Adult-onset Panhypopituitarism in Animals
Endocrinologically inactive, nonfunctional pituitary tumors develop most commonly in adult to aged animals; there is no apparent breed predisposition. The most common cause is a chromophobe adenoma arising in the pars distalis. Other infrequent causes include extensive inflammatory destruction of pituitary tissue, ischemic necrosis of the pituitary due to infarction from invasion of tumor cells, parasitic or septic emboli, diffuse necrosis associated with toxemia, invasion by neoplasms arising in adjacent structures (eg, meninges, sphenoid bone, nasal cavity, etc), and widespread hemorrhage and subsequent scarring after traumatic injury. Dogs and cats with nonfunctional adenomas develop clinical disturbances related to a lack of secretion of pituitary trophic hormones and diminished target organ function or to dysfunction of the CNS.
Affected animals often are depressed and uncoordinated and collapse with exercise. Occasionally, they exhibit a change in attitude, become unresponsive to people, and develop a tendency to hide at the slightest provocation. In chronic cases, there may be evidence of blindness, with dilated and fixed pupils due to compression and disruption of optic nerves by dorsal extension of the pituitary tumor. Affected dogs often show a progressive weight loss with muscle atrophy due to loss of the protein anabolic effect of growth hormone. Compression of the cells that secrete gonadotropic hormones or the corresponding releasing hormone from the hypothalamus results in atrophy of the gonads. Disturbances of water balance result from interference with the synthesis of antidiuretic hormone (ADH) or its release into capillaries of the pars nervosa. The posterior lobe, infundibular stalk, and hypothalamus are compressed or disrupted by neoplastic cells.
Animals with panhypopituitarism appear dehydrated despite increased water consumption. Dogs and cats with large nonfunctional pituitary tumors usually excrete large volumes of dilute urine with a low specific gravity (≤1.007) and may break housetraining. Clinical signs are not highly specific and can be confused with those of other CNS disorders (eg, brain tumors or encephalitis) or chronic renal disease.
Hypopituitarism caused by pituitary tumors should be included in the differential diagnosis of diseases characterized by incoordination, depression, polyuria, blindness, and sudden behavioral changes in adult or aged animals. Because the blindness is central in origin, ophthalmoscopic examination usually does not reveal significant lesions. There is no effect on body stature associated with compression of the pars distalis and probable interference of growth hormone secretion, because these tumors usually arise in dogs that have already completed their growth. Parakeets with chromophobe adenomas often develop exophthalmos due to extension of neoplastic cells along the optic nerve.
Endocrinologically inactive pituitary adenomas usually reach considerable size before they cause obvious signs or death. The proliferating tumor cells incorporate the remaining structures of the adenohypophysis and infundibular stalk. The entire hypothalamus may be compressed and replaced by tumor.
Thyroid glands in dogs and cats with large pituitary adenomas often are smaller than normal, although to a much lesser degree than the adrenal cortex. The adrenal glands are small and consist primarily of medullary tissue surrounded by a narrow zone of cortex. Seminiferous tubules are small and show little evidence of active spermatogenesis.
Skin atrophy and loss of muscle mass may be related to a lack of protein anabolic effects of growth hormone in an adult dog or cat. Interference with the secretion of pituitary trophic hormones often results in gonadal atrophy, resulting in either decreased libido or anestrus.
Endocrinologically inactive pituitary adenomas and adult-onset panhypopituitarism are rare disorders in dogs and cats.
Clinical signs are usually associated with local tissue compression or edema associated with large tumors that act as space-occupying lesions.
Signs of secondary endocrine deficiency, such as secondary hypoadrenocorticism or hypothyroidism, can be treated with supplementation of the affected hormone.