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What's the Big Deal About the Little Thyroid?

That is a question that many of us have been asking lately. The following is a list of clinical signs of hypothyroidism compiled by W. Jean Dodds, DVM. It originally appeared in ROTT N CHATTER, October 1992, V.1, N.3, and November 1992, V.1, N.4 (may be reproduced). Once you realize how broad the problems can be, you may want to learn more about this little gland!

 

Clinical Signs of Hypothyroidism
By W. Jean Dodds, DVM

Alterations in Cellular Metabolism

• lethargy

• mental dullness

• exercise intolerance

• neurologic signs (polyneuropathy, seizures)

• weight gain

• cold intolerance

• mood swings

• hyperexcitability

• stunted growth

• chronic infections

Hematologic Disorders

 

• bleeding

• bone marrow failure

• low red blood cell count (anemia)

• low white blood cell count

• low platelet

Occular Diseases

• corneal lipid deposits

• corneal ulceration

• uveitis

• keraconjunctivitis sicca ("dry eye")

• infections of the eyelid gland (meibomian gland)

Neuromuscular Problems

• weakness

• stiffness

• laryngeal paralysis

• facial paralysis

• "tragic expression"

• knuckling or dragging feet

• muscle wasting

• megaesophagus

• head tilt

• drooping eyelids

Dermatologic Diseases

• dry, scaly skin and dandruff

• coarse, dull coat

• bilaterally symmetrical hair loss

• "rat tail" or "puppy coat"

• hyperpigmentation

• seborrhea or greasy skin

• pyoderma or skin infections

• myxedema

• chronic offensive skin odor

Cardiac Abnormalities

• slow heart rate (bradycardia)

• cardiac arrhythmias

• cardiomyopathy

Gastrointestinal Disorders

• constipation

• diarrhea

• vomiting

Reproductive Disorders

• infertility of either sex

• lack of libido

• testicular atrophy

• hypospermia

• aspermia

• prolonged interestrus interval

• absence of heat cycles

• silent heat

• pseudopregnancy

• weak, dying or still born pups

Other Associated Disorders

• IgA deficiency

• loss of smell (dysosmia)

• loss of taste

• glycosuria

• chronic, active hepatitis

• adrenal endocrinopathies

• parathyroid endocrinopathies

Now that we have your attention...would you like to learn more? Please read on.

Introduction

The thyroid gland is located on the dogs trachea, just below the larynx. The thyroid gland makes two hormones, L-thyroxine (T4) and triiodothyronine (T3). These two hormones regulate the body's basic metabolism - including control of growth and development and maintenance of protein, carbohydrate, and lipid metabolism. More T4 is produced, however, T3 is the more active form and most of T4 is converted into T3 in the tissues. The majority of the hormones travel in the blood bound to protein, but a small proportion is unbound (free). Only the unbound or free hormones are available for physiologic action.

Hypothyroidism is the most common endocrine disease in dogs. The majority of cases are due to autoimmune thyroiditis. Idiopathic thyroid atrophy is characterized by loss of thyroid tissue, which is replaced by fat and connective tissue. This differs from lymphocytic thyroiditis, in which inflammatory cells invade and eliminate the thyroid tissue. Clinical signs of hypothyroidism become apparent as the thyroid gland is progressively destroyed. This is an inherited disease (genetic) in dogs and effects both males and females equally. The familial tendency has been demonstrated in Great Danes, Beagles and Borzois. More recently, many other breeds have been added to this list.

History

For many years the only test for thyroid function was the total T4 (TT4) test, which measured all the T4, bound and free. This was an insensitive measure of thyroid function as it usually does not go low until at least two-thirds of the functional thyroid tissue has been lost. Total T4 (TT4) and total T3 (TT3) levels may also be suppressed by liver and kidney disease, tumors and other physical diseases, as well as by various drugs, including steroids, Phenobarbital, anti-inflammatory drugs, and certain antibiotics. Free T3 and T4 (FT3 and FT4) levels are less likely to be affected by disease or drugs. In the past, thyroid stimulating hormone (TSH) was injected in order to measure the hormonal response. This thyroid stimulation test is rarely done now as TSH is expensive and the dog is required to remain at the vets to have 2 blood samples drawn throughout the day. This test was not very accurate and was influenced by many factors including stress and reproductive status. Later test for endogenous thyrotropin (eTSH) were incorporated in most thyroid screening panels. However, there were a significant number of cases were the T4 was normal and the eTSH was elevated or T4 depressed and eTSH normal. This led to considerable diagnostic problems.

In August of1996, the American Kennel Club Canine Health Foundation hosted an international symposium on canine hypothyroidism at the University of California at Davis. A group of approximately 100 people gathered at the university for the symposium. Presenters included leading researchers in canine endocrinology. Craig Sparkes, an English Setter Fancier, spoke about issues of hypothyroidism that affect breeders. Representatives from the AKC and the AKC Canine Health Foundation (AKC/CHF), which helped sponsor the event, included Dr. Sheldon Adler, chairman of the Delegates Committee on Canine Health Research and Education; Robert Kelly, a Board Member of the AKC/CHF, Ed Gilbert, an AKC Delegate; and Deborah Lynch, executive director of the AKC/CHF. These experts in their fields, got together to discuss the problems associated with testing and diagnosing thyroid disorders. The proceedings of the conference were published in Canine Practice, Vol. 22 No. 1, January/February 1997. The AKC Gazette also published an article summarizing the findings of the conference in February 1997. The AKC Canine Health Foundation decided to provide a summary directed to dog breeders. Elizabeth Bodner, DVM, reviewed all of the material from the conference proceedings and produced the first "white paper" for the Foundation. It summarizes the proceedings in lay language and captures the primary principles expressed at the conference in a shortened format.

Findings

• Lymphocytic thyroiditis affects male and female dogs equally.

• A familial tendency has been demonstrated in Great Danes, Beagles and Borzois.

• The most clearly defined neurologic disease associated with canine hypothyroidism is hypothyroid polyneuropathy, which causes generalized weakness.

• The disease may or may not be associated with clinical signs of reproductive dysfunction.

• Hypothyroidism can effect hemostasis, or the ability to control bleeding.

• Hypothryoidism can cause slowing of the heart and cardiac arrhythmias.

• The most common biochemical abnormality in hypothyroid dogs is hyperlipidemia, or high serum lipid levels. High cholesterol is observed in 66-80% of hypothyroid dogs.

• Numerous drugs can depress thyroid hormone concentrations.

The most significant outcome was the establishment of a practical approach to diagnosing and monitoring hypothyroidism. Out of this was born the OFA thyroid screening panel and certification registry.

Recommendations

For all dogs, the initial work-up begins with a complete blood count (CBC), blood chemistry panel, urinalysis, case history and physical examination. After this initial database is developed, testing depends on whether the dog is a pet, performance or breeding dog.

Breeding and Performance Dogs. The work-up includes the following tests: total T4 (TT4), free T4 measured by equilibrium dialysis (fT4d), thyroglobulin autoantibodies (TgAA) and canine thyroid stimulating hormone (cTSH). In normal dogs, these tests should be repeated annually. In dogs where the tests are normal but there are clinical signs, withhold from breeding and repeat the tests in 2-6 months. If the results are abnormal, do not breed, and retest in 3-6 months or initiate treatment, and retest in 6-8 weeks to monitor treatment.

 

Pet Dogs. The diagnostic protocol for pet dogs calls for a TT4 test after creation of the initial database. A normal result, in the absence of clinical signs, means there is no current hypothyroid disease. A normal result in conjunction with clinical signs, however, should lead to a cTSH and fT4d test. At this point, if the results of those additional tests are normal, the testing ends. If the cTSH and fT4d test yield abnormal results, the dog should be treated with thyroid supplementation. The pet dog that has clinical signs of hypothyroidism and an abnormal result on its initial TT4 test should also be treated. Retest in 6-8 weeks to monitor treatment.

Current

Much research has been conducted since the publication of the white paper in March 1997. Large studies have been conducted at Michigan State University supporting the familial incidence of autoimmune thyroiditis. One of the most significant findings to date has been the hypothesis that idiopathic hypothyroidism may be the end stage of autoimmune thyroiditis. Previously these were considered to be two separate diseases. Recent data from Michigan State University shows that 50% of dogs shown to have idiopathic primary hypothyroidism may actually have had autoimmune thyroiditis as the original problem. As the thyroid is destroyed by the lymphocytes, thyroglobulin is no longer around to stimulate the autoantibody production. Hence, the dogs become TgAA negative and are placed under the classification of idiopathic hypothyroids. It appears that the end stage of autoimmune thyroiditis is "idiopathic" hypothyroidism. This reinforces the justification for routine annual screening of all breeding stock. The development of the TgAA test offers breeders an accurate, reliable, and cost effective option for routine testing. TgAA is the FIRST indicator of autoimmune thyroiditis and can be positive long before clinical signs of the disease occur. Hypothyroidism usually manifests itself between the ages of three and five years, however, the TgAA test can detect problems in dogs as young as one year. . TgAA is a very stable gamma globulin and therefore is not effected by changes is temperature like fT4d. The TgAA assay has been found to be 96% accurate.

Statistics

• A 1998 MSU study tested five hundred consecutive samples for TgAA and found 9.9% of the samples were positive.

• Another study at MSU tested 91 random-source dogs and found that 3.3% had positive TgAA. Only 2.2% of these dogs had clinical signs of hypothyroidism.

• As of April 15, 1998, MSU had run 2,321 TgAA Assays using blood samples from Great Danes, and 4% of those were positive.

• Since its inception in 1996, the OFA thyroid registry has only registered 26 Great Danes.

• Of the 26 certified Danes, 10 are fawn, 3 brindle, 6 black, and 6 blue.

• Of the 26 certified Danes, 14 are male and 11 are female.

Current Testing Recommendations

OFA thyroid panel: this includes fT4d, TSH, and TgAA. The minimum testing requirement for all dogs is TgAA.

The blood sample should be taken when the dog is otherwise healthy, is not approaching or in a heat cycle, and is not taking pharmaceuticals such as steroids, non-steroidal anti-inflammatories, or anti-seizure drugs. Dogs currently on thyroid replacement therapy can not be tested and should be free of drug for at least 3 months prior to testing.

Dogs should be tested at 1, 2, 3, 4, 5, 7 and 9 years of age. Since this is an autoimmune disease, dogs can test negative at one age and develop the disease at a later time. If a dog does not acquire this disease by 5 years of age, odds are very good that it will remain negative.

Breeders have the option of having the data from positive TgAA (thyroiditis) dogs reported in the open OFA registry or not. Practically, most breeders chose not to report this data. This defeats the purpose of an "open" registry. The registry can help identify dogs that are phenotypically normal for breeding programs and help gather data on the prevalence of the disease within our breed. Testing of all dogs is just the first step. Sharing of this information is what is necessary in order to eliminate this disease from our breed.

Teresa La Brie
Norwich, NY

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References

Graham, P.A., Nachreiner, R.F., Refsal, K.R,, Hauptman, J., and Watson, G.L. Thyroglobulin autoantibody is an effective Marker for thyroiditis in dogs. Am J Vet Res (submitted).

Nachreiner, R.F., Refsal, K.R., Graham, P.A., et al. Prevalence of autoantibodies to thyroglobulin in dogs with non-thyroidal illness. AM J Vet Res, Vol. 59, No. 9, August 1998.

Thacker, E.L., Refsal, K.R., and Bull, R.W. Prevalence of autoantibodies to thyroglobulin, thyroxine or triiodothyronine and and relationship of autoantibodies and serum concentrations of iodothyronines in dogs. AM J Vet Res, Vol. 53, No. 4, 449-453, 1992.

Nelson, R .W., Et al: Serum free thyroxine concentration in healthy dogs, dogs with hypothyroidism and euthyroid dogs with concurrent illness. J AM Vet Med Assoc. Vol. 198, 1401-1407, 1991.

Additional information was obtained from the following:

Thyroid Testing in Dogs: A Reference for Dog Breeders and Owners
Wolfsheimer, DVM, PhD
Diplomate, American College of Veterinary Internal Medicine
Associate Professor, Dept. of Physiology, Pharmacology & Toxicology

Colleen Brady, B.A., Veterinary Student
School of Veterinary Medicine
Louisiana State University
Baton Rouge, LA 70803

Orthopedic Foundation for Animals
Canine Thyroid Registry
Ray Nachreiner, DVM, PhD
2300 Nifong Blvd.
Columbia, MO 65201

Oxford Laboratories
P.O. Box 558
Oxford, MI 48371

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