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Canine Hypothyroidism
Dan Schlesinger, DVM, MVSc,
Diplomate American College of Veterinary Internal Medicine (Internal Medicine)
the European
College of
Veterinary
Surgeonsin dogs. Although it is
Hypothyroidism is one ofDiplomate
the most of
commonly
diagnosed
endocrine
disorders
often a clinically obvious diagnosis, it is also frequently misdiagnosed or inappropriately treated.
Thyroid hormones (thyroxine {T4}, triiodothyronine {T3}, and reverse T3) are produced by the
thyroid glands in response to stimulation from thyroid stimulating hormone (TSH from the pituitary)
which in turn, has responded to stimulation by thyrotropin releasing hormone (TRH from the
hypothalamus). Hypothyroidism occurs when there is a failure of appropriate secretion at any one of
these stages.
Primary hypothyroidism is a result of failure of the thyroid gland to produce thyroid hormone. This is
most commonly thought to be mediated by progressive immune destruction of the thyroid gland
(lymphocytic thyroiditis). Clinical signs are not evident until more than 75% of the gland is
destroyed. Laboratory abnormalities may take 1-3 years to develop. Other reported causes of primary
hypothyroidism include idiopathic (possibly an end stage of lymphocytic thyroiditis), neoplasia, and
iatrogenic (surgery, antithyroid medications, radiation, sulfa drugs).
Secondary hypothyroidism results from a failure of the pituitary gland to secrete adequate TSH.
Reported causes include pituitary malformation/cysts, neoplasia, and suppression of thyrotropic cells
(euthyroid sick, Cushing’s disease, steroid therapy), and iatrogenic causes (radiation therapy,
hypophysectomy). Euthyroid sick syndrome is the most common type of secondary hypothyroidism
and generally does not require thyroid hormone supplementation. Instead, one should concentrate
on treating the underlying disease. Tertiary hypothyroidism is caused by a failure in TRH production.
This has not been documented in dogs.
Commonly Used Diagnostic Tests:
Clinical signs of hypothyroidism are extremely varied and can affect virtually all body systems.
Classically we think of the overweight, lethargic, cold intolerant patient with very bad hair. However,
most obese patients are not hypothyroid, nor are most patients with recurrent skin problems.
Diagnosis should generally be confirmed with laboratory testing. Approximately 95% of hypothyroid
dogs will have a [T4] below the reference range for the laboratory. Unfortunately, a large number of
“normal” dogs will have low [T4] and overlap. Consequently, a baseline serum [T4] can generally be
used to rule out hypothyroidism, but not to diagnose it. Additional tests should be used to make a
definitive diagnosis.
-2Free T4 is the non-protein bound fraction of T4 in circulation. Free T4 is thought to be less affected
by non-thyroidal illness and medications (but not unaffected). The positive predictive value of free T4
is improved if patients clinically appear hypothyroid and are not severely ill at the time of testing.
TSH concentration should theoretically be elevated in a patient with inadequate T4 or fT4. It should
not be used on its own to diagnose hypothyroidism. Although it is theoretically possible for TSH to be
elevated with normal [T4] in early hypothyroidism, we do not know what percentage of dogs will go
on to become truly hypothyroid. The accuracy of testing is improved by combining T4, fT4 and TSH
together.Other tests:
In the past, TSH stimulation and TRH stimulation tests were performed. The idea was to test the
ability of the pituitary or the thyroid gland to respond adequately to stimulation. However, the agents
are not easily or inexpensively obtained. Furthermore, the performance of these tests has not really
increased our ability to accurately diagnose the disease.
Autoantibody tests for lymphocytic thyroiditis are available and may be useful in the diagnosis.
However, not all patients with positive antibody tests progress to clinical hypothyroidism.
Ultimately, if one is faced with a clinically hypothyroid patient and discordant test results, trial
therapy may be warranted. This is generally quite safe, but one needs to use an adequate dose to
assess response (the doses are available in most textbooks). A positive response to therapy,
however, does not confirm the diagnosis. There are many conditions that can be thyroid responsive,
but patients are not hypothyroid. To truly be considered “therapeutic trial confirmation” of
hypothyroidism, the patient must improve with thyroid supplementation, and then get worse when
the supplementation is discontinued.
Monitoring:
I generally allow about 4 weeks to determine if I am seeing a clinical response. I usually start on a
q12h dose and check a 4-6 hour post pill sample at 4-6 weeks. If the clinical response is good and
the post pill T4 is well above the reference range, I generally try once daily dosing. On the other
hand, if the clinical response is poor, I may check both a post pill T4 and TSH concentration. If the
TSH is still elevated or the T4 is low, I may increase the dose of thyroxine. On the other hand, if the
T4 is elevated, the TSH immeasurable in the face of poor clinical response, the diagnosis should be
re-evaluated.