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PubMed2003

Endocrine diseases in dogs and cats: similarities and differences with endocrine diseases in humans.

Over several millennia, humans have created hundreds of dog and cat breeds by selective breeding, including fixation of mutant genes. The domestic dog is unique in the extent of its variation in height, weight and shape as well as its behavior. It is primarily the relatively long persistence of high levels of growth hormone (GH) release at a young age that accounts for the large body size in giant breeds of dogs. Several of the endocrine diseases of humans are also known to occur as similar entities in dogs and cats. With some variations, this is true for conditions such as diabetes mellitus and the hypofunction syndromes of the thyroid and adrenal cortex. Also, the hyperfunction syndromes of hypercortisolism and hyperparathyroidism in dogs and cats have many similarities with their human counterparts. The exception seems to be Graves' disease. This condition, which is due to production of thyroid-stimulating hormone (TSH)-receptor antibodies, has not been observed in dogs and cats. The very common form of hyperthyroidism in cats is due to toxic adenomas. In the 1980s it was discovered that in dogs exogenous progestins and endogenous progesterone can induce GH excess. This GH excess originates form the mammary gland and may give rise to acromegaly and insulin resistance. GH production by the mammary gland is not unique to the dog. It has become clear that cats and humans also express the GH gene in the mammary gland. There is increasing evidence that this locally produced GH not only plays a role in the morphologic changes of the mammary gland associated with the ovarian cycle and gestation, but that it is also involved in the development of breast cancer. In dogs, induction of mammary GH production by progestin administration allows for treatment of GH deficiency.

Animals↗
PubMed1976

Sheehan's syndrome of hypothalamic origin in a woman with juvenile diabetes mellitus.

A 25-year-old woman with severe diabetes mellitus since the age of 7 developed anterior pituitary insufficiency after pregnancy toxaemia with hypofunction of the thyroid, ovaries and adrenal cortex. Following the development of Sheehan's syndrome, her insulin requirment decreased dramatically. I.v. administration of TRH, LRH and vasopressin induced nearly normal pituitary response levels of TSH, LH and plasma cortisol, indicating a hypothalamic damage as the primary aetiological factor.

Adult↗