Hypoparathyroidism
Basic Information 
Clinical Presentation
Disease Forms/Subtypes
• Hypoparathyroidism can be primary or secondary.
• Primary hypoparathyroidism: Few cases have been documented in horses. These horses have clinical signs consistent with hypocalcemia, including muscle tremors and fasciculations, synchronous diaphragmatic flutter (thumps), cardiac arrhythmias, hyperexcitability, seizures, ileus, and (in severe cases) death.
• In secondary hypoparathyroidism, parathyroid gland dysfunction is the consequence of a primary problem elsewhere, typically sepsis or hypomagnesemia.
• In sepsis, hypoparathyroidism may also be associated with high concentrations of inflammatory systemic mediators (interleukin-1 [IL-1]) that decrease parathyroid gland function in horses.
• In hypomagnesemia, hypoparathyroidism may be subclinical, and horses will not show improvement until magnesium is supplemented.
Etiology and Pathophysiology
• PTH is secreted by the chief cells of the parathyroid gland in response to hypocalcemia. PTH increases renal reabsorption of calcium and excretion of phosphorus. Thus, an appropriate response to hypocalcemia would be an increase in PTH concentrations.
• Horses with hypoparathyroidism have hypocalcemia and hyperphosphatemia and low or normal PTH concentrations. This is indicative of parathyroid gland dysfunction.
• The cause of primary hypoparathyroidism in horses remains unknown.
• Hypoparathyroidism secondary to sepsis occurs in horses.
• Inflammatory mediators such as IL-1 have been shown to decrease PTH secretion in horses.
• Hypomagnesemia is a frequent finding in critically ill horses.
• Magnesium is required for PTH secretion and PTH action.
• In hypomagnesemia, PTH concentrations are low until the magnesium status is restored.
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