Doc, why is my" ferret going bald?" This is easily the most often asked question in ferret medicine, and a question that most ferret practioners hear on a daily basis.

Alopecia, or hair loss, is the most common sign of a very prevalent syndrome in American ferrets known as adrenal-associated endocrinopathy, or AAE. (The disease may also be referred to as hyperadrenocorticism in the ferret, but as discussed below, NOT Cushing's disease.)

AAE is caused by the presence of a proliferative lesion within the adrenal cortex, the region which is responsible for secreting a number of important hormones. The adrenal cortex secretes steroids that regulate mineral balances in the body, steroids that moderate the "fight or flight" syndrome and our responses to stress, and also secretes small amounts of sex steroids, such as estrogen. It is this last hormone, estrogen, which results in all of the signs of AAE in the ferret.

Estrogen is a hormone which is normally produced in the ovary of females, the testis of males (in small amounts) and the adrenal glands of both sexes (also in small amounts). At normal levels, estrogen regulates many parts of the reproductive cycle in both males and females ferret; however, in excessive amounts, estrogen can cause serious, even life-threatening health problems in ferrets.

The source of the hyperestrogenism in affected animals is a proliferative lesion in one (or in approximately 15% of cases, both) adrenals. (Please note: The term "proliferative lesion" is preferable to adrenal "cancer" or even the less objectionable term adrenal "tumor", as only about half of these lesions are true neoplasms, the rest being nodules of adrenocortical hyperplasia.)

Clinical signs exhibited by ferrets with AAE include a spectrum of cutaneous, reproductive, or behavioral symptoms, all related to high serum levels of estrogen and/or its precursors. Cutaneous signs are most commonly observed by owners and are characterized by bilaterally symmetric alopecia beginning over the tailhead and progressing forward along the body, generally sparing the head, neck, and distal extremities (see picture). Reproductive abnormalities include swelling of the vulva, vaginal discharge, and stump pyometra in spayed females, and dysuria in males as a result of cystic prostatic disease, secondary to hyperestrogenism and squamous metaplasia of glandular epithelium. Behavioral abnormalities include increased mounting behavior or aggression in both males and females, and marking behavior in males. Longstanding cases may show mild anemia and petechiation (small hemorrhages) as a result of estrogen's suppressive effect on the bone marrow, muscle wasting, and other non-specific signs such as lethargy and posterior paresis.

In most cases, diagnosis is based on clinical signs. Complete blood counts and chemistry panels will be within normal limits in the vast majority of animals, except in longstanding cases in which anemia or decreased platelet numbers may be seen. As the elevated hormone in AAE is estrogen, not cortisol, practitioners should be aware that serum cortisol is rarely if ever elevated, and diagnostic testing for Cushing's disease will be of little or no diagnostic value. While serum levels of estradiol may be measured at commercial labs, elevation of estradiol precursors or intermediates are responsible for clinical signs in many cases, and estradiol measurements may be within normal ranges. A new blood panel is available at the Department of Endocrinology at the University of Tennessee College of Veterinary Medicine which measures not only levels of serum estradiol but six other intermediates. Although the test is extremely sensitive (resulting in positive diagnosis in over 90% of cases) it is expensive and takes several weeks to complete, and should be reserved for cases in which clinical signs are marginal.

The most effective treatment of AAE is surgical removal of the affected adrenal gland. Exploratory laparotomy often reveals unilateral enlargement of one or both adrenal glands beyond the normal 3-5 mm. For unknown reasons, over 80% of proliferative adrenal lesions are located in the left adrenal gland. In approximately 15% of cases, lesions are bilateral. Unilateral adrenalectomy results in a cessation of clinical signs and hair regrowth in the majority of cases. Hair regrowth should begin within 2-6 weeks, or may be delayed until the next shedding cycle. However, in animals in with bilateral disease, hair regrowth may be shortlived, or not seen at all. In these cases, hemiadrenalectomy of the remaining adrenal gland should be strongly considered. Recently, a protocol was published in Modern Ferret for corticosteroid replacement in animals having undergone bilateral adrenalectomy by Dr. Joseph Bock. Bilateral adrenalectomy may be required in cases in which bilateral adrenocortical carcinomas develop. While much more research is required in this area, the possibility of exogenous maintenance of adrenalectomized ferrets now gives added hope in the treatment of adrenal neoplasia in ferrets.

Medical treatment of hyperadrenocorticism is reserved only for those animals who present a poor surgical risk, as it is generally symptomatic. while it may promote hair regrowth and lessen lethargy in affected animals, it generally does little to stop the growth of potentially malignant neoplasms in affected animals. Recently, there has been some success with Lupron . However, it is very expensive, and that is always a consideration.

Adrenal-associated endocrinopathy is a very common, and very treatable disease in the ferret. The diagnosis and treatment of this condition is something with which every ferret practitioner must be familiar. Every bald ferret is a ferret that can be helped