Three forms of hyperparathyroidism are recognized in dogs:
- Primary hyperparathyroidism - ↑Ca, ↓P, ↑PTH - benign parathyroid neoplasia, parathyroid adenoma, parathyroid carcinoma
- Secondary nutritional hyperparathyroidism - ↓Ca, ↓P, ↑PTH - parathyroid hyperplasia
- Secondary renal hyperparathyroidism - ↓Ca, ↑P, ↑PTH - parathyroid hyperplasia
Primary hyperparathyroidism is caused by autonomously functioning neoplastic or hyperplastic parathyroid 'chief' cells. Keeshonden are predisposed due to an autosomal-dominant genetic mutation with age-related penetrance.
Nutritional secondary hyperparathyroidism is usually caused by dietary mineral imbalances, such as diets that are low in calcium or vitamin D, or diets containing an excessive amount of phosphorus, such as feeding an all-meat diet. This condition may also be caused by type II rickets (vitamin D-independent).
Secondary renal hyperparathyroidism results from decreased calcitriol production resulting in phosphorus retention and resultant calcium excretion due to chronic renal disease or juvenile renal dysplasia or polycystic kidney disease. In dogs, young growing animals are preferentially affected, likely because their bones are more sensitive to the action of PTH.
Clinically affected dogs present with polyuria, polydipsia, reduced activity and stiff gait (due to bone changes). Spontaneous fractures of limb and jaw are not uncommon and facial swelling due to 'rubber jaw' has been reported.
Blood tests usually reveal hypercalcemia (normal 1.0 - 3.0 mmol/L), hypophosphatemia and normal or increased serum parathyroid hormone (normal 3 - 17 μmol/L) and parathyroid hormone-related protein levels. Calcitriol levels may be normal or elevated (normal 60 - 250 nmol/L). Elevated parathyroid hormone levels can be elevated in other diseases such as hyperadrenocorticism.
Serum calcium exists as ionized calcium (up 56% of total serum calcium) protein bound calcium (30%) and complexed calcium. Free calcium is the portion of total serum calcium that is biologically active and should be measured when assessing pathology.
Radiographs often reveal diffuse osteopenia of limb and skull and thinning of the cortices, polyostotic deformities associated with fracture remodeling, along with a floating dental arcade.
A differential diagnosis would include other causes of polyuria/polydipsia such as diabetes insipidus or causes of persistent hypercalcemia such as paraneoplasitc hypercalcemia (polyostotic lymphoma, osteosarcoma, anal sac adenocarcinoma), chronic renal disease, hypoadrenocorticism and vitamin D toxicosis. Additionally, parathyroid hormone levels can be elevated in association with inflammatory bowel disease and hypoalbuminaemia, usually with a concurrent hypocalcemia. Bone abnormalities can also be observed in rickets and osteogenesis imperfecta.
Primary hyperparathyroidism is usually treated by surgical thyroidectomy, percutaneous ultrasound-guided ethanol ablation or percutaneous ultrasound-guided heat ablation. These procedures have a relative risk of complications, most commonly hypocalcemia. Treatment with calcitriol and vitamin D supplements can be instituted to help avoid this postoperative complication.
Secondary renal hyperparathyroidism can be treated with dietary phosphorus restriction, intestinal phosphate binders, and calcitriol supplementation, which may slow the progression of renal disease.
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