Adrenal disease of ferrets

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The adrenal disease of ferrets (adrenocortical disease, ACD) is a castrated ferrets frequently occurring disease caused by an overproduction of sex hormones by the adrenal cortex caused. Removal of the sex glands in the castration (ovarian and testicular) a homo tional feedback mechanism is overridden, so the pituitary intensified luteinizing hormone (LH) release. Since the adrenal cortex of ferrets, unlike most other mammals, contains LH receptors , it stimulates the production of sex hormones. The condition is also known as adrenal-associated endocrinopathy .


Ferret with adrenal disease and severe hair loss

Castrated ferrets of both sexes that are kept as pets develop adrenal gland disease. Middle-aged to older animals are mainly affected by the disease. The animals usually reach sexual maturity in the first spring after birth at an age of approx. 4½ to 6 months. If the females are not mated during the oestrus , they often develop a permanent oestrus that lasts for several months and can lead to health problems, particularly estrogen-induced anemia . Male ferrets develop an intense musky odor at sexual maturity and display sexually motivated, aggressive behavior. For these reasons, most ferrets that are kept as pets and are not intended to be used for breeding are neutered.

By removing the sex glands (testes or ovaries), there is no negative feedback in the pituitary gland of the sex hormones synthesized by these organs, which is why it releases more luteinizing (LH) and follicle-stimulating hormone (FSH). Unlike most mammals, the adrenal cortex in ferrets has receptors for LH, which are stimulated by the high LH levels in the blood of castrated animals and lead to the production of the sex hormones estradiol , 17-hydroxyprogesterone and androstenedione in the adrenal cortex. The increased blood levels of these hormones cause adrenal disease, which manifests itself through symptoms such as bilateral symmetrical hair loss, itching, muscle wasting , weakness in the hind quarters, sexually motivated behavior and aggression. In females there is often a swelling of the vulva, secretion of vaginal secretions and sexual attractiveness for males. In male animals, prostate cysts, prostatitis and obstruction of the urethra occur. In rare cases, fatal estrogen-induced bone marrow depression develops .

In sick animals there is also an enlargement of the adrenal gland, which is limited to one side in 85% of the animals. While it is initially nodular hyperplasia in response to the permanent hormonal stimulation, tumors often develop over time, which are benign adenomas . Malignant adenocarcinomas also occur in around 10% of cases . The latter have a strong tendency to metastasize , which ultimately leads to the death of the affected animals.

Under natural conditions, ferrets are seasonally polyestrial between March and August, which means that the females go through a regular sexual cycle during this time. The duration of the propagation time is controlled by the intensity and duration of daylight. The secretion of LH from the pituitary gland is promoted by light, which is why the symptoms of adrenal disease are often more pronounced during periods of prolonged daylight than in seasons with short days.

There is a close correlation between the age at which animals are castrated and the frequency with which adrenal disease occurs. In countries such as the USA or Japan, where it is common to castrate ferrets as early as 4 to 6 weeks of age, the incidence of the disease is 15% to 22%. In countries where ferrets are typically not neutered until they are 6 to 12 months old, e.g. B. in the Netherlands or England, the incidence of the disease is significantly lower. The average age of the animals diagnosed with the disease is also higher.

A high inbreeding factor in commercial ferret breeding and diet are discussed as further predisposing factors . The unnatural lighting conditions when keeping ferrets in apartments is also assigned a predisposing role in the development of the disease. The artificial light simulates a permanent long-day season in animals kept in the apartment, so that there is a permanently increased LH secretion and the entry of female animals into the anestrus is delayed.


Diagnosis is made by examining blood levels of the hormones estradiol, 17-hydroxyprogesterone, and androstenedione. The increase in just one of these three parameters in conjunction with the clinical symptoms suggests the diagnosis of adrenal disease in a castrated animal. Adrenal gland disease can only be ruled out if all three parameters are within the normal range. Other clinico-chemical parameters and the blood count are mostly unchanged, but in the presence of estrogen-induced anemia the parameters of the red blood count are changed.

If one or both adrenal glands are enlarged as a result of the disease, experienced examiners can often feel them through the abdominal wall. The changed adrenal glands can be visualized with the help of an ultrasound examination ; The right adrenal gland is affected, it can also be investigated whether there is already a slump in the nearby posterior vena cava ( inferior vena cava has come), which is associated with a poor prognosis. In about 50% of the cases, the diagnosis is made by ultrasound.

After surgical removal of one or both of the altered adrenal glands, a patho-histological examination of the removed organs can be used to diagnose whether it was hyperplasia, a benign or malignant tumor. The differentiation between benign and malignant tumors is sometimes not possible with certainty, since the histological appearance of the two forms can be very similar. If both adrenal glands are changed, both organs should be examined histopathologically, as they can develop different tumors independently of one another.


Therapy consists of surgical removal of the affected adrenal glands. While the left adrenal gland is relatively easy to remove surgically, the right adrenal gland is located near the posterior vena cava , which is why its surgical removal is associated with an increased surgical risk. If both adrenal glands are affected, at least one adrenal gland should only be partially removed in order to avoid the development of hypoadrenocorticism . Only a small proportion of the animals require medical substitution with gluco- and / or mineralocorticoids after unilateral or incomplete bilateral removal of the adrenal glands .

To treat adrenal disease, GnRH analogues can also be used, which have a higher binding to the GnRH receptors than the body's own GnRH, which leads to a decrease in LH and FSH production in the pituitary gland. A hormone chip approved for the "homonal castration" of male ferrets, which continuously releases small amounts of the active ingredient Deslorelin , can be used. This procedure is a therapeutic option, especially for animals that cannot or should not be operated on. However, this is an off-label use .

Newer approaches to treatment include immunization against GnRH . The antibodies thus formed bind to the GnRH, which can then no longer stimulate the release of LH from the pituitary gland.

Individual evidence

  1. a b c Lowell A. Miller, Kathleen A. Fagerstonea, Robert A. Wagner, Mark Finkler: Use of a GnRH vaccine, GonaConTM, for prevention and treatment of adrenocortical disease (ACD) in domestic ferrets. In: Vaccine (31), 2013, pp. 4619-4623
  2. a b c d Colette L. Wheler, Carole L. Kamieniecki: Ferret adrenal-associated endocrinopathy. In: Canadian Veterinary Journal Volume 39, March 1998, pp. 175-176
  3. ^ A b c d e Felix Beuschlein, Sara Galac, David B. Wilson: Animal models of adrenocortical tumorigenesis . In: Molecular and Cellular Endocrinology, Volume 35 (1), March 31, 2012, pp. 78-86
  4. ^ Karen L. Rosenthal, Mark E. Peterson, KE Quesenberry, EV Hillyer, NL Beeber, SD Moroff, CD Lothrop: Hyperadrenocorticism associated with adrenocortical tumor or nodular hyperplasia of the adrenal gland in ferrets; 50 cases (1987-1991) . In: Journal of the American Veterinary Medical Association (JAVMA) Volume 203, Issue 2, August 1993, pp. 271-275.
  5. ^ In: Walter Baumgartner: Clinical propaedeutics of internal diseases and skin diseases of domestic animals. P. 312
  6. ^ Nico J. Shoemaker, Marielle Schuurmans, Hanneke Moorman, J. (Sjeng) T. Lumeij: Correlation between age at neutering and age at onset of hyperadrenocorticism in ferrets . In: Journal of the American Veterinary Medical Association (JAVMA), Vol 216, No. 2, Jan 15, 2000, pp. 195-197
  7. M. Bielinska, S. Ielinska, S. Kiiveri, H. Parviainen, S. Mannisto, M. Heinkinheimo, DB Wilson: Gonadectomy-induced Adrenocortical Neoplasia in the Domestic Ferret (Mustela putorius furo) and Laboratory Mouse . In: Veterinary Pathology. Volume 43, 2006, pp. 97-117
  8. ^ S. Chen: Advanced diagnostic approaches and current medical management of insulinomas and adrenocortical disease in ferrets (Mustela putorius furo) . In: Veterinary Clinics in North America: Exotic Animal Practice. Volume 13 (3), September 2010, pp. 439-52
  9. ^ CA Weiss, BH Williams, JB Scott, MV Scott: Surgical treatment and long-term outcome of ferrets with bilateral adrenal tumors or adrenal hyperplasia: 56 cases (1994–1997) . In: Journal of the American Veterinary Medical Association (JAVMA), Volume 215 (6), September 15, 1999, pp. 820-823
  10. ^ RA Wagner, CA Piché, W. Jöchle, JW Oliver: Clinical and endocrine responses to treatment with deslorelin acetate implants in ferrets with adrenocortical disease . In: American Journal of Veterinary Research. Volume 66 (5), May 2005, pp. 910-914