This disease is far more commonly observed than hyperthyroidism in canine patients.
The disease results in reduced levels of thyroxine (T4; often around 9 pmol/L) and triiodothyronine (T3), accompanied by changes in intermediary metabolism including alterations in bodyweight, insulin resistance, reduced leptin and adiponectin (lipid hormone) activity as well as interruption of normal blood-brain barrier function.
Three forms have been characterized:
- Congenital hypothyroidism - usually result from anomalies of the thyroid gland or pituitary
- Primary hypothyroidism - adult onset lymphocytic thyroiditis or idiopathic thyroid atrophy
- Secondary hypothyroidism - due to underlying myasthenia gravis or deficiency of thyroid-stimulating hormone (rare)
Hypothyroidism commonly occurs in older dogs, and certain breeds are predisposed, including the Boxer (with concurrent glomerulonephritis), Beagle (up to 40% affected), Tenterfield Terriers, Borzoi, Golden Retriever, Great Dane, Irish Setter, Doberman, Australian Shepherd Dog and Old English Sheepdog. In Golden Retrievers, progression of disease can be quite rapid.
Congenital hypothyroidism usually presents as cognitive deficits (due primarily to atherosclerosis) and skeletal developmental abnormalities, resulting in disproportionate dwarfism. Goitre may or may not be present and thyroid hormones levels are usually normal.
In adult dogs, clinical symptoms are often mild and nonspecific and can include lethargy, weight gain, dull coat, nonpruritic, symmetrical truncal and distal tail alopecia, superficial pyoderma, infertility, cold intolerance, cardiac abnormalities, ataxia, hemiparesis, seizures, vestibular disease and polyneuropathy.
The peripheral polyneuropathy is more commonly observed in large-breed dogs as a pelvic limb paresis, postural reaction deficits, hyporeflexia and muscle atrophy which may progress to tetraparesis over a course of 1 - 2 months.
In entire dogs, gynecomastia, reduced sperm motility, azoospermia is seen and in bitches, failure to conceive, prolonged interestrus length, silent estrus, anestrus and spontaneous abortions have been noted.
The subtle neurological changes seen in some dogs with hypothyroidism may be related to hyperlipidemia and hypercholesterolemia resulting in peripheral and central nerve ischemia, atherosclerosis and compression by myxedematous deposits
Blood analysis may be unremarkable, but alterations such as a normocytic, normochromic, nonregenerative anemia, hyperlipidemia, hypercholesterolemia, hypernatremia and hypercalcemia are not uncommon. In 20% to 30% of hyperthyroid dogs, serum creatine kinase levels may be elevated due to hypothyroid myopathy or changes in muscle metabolism.
Diagnosis is based on blood evaluation for T4 and TSH (thyroid stimulating hormone) levels, which are usually indicative.
Provocative thyroid function test and antibody ELISA testing for thyroiditis may assist a diagnosis but are relatively expensive.
Technetium thyroidal uptake appears to be unreliable.
Thyroid biopsy and histopathology are usually required for a definitive diagnosis.
Treatment usually involves dietary supplementation with levothyroxine (20 μg/kg every 12 hours). Clinical signs usually resolve with treatment. Failure of a response to this medication may require a re-evaluation of the underlying disease(s) process.
The use of antioxidants (vitamins E and C, fruits and vegetables) and mitochondrial cofactors (e.g. Co-Q10, S-adenosylmethionine, lipoic acid and carnitine) have been shown to significantly improve cognitive function in aged dogs and may assist the associated polyneuropathy associated with this condition.
Additional pharmacotherapy with drugs such as selegiline (a selective irreversible MAO-inhibitor) have shown benefit in canine cognitive disorders and should be considered as an adjunct therapy in advanced clinical cases.
- Animal Endocrine
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