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.


Figure 1. Regulation of parathyroid hormone (PTH). This illustration shows the direct (solid lines) and indirect (dashed line) effects of PTH on bone, kidneys, and intestines. PTH's net effect is to increase serum calcium and decrease serum phosphorus concentrations.
PTH mobilizes both calcium and phosphorus from bone, causes the kidneys to retain calcium and excrete phosphate, and indirectly increases intestinal absorption of calcium and phosphate (Figure 1).1,2,9 PTH has both rapid and long-term effects on bone.7 In acute hypocalcemic situations, the rate of bone breakdown and subsequent calcium release into the blood is increased, and changes in serum calcium can be noted within minutes.7,9 Initially, calcium salts (about 1% of total body calcium), particularly CaHPO4, serve as a readily exchangeable reservoir of calcium.7,8 If hypocalcemia and elevation in PTH continue for several days to weeks, PTH causes proliferation of osteoclast-mediated breakdown of existing bone (osteolysis). Osteoclasts, unlike osteoblasts and osteocytes, lack receptors for PTH, so osteoclast activation is likely indirect through cytokines (e.g. insulin-like growth factor 1, interleukin 6, granulocyte-macrophage stimulating factor) released by activated osteoblasts and osteocytes.7,9 Osteolysis results in increased serum phosphorus and calcium concentrations.

In normal animals, ionized and complexed calcium (but not protein-bound calcium) passes into the glomerular filtrate.7 Ninety-nine percent of this calcium is eventually reabsorbed.7,13 About 90% of the reabsorption of calcium occurs in the proximal tubules, loop of Henle, and early distal tubules.7 In the thick ascending limb of the loop of Henle, there is marked reabsorption of calcium because of the positive charge within the lumen of the tubules compared with the surrounding interstitial fluid.7 The reabsorption of the final 9% or 10% of calcium depends on the serum ionized calcium concentration and presence of PTH, which if present increase the degree of calcium reabsorption in the late distal tubules and early collecting ducts.1,7,9,13 In the proximal tubule, phosphate reabsorption is inhibited by PTH.7,9,13 PTH in the proximal tubule also stimulates the enzyme 1-alpha-hydroxylase, vital in the final conversion of the vitamin D precursor to its most active form, calcitriol (discussed later).9,11 The net effects of PTH on the kidneys are to decrease the serum phosphorus concentration and increase the serum calcium concentration.


Calcitonin's activity further controls the effects of PTH on calcium. Calcitonin, the hormone produced by the parafollicular cells (also called C cells) of the thyroid gland, antagonizes the actions of PTH, particularly on bone.7 The effects of calcitonin are relatively weak compared with PTH.7


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