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Suspected Case of Hyperadrenocorticism
in a Golden Hamster
(Mesocricetus auratus)
Filipe Martinho, DVM
Clı´nica Me
´dico-veterina
´ria, R. Ma
´rio Viegas Lt. 1 Lj. 2, 2755-057 Alcabideche, Portugal
Skin problems are common in pet rodents. Their causes are diverse, in-
cluding bacterial, fungal, and parasitic infection, behavior, and nutrition is-
sues. However, little is known about the effects of endocrine disease on the
skin in these animals.
In other mammal species (cat, dog) the cutaneous changes caused by hy-
peradrenocorticism (or Cushing’s disease) are well described, as are other
clinical signs and its causes, pathology, and diagnosis. In laboratory set-
tings, hamsters are reported to have a high incidence of adrenal adenomas
and adrenocortical hyperplasia, but there are few reported cases of hypera-
drenocorticism in pet hamsters in the literature [1,2].
Pet hamsters with a history and clinical signs similar to those of dogs with
hyperadrenocorticism are often presented to clinicians. The diagnosis in
these cases is usually based on history and signs.
Theoretically, the laboratory diagnosis could be based on the serum mea-
surement of alkaline phosphatase and cortisol. However, blood collection
may be limited by the occasional difficulty of venous access, small vein
size, and the volume of the sample required for analysis. Additionally, ham-
sters secrete cortisol and corticosterone in similar proportions [3], and the
diagnostic significance of cortisol is not yet fully understood.
The cause of hyperadrenocorticism in this species (adrenal neoplasia or
hyperplasia or excessive production of corticotropin through a pituitary ad-
enoma) is even more difficult to determine.
In the case described here, a presumptive diagnosis of hyperadrenocorti-
cism was made after excluding other possible causes of the observed skin
changes and by determining the urine cortisol/creatinine ratio. In addition
E-mail address: martinhofilipe@sapo.pt
1094-9194/06/$ - see front matter Ó2006 Elsevier Inc. All rights reserved.
doi:10.1016/j.cvex.2006.05.021 vetexotic.theclinics.com
Vet Clin Exot Anim 9 (2006) 717–721
to correcting other problems present, the author initiated therapy with
ketoconazole, with no apparent success.
Case report
The patient was an 18-month-old male golden hamster, kept in a wire
cage with bedding made of wood shavings. It was fed a diet composed of
a mixture of seeds ad libitum and supplemented with occasional fresh fruits
and vegetables. Water was supplied by a bottle and changed daily. There
were no previous health issues or contact with other animals.
In the few weeks before presentation, the hamster had developed a pro-
gressive, nonpruritic alopecia, and the owners had noticed increased drink-
ing and urine output and abdominal distension. No respiratory or digestive
disorder was noted, and appetite and behavior remained normal.
The patient had already been seen by another veterinarian and was being
treated for external parasites with ivermectin injections weekly for a total of
three injections. Benzyl benzoate (Acarilbial, Bial) was also being applied
topically to the lesions, but there was no change in the condition.
The hamster was bright and alert; no problems were detected on exami-
nation of the head and mouth. Some degree of abdominal distension was
observed, but no abnormalities could be detected on palpation. The alopecia
was bilaterally symmetric; the skin was slightly erythematous, with areas of
hyperpigmentation, comedones, and ulcerations of variable diameter
(Fig. 1).
At this point, the differential diagnosis included demodecosis (Demodex
criceti or D auratus), mange, ringworm, pyoderma, epitheliotropic lym-
phoma, and hyperadrenocorticism.
A number of skin scrapings, taken from several areas of the skin, were
negative for mites. Hair was collected from the periphery of the lesions
and placed in Saboraud’s growth media for detection of fungal organisms,
with no growth detected after 7 days. Skin cytology revealed some nonde-
generate neutrophils and a mixed population of bacteria, suggestive of
a mild pyoderma.
Whole-body radiographs revealed loss of abdominal contrast and some
intestinal gas. A small radiodense area (1 mm in diameter) was detected
in midabdomen (Fig. 2).
The owners were asked to collect a urine sample at home, to reduce the
effect that stress might have on cortisol levels when the sample was collected
in the clinic. This was achieved by removing all the wood shavings from the
floor of the cage and collecting urine over a 24-hour period, which was then
refrigerated. The sample was submitted for determination of the urine cor-
tisol/creatinine ratio (Table 1).
The patient was started on 30 mg/kg of trimethoprim plus sulfamethox-
azole orally twice daily and topical treatment with chlorhexidine 0.2% for
the pyoderma.
718 MARTINHO
A week later, the hamster was re-evaluated. Some improvement of the
skin condition was noted (healing of some of the ulcers and a decrease in
erythema). The antibiotic and chlorhexidine were maintained for another
week, and therapy with 5 mg/kg of ketoconazole orally every 12 hours
was initiated.
Two weeks later, further re-evaluation revealed that the pyoderma was
mostly localized in the ventral neck area. There was no progression of the
alopecia, and the abdominal distension was reduced, but the other signs
were not improved. Behavior, level of activity, and appetite remained
unaltered.
Two weeks after this evaluation, the author was notified by the owner
that the hamster had died. Its body was not available for autopsy.
Fig. 1. (A,B) Skin lesions seen in the golden hamster include erythema, hyperpigmentation,
comedones, and ulcers.
719
HYPERADRENOCORTICISM IN A HAMSTER
Discussion and summary
Dermatologic disease is common in pet rodents, including golden ham-
sters. Most of the cases are related to husbandry or to bacterial, fungal,
or parasitic disease. Other causes are more obscure.
Adrenal disease has been recognized in golden hamsters and well described
in laboratory animals, but its effect on the skin is not well understood. Al-
though individuals with signs consistent with hyperadrenocorticism are occa-
sionally reported, few have been definitively diagnosed, and the presumptive
diagnosis of hyperadrenocorticism is based on history and clinical signs.
The urine cortisol/creatinine ratio has been used as a screening test for
hyperadrenocorticism in dogs and cats [4,5], where it is significantly in-
creased in both random and 24-hour urine samples taken from individuals
with confirmed hyperadrenocorticism. However, the test has a low specific-
ity, because the ratio may be increased in animals with nonadrenal illness
and in animals that have signs compatible with hyperadrenocorticism but
normal pituitary-adrenocortical function. As such, it is more useful as
a screening test for normal individuals. Urine samples should be collected
at home or in a familiar environment to reduce the effect of stress on cortisol
excretion, which could increase the urine cortisol/creatinine ratio.
Fig. 2. Whole-body lateral radiograph shows loss of abdominal detail, small amount of intes-
tinal gas, and presence of a small radiodense area in the midabdomen.
Table 1
Urine concentration of cortisol and cortisol/creatinine ratio in this patient Mesocricetus auratus
Urine cortisol
(mg/dL)
Urine creatinine
(g/dL)
Cortisol/
Creatinine ratio Comments
Patient 3.74 0.25 45.6 Cushing?
The laboratory reference range for cortisol/creatinine ratio was !20 higher values were con-
sidered pathologic.
720 MARTINHO
This article describes a case of a golden hamster with ‘‘classic’’ signs of
hyperadrenocorticism. Although the determination of blood cortisol level
could be used to test for hyperadrenocorticism, there are few clinical reports
of its use. Because of the patient’s small size and the comparatively large vol-
ume of blood required to run some adrenal function tests, it was decided to
use the urine cortisol/creatinine ratio as a screening test. The urine cortisol/
creatinine ratio was significantly increased compared with the reference
range used by the laboratory.
Because o,p0-DDD is unavailable in Portugal, therapy with ketoconazole
was attempted, by adapting protocols for treating dogs with hyperadreno-
corticism. Although some of the clinical signs resolved, recovery was not
complete by the fifth week of treatment. Because it was not possible to do
a necropsy, it remains unknown whether the death of the patient was caused
by complications related to adrenal dysfunction, some other health problem,
or drug toxicosis during treatment.
Further measurements of urine cortisol and creatinine levels, from both
normal and affected individuals, would be useful in determining the applica-
bility of this test to diagnosis of hamsters (and other rodents) suspected of
having hyperadrenocorticism. It is also important to try different treatment
protocols with ketoconazole in this species, to access its efficacy in control-
ling this pathologic condition.
References
[1] Bauck L, Orr JP, Lawrence KH. Hyperadrenocorticism in three teddy bear hamsters. Can Vet
J 1985;25:247–50.
[2] Donnelly TM. Disease problems of small rodents. In: Quesenberry KE, Carpenter JW, edi-
tors. Ferrets, rabbits and rodents: clinical medicine and surgery. 2nd edition. WB Saunders;
2005.
[3] Ottenweller JE, Tapp WN, Burke JN, et al. Plasma cortisol and corticosterone concentrations
in the golden hamster. Life Sci 1985;37:1551–8.
[4] Goossens MM, Meyer HP, Voorhout G, et al. Urinary excretion of glucocorticoids in the
diagnosis of hyperadrenocorticism in cats. Domest Anim Endocrinol 1995;12:355–62.
[5] Jensen AL, Iversen L, Koch J, et al. Evaluation of the urinary cortisol:creatinine ratio in the
diagnosis of hyperadrenocorticism in dogs. J Small Anim Pract 1997;38:99–102.
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HYPERADRENOCORTICISM IN A HAMSTER
