Hypoparathyroidism is an uncommon endocrine disease characterized by a physical or physiological inactivity of parathyroid hormone (PTH) by the parathyroid gland.
Hypoparathyroidism may be a primary disease or secondary to other systemic disease(s). With primary hypoparathyroidism, the common cause is idiopathic (immune-mediated) lymphocytic parathyroiditis.
Parathyroid hormone (parathormone) is secreted by the chief cells of the parathyroid glands and causes an increase in blood concentration of ionized calcium, whereas calcitonin (a hormone produced by the parafollicular cells (C cells) of the thyroid gland) acts to decrease calcium concentration.
The contrary condition, hyperparathyroidism also occurs frequently in dogs.
This condition can occur as a result of:
- congenital agenesis (Primary hypoparathyroidism)
- dietary calcium deficiency
- Immune-mediated disease
- - lymphocytic parathyroiditis (idiopathic hypoparathyroidism)
- Protein-losing enteropathy and secondary hypomagnesemia
- Chronic hypercalcemia
- Tumor lysis syndrome associated with chemotherapy or surgical lumpectomy
Clinical symptoms is affected dogs develop over 1 - 4 weeks due to progressive hypocalcemia, and present initially with muscle twitching, polyuria, polydipsia, anorexia, and sometimes periocular alopecia.
As the condition worsens, mental depression, seizures, muscle tremors and fasciculations, stiff gait, tetany, muscle cramping, behavioural changes and cataracts (posterior lenticular cataract formation secondary to hypocalcemia) may develop.
A tentative diagnosis can be made from blood results which usually show severe hypocalcemia (less than 6.5 mg/dl; normal 9 - 11.4), mild hyperphosphatemia (due to increased renal tubular reabsorption) and reduced intact parathyroid hormone levels.
Radiography may elucidate calcification of microvasculature, intracerebral calcification, osteopenia and ligamentous ossification.
Electrocardiographys often exhibit prolonged QT intervals due to a ST-segment prolongation.
In the early stages of immune-mediated lymphocytic parathyroiditis in dogs, there is infiltration of the gland with lymphocytes and plasma cells and nodular regenerative hyperplasia of remaining chief cells. Later, the parathyroid gland is replaced by lymphocytes, fibroblasts, and capillaries, with only an occasional viable chief cell.
A response to therapy may also suggest a diagnosis of primary hypoparathyroidism.
A differential diagnosis would include neoplasia and milk fever (perparturient hypocalcemia; usually has concurrent hypophosphatemia).
Treatment involves addressing the acute hypocalcemia with parenteral calcium gluconate (10 mL of 10% calcium gluconate in 250 mL of 0.9% saline administered at 2.5 mL/kg/hr for 8 – 12 hours) and intravenous anticonvulsants.
Chronic therapy included oral vitamin D analogues (calcitriol ≥25,000 – 50,000 U/day), dihydrotachysterol and dietary calcium supplementation, with monitoring of blood calcium to minimize risk of secondary vitamin D toxicosis and calcinosis cutis.
Once the blood calcium has returned to normal, substantially lower doses of vitamin D are indicated for longterm maintenance; in some dogs, only dietary calcium supplementation is required for longterm stabilization.
Levels of parathyroid hormone may remain suppressed for some time post-therapy, especially in older dogs.
- Vet Grad
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