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Hypothyroidism in dogs (Proceedings)

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Nov 01, 2010

Background

Thyroid hormones influence many body systems. Thyroid hormones are involved in the development of the nervous and musculoskeletal systems. Thyroid hormones are also important to normal cardiorespiratory function, other hormones and enzyme systems, and red cell synthesis to name a few. The hypothalamus secretes thyrotropin-releasing hormone in response to nervous stimuli. The TRH then stimulates the pituitary gland to secrete thyrotropin-secreting hormone (TSH).1 The follicular cells of the thyroid gland then release thyroid hormone in response to TSH. Thyroxine (T4) and tri-iodothyronine (T3) provide negative feedback primarily at the level of the pituitary. Thyroxine is the primary iodothyronine, or thyroid hormone, released from the thyroid gland.2 Tri-iodothyronine is also released in a much smaller quantity. Thyroid hormones consist of both free and bound fractions. Ninety-nine percent are bound to albumin, prealbumin and thyroid hormone-binding globulin and act as a storage reservoir. It is the free fraction of T4 that can enter cells where it is converted to the biologically active portion, T3 as well as rT3.

Signalment

There are certain breeds that have an increased incidence of hypothyroidism including the golden retriever and Doberman pinscher. Other breeds have a similar incidence as mixed breed dogs. There are also breeds with a higher incidence of autoantibodies to thyroglobulin and thyroid hormones including pointers, English Setter, Old English Sheepdog, Skye Terrier, boxers, giant schnauzers and maltese amongst others.

Etiology

Hypothyroidism is classified as primary (problem in thyroid gland) or secondary (problem in pituitary). Primary hypothyroidism is most commonly due to lymphocytic thyroiditis or idiopathic atrophy with rare cases of neoplasia (mixed tumor, medullary thyroid carcinoma).

Lymphocytic thyroiditis is defined by infiltration of lymphocytes, plasma cells and macrophages throughout the thyroid gland that results in progressive destruction and fibrosis. Clinical signs don't usually appear until over 75% of the gland is destroyed. Antibodies to thyroglobulin and thyroid hormones may be seen prior to clinical signs and at diagnosis. Lymphocytic thyroiditis has occasionally occurred with other autoimmune disorders as part of a polyglandular syndrome.

Idiopathic fibrosis is characterized by replacement of thyroid parenchyma with fat. There are no autoantibodies present and on histopath no inflammatory cells. Idiopathic fibrosis may result from degeneration of thyroid follicles or the progression of LP thyroiditis.This is usually a diagnosis of exclusion so in a dog with primary hypothyroidism that fails to produce autoantibodies, idiopathic atrophy is presumed. Histopathology would be required to differentiate idiopathic atrophy from lymphocytic thyroiditis.

Rarely, neoplasia (discussed above), surgery (bilateral thyroidectomy), dietary iodine deficiency/excess, and hormone dysgenesis can cause primary hypothyroidism.

Secondary hypothyroidism indicates a problem with the pituitary thyrotrophs. The most common cause is suppression of TSH production from the thyrotrophs by exogenous or endogenous glucocorticoids (HAC, illness). Pituitary malformations/cysts and neoplasia can sometimes cause secondary hypothyroidism. Malformation and neoplasia often involve other hormones (CRH, GH, FSH, LH) so other symptoms may be present. Secondary hypothyroidism may also occur with pituitary irradiation and has been reported following hypophysectomy for pituitary-dependent hyperadrenocorticism.

Congenital hypothyroidism is rare but can occur as a result of iodine deficiency (primary), defects in organification of iodine (primary), thyroid dysgenesis (primary), TSH deficiency (secondary) and pituitary dwarfism (secondary).

Goiter refers to an enlarged thyroid gland and is rare in dogs. It can occur with organification defects (primary), thyroid peroxidase defects (primary) and trimethoprim-sulfa administration (primary).