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Canine Hypothyroidism, An Overview

Erin Bell, DVM; Kenneth S. Latimer, DVM, PhD; Bruce E. LeRoy, DVM, PhD; Holly Moore, DVM

Class of 2005 (Bell) and Department of Pathology (Latimer, LeRoy, Moore) College of Veterinary Medicine, Universityof Georgia, Athens, GA 30602-7388

Introduction

Hypothyroidism is due to impaired production and secretion of the thyroid hormones, which results in a decreased

metabolic rate.1 It is the most common endocrinopathy of the dog. The clinical signs are quite variable and almostany organ system may be involved. Veterinarians have many options for diagnostic tests of thyroid function, howeverno one test is optimal for all clinical situations. Therefore, clinicians also must be careful in interpretation of the test

results. However, there are likely to be more specific and sensitive tests of thyroid function to clinical use.8 Thefollowing manuscript presents a general overview of canine hypothyroidism, with special emphasis on the diagnostictests that are currently available as well as their advantages and disadvantages.

Etiology

Although dysfunction anywhere in the hypothalamic-pituitary-adrenal axis may result in thyroid hormone deficiency, >95% of the clinical cases of hypothyroidism in dogs appear to result from destruction of the thyroid gland (primary

hypothyroidism).1 The normal thyroid gland contains numerous follicles lined by cuboidal to columnar epitheliumsurrounding lakes of colloid (Fig. 1). Primary hypothyroidism results from lymphocytic thyroiditis, idiopathic thyroid

atrophy, or, more rarely, neoplasia.15 Approximately 50% of the cases of primary hypothyroidism are due to

lymphocytic thyroiditis.7 Canine thyroiditis is believed to be immune-mediated and is characterized histologically by adiffuse infiltration of the gland by lymphocytes, plasma cells, and macrophages (Fig. 2). Infiltration subsequently

results in progressive destruction of follicles and secondary fibrosis.1, 11 Antithyroglobulin antibodies are present in

42% to 59% of dogs with thyroiditis.7

Figure 1: normal thyroid gland composed of colloid-laden follicles, thyroid follicular epithelial cells (blackarrow) and parafollicular C-cells (white arrow).

Figure 2: thyroid gland with lymphocytic thyroiditis. Afollicle (black arrow) is surrounded by a denselycellular infiltrate of lymphocytes and plasma cells

(white arrow).

Idiopathic thyroid atrophy is characterized histologically by loss of thyroid parenchyma and replacement of the normal

colloid-filled follicles (Fig. 3) with adipose tissue.1 Most dogs with thyroid neoplasia are euthyroid because

hypothyroidism does not occur until at least 75% of the thyroid parenchyma has been destroyed.7 However, some

dogs have been reported to be hyperthyroid due to the presence of functional thyroid carcinomas.8

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Figure 3: an atrophic thyroid gland composed ofdegenerate thyroid epithelial cells. A single folliclecontaining colloid and degenerate cells is present (whitearrow).

Secondary hypothyroidism, resulting from inadequate secretion of thyrotropin (thyroid stimulating hormone or TSH)from the pituitary gland, is less commonly recognized, probably because a validated assay for canine TSH has beenunavailable until recently. Causes of acquired secondary hypothyroidism include pituitary neoplasia and pituitary

malformations such as a cystic craniobuccal (Rathke’s) pouch.15 Because of the nonselective nature of the resultingcompressive atrophy and replacement of pituitary tissue by such large tumors, deficiencies of other (one or more)

pituitary hormones also usually occur.1

Tertiary hypothyroidism results from a deficiency of hypothalamic thyrotropin-releasing hormone (TRH). This entity

has yet to be documented in the dog.7

Congenital hypothyroidism (cretinism) is rarely diagnosed in dogs. Congenital primary hypothyroidism may resultfrom iodine deficiency, thyroid dysgenesis, or dyshormonogenesis (inability to organify iodide). Congenital secondaryhypothyroidism (associated with disproportionate dwarfism, lethargy, gait abnormalities, and constipation) due to TSH

or TRH deficiency has been documented in a family of Giant Schnauzers and in a young Boxer.7

Iatrogenic causes of hypothyroidism include radioactive 125I treatment, administration of antithyroid drugs, andsurgical thyroidectomy. Because of the presence of accessory thyroid tissue, permanent hypothyroidism is rare after

thyroidectomy.7

Clinical Signs

Although the age of onset is variable, hypothyroidism most commonly occurs in dogs from 4 to 10 years of age. It

usually affects mid- to large-size breeds and is rare in toy and miniature breeds.1 The clinical signs of hypothyroidismmay be vague and insidious in onset, therefore hypothyroidism may be considered in the differential diagnosis of awide range of medical problems. Lethargy, mental dullness, weight gain, unwillingness to exercise, and coldintolerance are classical signs of hypothyroidism and are the result of a decreased metabolic rate. Dermatological

manifestations occur in 60% of hypothyroid dogs.7 These may include a dry hair coat, seborrhea, alopecia,hyperpigmentation, and pyoderma (Fig. 4). While hair loss occurs in a bilaterally symmetrical pattern, it initially occursin areas of friction such as the tail, around the neck, lateral trunk, and ventral thorax. Accumulation of excessiveamounts of glycosaminoglycans (mostly hyaluronic acid) in the dermis results in the myxoedematous appearance

(tragic facial expression) found in some dogs.13 Glycosaminoglycan accumulation may also occur in thegastrointestinal tract, heart, and skeletal muscles. Neurological, cardiovascular (bradycardia), and reproductivemanifestations have also been recognized. Myxedema coma, a rare syndrome, is the extreme expression of severe

hypothyroidism.1

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Figure 4: generalized alopecia in a hypothyroid dog.

Diagnosis

Hypothyroidism in dogs is probably one of the most over diagnosed diseases in small animal practice. The clinicalsigns of many diseases and conditions can mimic those of hypothyroidism, and some of these clinical signs, even in

dogs with normal thyroid function, can improve after administration of exogenous thyroid hormone.1 For this reason,clinicians need to have a clinical suspicion for hypothyroidism prior to ordering diagnostic tests. There is no singlehematologic or biochemical test that is conclusive for hypothyroidism and even hormonal tests must be interpreted in

light of historical and physical findings.8 The wide variety of clinical signs and findings associated with hypothyroidismnecessitates specific testing of thyroid function to establish a definitive diagnosis. Tests currently available fordiagnosing thyroid disease include total thyroxine (TT4), total 3,5,3’-tri-idothyronine (TT3), free T4 (fT4), endogenouscanine thyroid stimulating hormone (cTSH), TSH response test, TRH response test, T4 and T3 autoantibodies,

antithyroglobulin antibodies, nuclear scintigraphy, and thyroid gland biopsy.13 TT4, fT4 by dialysis, and cTSH are teststhat are recommended routinely.

Factors affecting thyroid hormone concentrations: Age, breed, obesity, systemic illness, and drugs may allaffect thyroid hormone concentrations. Thyroid hormone concentrations may be elevated from 2 to 5 times the adultlevel during the first three months of a puppy’s life. Information is accumulating that certain breeds have considerablylower ranges of normal thyroid hormone concentrations. Greyhounds and Scottish Deerhounds have serum T4concentrations considerably lower than the reference ranges commonly used by most diagnostic laboratories. Mildincreases in T3 and T4 concentrations have been reported in obese, euthyroid dogs due to excessive caloric intake.The effects of nonthyroidal illnesses that depress thyroid hormone concentrations are collectively called the "euthyroidsick syndrome." A lowering of TT3 alone (low T3 syndrome) is less likely to be observed than is the lowering of TT4and TT3 (low T4 state of medical illness). Drugs used in veterinary medicine which lower thyroid hormoneconcentrations include the glucocorticoids, anticonvulsants, quinidine, salicylates, phenylbutazone, sulfa antimicrobials,

and radiocontrast agents.4, 7 , 8

Nonspecific clinicopathologic abnormalities: The severity of these nonspecific abnormalities usually correlateswith the severity and chronicity of the hypothyroid state. These abnormalities may be associated with many otherdiseases, but their presence adds supportive evidence for a diagnosis of hypothyroidism in a dog with appropriateclinical signs. The classic hematologic finding associated with hypothyroidism is a mild, normocytic, normochromic,nonregenerative anemia. The classic serum biochemical abnormality is hypercholesterolemia, which occurs in about80% of dogs with hypothyroidism, making it an excellent screening test. Other clinicopathologic abnormalities mayinclude high serum concentrations of triglycerides and increased activity of alkaline phosphatase and creatine kinase.

The electrocardiogram may show low amplitude and inverted T waves with bradycardia.1, 8

Total T4 Concentration: Measurement of serum TT4 concentrations remains a useful screening test forhypothyroidism. Accuracy of TT4 in evaluating thyroid function is 85 to 90%. However, it is important to remember

that several factors can artificially affect serum TT4 values.2 TT4 infrequently is within the reference interval inhypothyroid dogs, although early hypothyroidsm does result in a low normal TT4. TT4 is, however, frequently belowthe reference interval in dogs with normal thyroid function. This occurs because of physiological fluctuations in thyroid

hormone concentrations as well as the effects that drugs and non-thyroidal illness have on TT4.13 The soledetermination of TT4 concentration by radioimmunoaassay is truly diagnostic only if the value is within the referenceinterval or elevated, in which case, hypothyroidism can be excluded. Dogs with hypothyroidism can, in most cases, bedistinguished from healthy dogs on the basis of a low resting TT4 concentration. However, nonthyroidal conditions onthe list of differential diagnoses, certain drugs, and even the time of day may also lower baseline TT4 and TT3concentrations. Therefore, reduced basal TT4 or TT3 concentrations are not specific enough to serve as reliableindicators of hypothyroidism. It is always wise to confirm the diagnosis of hypothyroidism with a more specific test,

such as fT4, cTSH, or TSH response.8

Total T3 Concentration: As T3 is the most potent thyroid hormone at the cellular level, it would seem logical to

measure its concentration for diagnostic purposes.8 However, measurement of TT3 concentrations is less accuratethan TT4 measurement for distinguishing euthyroid from hypothyroid dogs. T3 concentrations undergo normal

fluctuations out of the reference interval to a greater extent than T4 concentrations in euthyroid dogs.7 Although

concentrations of T4 are low in the late stages of hypothyroidism, concentrations of T3 are often within the referenceinterval in many hypothyroid dogs. One likely reason for this involves the compensatory mechanisms occurring in thefailing thyroid and its ability to shift secretion, releasing more T3 as failure progresses. Additionally, elevated ornondetectable results may occur owing to anti-T3 antibodies. For this reason it is not recommended to measure TT3 in

the evaluation of hypothyroidism in dogs.7, 10

Free T4 Concentration: Serum fT4 is a better test of thyroid function than TT4 concentrations because it is lessaffected by factors that alter protein binding. The accuracy of fT4 measurement is largely dependent on the assaymethod. The most accurate method of measurement available in clinical laboratories is a modified equilibrium dialysis

technique.13 The diagnostic sensitivity of fT4 equilibrium dialysis is 98%, specificity is 93%, and accuracy is 95%.2

Because fT4 by dialysis is expensive and time consuming, single-stage solid-phase (analog) radioimmunoassays forhuman fT4 are commonly used for measurement of canine fT4. However, canine fT4 concentrations measured byanalog methods are lower than those measured by equilibrium dialysis and have no diagnostic advantage over

measurement of TT4.7

Endogenous Canine Thyrotropin (cTSH) Concentration: The recently developed assay to measure cTSH wasanticipated as a potentially accurate and sensitive method of assessing thyroid function. Serum TSH is the mostaccurate test of thyroid function in humans, where it allows diagnosis of hypothyroidism at a very early, evensubclinical, stage. Unfortunately, assay performance of cTSH in the dog has been disappointing when it is used as a

single test.12 Serum TSH concentrations would be expected to be high in dogs with primary hypothyroidism becauseof the loss of negative feedback of T4 and T3 on the pituitary gland. Unfortunately, from 18 to 38% of dogs withprimary hypothyroidism have cTSH concentrations within reference intervals. Furthermore, 0 to 14% of euthyroid

dogs have an elevated cTSH.13 This results in an assay sensitivity of only 63 to 82%. Possible reasons that dogs withhypothyroidism might have a cTSH concentration within the reference interval include secondary or tertiary

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hypothyroidism might have a cTSH concentration within the reference interval include secondary or tertiary

hypothyroidism, effects of drugs or concurrent illness, and diurnal fluctuation of cTSH concentration.3 In secondary

and tertiary hypothyroidism, TSH concentrations range from the low end of the reference interval to undetectable.15

Since the TSH concentration is within reference interval in 20 to 40% of hypothyroid dogs, it cannot be used alone for

a diagnosis.2, 14 Use of T4 in combination with TSH should increase the accuracy of diagnosis.15 While serum TT4 is agood screening test, fT4 and cTSH are the primary tests to confirm the diagnosis of hypothyroidism. When cTSH ismeasured with fT4, it can provide valuable evidence supporting hypothyroidism by increasing the diagnostic specificityto 98%. Test results within the reference interval indicate that the dog is not hypothyroid. Decreased fT4 andincreased cTSH identify clinical hypothyroidism. The serum TT4 can be within the reference interval and TSH can beelevated in true hypothyroidism if there are circulating thyroid autoantibodies, as these often cross-react with TT4

assays.2 Measurement of cTSH concentration is a valuable adjunct to T4 assessment in the diagnosis of caninehypothyroidism but should not be used alone. Serum fT4 concentrations are more specific but may be less sensitivethan TT4 estimations in the diagnosis of hypothyroidism. Given the expense of fT4 estimations, TT4 measurements

are currently considered adequate in evaluating thyroid function.5

Thyrotropin (TSH) Response Test: The TSH response test has long been recognized as an accurate measure of

thyroid function and serves as the "gold standard" measurement in many studies evaluating thyroid function tests.13

This is because it provides important information about thyroid secretory reserve.8 Measurement of TT4 before andsix hours after intravenous administration of 0.1 U/kg bovine TSH is the recommended protocol. Post-TSH TT4concentrations above 30 mmol/L are normal in most laboratories, while TT4 less than 20 mmol/L is diagnostic for

hypothyroidism.13 In pituitary forms of hypothyroidism, the thyroid gland should remain responsive to TSH. With theTSH response test, depression of baseline serum T4 concentrations due to drugs and illness may be distinguishedfrom advanced primary hypothyroidism but not from other forms of hypothyroidism or from earlier stages of primaryhypothyroidism. The rare cases of long-standing secondary (pituitary) or tertiary (hypothalamic) hypothyroidism withsubsequent thyroid atrophy may require 2 or 3 consecutive daily doses of TSH to eventually demonstrate thyroid

responsiveness.8 Unfortunately, although the TSH response test is accurate, bovine TSH is not licensed for use in the

dog and is difficult and expensive to obtain.5 There have also been occasional reports of anaphylactic responses afterbovine TSH administration. The TSH response test cannot be used to evaluate thyroid function in dogs receiving L-thyroxine because treatment causes thyroid atrophy. Supplementation must be discontinued 6 to 8 weeks before

testing.7

Thyrotropin Releasing Hormone (TRH) Response Test: The TRH response test is used in humans to differentiateprimary from secondary hypothyroidism. In people with primary hypothyroidism, response of TSH to TRHadministration is exaggerated, whereas in secondary hypothyroidism there is no response. In dogs, the test has been

used in place of the TSH response test, and change in TT4 has usually been measured.7 The TRH response test isperformed by measurement of TT4 before and four hours after intravenous administration of suggested doses ofsynthetic TRH that range from 0.2 mg/dog to 0.1 mg/kg. A normal response has been stated to be 1.5 times thebaseline T4 concentration, but a very low baseline T4 could increase to that degree by normal fluctuations in hormone

concentration over time.13 In theory, the administration of TRH should lead to an increase in T4 only if the pituitary-thyroid axis is intact. Therefore, responsiveness to TRH should only be observed in healthy dogs and dogs withtertiary (hypothalamic) thyroid insufficiency, a condition not yet documented. Perhaps the main limitation of the TRH

response test is that little information has been published on the effects of drugs or nonthyroidal illness.8 Results ofthe TRH response test are variable, with a significant percentage of dogs failing to respond with a substantial increase

in T4.13 The TRH response test is incapable of accurately separating hypothyroid dogs from euthyroid dogs with non-

thyroidal illness and can no longer be recommended.5, 10

Antithyroglobulin Antibody (ATA): ATA is found in 42 to 59% of hypothyroid dogs and is believed to be the resultof leakage of thyroglobulin into circulation owing to lymphocytic thyroiditis. A commercially available ELISA for ATA is

a sensitive and specific indicator of thyroiditis; false-positive results occur in < 5% of dogs with other endocrinedisorders. It is important to recognize that a positive ATA titer is not an indicator of abnormal thyroid function.

Whether all dogs with ATA ultimately develop hypothyroidism is unknown.7, 9

Anti-T3 and -T4 Antibodies: Antibodies directed against T3 and T4 also occur in canine thyroiditis, although theyare less prevalent than ATA. The incidence or recognition of anti-T3 antibodies appears to be greater than for anti-T4antibodies. Because dogs with thyroiditis may still have adequate thyroid reserve, antithyroid antibodies are notindicators of hypothyroidism. Antibodies directed against T3 and T4 may interfere with hormone assays, leading to a

spurious increase or decrease in the measured hormone concentration.7 The clinical significance of antithyroidhormone antibodies is primarily in their indication of the diagnosis of lymphocytic thyroiditis and the confusion they

create for the interpretation of thyroid function tests.8

Scintigraphy: Nuclear scintigraphy using radioiodine or technetium is rarely used as a method of diagnosinghypothyroidism because of the limited availability of the technique, exposure of the patient and personnel to

radioactive isotopes, and accuracy of the procedure.13 Available only at referral institutions, thyroid uptakedeterminations are no longer used as a general screening test for canine hypothyroidism but are reserved as an aid in

characterizing congenital defects of thyroid hormone synthesis.8

Thyroid Biopsy: Thyroid gland biopsy is another rarely used tool for diagnosis of hypothyroidism. Thyroid glandbiopsy may be a better method of diagnosing lymphocytic thyroiditis than primary hypothyroidism because earlyfollicular atrophy may be difficult to detect in an incisional biopsy of one thyroid gland. It may be a useful method ofdifferentiating primary from secondary hypothyroidism where enlarged follicles and flattened follicular epithelial cellsare found because of deficient TSH secretion. Risks of thyroid gland biopsy include general anesthesia and damage to

surrounding tissue such as the parathyroid glands and recurrent laryngeal nerves.13

Therapeutic Trial: When diagnostic tests do not provide a clear diagnosis of hypothyroidism, thyroid replacementtherapy has been suggested as a valid diagnostic step. The cost of the diagnostic testing is often cited as hardship forthe owner, but it should be emphasized that replacement therapy is generally required for the remainder of theanimal’s life. Therefore, an incorrect diagnosis can also be quite expensive, a delayed diagnosis of another diseasecould be detrimental, and diagnostic procedures following a therapeutic trial with equivocal results can be quite difficult

to interpret because secretion of the healthy thyroid gland is inhibited by this procedure.8 A positive response totherapy should be interpreted with caution because clinical signs may also improve in euthyroid animals treated with

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therapy should be interpreted with caution because clinical signs may also improve in euthyroid animals treated withL-thyroxine. A diagnosis of hypothyroidism based on response to therapy should be confirmed by recurrence of

clinical signs after withdrawal of supplementation.7

Treatment

Note: Treatment of animals should only be performed by a licensed veterinarian. Veterinariansshould consult the current literature and current pharmacological formularies before initiating anytreatment protocol.

The initial treatment of choice is synthetic L-thyroxine, because it results in normalization of both T4 and T3concentrations. Risk of iatrogenic hyperthyroidism is low because physiologic regulation of conversion of T4 to T3 ispreserved. Bioavailability may vary greatly from one product to another, so it is advisable to use a brand-nameproduct for initial treatment. It also is advisable to measure TT4 concentrations 4-8 weeks after changing the brand of

supplement, particularly if a generic product is substituted for a name-brand product.7 With few exceptions,

replacement therapy is necessary for the remainder of dog’s life.1

Optimal dose and frequency of supplementation vary among dogs because of variability in L-thyroxine absorption andserum half-life. Treatment should be initiated at a dose of 0.02 mg/kg orally every 12 hours, and then the dose shouldbe adjusted based on results of therapeutic monitoring. Using twice-daily treatment initially improves the likelihood ofresponse to treatment in all dogs. After clinical signs resolve and TT4 concentrations stabilize within the therapeutic

range, the majority of dogs can be maintained on 0.02 mg/kg once daily.6, 7

The most important indicator of the success of therapy is clinical improvement. Clinical resolution of metabolic signssuch as lethargy and mental dullness can be expected within two weeks of starting therapy, while other abnormalities,

including dermatologic signs, may take up to three months to resolve.6

Biochemical therapeutic monitoring is required because of variable individual response to treatment; dose

adjustments are required in approximately half of all patients.6 Therapeutic monitoring of serum TT4 and cTSH levelsshould be started beginning four to eight weeks after starting supplementation. Serum TT4 concentrations should bemeasured at six- to eight-week intervals during the first six to eight months of treatment, because metabolism of T4will change when the metabolic rate normalizes and dosage adjustments may be necessary. Once adequate serumTT4 concentrations are documented and the dog’s dosage has stabilized, frequency of measurement of serum TT4

may be decreased to once or twice a year.7

With once-daily administration of T4, the peak serum concentration of T4 generally should be slightly high to high-normal four to eight hours after dosing and low-normal to normal 24 hours after dosing. Animals on a twice-dailyadministration probably can be checked at any time, but peak concentrations can be expected at the middle of the

dosing interval (4 to 8 hours) and the nadir just before the next dose.1 Six hours after Soloxine administration on aonce daily administration program, a median total T4 value of approximately 55 mmol/L is associated with goodclinical control in most dogs, whereas values of less than 35 mmol/L usually indicate the need for an increase in

dosage. Maintenance of an elevated circulating cTSH concentration is a reliable predictor of an increased therapeuticrequirement but suppression of cTSH concentration into the reference interval does not guarantee the adequacy oftherapy. A decrease in circulating cholesterol and triglyceride concentration and an increase in the RBC count can beused to indicate an overall effect of thyroid hormone replacement therapy but is not valuable in reliably confirming

therapeutic efficacy.6

Prognosis

Prognosis for return to normal function following treatment is excellent in most adult hypothyroid dogs. Prognosis inmyxedema coma is dependent on early recognition. Resolution of clinical signs in puppies with congenital

hypothyroidism is dependent on the age at which treatment is initiated.7

References

1. Aiello, SE (ed): Merck Veterinary Manual, 8th ed. Whitehouse Station, Merck & Co, 1998, pp 415-418.

2. Beaver, BV, Haug, LI: Canine behaviors associated with hypothyroidism. J Am Anim Hosp Assoc 39:431-437, 2003.

3. Bruner, JM, Scott-Moncrieff, JC, Williams, DA: Effect of time of sample collection on serum thyroid-stimulatinghormone concentrations in euthyroid and hypothyroid dogs. J Am Vet Med Assoc 212:1572-1577, 1998.

4. Daminet, S, Ferguson, DC: Influence of drugs on thyroid function in dogs. J Vet Intern Med 17:463-466, 2003.

5. Dixon, RM, Mooney, CT: Evaluation of serum free thyroxine and thyrotropin concentrations in the diagnosis ofcanine hypothyroidism. J Small Anim Pract 40:72-74, 1999.

6. Dixon, RM, Reid, SW, Mooney, CT: Treatment and therapeutic monitoring of canine hypothyroidism. J Small AnimPract 43:334-344, 2002.

7. Ettinger, SJ, Feldman, EC (eds): Textbook of Veterinary Internal Medicine, Diseases of the Dog and Cat, 5th ed.Philadelphia, WB Saunders, 2000, pp 1420-1427.

8. Feldman EC, Nelson RW. Canine and Feline Endocrinology and Reproduction, 3rd ed. St. Louis, Saunders, 2004, pp.244-245.

9. Ferguson, DC: Update on the diagnosis of canine hypothyroidism. Vet Clin North Am Small Anim Pract 24:515-519,1994.

10. Iverson, L, Jenson, AL, Hoier, R, Skydsgaard, M, Kristensen, F: Development and validation of an improvedenzyme-linked immunosorbent assay for the detection of thyroglobulin autoantibodies in canine serum samples.Domest Anim Endocrinol 15:525-532, 1998.

11. Kemppainen, RJ, Behrend, EN: Diagnosis of canine hypothyroidism. Perspectives from a testing laboratory. Vet

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11. Kemppainen, RJ, Behrend, EN: Diagnosis of canine hypothyroidism. Perspectives from a testing laboratory. VetClin North Am Small Anim Pract 31:951-956, 2001.

12. Lucke, VM, Gaskell, CJ, Wotten, PR: Thyroid pathology in canine hypothyroidism. J Comp Pathol 93:415-420,1983.

13. Marca, MC, Loste, A, Orden, I, Gonzalez, JM, Marsella, JA: Evaluation of canine serum thyrotropin (TSH)concentration: comparison of three analytical procedures. J Vet Diagn Invest 13:106-111, 2001.

14. Panciera, DL: Is it possible to diagnose canine hypothyroidism? J Small Anim Pract 40:152-155, 1999.

15. Ramsey, IK, Evans, H, Herrtage, ME: Thyroid-stimulating hormone and total thyroxine concentrations in euthyroid,sick euthyroid, and hypothyroid dogs. J Small Anim Pract 38:540-544, 1997.

16. Scott-Moncrieff, JC, Nelson, Rw, Bruner, JM, Williams, DA: Comparison of serum concentrations of thyroid-stimulating hormone in healthy dogs, hypothyroid dogs, and euthyroid dogs with concurrent disease. J Am Vet MedAssoc 212:387-494, 1998.

Acknowledgement

The watercolor "Dog on Beach" by Chriss Pagani is from her website Paintings: Oregon Impressions. The image iscopyrighted and used with permission.

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