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CANINE
AUTOIMMUNE THYROID DISEASE: COMMON PROBLEM OF PUREBRED DOGS
by W. Jean Dodds DVM
The
information provided here outlines an approach that has been used successfully
by the author to reduce the prevalence of clinically expressed canine thyroid
disease within susceptible families or breeds.
EARLY
THYROID DISEASE (THYROIDITIS)
COMPENSATORY AND CLINICAL CANINE HYPOTHYROIDISM
Most of the confusion about the diagnosis and treatment of thyroid disease in
purebred or mixed breed dogs today stems from the expectation that affected
animals must show clinical signs of inadequate thyroid hormonal production (i.e.
hypothyroidism) in order to have the disease. 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. But let's start at the
beginning.
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.
The above explanation helps us to appreciate existing confusion and controversy
within the veterinary profession regarding whether or not testing or treatment
is indicated for dogs that fail to show typical signs of hypothyroidism. In
fact, we have only recently begun to recognize the subtle signs of early thyroid
dysfunction in dogs as prevalence of the autoimmune form of the condition has
increased within and among dog breeds. Today, some 50 breeds are genetically
predisposed to develop thyroid disease.
GENETIC SCREENING FOR THYROID
DISEASE
These thyroid panels and antibody tests can also be used for genetic screening
of apparently healthy animals to evaluate their fitness for breeding. A bitch
with antithyroid antibodies in her blood may pass these along to her puppies in
her colostral milk. Also, any dog having circulating antithyroid antibodies can
eventually develop clinical symptoms of thyroid or other autoimmune diseases.
Therefore, thyroid screening can be very important for potential breeding stock.
Thyroid testing for genetic screening purposes is less likely to be meaningful
before puberty. Screening is initiated, therefore, once healthy dogs and bitches
have reached sexual maturity (between 10-14 months in males and during the first
anestrus period for females following their maiden heat). Anestrus is a
time when the female sexual cycle is quiescent, thereby removing any influence
of sex hormones on baseline thyroid function. This period generally begins 12
weeks from the onset of the previous heat and lasts one month or longer. The
interpretation of results from baseline thyroid profiles in intact females is
more reliable when they are tested in anestrus. Testing for health screening is
performed at 12-16 weeks from the onset of the previous heat. In fact, genetic
screening of intact females for other parameters like von Willebrand's disease
or wellness health and reproductive checkups should also be scheduled in
anestrus females. Once the initial thyroid profile is obtained, dogs and bitches
should be rechecked on an annual basis to assess their own health. Annual
results permit comparisons that should reveal early evidence of developing
thyroid disease or dysfunction. This also allows for early treatment where
indicated to abort the development or advancement of clinical signs associated
with hypothyroidism.
Healthy young dogs (less than 15-18 months of age) should have thyroid baseline
levels for all parameters in the upper 1/2 to 1/3 of the adult normal ranges. In
fact, for optimum thyroid function in screening breeding stock, levels should be
at least at the midpoint of the laboratory normal ranges, because lower levels
may well be indicative of the early stages of thyroiditis among relatives of dog
families known to have thyroid disease.
TREATMENT OF THYROID DISEASE
The new information summarized here has changed our approach to treatment and
control of thyroid disease. In addition to providing thyroid supplementation for
dogs showing the typical signs of thyroid disease, we now know that treatment of
dogs showing the early stages of thyroiditis (based on the testing described
above) is necessary and important to correct the underlying thyroid imbalance,
reduce the risk of developing other related immune-mediated disorders, and to
control or prevent the process of thyroiditis from progressing to depletion and
exhaustion of the thyroid gland.
1. Type of Treatment
The treatment of choice because of its wide safety margin and efficacy is T4
hormone (L - or levothyroxine). The most commonly used brand names are Soloxine
(Daniels) and Synthroid (Flint) and we recommend either of these over generics
especially for the smaller breeds. Use of T3 hormone (triiodothyronine) is not
recommended for initial use because toxicity can more easily develop with this
product; T3 is the intercellular hormone whereas most of T4 must be first
converted to T3 before it achieves its metabolic effect. In some cases where the
animal's body cannot properly convert T4 to T3, the dog will need both T4 and T3
therapy to correct the problem. For this purpose, the general rule of thumb is
to give from 2/3 to a full dose of T4 and a 1/3 dosage of T3 (i.e., 0.1 mg
per 10-20 pounds of T4 plus 1 ugm per pound of T3 twice daily). However,
no dog should be treated with these thyroid hormonal preparations without having
proper veterinary testing, medical examination and follow-up.
2. Frequency of Treatment
Thyroid hormones should always be given twice daily to effect the best response.
Until recently, veterinarians have been advised to give treatment to effect
either once or twice daily because data on this point was unclear. We now
know that the half-life of T4 in the dog is about 10-12 hours (much shorter than
humans); for T3, it's only 6-8 hours. Thus, about half of the hormone is
metabolized and excreted from the body within 12 hours. Furthermore, twice
daily dosing aids in controlling thyroiditis because it shuts off pituitary
production of TSH by negative feedback in concert with the half-life of the
hormone. In other words, the dog's own thyroid follicular cells become quiescent
and are less likely to stimulate production of the antithyroid antibodies
responsible for the disease. (Obviously these are simplistic explanations of the
complex metabolic, immunologic and biochemical events involved.) Contrary
to some popular wisdom, treatment with thyroid hormone does not destroy or
suppress the potential of the gland to respond on its own once treatment is
stopped for whatever reason. The latest veterinary research shows that it takes
the thyroid gland up to 30 days to recover its full potential once therapy is
withdrawn. Therefore if an animal has been medicated, where the diagnosis is
unclear, treatment should be withdrawn (if it's clinically safe to do so) for 30
days before the animal is retested with the complete type thyroid profile
described above.
Follow-up testing after initiating treatment is usually performed after four to
eight weeks of therapy. The sample should be taken 4-6 hours after the morning
dosage and optimum results will show thyroid values in the upper third of normal
ranges at the peak time of absorption. Dosage can then be adjusted accordingly
if needed. Dogs on long term therapy with thyroid hormones should be monitored
with complete panels (not just T4 as you need to be sure the dog's body is
converting the T4 medication properly to T3) on a regular basis (every 6-12
months).
CLINICAL SIGNS OF CANINE
HYPOTHYROIDISM
| Alterations
in Cellular Metabolism |
weakness / stiffness / laryngeal paralysis / facial paralysis
/ tragic expression / knuckling or dragging feet / muscle wasting /
megaesophagus / head tilt / drooping eyelids
Neuromuscular Problems
seizures / mental dullness / exercise intolerance / neurologic signs
polyneuropathy / lethargy / weight gain / cold intolerance / mood swings
hyperexcitability / stunted growth / chronic infections
Dermatologic Diseases
dry, scaly skin and dandruff / coarse, dull coat / bilateral symmetrical hair
loss / rat tail, puppy coat / hyperpigmentation / seborrhea or greasy skin
pyoderma or skin infections / myxedema / chronic offensive skin odor
Reproductive Disorders
infertility of either sex / lack of libido / testicular atrophy / hypospermia
aspermia / prolonged interestrus interval / absence of heat cycles / silent
heats / pseudopregnancy / weak, dying or stillborn pups
Cardiac Abnormalities
slow heart rate (bradycardia) / cardiac arrhythmias / cardiomyopathys
Gastrointestinal Disorders
constipation / diarrhea / vomiting
Hematological Disorders
bleeding / bone marrow failure / low red blood cells / low white blood cells /
low platelets
Ocular Diseases
corneal lipid deposits / corneal ulceration / uveitis Keratococonjunctivitis /
sicca or dry eye / infections of eyelid glands (Meibomian gland)
Other Associated Disorders
lgA deficiency / loss of smell (dysosmia) / loss of taste / glycosuria / chronic
active hepatitis / other endocrinopathies adrenal, pancreatic, parathyroid
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