ABSTRACT
More than 95% of canine cases are classified as acquired primary hypothyroidism, which results in compensatory increases in both TRH and TSH because the typical negative feedback of thyroid hormones on the hypothalamus and pituitary is lacking (Part A). Antibodies against the TSH receptor have been found in human patients, and lead to thyroid gland atrophy. As TRH is a stimulator of prolactin release from the anterior pituitary, primary hypothyroidism may lead to galactorrhea (i.e., excessive or spontaneous flow of milk irrespective of nursing) in sexually intact bitches. Destruction of the thyroid in animals has been reported to result from lymphocytic thyroiditis, idiopathic thyroid atrophy, or (rarely) neoplastic invasion. Lymphocytic thyroiditis may also be associated with the formation of antibodies to thyroglobulin, T4 and T3. Secondary hypothyroidism (decreased TSH) is seen in humans, but is uncommonly recognized in dogs (probably due to inadequate assay for TSH) (see Part A). Causes of acquired secondary hypothyroidism in dogs include pituitary neoplasia and pituitary malformations such as cystic Rathke’s pouch, and hyperadrenocorticism. High levels of circulating glucocorticoids suppress the pituitary response to TRH (Ch. 36). Tertiary hypothyroidism (decreased TRH) has not been documented in dogs (see Part A).
