Hyperadrenocorticism in a cat

A diabetic cat with hyperadrenocorticism had polydipsia, polyuria, ventral abdominal alopecia, thin dry skin, and a pendulous abdomen. Results of laboratory testing indicated persistent resting hypercortisolemia, hyperresponsiveness of the adrenal glands (increased cortisol concentration) to ACTH gel, and no suppression of cortisol concentrations after administration of dexamethasone at 0.01 or 1.0 mg/kg of body weight. Necropsy revealed a pituitary gland tumor, bilateral adrenal hyperplasia, hepatic neoplasia, and demodicosis. Adrenal gland function was concurrently assessed in 2 cats with diabetes mellitus. One cat had resting hypercortisolemia, and both had hyperresponsiveness to ACTH gel (increased cortisol concentration) at one hour. After administration of dexamethasone (0.01 and 1.0 mg/kg), the diabetic cats appeared to have normal suppression of cortisol concentrations. The effects of mitotane were investigated in 4 clinically normal cats. Adrenocortical suppression of cortisol production occurred in 2 of 4 cats after dosages of 25, 37, and 50 mg/kg. Three cats remained clinically normal throughout the study. One cat experienced vomiting, diarrhea, and anorexia.     

Hyperadrenocorticism in six cats

The case records of six cats with hyperadrenocorticism presented to the Department of Clinical Veterinary Medicine, University of Cambridge, over an 11-year period were reviewed. Signalment and clinical signs were similar to previous reports but, in contrast to other reports, only three cats had diabetes mellitus on presentation. Abdominal radiographs revealed an adrenal mass in one case, obesity in all cases but no hepatomegaly. The adrenal glands were identified ultrasonographically in three out of six cases. Clinicopathological findings were non-specific. The diabetic cats had a significantly lower serum potassium concentration than the non-diabetic cats (P<0·05). Results of adrenocorticotrophic hormone (ACTH) stimulation tests were supportive of a diagnosis of hyperadrenocorticism in the five cats in which they were performed. Five cats had pituitary-dependent hyperadrenocorticism (PDH) and one had an adrenal tumour. Differentiation between the two forms of hyperadrenocorticism was possible preoperatively in five out of six cats. Adrenal histopathology confirmed hyperplasia in four cats and adenocarcinoma in one cat. Three cats with PDH underwent bilateral adrenalectomy and two of these cats had low, flat ACTH stimulation tests postoperatively and survived for significant periods. The cat with an adrenal tumour underwent partial unilateral adrenalectomy, maintained a positive ACTH stimulation test postoperatively and was euthanased one week after surgery.     

Cyclic estrous-like behavior in a spayed cat associated with excessive sex-hormone production by an adrenocortical carcinoma

A 15-year-old, spayed female domestic shorthair cat was evaluated for 1-year duration of cyclic intermittent estrous behavior. Diagnostic testing performed before referral, including baseline progesterone concentration, human chorionic gonadotropin (hCG) hormone stimulation test and surgical exploratory laparotomy, had remained inconclusive for a remnant ovary. Evaluation of sex hormones before and after adrenocorticotropic hormone (ACTH) administration revealed increased basal concentrations of androstenedione, estradiol, progesterone, and 17α-hydroxyprogesterone and normal ACTH-stimulated hormone concentrations. Enlargement of the right adrenal gland was identified by abdominal ultrasound. The cat underwent an adrenalectomy and histopathology of the excised adrenal gland was consistent with an adrenocortical carcinoma. Clinical signs resolved immediately following surgery, and most hormone concentrations declined to within or below the reference interval (RI) by 2 months after surgery.     

Steroidogenic response of adrenal tissues after administration of ACTH to dogs with hypercortisolemia

OBJECTIVE: To evaluate adrenal sex hormone concentrations in neutered dogs with hypercortisolemia. DESIGN: Case series. ANIMALS: 11 neutered dogs with hypercortisolemia. PROCEDURE: Serum samples obtained before and 1 hour after administration of ACTH were evaluated for concentrations of cortisol, progesterone, testosterone, dehydroepiandrosterone sulfate or androstenedione or both, and 17-hydroxyprogesterone. RESULTS: For all dogs, concentrations of 1 or more adrenal sex hormones were substantially greater than reference range values before or after administration of ACTH. Testosterone concentration was not greater than reference range values in any of the dogs. CONCLUSIONS AND CLINICAL RELEVANCE: Results emphasize the importance of ruling out hypercortisolemia before measuring adrenal sex hormone concentrations as a means of diagnosing adrenal hyperplasia syndrome (alopecia X) in dogs.     

Progesterone secreting adrenal mass in a cat with clinical signs of hyperadrenocorticism

A 7-year-old 7-kg (16-lb) neutered male Himalayan cat had nonpruritic progressive alopecia of 9 months' duration. The cat had hyperglycemia and glucosuria. Physical examination revealed complete alopecia along the abdomen, inguinal area, medial and caudal areas of the thighs, ventral area of the thorax, and axilla. Clinical signs were consistent with endocrine-induced alopecia and hyperadrenocorticism, however, results of diagnostic tests (ACTH stimulation and low-dose dexamethasone suppression) were not supportive of hyperadrenocorticism. Abdominal ultrasonography revealed a mass cranial to the left kidney. Blood samples were obtained before and after ACTH stimulation to measure sex hormone concentrations. Analysis revealed markedly high blood progesterone concentrations before and after ACTH stimulation. An adrenalectomy was performed and histologic examination of the mass revealed a well-differentiated adrenocortical carcinoma. The right adrenal gland could not be viewed during surgery and was assumed to be atrophic. Following surgery, the hyperglycemia and glucosuria resolved. Within 4 months of surgery, the hyperprogesteronemia had resolved, and at 12 months the cat's coat quality appeared normal. Findings suggest that cats with signs of hyperadrenocorticism should be evaluated not only for abnormal cortisol concentrations, but also for sex hormone abnormalities.     

Diagnosis and treatment of naturally occurring hypoadrenocorticism in 42 dogs

Hypoadrenocorticism was diagnosed in 42 dogs over a two-and-a-half-year period. The disease occurred more commonly in young to middle-aged dogs, with a female:male ratio of 2:1. Most dogs had chronic intermittent signs (eg, poor appetite, lethargy and vomiting), but more than a third were in acute adrenal crisis at the time of diagnosis. Serum biochemical testing revealed azotaemia, hyperphosphataemia, hyper-kalaemia and hyponatraemia in almost all the dogs. In all dogs, results of adrenocorticotrophic hormone (ACTH) stimulation testing revealed a low to low-normal serum baseline Cortisol concentration that failed to increase after ACTH administration. In two dogs with persistently normal serum electrolytes concentration, one had a markedly high plasma ACTH concentration diagnostic for primary hypoadrenocorticism, whereas the other had a low concentration confirming secondary hypoadrenocorticism. Fludrocortisone acetate was initially used for mineralocorticoid replacement in 33 of the 37 treated dogs withprimary hypoadrenocorticism (final median dosage, 27-0 μg/kg/day), but supplementation was changed to desoxycorticos-terone pivalate (DOCP) in four dogs because of poor response or adverse effects. Seven dogs with primary hypoadrenocorticism were treated with DOCP (final median dosage, 2-02 mg/kg/month). Prednisone, initially administered to 36 dogs, was discontinued in 11 dogs because of side effects. Of the dogs treated with fludrocortisone, the response was considered good to excellent in 26 dogs (78.8 per cent), fair in three, and poor in four. All dogs treated with DOCP responded well.     

Hyponatremia and hyperkalemia associated with peritoneal effusion in four cats

Four cats with considerable peritoneal effusion and corresponding hyponatremia and hyperkalemia were evaluated. The Na:K ratio in all cats was < 25, which is suggestive of adrenal insufficiency. An ACTH stimulation test was performed on 3 cats for evaluation of adrenal gland function. Serum cortisol and aldosterone concentrations did not support a diagnosis of adrenal gland insufficiency. In 1 cat, histologic evaluation of the adrenal glands at necropsy also failed to support a diagnosis of hypoadrenocorticism. On the basis of these findings, and because hyponatremia and hyperkalemia could not be readily explained by another cause, the electrolyte abnormalities were presumed to be secondary to peritoneal effusion.     

Pituitary dependent hyperadrenocorticism in a cat.

A cat that was suspected some insulin resistance was diagnosed as pituitary dependent hyperadrenocorticism from an adrenocorticotropic hormone (ACTH) stimulation test, dexamethasone suppression test and measure of endogenous plasma ACTH concentration. Histopathological examination revealed chromophobe adenoma in pituitary gland and hyperplasia in adrenal cortex.     

Hyperadrenocorticism in cats: seven cases (1978-1987)

Hyperadrenocorticism was diagnosed in 7 cats with concurrent diabetes mellitus. Four cats had pituitary adenoma with bilateral adrenocortical hyperplasia, 1 cat had pituitary carcinoma with bilateral adrenocortical hyperplasia, 1 cat had adrenocortical carcinoma, and 1 cat had adrenocortical adenoma of the left adrenal gland. One year later, adrenocortical adenoma involving the right adrenal gland also was diagnosed in this cat. Clinical signs included polyuria and polydipsia (n = 7), development of pot-bellied appearance (n = 5), dermatologic alterations (n = 5), lethargy (n = 3), weight loss (n = 3), dyspnea/panting (n = 2), and recurrent bacterial infections (n = 2). In 6 cats, the diagnosis of hyperadrenocorticism was established before death on the basis of results of the ACTH stimulation test (n = 3) and the dexamethasone screening test (n = 5). Pituitary-dependent hyperadrenocorticism was differentiated from adrenocortical neoplasia on the basis of results of the dexamethasone suppression test (n = 4), endogenous ACTH concentration (n = 3), results of abdominal radiography and ultrasonography (n = 3), and exploratory celiotomy (n = 1). Four cats died or were euthanatized without treatment attempts. Treatment with mitotane followed by 60Co teletherapy was ineffective in one cat with pituitary adenoma. One cat with pituitary carcinoma died one week after bilateral adrenalectomy. Bilateral adrenocortical adenomas were removed surgically in the affected cat.     

Histopathologic features, environmental factors, and serum estrogen, progesterone, and prolactin values associated with ovarian phase and inflammatory uterine disease in cats.

Forty-four female American Shorthair cats with inflammatory uterine disease or infertility were evaluated. Data collected included age, month of diagnosis, housing, reproductive history, results of bacteriologic culture of uterine specimens, serum concentrations of estrogen, progesterone, and prolactin and histopathologic features of the ovaries and uterus. Histologically, the ovaries of 19 cats were dominated by active or cystic follicles, whereas 25 cats had luteal-phase ovaries. Of the 25 cats with active corpora lutea, 20 had either recently weaned litters (n = 11) without subsequent exposure to a male cat, or had been housed individually for lengthy periods (n = 9). The finding of active corpora lutea under these circumstances indicates that in queens, ovulation may occur by mechanisms not involving coitus. Prominent, active corpora lutea on the ovaries were associated with adenomatotic proliferative changes in the superficial and glandular epithelium of the uterus and with myometrial hyperplasia, compared with the uterus of cats with follicular ovaries (P less than 0.01). Serum progesterone concentration greater than or equal to 1.87 ng/ml was consistently associated with luteal-phase ovaries. Serum progesterone values less than or equal to 0.15 ng/ml were consistently associated with follicular-phase ovaries. Escherichia coli was the organism most commonly isolated from uterine contents.     

Treatment of fibroepithelial hyperplasia (FEH) of the mammary gland in the cat with the progesterone antagonist Aglépristone (Alizine)

Three cases of fibroepithelial hyperplasia (FEH) of the mammary gland in the cat are reported. A one year old female cat had a distinct enlargement of the middle mammary glands, one on each side, 5 days after the first estrus. One week later the cat was treated with medroxyprogesterone acetate (Depo-Promone). The affected glands, along with the remaining glands, increased further in size. A five year old female cat was treated with Proligeston (Covinan) for the suppression of estrus. Two weeks later fibroepithelial hyperplasia occurred in two glands, one with a well demarcated ulceration. A seven months old male cat was treated with delmadinon acetate (Tarden) because of urine spraying. Two months later he had enlargement of all mammary glands. All three cats were treated with the progesterone antagonist Aglépristone (Alizine). Within 5 to 11 weeks the mammary glands had regressed to normal.     

Effects of delmadinone acetate on pituitary-adrenal function, glucose tolerance and growth hormone in male dogs

Objective To characterise the effects of delmadinone acetate on the pituitary-adrenal axis, glucose tolerance and growth hormone concentration in normal male dogs and dogs with benign prostatic hyperplasia.
Design A prospective study involving nine normal male dogs and seven with prostatic hyperplasia.
Procedure Delmadinone acetate was administered to six normal male dogs and seven dogs with benign prostatic hyperplasia at recommended dose rates (1.5 mg/kg subcuta-neously at 0, 1 and 4 weeks). Three normal controls received saline at the same intervals. Blood concentrations of ACTH, cortisol, glucose, insulin and growth hormone were measured over 50 days. Intravenous glucose tolerance and ACTH response tests were performed before and after treatment in the nine normal animals.
Results A substantial suppression of basal and 2 h post-ACTH plasma cortisol secretion was demonstrated after one dose in all dogs given delmadinone acetate. Individual responses after the second and third administration varied between recovery in adrenal responsiveness to continued suppression. Plasma ACTH concentration was also diminished after one treatment. No effects were evident on glucose tolerance or serum growth hormone concentrations.
Conclusion Delmadinone acetate causes adrenal suppression from inhibition of release of ACTH from the pituitary gland. Treated dogs may be at risk of developing signs of glucocorticoid insufficiency if subjected to stressful events during or after therapy. Neither glucose intolerance nor hyper-somatotropism seems likely in male dogs given delmadinone acetate at the recommended dose rate, but the potential for excessive growth hormone secretion in treated bitches remains undetermined.     

Passive immunization with antiserum to adrenocorticotropin increases weight gain in normal female rats.

Passive immunization against ACTH was used to test the hypothesis that growth in female rats is constrained by physiological concentrations of glucocorticoids. When animals were stressed by 15-min exposure to ether before blood sampling by cardiac puncture, serum concentrations of corticosterone were lower (P less than .05) in immunized rats than in stressed controls. The maximum effect was apparent 2 h after injection of ACTH antiserum, and no effect was apparent 6 h after injection. To examine the effects of ACTH immunization on growth, rats received daily injections of either saline, sheep immunoglobulin G, or ACTH antiserum, 2 h before the afternoon peak in plasma concentrations of corticosterone. After 7 d of treatment, rats treated with ACTH antiserum had gained 37% more body weight than saline-injected controls, and this effect was accompanied by a 59% reduction in peak plasma concentrations of corticosterone. Immunoglobulin G purified from normal sheep serum had no effect on weight gain. It is concluded that growth rate in normal female rats can be stimulated through the suppression of adrenal activity.     

Hyperadrenocorticism treated with metyrapone followed by bilateral adrenalectomy in a cat

A 6-year-old spayed female cat was evaluated for uncontrolled diabetes mellitus and poor hair coat. Clinicopathologic abnormalities included high serum activity of liver enzymes, hyperglycemia, hypercholesterolemia, glucosuria, and an exaggerated response to ACTH stimulation. Abdominal ultrasonography revealed large adrenal glands. Hyperadrenocorticism was diagnosed. Treatment for a facial abscess was instituted along with administration of metyrapone for hyperadrenocorticism. After stabilization, bilateral adrenalectomy was performed. The cat recovered without complications and has remained clinically normal for 5 months with treatment of desoxycorticosterone pivalate and prednisone. Treatment with metyrapone appeared to stabilize the cat metabolically and clinically prior to surgery.     

Hyperadrenocorticism associated with excessive sex hormone production by an adrenocortical tumor in two dogs.

An 11-year-old spayed female Labrador Retriever and a 9-year-old castrated male miniature Poodle were evaluated because of clinical signs of hyperadrenocorticism. Cortisol testing did not support a diagnosis of hypercortisolemia in either dog; however, imaging studies revealed unilateral adrenal tumors in both dogs. Serum concentrations of 17-hydroxyprogesterone, progesterone, and estradiol were high in both dogs, and androstenedione concentrations were also high in 1 dog. It is suspected that sex hormone secretion by the adrenal tumors in these dogs resulted in clinical signs of hyperadrenocorticism. Clinical signs and hormonal abnormalities resolved in the male dog after surgical resection of the tumor. There was no improvement in clinical signs after treatment with mitotane in the female dog, which died 2 months after diagnosis. Histologic evaluation confirmed the presence of adrenocortical carcinoma in both dogs.     

Pituitary-dependent hyperadrenocorticism in a cat

Pituitary-dependent hyperadrenocorticism was diagnosed in a 9-year-old, male castrated cat that had polyuria, polyphagia, pendulous abdomen, truncal hair loss, congestive heart failure, and insulin-resistant diabetes mellitus. Results of pituitary-adrenal function testing revealed inadequate serum cortisol suppression following dexamethasone administration, exaggerated serum cortisol responses after exogenous ACTH stimulation, and high plasma ACTH concentrations. The pathologic findings of bilateral adrenocortical hyperplasia and a pituitary adenoma that immunostained well for ACTH-related peptides confirmed pituitary-dependent hyperadrenocorticism.     

Hyperadrenocorticism and hyperprogesteronemia in a cat with an adrenocortical adenocarcinoma

A seven-year-old, neutered male domestic shorthair cat was evaluated for poorly regulated diabetes mellitus and increased skin fragility. Imaging studies revealed a right adrenal gland tumor, but cortisol testing did not support a diagnosis of hyperadrenocorticism. Serum concentrations of progesterone and testosterone were increased compared with a group of normal cats, and the clinical signs were attributed to hyperprogesteronemia. At necropsy, a diagnosis of adrenocortical adenocarcinoma was confirmed, and immunohistochemical staining confirmed the presence of progesterone within the tumor. Clinical signs of hyperadrenocorticism in cats may occur due to increased serum concentrations of hormones other than cortisol.     

Luteinizing hormone-dependent Cushing's syndrome in a pet ferret (Mustela putorius furo)

Hyperadrenocorticism in ferrets is associated with increased circulating concentrations of adrenal androgens, whereas plasma concentrations of cortisol and ACTH are usually not affected. Here, we report on a 5-year-old castrated male pet ferret (Mustela putorius furo) in which the major presenting signs were polyuria and polyphagia. Routine biochemistry values were within their reference ranges. The urinary corticoid:creatinine ratio (UCCR) was increased and the plasma ACTH concentration was suppressed. Abdominal ultrasonography revealed an enlarged right adrenal gland and atrophy of the left adrenal gland. Administration of hCG resulted in an increase of plasma cortisol and androstenedione concentrations. Based on these findings LH/hCG-dependent hypercortisolism and hyperandrogenism were suspected and treatment was started with a depot GnRH-agonist implant containing 9.4mg deslorelin. Within 3 weeks after placement of the implant all clinical signs had disappeared. Three months later the endocrine parameters had normalized, while abdominal ultrasonography revealed that the right adrenal gland had diminished in size and the left adrenal gland was considered of normal size. No recurrences of clinical signs were seen within 2 years after placement of the deslorelin implant. At that time urinary corticoid and plasma hormone concentrations were within their reference ranges, and no further change in the size of the adrenal glands was seen. In conclusion, this is the first confirmed case of LH-dependent hypercortisolism in a ferret that was treated successfully with a depot GnRH-agonist.     

Functioning unilateral adrenocortical carcinoma in a dog

An 11-year-old, 24-kg, intact female Siberian husky dog in anestrus had a 2-month history of polyuria and polydipsia. The dog had signs of mineralocorticoid excess such as hypertension and hypokalemia refractory to potassium supplementation. Abdominal ultrasound revealed an irregular mass in the left adrenal gland. The ACTH stimulation test for aldosterone concentration did not reveal hyperaldosteronism. Unilateral adrenalectomy was performed and histopathology identified adrenal cortical carcinoma. All clinical signs of mineralocorticoid excess ceased after surgery.     

Steroid hormone concentration profiles in healthy intact and neutered dogs before and after cosyntropin administration

The purpose of this study was to determine steroid hormone concentration profiles in healthy intact and neutered male and female dogs. Seventeen intact female dogs, 20 intact male dogs, 30 spayed female dogs, and 30 castrated male dogs were used in this study. Serum samples were collected before and 1h after cosyntropin administration, and serum concentrations were determined for cortisol, progesterone, 17-OH progesterone (17-OHP), dehydroepiandrosterone sulfate (DHEAS), androstenedione, testosterone, and estradiol. Intact male dogs had greater concentrations of DHEAS, androstenedione, and testosterone. Intact female dogs had greater concentrations of progesterone. There was no significant difference in estradiol concentration among the four groups. Intact male dogs had lower concentrations of cortisol post-stimulation. DHEAS and testosterone did not increase in response to ACTH in intact males, and estradiol concentrations did not increase in response to ACTH in any group. Results from this study will enhance interpretation of suspected adrenal and/or gonadal disorders of dogs. Because estradiol concentrations were similar in all groups of dogs, measuring estradiol may not be a useful diagnostic test. Cortisol concentrations for intact male dogs with hyperadrenocorticism may be lower than those of female or neutered dogs.