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Symmetrical alopecia associated with hypothyroidism[1]
Distal alopecia of the tail associated with hypothyroidism[1]
Brain of a 2-year-old Australia Shepherd which died from acute neurological signs secondary to hypothyroidism, showing severe atherosclerosis of the brain and spinal cord[2]

Hypothyroidism is a neuroendocrine disease of dogs characterized by thyroid inactivity or reduced activity.

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[3], reduced leptin and adiponectin (lipid hormone) activity[4] as well as interruption of normal blood-brain barrier function[5].

All serum T4 is produced by the thyroid glands and T4 accounts for most of the hormones secreted by the thyroid gland, with only small quantities of T3 and reverse T3 (rT3) released. The majority of T4 is bound to plasma proteins, and only 1% is unbound as the active form, which exerts a positive effect on cells throught the body except for the pituitary, where it exerts a negative feedback effect on TSH secretion. The function of plasma-bound T4 is to act as a reservoir and buffer to maintain a steady level of circulatory free T4. Within most cells, free T4 is deiodinated to T3 or rT3. The latter is primarily utilized during illness, starvation or excessive endogenous catabolism. Intracellular T3 binds to receptors on the mitochondria, nucleus and plasma membrane, resulting in heightened intracellular activity.

Three forms have been characterized:

  • Congenital hypothyroidism - usually result from anomalies of the thyroid gland or pituitary[6]
  • Primary hypothyroidism - adult onset lymphocytic thyroiditis or idiopathic thyroid atrophy
  • Secondary hypothyroidism - due to underlying myasthenia gravis[7][8] or deficiency of thyroid-stimulating hormone (rare)

Hypothyroidism commonly occurs in older dogs, and certain breeds are predisposed, including the Boxer (with concurrent glomerulonephritis[9]), Beagle (up to 40% affected), Tenterfield Terriers[10], 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.

Concurrent age-related diseases such as hypoadrenocorticism[11] and diabetes mellitus[12] often aggravate clinical symptoms[13].

Schmidt syndrome (hypoadrenocorticism, hypothyroidism and diabetes mellitus) appears relatively uncommon in dogs compared with humans[14].

Megaesophagus has been shown to not be associated with or occur as a result of hypothyroidism in dogs[15].

Clinical signs

Congenital hypothyroidism usually presents as cognitive deficits (due primarily to atherosclerosis) and skeletal developmental abnormalities, resulting in disproportionate dwarfism[16]. Goitre may or may not be present and thyroid hormones levels are usually normal[17].

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.[18][19]

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[20].

Symmetrical alopecia areata, superficial pyoderma, comedones, hypertrichosis, ceruminous otitis externa and poor wound healing are also commonly observed.

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[21].

Rare symptoms such as megaesophagus[22] and xanthoma[23] and cognitive deficits have also been reported.

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[24] and compression by myxedematous deposits[25]

Blood analysis may be unremarkable, but alterations such as a normocytic, normochromic, nonregenerative anemia, hyperlipidemia, hypercholesterolemia, hypernatremia and hypercalcemia[26] 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[27].


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[28] for thyroiditis may assist a diagnosis but are relatively expensive.

Technetium thyroidal uptake appears to be unreliable[29].

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 prednisolone given concurrently for other diseases does not appear to significantly interfere with therapy[30].

The use of antioxidants (vitamins E and C, fruits and vegetables) and mitochondrial cofactors (e.g. Co-Q10, S-adenosylmethionine[31], lipoic acid and carnitine)[32] have been shown to significantly improve cognitive function in aged dogs[33] 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[34].


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