Diseases of the Thyroid Gland

Chapter 31 Diseases of the Thyroid Gland



David L. Panciera, Mark E. Peterson, Stephen J. Birchard



HYPOTHYROIDISM IN DOGS


Hypothyroidism is a common, multisystemic disease in dogs. Thyroid hormone deficiency affects virtually all body systems, resulting in a wide array of clinical signs. It occurs predominantly in middle-aged, pure-breed dogs, including the golden retriever, Doberman pinscher, Irish setter, boxer, miniature schnauzer, dachshund, and cocker spaniel. There is no strong sex predilection.



Etiology



Primary Hypothyroidism


Primary hypothyroidism, resulting from gradual destruction of the thyroid gland, is responsible for over 95% of cases.



Lymphocytic Thyroiditis



• Immune-mediated destruction

• Circulating antithyroglobulin antibodies in most cases

• Lymphocytic infiltration in the thyroid gland


Idiopathic Thyroid Gland Atrophy



• Replacement of thyroid parenchyma by adipose tissue without inflammation

• Unknown cause

• Not associated with antithyroglobulin antibodies


Other Causes



• Uncommon causes of primary hypothyroidism include congenital types (e.g., dyshormonogenesis and thyroid dysgenesis), replacement of thyroid gland parenchyma by nonfunctional neoplastic tissue, surgical thyroidectomy, and radioiodine treatment.


Secondary (Pituitary) Hypothyroidism


Secondary (pituitary) hypothyroidism is caused by impaired secretion of thyroid-stimulating hormone (TSH). This etiology accounts for less than 5% of cases.


• Pituitary tumors: Destruction of normal pituitary thyrotrophs by neoplastic invasion.

• Cystic Rathke pouch: This form occurs in German shepherd pituitary dwarfs and is associated with concurrent hormone deficiencies including growth hormone deficiency, hypoadrenocorticism, and hypogonadism (see also Chapter 36).

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Figure 31-3 Extracapsular dissection for removal of a thyroid lobe in a cat. Incise the thyroid capsule immediately adjacent to the parathyroid gland. Carefully cauterize capsular blood vessels if necessary. Bluntly separate the thyroid gland from the parathyroid gland using a sterile cotton-tipped applicator. After ligating or cauterizing blood vessels as necessary, remove the thyroid gland and its capsule.



Tertiary (Hypothalamic) Hypothyroidism


Tertiary (hypothalamic) hypothyroidism resulting from deficient production or release of thyrotropin-releasing hormone (TRH) has not yet been documented in dogs.




Key Point


The majority of hypothyroid dogs have primary disease due to lymphocytic thyroiditis or atrophy.



Clinical Signs


The clinical signs of hypothyroidism are insidious in onset because of the gradual destruction of the thyroid gland. Signs are diverse and range from mild to severe (Table 31-1).


Table 31-1 CLINICAL SIGNS AND LABORATORY FINDINGS IN DOGS WITH HYPOTHYROIDISM













































Common Findings Uncommon Findings
Dermatologic Abnormalities Neuropathy
  Seborrhea Vestibular
Alopecia Facial
Pyoderma Generalized
Myxedema Laryngeal paralysis
Obesity Myopathy
Lethargy Megaesophagus
Weakness/exercise intolerance Central nervous system abnormalities
Low-voltage ECG complexes Dwarfism
Bradycardia Reproductive abnormalities (anestrus)
Hypercholesterolemia Insulin-resistant diabetes mellitus
Nonregenerative anemia Ocular abnormalities
Myxedema stupor or coma

ECG, electrocardiographic.



General Appearance and Behavior



• Weight gain (mild to marked obesity)

• Lethargy, dullness, and exercise intolerance

• Cold intolerance and hypothermia (uncommon)


Integument



• The majority of hypothyroid dogs have dermatologic abnormalities.

• Excessive scaling and dry haircoat are often the earliest changes.

• Excessive shedding.

• Alopecia.

• Often begins on the tail and neck (areas of friction).

• May progress to bilaterally symmetric truncal alopecia sparing the head and extremities.

• Cutaneous hyperpigmentation.

• Recurrent otitis externa or pyoderma.

• Myxedema: Thickening of the skin, especially facial, secondary to glycosaminoglycan accumulation, leading to a “tragic” facial expression.

• Pruritus is not present except when associated with secondary pyoderma, seborrhea, or Malassezia infection.


Nervous System and Muscle



• Uncommon finding in hypothyroidism.

• Peripheral neuropathy.

• Generalized neuropathy can cause weakness, ataxia, and abnormal proprioception.

• Vestibular neuropathy.

• Facial neuropathy, often concurrent with vestibular signs.

• Unilateral forelimb lameness with pain in the glenohumeral joint.

• Megaesophagus is very rare and may occur secondary to myopathy, neuropathy, or concurrent myasthenia gravis.

• Nonspecific weakness and exercise intolerance may be caused by myopathy or mild neuropathy.

• Behavioral abnormalities including aggression have been reported with hypothyroidism.


Cardiovascular System



• Bradycardia, weak apex beat, and weak pulses.

• Decreased amplitude of R wave or first-degree atrioventricular block on electrocardiogram.

• Atrial fibrillation may occur rarely in dogs with hypothyroidism.

• Decreased myocardial contractility (mild and subclinical).


Reproductive System



• No clinically significant effects on male reproduction.

• Anestrus, infertility, and abortion are possible in females.

• Inappropriate galactorrhea in intact females.


Eyes



• Ocular manifestations of hypothyroidism are rare and appear to be associated with hyperlipidemia.

• Corneal lipid deposits.

• Chronic uveitis.


Bleeding Disorders



• Bleeding tendencies are not caused by hypothyroidism.

• Thyroid hormone administration does not increase the von Willebrand factor in dogs with congenital von Willebrand disease.


Congenital Hypothyroidism



• Lethargy, mental dullness, weak nursing, and constipation.

• Disproportionate dwarfism, broad skull, macroglossia, delayed dental eruption, hypothermia, distended abdomen, retention of puppy haircoat, dry skin, and gait abnormalities.

• Some abnormalities (e.g., short stature, osteoarthritis, and impaired mental function) may persist despite treatment.


Myxedema Stupor and Coma



• Most severe and rarest form of hypothyroidism

• Stupor or coma, hypothermia without shiver-ing, bradycardia, hypotension, and hypoventil-ation, in addition to the more common signs of hypothyroidism

• Hypercholesterolemia, hyponatremia, hypoglycemia, and high creatine kinase level



Key Point


Dogs may develop various clinical signs of hypothyroidism. Although one sign may predominate, cutaneous abnormalities, lethargy, and/or weight gain are present in most cases.



Diagnosis


Because of the diverse clinical signs and difficulty in interpreting thyroid function tests, hypothyroidism is often diagnosed inappropriately.




Key Point


Many non-thyroidal factors can influence thyroid function tests, resulting in low serum thyroid hormone concentrations in euthyroid dogs.


Diagnosis is dependent on both compatible clinical signs and abnormal thyroid function tests, not either alone.



Screening Laboratory Tests



• Complete blood count shows normocytic, normochromic anemia in 30% of cases.

• Serum biochemical analysis shows hypercholesterolemia in 75% of cases. Hypertriglyceridemia is also common.


Basal Total Thyroid Hormone Concentration (T4 and T3)



• Normal serum thyroxine (T4) concentration infrequently occurs in the hypothyroid dog.

• Serum T4 is in the low-normal range in about 10% of hypothyroid dogs.

• Serum triiodothyronine (T3) concentration is unreliable in the diagnosis of hypothyroidism since it is often within the reference range in hypothyroid dogs.

• Serum T4 is often below normal in euthyroid dogs for the following reasons:

• Normal daily fluctuation can result in low serum T4 on repeated sampling of normal dogs.

• Breed differences result in low serum T4 in greyhounds, deerhounds, Alaskan sled dogs, and probably other breeds.

• Non-thyroidal illness (e.g., hyperadrenocorticism, renal disease, or neoplasia) causes a decrease in total T4 and T3.

• Administration of various drugs, including glucocorticoids, sulfonamides, anticonvulsants, nonsteroidal anti-inflammatory drugs, and radiocontrast agents, lowers serum T4 and T3.



Key Point


Low total T4 concentration is almost always present in hypothyroidism. If total T4 is normal, hypothyroidism is very unlikely.



Free Thyroxine Concentration



• Free T4 is the portion of T4 that is not bound to plasma carrier proteins (normally 0.1% of total T4).

• Free T4 is not affected by most non-thyroidal illnesses and drugs.

• Equilibrium dialysis is the only reliable method for measurement of free T4 in dogs with non-thyroidal illness. Free T4 by equilibrium dialysis is the most accurate single test for diagnosing hypothyroidism (see the Endocrine Diagnostic Laboratory of the Michigan State University website: www.ahdl.msu.edu).

• Hypothyroid dogs rarely have a normal serum, free T4 concentration.


Serum Endogenous Canine Thyroid-Stimulating Hormone Concentration



• Serum TSH concentration is increased in most cases of primary hypothyroidism due to loss of negative feedback of T4 and T3 on the pituitary gland.

• High serum TSH and low serum T4 or free T4 are diagnostic of hypothyroidism.

• Serum TSH concentration is normal in 20% to 40% of hypothyroid dogs.

• Serum TSH concentration may occasionally be increased in euthyroid dogs with non-thyroidal illness.


Thyroid-Stimulating Hormone Stimulation Test



• The most reliable method of confirming the diagnosis of hypothyroidism in dogs is by demonstrating a low resting T4 that fails to increase following TSH administration.

• Test protocol: Collect blood for measurement of serum T4 before and 4 hours after IV administration of 100 μg human recombinant TSH.

• Human recombinant TSH is very expensive, making this test impractical in most cases. Use should be reserved for cases in which the diagnosis cannot be made by measurement of baseline serum hormones.


Thyrotropin-Releasing Hormone Stimulation Test



• TRH administration results in a small and inconsistent increase in serum T4 and free T4 in dogs, making this test inadequate for routine use.


Antithyroglobulin Antibodies



• Autoimmune thyroiditis is associated with serum antibodies directed against thyroglobulin.

• Antithyroglobulin antibodies can be present in euthyroid dogs, and they do not indicate hypothyroidism.

• This assay may be useful to identify dogs affected with autoimmune thyroid disease prior to development of hypothyroidism to help plan breeding, but it is not clear if the antibodies predict hypothyroidism in the future.


Thyroid Hormone Autoantibodies



• Antibodies occasionally form against T3 and T4 that interfere with radioimmunoassay of these hormones.

• These antibodies cause a false increase in T3 or T4 in most assays, with apparent elevation of the hormone into the normal or hyperthyroid range.

• Dogs with thyroid hormone autoantibodies may or may not have signs of hypothyroidism.

• Measurement of free T4 by equilibrium dialysis is not affected by T4 autoantibodies.



Key Point


The most reliable method of confirming a diagnosis of hypothyroidism in a dog with compatible clinical signs is the demonstration of decreased serum total T4 or free T4 by equilibrium dialysis combined with elevated serum endogenous TSH.



Treatment


Treat dogs with hypothyroidism with daily administration of thyroid hormone. Response to treatment is usually noted within 1 to 2 weeks with an increase in activity and improvement in attitude. Weight loss and neurologic abnormalities usually begin to resolve within 1 to 4 weeks of initiating treatment, whereas dermatologic changes may require 4 to 6 weeks to improve and months to completely resolve. Failure to respond within 6 to 8 weeks of initiating treatment should prompt reevaluation of the diagnosis and reasons for possible therapeutic failure.



Synthetic L-Thyroxine


Synthetic L-thyroxine (levothyroxine) is the treatment of choice in all cases of hypothyroidism. Synthetic L-triiodothyronine (L-T3), combinations of synthetic L-T4 and L-T3, and desiccated thyroid gland preparations or extracts are not indicated in the treatment of canine hypothyroidism.


• The initial dosage of L-T4 is 0.022 mg/kg q12h PO. Once-daily treatment at the same dose is usually adequate for resolution of clinical signs and can be used initially or after twice-daily treatment has resulted in a good clinical response.

• Decrease the dosage slightly in dogs over 30 kg.

• Reevaluate after 6 to 8 weeks of treatment by examining for resolution of clinical signs and measuring serum T4.

• A serum T4 concentration collected 4 to 6 hours after pill administration should be near the upper limit or slightly above the reference range; T3 concentration may be low despite normal or high T4.

• If signs of hyperthyroidism occur, such as polyuria, polydipsia, tachycardia, weight loss, diarrhea, or tachycardia, measure serum T4 and T3, stop treatment for 1 to 2 days, and reduce the dosage based on this evaluation.

• Treatment for myxedema stupor and coma consists of IV administration of L-T4 (0.66 mg/kg), passive warming, judicious fluid therapy, glucocorticoid supplementation, and mechanical ventilation if necessary. The prognosis is guarded.


HYPOTHYROIDISM IN CATS




Key Point


Spontaneous hypothyroidism is extremely uncommon in cats.


Most clinical cases of feline hypothyroidism occur as a rare complication of treatment for hyperthyroidism. Non-iatrogenic feline hypothyroidism has been reported primarily in kittens with dwarfism. Cretinism is the most common cause of endocrine congenital dwarfism in cats (growth hormone deficiency has not been reported in cats). Adult onset spontaneous hypothyroidism has been proven in only one cat.



Etiology



• Congenital hypothyroidism is associated with thyroid gland atrophy or defective thyroid hormone biosynthesis. In many kittens, this may go undetected and may result in early death.

• Primary iatrogenic hypothyroidism results from surgical removal of thyroid glands or their destruction by radioactive iodine in the treatment of feline hyperthyroidism.


Clinical Signs



Congenital Hypothyroidism



• Disproportionate dwarfism (stunted growth of long bones, enlarged head).

• Lethargy and mental dullness.

• Hypothermia.

• Bradycardia.

• Bilaterally symmetric alopecia does not occur.


Primary Iatrogenic Hypothyroidism



• History of treatment for hyperthyroidism.

• Lethargy.

• Seborrhea sicca and dry haircoat.

• Obesity is common.

• Bilaterally symmetric alopecia does not occur.


Diagnosis



• Strong index of suspicion based on history and clinical signs.

• Confirmed by finding subnormal resting serum T4 concentration that fails to increase 4 to 6 hours after IV administration of TSH (see “Hypothyroidism in Dogs”).

• Can also be confirmed by finding low serum concentrations of total T4 and free T4 (see “Hypothyroidism in Dogs”).

• Determination of serum TSH concentration is not generally useful in diagnosis of hypothyroidism in cats, inasmuch as most available TSH assays do not measure feline TSH.


Treatment



• Treatment for congenital cretinism is not very rewarding because growth abnormalities and mental deficiencies may not be reversible.

• Treat iatrogenic hypothyroidism with daily T4 supplementation using an initial dosage of T4 of 0.01 to 0.02 mg/kg/day (10-20 μg/kg/day) PO.

• Adjust the dosage based on resolution of clinical signs and on postpill serum T4 concentrations.


HYPERTHYROIDISM IN CATS


Feline hyperthyroidism, a multisystemic metabolic disorder resulting from excessive circulating concentrations of thyroid hormone, is the most common endocrinopathy of middle-aged and older cats. First described in 1979, hyperthyroidism has emerged as the most common endocrine disorder of this species and a disease frequently diagnosed in small animal practice. There is no breed or sex predilection. The clinical signs of the disease are the result of increased basal metabolic rate and the body’s inability to meet excessive metabolic demands.



Etiology



Adenomatous Hyperplasia


Functional adenomatous hyperplasia of one or both lobes of the thyroid gland, causing high circulating concentrations of T4 and T3, is the most common cause. Both lobes are enlarged in approximately 70% of cases. The pathogenesis of this adenomatous hyperplasia is unknown.


• In cats, the disease most closely resembles toxic nodular goiter in human patients, which is caused by hyperfunctioning adenomatous thyroid nodules.

• Hyperthyroidism in cats is not analogous to the autoimmune disorder Graves disease, the most common form of hyperthyroidism in human patients.


Thyroid Carcinoma


Thyroid carcinoma occurs in only 1% to 2% of cats with hyperthyroidism.



Clinical Signs


All of the clinical manifestations of hyperthyroidism are due to the effects of excessive thyroid hormone. These effects are generally stimulatory. They cause increased heat production and heightened protein, carbohydrate, and lipid metabolism in virtually all body systems and tissues. Clinical signs can range from mild to severe (Table 31-2).


Table 31-2 FREQUENCY OF HISTORICAL AND CLINICAL SIGNS IN CATS WITH HYPERTHYROIDISM






















































Clinical Finding Percentage of Cats
Weight loss 95–98
Hyperactivity/difficult to examine 70–80
Polyphagia 65–75
Tachycardia 55–65
Polyuria/polydipsia 45–55
Cardiac murmur 20–55
Vomiting 33–50
Diarrhea 30–45
Increased fecal volume 10–30
Decreased appetite 20–30
Lethargy 15–25
Polypnea (panting) 15–30
Muscle weakness 15–20
Muscle tremor 15–30
Congestive heart failure 10–15
Dyspnea 10–15



Key Point


The classic clinical signs of feline hyperthyroidism include weight loss despite an increase in appetite.



General Appearance and Behavior



• Weight loss.

• Restlessness, hyperexcitability, and difficulty in examining.

• Impaired stress tolerance. The hyperthyroid cat is prone to respiratory distress and weakness when stressed. Cardiac arrhythmias or arrest can occur in extreme cases.

• Unkempt haircoat, excessive shedding, and matting of hair, especially in long-haired cats.


Thyroid Gland



• Enlargement of one or both lobes of the thyroid gland is palpable in >90% of cats with hyperthyroidism. To palpate the thyroid gland, extend the cat’s neck and tilt the head back slightly. Using the thumb and forefinger, gently palpate the tissues on either side of the trachea, starting at the larynx and moving caudally to the thoracic inlet (see Fig. 1-3 in Chapter 1).

• A small percentage of cats have intrathoracic thyroid nodules that evade palpation.


Nervous System and Muscle



• Hyperactivity

• Weakness and increased fatigability


Gastrointestinal System



• Increased appetite is due to increased energy utilization and high metabolic demands. The increased caloric intake observed in most cats is, however, inadequate to compensate for increased demand.

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  4. Otitis Media and Otitis Interna

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Aug 27, 2016 | Posted by in SMALL ANIMAL | Comments Off on Diseases of the Thyroid Gland

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