Equis ISSN 2398-2977

Endocrine: hypoparathyroidism

Contributor(s): Janice Sojka, Ramiro Toribio, Han van der Kolk

Introduction

  • Cause: deficiency in parathyroid hormone (PTH). Inappropriate or low response (PTH secretion) of the parathyroid gland chief cells to hypocalcemia. Both primary and secondary hypoparathyroidism have been reported in horses.
  • Signs: depends if primary or secondary hypoparathyroidism. Often there is ileus, muscle fasciculations, synchronous diaphragmatic flutter, cardiac arrhythmias.
  • Diagnosis: serum electrolyte determination (hypocalcemia, hyperphosphatemia) and assay for endogenous intact PTH.
  • Treatment: IV calcium borogluconate, dietary calcium supplementation.
  • Prognosis: guarded to good depending if primary or secondary and response to treatment.

Pathogenesis

Etiology

Primary hypoparathyroidism

  • Caused by a failure of the chief cells in the parathyroid gland to secrete appropriate amounts of PTH relative to blood ionized calcium concentrations. In man and dogs, decreased PTH secretion can be due to either surgical removal of the parathyroid gland, immune-mediated, adverse reaction to chemotherapeutic agents, prolonged hypomagnesemia, and genetic (in humans). Similar underlying factors have not been identified in horses yet.

Secondary hypoparathyroidism

  • Sepsis and endotoxemia are also associated with abnormal parathyroid gland function characterized by hypocalcemia and low PTH concentrations.
  • Inflammatory mediators such as interleukin-1 decrease parathyroid chief cell function in horses.
  • Hypomagnesemia and magnesium depletion also result in secondary hypoparathyroidism as magnesium is required for PTH synthesis and release.
  • The hypercalcemia of chronic renal failure may result in low blood levels of PTH, although clinical signs are referable to renal disease rather than hypercalcemia.

Predisposing factors

General
  • Although there are no clear predisposing factors for primary hypoparathyroidism, all of the horses described in the case reports were in race training at the time the condition was identified.
  • Sepsis, endotoxemia, magnesium deficiency predispose to secondary hypoparathyroidism.

Pathophysiology

  • The disease results from the failure of the chief cells of the parathyroid gland to secrete PTH in response to decreased blood calcium concentrations   Blood: biochemistry - calcium  .
  • Inflammatory mediators such as interleukin-1 decrease parathyroid chief cell function in the horse.
  • Magnesium is required for PTH synthesis and release and magnesium depletion may result in secondary hyperparathyroidism.

Diagnosis

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Treatment

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Outcomes

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Further Reading

Publications

Refereed papers

  • Recent references from PubMed and VetMedResource.
  • Schwarz B & van den Hoven R (2012) Seizures in an Arabian foal due to suspected prolonged transient neonatal hypoparathyroidism. Equine Vet Educ 24 (5), 225-232.
  • Toribio R E, Kohn C W, Hardy J & Rosol T J (2005) Alterations in serum parathyroid hormone and electrolyte concentrations and urinary excretion of electrolytes in horses with induced endotoxemia. J Vet Intern Med 19 (2),223-231 PubMed.
  • Toribio R E, Kohn C W, Capen C C & Rosol T J (2003) Parathyroid hormone (PTH) secretion, PTH mRNA and calcium-sensing receptor mRNA expression in equine parathyroid cells, and effects of interleukin (IL)-1, IL-6, and tumor necrosis factor-alpha on equine parathyroid cell function. J Mol Endocrinol 31 (3), 609-620 PubMed.
  • Aguilera-Tejero E, Estepa J C, Lopez I et al (2000) Polycystic kidneys as a cause of chronic renal failure and secondary hypoparathyroidism in a horse. Equine Vet J 32, 167.
  • Hudson N P H, Church D B, Trevena J et al (1999) Primary hypoparathyroidism in two horses. Aust Vet J 77 (8), 504-508 PubMed.
  • Couetil L L, Sojka J E & Nachreiner R F (1998) Primary hypoparathyroidism in a horse. J Vet Intern Med 12 (1), 45-49 PubMed.

Other sources of information

  • Toribio R E (2004) Calcium Disorders. In: Equine Internal Medicine. Eds: Reed S M, Bayly W M, & Sellon D C. 2nd edn. Saunders, USA. pp 1295-1327


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