Chronic Hyperadrenocorticalism in a Female Lowland Gorilla (Gorilla Gorilla)
IAAAM 2000
Ray L. Ball1, DVM; John H Olsen1, DVM; Peter Dunne2, MD; Genevieve Dumonceux1, DVM; Mike Burton1,VMD; Cathy Lynch3, MD
1Busch Gardens, Tampa, FL, USA; Departments of 2Neurology and 3Obstetrics and Gynecology, University of South Florida College of Medicine, Tampa, FL, USA

Abstract

A 20-yr-old nulliparous female lowland gorilla had developed severe truncal obesity over the course of 2 yr. This animal lived with a troop consisting of 2.2 conspecifics; an adult male was removed from the group in early 1997. Prior to this time this animal's medical history consisted of irregular menstrual cycle, polyuria, and hyperphagia actually contributing to social conflicts with other troop members. The female gorilla had a behavioral history of hair plucking that extended back to her previous facility 9 yr previously. In June 1998 she experienced a bout of lethargy and a fractured the right central incisor. During a cursory visual exam for that problem a petit mal seizure was witnessed wherein her eyes rolled back into her head, she slumped over, and she was non-responsive to tactile or auditory stimuli for about 45 sec. She was semi-catatonic and reluctant to use her right hand in the immediate post-ictal phase, but by late in the day was back to normal. The next morning she was found with wide bands of skin excoriations around her abdomen and right flank, and on her back. At this time all the skin lesions were localized to the right. Medial deviation of her left eye was also noted.

Several attempts were made to culture skin wounds, perform skin scrapes and treat the skin wounds with topical and systemic medications including antibiotics, astringents, and anti-histamines. No specific etiology could be gathered from these diagnostics and therapeutics, and the lesions grew as a result of self plucking. Urinary cortisol:creatinine ratios (UCCR) from this female suggested that the pituitary-adrenal axis warranted closer examination. A differential diagnosis list to include all of her findings at this point centered around hormonal dysfunction and included polycystic ovarian syndrome, hyperadrenocorticalism, hyperthyroidism, and possibly others endocrinopathies, such as acromegaly and hyperprolactinemia. A physical examination under general anesthesia 9 mo later included a general physical examination, a dermatology consultation, reproductive evaluation, and magnetic resonance imaging (MRI) of the skull. The physical examination revealed a grossly obese animal with the fat distributed primarily in the trunk and the back of the neck, severe bruises on the arm, and generalized muscle atrophy of the limbs. Diagnostics of the skin included biopsy for histopathology, bacterial, fungal, and viral culture. The histologic diagnosis was dermal fibrosis and a mild amount of Staphylococcus aureus was grown on culture. The reproductive exam was not informative. MRI with gadolinium contrast delivered i.v. demonstrated a 2.5-mm mass consistent with a microadenoma on the right side of the anterior pituitary. Serum biochemistry abnormalities were mild and consisted of hypocalcemia, hypernatremia, hyperkalemia, hyperchloremia, hyperlipasemia, and elevated testosterone. Based on the history, clinical signs and this examination, a tentative diagnosis of pituitary dependent hyperadrenocorticalism (Cushing's disease) was made.

During the next several months, many consultations were made with endocrinologists, neurologists, and neurosurgeons regarding this case. The presence of a presumptive pituitary lesion warranted investigation of the hormonal status of the adrenal gland. A low dose dexamethasone suppression test using urinary cortisol analysis was elected to evaluate the status of the pituitary B adrenal axis. This animal and a 31-yr-old female gorilla were given dexamethasone (1 mg p.o.) at midnight and all voided urine collected from a clean cafeteria tray at 0800 hr the next morning. Because the test animal suppressed to the same levels as the control, the possibility of Cushing's syndrome/disease (CD) seemed less likely. In November 1999, a follow-up examination was performed to specifically evaluate the reproductive status of this female. A corticotrophin stimulation test, 100 µg i.v. corticorelin ovine triflutate (ActhrelTM, Ben Venue Laboratories, Bedford, OH 44146 USA) was performed to rule out any possibility of hyperadrenalcorticalism. Transrectal ultrasonography examination exam revealed several small hypoechoic areas on the right ovary consistent with polycystic ovarian syndrome. The cervix had a moderate amount of mucosal congestion. Anesthesia was unremarkable until upon recovery, the gorilla became comatose and was placed on a ventilator overnight. Twelve hours into recovery her neurologic status became questionable and was in severe respiratory acidosis. Electrocardiogram tracings, peaked T waves, wide QRS complexes, and flattened P waves, suggested hyperkalemia. An electroencephalogram detected some very low amplitude activity but the animal expired shortly after the examination.

Gross necropsy revealed an obese gorilla with a truncal distribution of fat and little fat in the subcutaneous tissue of any limb. A large amount of fat was found in the thoracic cavity overlying the lung fields. The pituitary gland was swollen out of the sella dorsally. Several small tags of endometrial tissue were found in the abdomen on the serosal surface of the right side of the uterus. There was multifocal chronic active ulceration in the distal esophagus and stomach. The left adrenal was approximately three times normal size and had a severely necrotic center. The right adrenal could not be found. On histologic examination the left adrenal was necrotic and the pituitary demonstrated diffuse hyperplasia. Results of follicle stimulating hormone (FSH), luteinizing hormone (LH), thyrotropin stimulating hormone (TSH), growth hormone (GH), and adrenal-corticotrophin hormone (ACTH), prolactin staining are pending at the time of this writing. The corticotrophin stimulation test revealed a hyperresponsive elevation of plasma ACTH and serum cortisol levels that remained near baseline.

While clinical diagnosis and imaging modalities are extremely useful in the overall diagnosis and treatment plans for CD, laboratory confirmation is the hallmark of making a definitive diagnosis.6 Urinary cortisol:creatinine ratios (UCCR) have been utilized in ferrets,5 humans,3 and to some degree in dogs1,4 in an effort to diagnose hyperadrenocorticalism. Morning collections from all members of this gorilla troop showed elevations of UCCR (institutional normals = 25-45, n = 6 individuals), but this female had consistently elevated levels (50-65, institutional normals < 14, n = 6 individuals) at evening collections. This finding is not definitive for CD but does suggest some loss to a diurnal cycle in the affected female gorilla compared to the others. Another possibility for the lack of clinicopathologic support for clinical CD by UCCR values in this animal may have been related to progressive adrenal gland necrosis such that cortisol was falling into the normal range, as the animal was experiencing hyperadrenalcorticalism (Addison's disease). This theory may explain why suppression was noted after administration of p.o. low dose dexamethasone. The results of the corticotrophin stimulation also support this theory and are consistent with those of patients with Addison's disease. Macronodular adrenal hyperplasia also allows failure to suppress at a low dose in suspect clinical CD. Bilateral6 and unilateral2 hyperplasia have been reported in cases of chronic CD patients. The literature remains unclear whether the adrenal gland is responding to the pituitary stimulation or the adrenal gland is the primary problem. Familiar CD has been documented in humans but has not yet been pursued with this gorilla. The relationship between the seizure activity and CD is unclear still but steroid psychosis in chronic CD is not uncommon6 and may explain her tritrichomania and some other aberrant behaviors.

References

1.  Angles JM, EC Feldman, RW Nelson, MS Feldman. 1997. Use of urine cortisol:creatinine ratio versus adrenocorticotropic hormone stimulation testing for monitoring mitotane treatment of pituitary-dependent hyperadrenocorticism in dogs. J. Am. Vet. Med. Assoc. 211:1002-1004.

2.  Bunch FT, BA Warner. 1993. Cushing's disease with a unilateral adrenal macronodule: evolutive transition or incidental finding? South. Med. J. 86: 235-238.

3.  Corcuff JB, A Tabarin, M Rashedi, M Duclos, P Roger, D Ducassou. 1998. Overnight urinary free cortisol determination: a screening test for the diagnosis of Cushing's syndrome. Clin. Endocrinol. (Oxf) 48: 503-508.

4.  Galac S, HS Kooistra, E Teske, A Rijnberk. 1997. Urinary corticoid/creatinine ratios in the differentiation between pituitary-dependent hyperadrenocorticism and hyperadrenocorticism due to adrenocortical tumour in the dog. Vet. Q. 19: 17-20.

5.  Gould WJ, TJ Reimers, JA Bell, HJ Lawrence, JF Randolph, PH Rowland, JM Scarlett. 1995. Evaluation of urinary cortisol:creatinine ratios for the diagnosis of hyperadrenocorticism associated with adrenal gland tumors in ferrets. J. Am. Vet. Med. Assoc. 206: 42-46.

6.  Orth DN. 1995. Cushing's syndrome. N. Engl. J. Med. 332: 791-803.

Speaker Information
(click the speaker's name to view other papers and abstracts submitted by this speaker)

Ray L. Ball, DVM
Busch Gardens Tampa Bay
Tampa, FL


MAIN : All : Hyperadrenocorticolism
Powered By VIN
H
E
L
P

CONTACT US

777 W. Covell Blvd., Davis, CA 95616

mailto:vingram@vin.com

PHONE

  • Toll Free: 800-700-4636
  • From UK: 01-45-222-6154
  • From anywhere: (1)-530-756-4881
  • From Australia: 02-6145-2357
SAID=27