Thyroid Disease in the Dog—A Review: Part II

Bush, B. M.

doi:10.1111/j.1748-5827.1969.tb04036.x

Cited by 5 publications

(2 citation statements)

References 32 publications

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“…The category associated with goitre includes various forms of thyroid dyshormonogenesis such as iodide organification defects, defects in iodine transport, lack of iodotyrosinase activity and disorders of thyroglobulin and iodothyronine synthesis (Stanbury 1974;Fisher 1978;Fisher and Klein 1981;Chastain and Ganjam 1986). Goitrous hypothyroidism may also be caused by defective TSH metabolism (Fisher 1978;Fisher and Klein 1981) or a deficiency of dietary iodine (Bush 1969). With the exception of defective TSH metabolism, the enlargement of both thyroid glands in all these disorders follows a diminution of feedback inhibition by T, and T, on the hypothalamus and adenohypophysis leading to increased serum TSH levels.…”

Section: Discussionmentioning

confidence: 99%

“…Congenital hypothyroidism in dogs is rare (Belshaw 1983;Chastain and Ganjam 1986). Apart from those due to a deficiency of dietary iodine (Bush 1969), there appears to be only one documented case of hypothyroidism resulting from an inborn error of metabolism (Chastain et af 1983). In that particular case, the hypothyroidism was due to the failure to form organic iodine and the diagnosis was based on low serum thyroxine (T, and triiodothyronine (TJ, radiography and an abnormal perchlorate discharge test.…”

Section: Introductionmentioning

confidence: 99%

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Congenital hypothyroidism in Scottish Deerhound puppies

et al. 1988

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Two Scottish Deerhound puppies had clinical and pathological features consistent with the diagnosis of congenital non-goitrous hypothyroidism. They were from separate litters, but were the progeny of the same sire and dam. The puppies were smaller, had shorter limbs and shorter, broader heads than their littermates. They also had histories of weakness, difficulty in walking and somnolence. A characteristic radiographic feature was the absence of epiphyseal growth centres. Both had depressed serum thyroxine (T4) levels and one did not respond to exogenous thyroid stimulating hormone. On necropsy, the thyroid glands were small, the follicles varied in size and contained little or no colloid. The adenohypophysis contained many cells with markedly vacuolated cytoplasm. It is suggested that the clinicopathological pattern is the result of a primary thyroid abnormality. Possible mechanisms include either primary thyroid hypoplasia or an unresponsiveness to thyroid stimulating hormone.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%