Equis ISSN 2398-2977

Endocrine: hyperparathyroidism

Synonym(s): Bran disease, big head, Miller's disease

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

Introduction

  • Parathyroid hormone (PTH) is produced by the parathyroid gland in response to decreased calcium or increased phosphorus concentrations. Either PTH or PTH analogues are secreted in inappropriate levels in a variety of circumstances.
  • There are 2 pairs of equine parathyroid glands, namely one pair located near the bifurcation of the bicarotid trunk at the level of the first rib, and a smaller pair situated on the dorsolateral aspect of the thyroid glands.
  • Hyperparathyroidism (HPT) is the excessive, pathologic secretion of PTH by the parathyroid glands. It can be primary or secondary.
  • Cause:
    • Primary hyperparathyroidism:
      • Excessive secretion of PTH from the parathyroid glands autonomously. 
    • Secondary hyperparathyroidism:
      • Increased secretion of the parathyroid glands in response to excessive dietary phosphorus and oxalates, and low in calcium = nutritional secondary hyperparathyroidism (NSH).
      • Renal secondary hyperparathyroidism has NOT been described in horses. Rather horses develop hypercalcemia with renal disease as a result of calcium retention as the kidney eliminates large amounts of calcium in the horse.
    • Pseudohyperparathyroidism:
      • Many malignancies in horses (lymphome, cutaneous and gastric squamous cell carcinoma, myeloma) secrete large amounts of a PTH-like protein, parathyroid hormone-related protein (PTHrP).
      • PTHrP interacts with the PTH receptor to induce hypercalcemia.
      • Also known as humoral hypercalcemia of malignancy (HHM) - PTH in these horses is low.
  • Signs: anorexia, weight loss, lameness, soft-tissue mineralization, facial enlargement (osteodystriphia fibros) and polyuria/polydypsia.
  • Diagnosis: determination of serum/plasma intact PTH concentrations, serum ionized calcium concentrations, serum and urine chemistry, urinalysis, determination of fractional excretion of calcium and phosphorus and radiography.
  • Treatment: depends on whether the cause of primary or secondary hyperparathyroidism. For secondary, diet adjustments, decrease phosphorus intake, supplement with oral calcium, analgesia, fluid therapy, NSAIDs. In primary HPT surgical removal of the parathyroid glands, although indicated, it is difficult. Low doses of glucocorticoids to decrease intestinal calcium absorption and renal reabsorption should be considered in animals with clinical signs.
  • Prognosis: good for nutritional secondary hyperthyroidism (NSH); poor for other causes.

Pathogenesis

Etiology

  • In primary HPT, an abnormality of the parathyroid gland chief cells   →    excessive and autonomous synthesis and secretion of PTH, and the parathyroid gland does not respond to the negative feedback of calcium.
  • In secondary HPT, increased phosphate intake or decreased calcium absorption (oxalates, low calcium diet)   →   hyperphosphatemia and hypocalcemia, increasing PTH synthesis and secretion.
  • Certain equine malignancies (lymphoma, cutaneous and gastric squamous cell carcinomas, myelomas) secrete PTHrP, which stimulates PTH receptors to increase renal reabsorption of calcium and bone resorption.

Predisposing factors

General
  • Nutritional secondary hyperparathyroidism is caused by feeding a diet that has an absolute calcium deficiency or that has more phosphorus than calcium over an extended period of time. Diets with high oxalate content (>0.5% dry matter or a calcium:oxalate ratio <0.5 may result in nutritional secondary HPT).
  • Renal failure does not cause renal secondary hyperparathyroidism as in other species, but   →   hypercalcemia.
  • The presence of tumors    →   humoral hypercalcemia of malignancy or pseudohyperparathyroidism.

Specific

  • Ingestion of a diet that has more phosphorus than available calcium will cause a relative hyperphosphatemia. 
  • Phosphorus excretion from the kidney is stimulated by increased PTH secretion. As a result, serum calcium is conserved in the kidney and bone resorption is increased   →    hypercalcemia   Blood: biochemistry - calcium  .

Pathophysiology

  • Increased blood phosphorus and/or decreased blood calcium stimulates the secretion of PTH from the parathyroid glands.
  • PTH increases renal reabsorption of calcium and bone resorption   →    hypercalcemia.
  • Tumors that secrete PTHrP produce similar effects, ie hypercalcemia   Blood: biochemistry - calcium  , increased renal phosphorus excretion, and variable blood phosphorus concentrations.
  • Because there is hypercalcemia, which inhibits PTH secretion, serum PTH is low.

Timecourse

  • Most horses with clinical disease due to hyperparathyroidism have insidious diseases that have occurred over several weeks or months.
  • It is likely that alterations in blood PTH concentrations precede any clinical sign by a period of time.

Epidemiology

  • These conditions are too uncommon to draw meaningful conclusions as to epidemiology; they do tend to occur in older horses.

Diagnosis

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Treatment

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Prevention

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Outcomes

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Further Reading

Publications

Refereed papers

  • Recent references from PubMed and VetMedResource.
  • van der Kolk J H (2007)Humoral hypercalcemia of malignancy or pseudohyperparathyroidism in the horse.Equine Vet Educ19(7), 384-386 VetMedResource.
  • Benders N A, Junker K, Wensing T H, van den Ingh G A M & van der Kolk J H (2001)Diagnosis of secondary hyperparathyroidism in a pony using intact parathyroid hormone radioimmunoassay.Vet Rec149, 185 PubMed.
  • Frank N, Hawkins J F, Couetil L L & Raymond J T (1998)Primary hyperparathyroidism with osteodystrophia fibrosa of the facial bones in a pony.JAVMA212(1), 84 PubMed.
  • Peauroi J R, Fisher D J, Mohr F C & Vivrette S L (1998)Primary hyperparathyroidism caused by a functional parathyroid adenoma in a horse.JAVMA212(12), 1915 PubMed.
  • Marr C M, Love S & Pirie H M (1989)Clinical, ultrasonographic and pathological findings in a horse with splenic lymphosarcoma and pseudohyperparathyroidism.Eq Vet J 21(3), 221 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, St Louis. pp 1295-1327.


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