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Canine Autoimmune Thyroid Disease
by W. Jean Dodds, DVM
Common Problem of Purebred Dogs
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.
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.
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
seizures / mental dullness / exercise intolerance / neurologic signs / polyneuropathy / lethargy / weight gain / cold intolerance / mood swings hyperexcitability / stunted growth / chronic infections
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
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
slow heart rate (bradycardia) / cardiac arrhythmias / cardiomyopathys
constipation / diarrhea / vomiting
bleeding / bone marrow failure / low red blood cells / low white blood cells / low platelets
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
W. Jean Dodds, DVM is an internationally recognized authority on thyroid issues in dogs and blood diseases in animals. In the mid-1980's she founded Hemopet,11330 Markon Drive Garden Grove, CA 92841, the first nonprofit blood bank for animals. Dr. Dodds is a grantee of the National Heart, Lung, and Blood Institute, and author of over 150 research publications. Through Hemopet she provides canine blood components and blood-bank supplies throughout North America, consults in clinical pathology, and lectures worldwide. Reprinted with Dr. Dodds' kind permission.
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