Hyperparathyroidism

Also Known As – Parathyroid hyperplasia – Parathyroid adenoma - Fibrous Osteodystrophy – Grain Overload – Bran Disease – Bran-head Disease – Rubber Jaw

Introduction

Hyperparathyroidism is an endocrine disease caused by overactivity of the parathyroid gland and consequent raised body levels of parathyroid hormone (PTH). It occurs in many veterinary species and can be primary or secondary.

Primary hyperparathyroidism originates within the parathyroid gland itself and can be due to glandular hyperplasia or neoplasia. It is most commonly due to a solitary benign adenoma of either the internal or external parathyroid gland.

Secondary hyperparathyroidism can be either renal or nutritional in origin:

Secondary renal hyperparathyroidism is a complication of chronic renal failure. This is due to hyperphosphataemia developing as a result of impaired glomerular filtration rate. Renal production of Calcium#Calcitriol#calcitriol is also reduced, exacerbating the resulting hypercalcaemia.

Signalment

Primary hyperparathyroidism is seen infrequently in dogs and cats, but is documented in German Shepherd Dogs.

Secondary renal hyperparathyroidism is seen frequently in dogs and occasionally in cats.

Clinical Signs

The main effect of hyperparathyroidism is hypercalcaemia which causes a range of clinical signs. Polydipsia, polyuria, anorexia, lethargy and depression are the most common signs but animals may also be constipated, weak, stiff-gaited, shivering and vomiting. Mild hypercalcaemia may not generate any overt clinical signs.

Sequelae of hyperparathyroidism include fibrous osteodystrophy and

Osteodystrophy is the osteoclastic resorption of bone and replacement by weaker fibrous tissue. When this occurs in the long bones it causes lameness and weakened bones that are prone to fracture. Compression fractures may also occur spontaneously and if this occurs in the vertebrae, nerve dysfunction results.

Fibrous osteodystrophy in the flat bones of the skull and face causes facial hyperostosis. This is seen in Bran disease or grain overload in horses and also in dogs with primary hyperparathyroidism. The face and head become grossly disfigured by excessive amounts of fibrous tissue laid down in an attempt to consolidate the weakened lamellar bone. In advanced cases, the mandible may become pliant and teeth may loosen, hence the colloquial name, “rubber jaw”.

Animals affected by secondary renal HPT may exhibit classical signs of renal insufficiency such as polydipsia, polyuria, weight loss, vomiting and dehydration.

Diagnosis

Electrolyte imbalances on blood biochemistry profiles are highly suggestive. Hypercalcaemia with a normal to low serum phosphorus and a low urine specific gravity are fairly consistent findings.

Urinary excretion of phosphorus and sometimes also calcium is increased. This can result in urolithiasis in some cases.

Serum PTH levels may be useful in diagnosing primary hyperparathyroidism, but only in animals with normal renal function, i.e., those with normal creatinine and blood urea nitrogen. A high PTH assay along with high creatinine and blood urea nitrogen is indicative of possible renal secondary HPT.

Exploratory surgery of the cervical region may identify enlarged parathyroid glands if no other test is available or confirmatory.

Treatment

Treatment for primary hyperparathyroidism usually required surgical excision. Hypocalcaemia is a known post-operative complication and supplementation may be required in the short or long term management. If the hypercalcaemia persists, metastatic disease should be suspected and investigated.

Renal secondary HPT therapy is directed at control of the renal disease by way of specialised diet and rehydration along with supplementation of calcitriol and phosphorus binders.

Control

Hyperparathyroidism Learning Resources
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References

Lavoie, J-P., Hinchcliff, K. W (2008) Blackwell’s Five-Minute Veterinary Consult: Equine 2nd ed. Wiley-Blackwell, Oxford, pp.

Haskell, S (2008) Blackwell’s Five-Minute Veterinary Consult:Ruminant. Wiley-Blackwell, Oxford, pp.

Merck Vet Manual, Renal Secondary Hyperparathyroidism, accessed 25/07/2011 at http://www.merckvetmanual.com/mvm/index.jsp?cfile=htm/bc/90314.htm