Canine Hypothyroidism

J. Catharine R. Scott-Moncrieff, West Lafayette, Indiana

Clinical signs of hypothyroidism result from decreased production of thyroxine (T₄) and triiodothyronine (T₃) by the thyroid gland. Acquired primary hypothyroidism is most common in dogs and usually is caused by either lymphocytic thyroiditis or idiopathic thyroid atrophy. Secondary hypothyroidism (deficiency of thyroid-stimulating hormone [TSH]) is less commonly recognized in dogs.

Cause

Approximately 50% of cases of primary hypothyroidism are caused by lymphocytic thyroiditis. Grossly, the thyroid gland may be normal or atrophic, whereas histologically there is multifocal or diffuse infiltration of the thyroid gland by lymphocytes, plasma cells, and macrophages. As thyroiditis progresses, the parenchyma is destroyed and replaced by fibrous connective tissue. Initially, thyroiditis may be subclinical, but progression to overt hypothyroidism can occur. Idiopathic thyroid atrophy, in which there is loss of thyroid parenchyma and replacement by adipose and connective tissue, may represent end-stage thyroiditis rather than a separate disease process. Canine thyroiditis is believed to be immune mediated, and antithyroglobulin antibodies (ATAs) are a sensitive marker of thyroid inflammation. Approximately 50% of hypothyroid dogs have ATAs; however, the prevalence varies widely among breeds, which reflects a familial tendency for thyroiditis and resultant hypothyroidism.

Signalment

Any breed can develop hypothyroidism; however, some breeds, such as the golden retriever and the Doberman pinscher, have been reported to be at higher risk. Thyroiditis is clearly heritable in the beagle and the borzoi, and many other common breeds, such as the golden retriever, Great Dane, Irish setter, Doberman pinscher, and Old English sheepdog, have a high prevalence of ATAs. The rate of clinical progression of thyroiditis also varies among breeds. In beagles, the prevalence of thyroiditis can reach 40%, but if thyroiditis progresses to hypothyroidism, it occurs in middle age or later (Scott-Moncrieff et al, 2006). In other breeds, such as golden retrievers, thyroiditis appears to progress more rapidly, with some dogs diagnosed at 2 years of age. Middle-aged dogs generally are at increased risk of hypothyroidism. In one study, mean age at diagnosis was 7 years (range, 0.5 to 15 years).

Clinical Signs

Clinical features of hypothyroidism are insidious in onset, and hypothyroidism is commonly misdiagnosed because of nonspecific clinical signs affecting multiple body systems. Clinical signs attributable to decreased metabolic rate include lethargy, mental dullness, weight gain, unwillingness to exercise, and cold intolerance.

Dermatologic findings include dry scaly skin, changes in hair coat quality or color, symmetrical alopecia, seborrhea, and superficial pyoderma. Hyperkeratosis, hyperpigmentation, comedo formation, hypertrichosis, ceruminous otitis, poor wound healing, increased bruising, and myxedema also may occur. Alopecia is usually bilaterally symmetrical (see Chapter 39) and is first evident in areas of wear, whereas the head and extremities tend to be spared. The hair may be brittle and easily epilated, and loss of undercoat or primary guard hairs may result in a coarse appearance or a puppy-like hair coat. Fading of coat color may occur, and failure of hair regrowth after clipping is common. Hypothyroid dogs are also predisposed to recurrent bacterial infections of the skin.

Reproductive dysfunction has been attributed to hypothyroidism. There is little evidence for male reproductive dysfunction associated with hypothyroidism; however, bitches with radioactive iodine (¹³¹I)–induced hypothyroidism have reduced fertility, prolongation of parturition, and higher periparturient mortality compared with euthyroid bitches (Panciera et al, 2007).

Both the peripheral nervous system and the central nervous system may be affected by hypothyroidism. Subclinical myopathy is well documented in hypothyroid dogs (Rossmeisl, 2010). Peripheral nerve dysfunction also has been described in association with hypothyroidism. Affected dogs have exercise intolerance, generalized weakness, ataxia, tetraparesis or paralysis, deficits of conscious proprioception, and decreased spinal reflexes. Some affected dogs have multifocal dysfunction of cranial nerves (facial, trigeminal, vestibulocochlear). Clinical signs resolve with levothyroxine sodium (l-thyroxine) supplementation. Rarely, central neurologic dysfunction (seizures, central vestibular dysfunction, disorientation, and mentation changes) is observed as a result of cerebral or cerebellar infarction, atherosclerosis, myxedema, coma, and blood viscosity changes secondary to hyperlipidemia. Overall, hypothyroidism is a rare cause of seizure disorders in dogs (Higgins et al, 2006). Although laryngeal paralysis and megaesophagus have been reported in association with hypothyroidism, treatment of hypothyroidism does not consistently result in resolution of clinical signs, and a causal relationship has not been established. Behavioral abnormalities that have been attributed to canine hypothyroidism include aggression and cognitive dysfunction; however, evidence for a causal association between behavioral problems and hypothyroidism is lacking.

Hypothyroidism can cause cardiovascular changes, such as sinus bradycardia, weak apex beat, low QRS voltage, and inverted T waves. Reduced left ventricular pump function has been documented in hypothyroidism and may exacerbate clinical signs in dogs with underlying cardiac disease. Although hypothyroidism is rarely the primary cause of myocardial failure in dogs, dilated cardiomyopathy and hypothyroidism may occur concurrently.

Congenital hypothyroidism results in mental retardation and stunted, disproportionate growth caused by epiphyseal dysgenesis and delayed skeletal maturation. Affected dogs are mentally dull and have large broad heads, short thick necks, short limbs, macroglossia, hypothermia, delayed dental eruption, ataxia, and abdominal distention. A palpable goiter may be present, depending on the cause of the congenital defect. Other clinical signs include gait abnormalities, stenotic ear canals, sealed eyelids, and constipation. Congenital hypothyroidism with goiter (CHG) caused by a nonsense mutation in the thyroid peroxidase gene has been recognized in toy fox terriers and rat terriers (Fyfe et al, 2003; Dodgson et al, 2012). A different missense mutation of the thyroid peroxidase gene causes CHG in Tenterfield terriers. Both defects are autosomal-recessive traits, and a deoxyribonucleic acid test that detects carriers of the defects is available through the laboratory of comparative medical genetics at Michigan State University.