity of the clinical signs and the timing of their onset are a reflection of the duration and magnitude of the hypocalcemia.



Naturally occurring primary hypoparathyroidism tends to occur in middle-aged spayed female dogs.3 The average age at the time of presentation is 4.8 years, but it has been reported in dogs as young as 6 weeks and as old as 13 years.1,2 Sixty percent to 65% of the affected dogs are female.1-3 Toy poodles, Labrador retrievers, miniature schnauzers, German shepherds, and terrier breeds are predisposed to the condition.1-3

This condition was first reported in a cat in 1990,1 and few cases have been reported since.4,12,15,18 The average affected cat was just over 2 years old, and a sex predilection for male cats may exist, though a breed predilection has not been reported.1,4


The histopathologic changes in naturally occurring primary hypoparathyroidism depend on the stage in the course of the disease.1 Early in the process, there is a lymphocytic-plasmacytic parathyroiditis with degeneration of the chief cells, consistent with an immune-mediated pathogenesis.1,2,6 The remaining chief cells become hyperplastic and eventually become isolated in small areas at the periphery of the parathyroid gland.1,2,6 Later, fibrous connective tissue replaces the lymphocytic-plasmacytic infiltration of the parathyroid gland.1,2

Hypoparathyroidism is a lack of PTH resulting in decreased mobilization of minerals from bone, calciuresis, renal phosphate retention, and decreased absorption of both calcium and phosphorus from the intestines.1,2,5,7 The net effect of hypoparathyroidism is hypocalcemia and hyperphosphatemia.1

The severity of the signs and the timing of their onset reflect the duration, rate of change, and magnitude of the hypocalcemia.5,8 Calcium normally stabilizes nerve cell membranes by decreasing their permeability to sodium.1,2 Nerve fibers are sensitive to changes in the concentration of ionized calcium (the physiologically active form), which affects acetylcholine's release during neuromuscular transmission.1,2 The level of excitability increases as the ionized calcium concentration decreases.1 When the ionized calcium concentration reaches 50% below normal, there is spontaneous discharge of peripheral nerve fibers and skeletal muscle contraction.1,2,4-7

Mild hypocalcemia rarely causes overt clinical signs, and animals have some ability to adapt to hypocalcemia.1,4,5 An animal often does not show signs until its total serum calcium concentration drops below 6 to 6.5 mg/dl, but if the concentration drops even slightly lower, clinical signs may develop rapidly.1,4,5 In individual dogs, it is difficult to predict the exact onset of clinical tetany; in people, tetany generally occurs when the calcium concentration drops 35% to 40% below normal. This percentage of decrease would correspond to a total calcium concentration below 6 mg/dl or an ionized calcium below 0.7 mmol/L in dogs.1,7 Although rare, a total serum calcium concentration less than 4 mg/dl can be lethal because of hypotension, decreased myocardial contractility, and paralysis of the respiratory muscles leading to respiratory arrest.1,5,7 Even with a stable level of hypocalcemia, clinical signs are often intermittent. Exercise or excitement may cause a respiratory alkalosis (i.e. increased ventilation from tachypnea leads to decreased arterial carbon dioxide), reducing the ionized fraction of serum calcium by increasing the binding of calcium to albumin.1,4,5,8,10,11


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