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Common names or abbreviations:
 | Thyroid Dysfunction, Hypothyroidism, Thyroiditis,
Hashimoto's Disease |
Description or definition:
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Canine
hypothyroidism is the absence of sufficient thyroid hormone to maintain
healthy body functions. The term hypothyroidism has been loosely
applied to describe all stages of this disease process whereas strictly
speaking it should be reserved for the end-stages when the animal's
thyroid gland is no longer capable of producing sufficient hormone(s) to
sustain clinical health. At this point, the dog can express any number of
the non-specific multisystem signs of thyroid dysfunction. The age
of onset is usually between one and six years of age. Cases have
been reported in Golden Retriever, Great Dane, Beagle, Borzoi, Shetland
sheepdog, American Cocker Spaniel, Labrador retriever, Rottweiler, Boxer,
Doberman pinscher, German shepherd, Akita, Old English sheepdog, and Irish
setter. The incidence of autoimmune thyroiditis in males and females
is similar, so it is equally important to test both prior to breeding.
The most common cause of canine thyroid disease is autoimmune thyroiditis
(estimated 90% of cases). Thyroiditis is an immune-mediated process that
develops in genetically susceptible individuals and is characterized by
the presence of antithyroid antibodies in the blood or tissues.
Thyroiditis is believed to start in most cases around puberty, and
gradually progress through mid-life and old age to become clinically
expressed hypothyroidism once thyroid glandular reserve has been depleted.
During this process, the animal or person becomes more susceptible to
immune-mediated or other diseases affecting various target tissues and
organs. The prerequisite genetic basis for susceptibility to this disorder
has been in established in humans, dogs and several other species.
About
half of canine hypothyroidism has been reported to be associated with
autoimmune thyroiditis (positive TgAA- Thyroglobulin Autoantibody); the
majority of the remaining hypothyroidism is idiopathic (without apparent
cause and TgAA negative), while a small fraction is from a pituitary
disorder. A number of scientific publications have presented data to
support the genetic transmission of autoimmune thyroiditis, others have
reported the familial (occurring among relatives) incidence of the disease
and still others report cases from surgical removal of the gland, cancer,
low iodine in the diet and many other causes.
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Symptoms
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Typical
clinical signs can mimic other diseases like Degenerative Myelopathy and
include weight gain, skin abnormalities, weakness, unprovoked aggression
towards other animals and/or people, sudden onset of a seizure disorder in
adulthood, disorientation, moodiness, erratic temperament, periods of
hyperactivity, hypo-attentiveness, depression, fearfulness and phobias,
anxiety, submissiveness, passivity, compulsiveness and irritability.
After the episodes, a majority of the animals were noted to behave as if
they were coming out of a trance-like state and were unaware of their
previous behavior.
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Diagnosis:
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The
latest tests include measurement of two forms of the thyroid hormones T3 (triiodothyronine)
and T4 (levothyroxine) and a search for antibodies that could indicate
autoimmune thyroiditis, the genetic form of the disease. Interpretation of
the numbers recorded is as important as the numbers themselves, for the
relationship between the hormones is complex. In addition, normal ranges
of hormone vary somewhat with the breed or mix.
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The best
current marker for this disease is a positive TgAA (Thyroglobulin
Autoantibody) test result. Assuming a single gene disorder and
recessive trait, TgAA will be positive only in dogs having both genes for
thyroiditis. The Orthopedic Foundation for Animals (OFA)3 started a
Canine Thyroid Registry and has certified a number of regional veterinary
laboratories in the US and Canada qualified to perform the thyroid profile
for registry purposes. Oxford Laboratories4 began producing a commercially
available assay for TgAA so all reagents for the OFA profiles are standard
among certified laboratories.
For
further information on the Canine Thyroid Registry, contact the OFA:
Telephone: 1-573-442-0418.
Treatment:
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Treatment
consists of two daily doses of levothyroxine, the hormone identified in
the test as T4. Levothyroxine is converted to triiodothyronine by
the body; dogs that cannot make this conversion will need both
levothyroxine and triiodothyronine. The dosage is based on body
weight; thyroid hormones are quickly metabolized and excreted from the
body, so splitting the dose is most effective. The initial
improvements are usually seen during the first week of therapy (an
increased mental alertness, greater activity, more muscle strength, and
improved appetite). The improvements in the skin and hair take a bit
longer (several months) to return to normal. One to two months after
starting the dog on therapy, the veterinarian will redo the tests to make
sure the levels are within the normal range. Blood should be drawn
four-to-six hours after the morning dose. Dogs on long-term therapy
should have a complete panel of tests every six to 12 months.
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Prevention:
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There
is no DNA based testing procedure at this time, testing with the best
available marker, TgAA, can be beneficial. Selective breeding should
reduce the prevalence in high incidence breeds and prevent an increasing
prevalence in low incidence breeds. Although males were similar to females
in prevalence, you can imagine the impact one important but affected male
could have on the breed, especially a breed with small numbers. The TgAA
portion of the thyroid profile is most important during the first 5 years
of life as few dogs are found to have idiopathic hypothyroidism before
this age.
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While
there is a genetic predisposition for thyroid disorders, environmental
factors such as pollutants and allergies probably play a role as well.
Links to sites about this disease:
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