Nonfunctional tumors of the pituitary gland can lead to panhypopituitarism, as the growth of a neoplastic but nonsecretory cell type displaces other pituitary cells. Clinical signs related to the loss of gonadal, thyroid, and adrenocortical hormones result, along with neurological signs related to local compression of brain structures. Hormone assays and MRI can be useful for diagnosis. Signs related to endocrine deficiencies can be treated by supplementation with missing hormones.
"Panhypopituitarism" refers to decreased secretion of all pituitary hormones.
The most common cause of adult-onset panhypopituitarism 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 resulting from invasion by tumor cells, parasitic or septic emboli, diffuse necrosis associated with toxemia, invasion by neoplasms arising in adjacent structures (eg, meninges, sphenoid bone, nasal cavity), and widespread hemorrhage and subsequent scarring after traumatic injury.
Dogs and cats with nonfunctional adenomas develop clinical disturbances related to lack of secretion of pituitary tropic hormones and diminished target organ function, or to dysfunction of the CNS.
Epidemiology of Adult-Onset Panhypopituitarism in Animals
Endocrinologically inactive, nonfunctional pituitary tumors develop most commonly in adult to aged animals. There is no apparent breed predisposition.
Clinical Findings of Adult-Onset Panhypopituitarism in Animals
Animals with panhypopituitarism often are lethargic and uncoordinated, and they collapse with exercise. Occasionally, they exhibit a change in attitude, become unresponsive to people, and tend to hide at the slightest provocation. In chronic cases, they become blind and have dilated and fixed pupils due to compression and disruption of optic nerves by dorsal extension of the pituitary tumor.
Dogs with panhypopituitarism often show 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 can break housetraining. Clinical signs are not highly specific and can be confused with those of other CNS disorders (eg, brain tumors or encephalitis) or of chronic renal disease.
Hypopituitarism due to a pituitary tumor should be included in the differential diagnosis of diseases characterized by incoordination, lethargy, polyuria, blindness, and sudden behavioral changes in adult or aged animals. Because the blindness is central in origin, ophthalmoscopic examination usually reveals no lesions of consequence.
Compression of the pars distalis and probable interference of growth hormone secretion have no effect on body stature, because these tumors usually arise in dogs that have already completed their growth.
Parakeets and cockatiels with chromophobe adenomas often develop exophthalmos and blindness because of the extension of neoplastic cells along the optic nerve.
Lesions
Endocrinologically inactive pituitary adenomas usually reach considerable size before producing obvious clinical signs or death. The proliferating tumor cells incorporate the remaining structures of the adenohypophysis and infundibular stalk. The entire hypothalamus can be compressed and replaced by tumor.
In dogs and cats with large pituitary adenomas, the thyroid gland is often smaller than normal; however, the decrease in size is less than that of 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 can be related to a lack of protein anabolic effects of growth hormone in an adult dog or cat. Interference with the secretion of pituitary tropic hormones often results in gonadal atrophy, manifested either as decreased libido or as anestrus.
Diagnosis of Adult-Onset Panhypopituitarism in Animals
Hormonal testing can confirm hormone deficiencies associated with panhypopituitarism that include ADH, TSH, and ACTH deficiencies. CT or MRI can show a pituitary mass or, in some cases, a hemorrhage or scar tissue caused by sudden head trauma (eg, from being hit by a car).
Treatment of Adult-Onset Panhypopituitarism in Animals
Clinical signs of panhypopituitarism that are related to endocrine deficiencies (eg, secondary hypoadrenocorticism or hypothyroidism) can be treated by supplementation with glucocorticoids at a physiological dose (0.1–0.3 mg/kg, PO, every 24 hours) andlevothyroxine (22 mcg/kg, PO, every 12 hours, or 44 mcg/kg, PO, every 24 hours), depending on clinical response.
External beam radiotherapy can decrease pituitary tumor size and decrease clinical signs in some cats; however, experience with this kind of treatment is limited for cats with large pituitary tumors. Overall, the outlook is poor.
The prognosis for adult-onset panhypopituitarism in animals depends on the cause either of the pituitary mass or of the shrinking of pituitary tissue (eg, "empty sella syndrome," in which the pituitary shrinks and the bony sella turcica surrounding the pituitary fills with CSF). Neoplastic lesions carry a poor prognosis; however, other lesions, such as those caused by head trauma leading to a loss of pituitary hormone secretion, can be associated with a good prognosis with hormone replacement.
Key Points
Endocrinologically inactive pituitary adenomas and adult-onset panhypopituitarism are rare in dogs and cats.
Clinical signs are usually associated with local tissue compression or edema accompanying large tumors that act as space-occupying lesions.
Signs of secondary endocrine deficiency, such as secondary hypoadrenocorticism or hypothyroidism, can be treated with supplementation with missing hormones.
For More Information
Melmed S, Auchus RJ, Goldfine AB, Kopp PA, Rosen CJ. Principles of endocrinology. In: Melmed S, Auchus RJ, Goldfine AB, Rosen CJ, Kopp PA, eds. Williams Textbook of Endocrinology. 15th ed. Elsevier; 2025:1-11.
Maxie MG, Palmer NC, Maxie GM (ed.), Jubb KVF. Endocrine glands. In: Maxie MG, Palmer NC, Maxie GM (ed.), Jubb KVF, Jubb, Kennedy & Palmer's Pathology of Domestic Animals. 5th ed. Vol. 3. W. B. Saunders; 2007:325-428.
Also see pet owner content regarding adult-onset panhypopituitarism in dogs and cats.
