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Results for “Adrenocortical Hyperfunction”

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PubMed1998

Assessment of adrenal glucocorticoid function. Which tests are appropriate for screening?

The rapid cosyntropin stimulation test offers a simple means for detecting adrenal insufficiency. In contrast, assessment of suspected hypercortisolism (Cushing's syndrome) is difficult because cortisol levels fluctuate with intermittent release of corticotropin from the pituitary or from tumors. Also, a number of medications affect cortisol levels, leading to false-positive or false-negative results. The classic low-dose followed by high-dose dexamethasone test is cumbersome, and other, simpler studies, such as the overnight high-dose dexamethasone suppression test, may prove more practical and cost-effective. With both high and low levels of adrenal glucocorticoids, awareness and early recognition of the symptoms are important. An endocrinologist should be consulted when the overnight dexamethasone suppression test or the 24-hour urine cortisol collection is abnormal or if clinical suspicion is high despite normal results on screening tests.

Adrenal Cortex Function Tests↗
PubMedDate not supplied

The use of trilostane for the treatment of alopecia X in Alaskan malamutes.

Three Alaskan malamutes with hair loss and slightly elevated blood concentrations of 17-hydroxyprogesterone after stimulation with adrenocorticotropic hormone (ACTH) were treated with trilostane. Trilostane, an inhibitor of 3 beta-hydroxysteroid dehydrogenase, was given twice daily at a dose of 3.0 to 3.6 mg/kg per day orally for 4 to 6 months. Routine ACTH stimulation tests were performed over 8 months to evaluate the degree of adrenal function suppression. Treatment with trilostane led to complete hair regrowth in all three dogs within 6 months. No adverse effects associated with trilostane were recognized.

17-alpha-Hydroxyprogesterone↗
PubMedDate not supplied

Long-term efficacy of trilostane administered twice daily in dogs with pituitary-dependent hyperadrenocorticism.

Trilostane is considered an efficacious and safe medication for canine pituitary-dependent hyperadrenocorticism (PDH). Its recommended frequency of administration is once daily. In this prospective study, the efficacy, toxicity, and long-term outcome of trilostane administered twice daily per os were evaluated in 44 dogs with PDH. Mean initial dose was 3.1 mg/kg q 12 hours, and mean final dose was 3.2 mg/kg q 12 hours. The final total daily dose was lower than previously reported for once-daily administration. The mean survival time for affected dogs was 930 days.

Adrenocortical Hyperfunction↗
PubMedDate not supplied

Acute hepatopathy associated with mitotane administration in a dog.

An adult dog with a persistent elevation in alkaline phosphatase enzyme activity was started on mitotane for suspected hyperadrenocorticism. One month later, the dog was presented for intermittent anorexia and acute icterus. The dog's liver enzyme activities and total bilirubin were markedly elevated, prothrombin time was prolonged, and blood urea nitrogen and glucose were low. Histopathology revealed marked, centrilobular, hepatocellular loss. After discontinuation of the mitotane, the dog recovered with supportive care and was normal 3 months later, which was consistent with mitotane-associated hepatic failure.

Adrenocortical Hyperfunction↗
PubMedDate not supplied

Iatrogenic hyperadrenocorticism in 12 cats.

Iatrogenic hyperadrenocorticism is an extremely rare condition in cats. Twelve cats with a medical history of progressive skin lesions and long-term treatment with corticosteroids were retrospectively studied. Noncutaneous signs in the cats were variable and included anorexia, lethargy, polydipsia, polyuria, and atrophy of the thigh muscles. Laboratory abnormalities included leukocytosis, elevated alanine aminotransferase levels, and hyperglycemia. Transient diabetes mellitus was a secondary complication in four cats, and transient hypothyroidism was suspected in four cats. The mean time for regression of signs was 4.9 months after corticosteroid withdrawal.

Adrenal Cortex Hormones↗
PubMedDate not supplied

Clinical aspects and surgical treatment of hyperadrenocorticism in the domestic ferret: 94 cases (1994-1996).

The signalment, clinical findings, laboratory values, and histopathological results of 96 ferrets with signs (i.e., bilaterally symmetrical alopecia, return to male sexual behavior, or an enlarged vulva) suggestive of hyperadrenocorticism were evaluated retrospectively. Of these 96 ferrets, 94 (98%) were diagnosed with hyperadrenocorticism histologically. Treatment consisted of unilateral adrenalectomy for unilateral tumors (84%) and subtotal bilateral adrenalectomy for bilateral adrenal tumors (16%). The histopathological diagnosis included nodular hyperplasia (56%), adrenocortical carcinoma (26%), and adrenocortical adenoma (16%). Common concurrent diseases included splenomegaly (87%), islet-cell tumor (27%), and cardiomyopathy (10%).

Adenoma↗
PubMedDate not supplied

Diabetes mellitus, hyperadrenocorticism, and hypothyroidism in a dog.

An unusual combination of three endocrinopathies found in one dog is described. A six-year-old, spayed female, mixed-breed dog presented with polyuria, polydipsia, polyphagia, and weight loss. She was diagnosed with diabetes mellitus but was suspected of having insulin resistance and was diagnosed subsequently with hyperadrenocorticism. Persistent hypercholesterolemia led to the suspicion and eventual diagnosis of hypothyroidism. The dog has responded well to medical therapy, and her clinical signs and biochemical changes have resolved. A literature search did not identify a similar-reported polyendocrinopathy.

Adrenocortical Hyperfunction↗
PubMedDate not supplied

Ultrasonographic characteristics of both adrenal glands in 15 dogs with functional adrenocortical tumors.

Ultrasonographic examination of both adrenal glands was performed in 15 dogs with functional adrenocortical tumors (FAT). Bilateral adrenal tumors were diagnosed in three of 15 dogs, and unilateral tumors were diagnosed in 12 of 15 dogs. Adrenal tumors were characterized by adrenal gland enlargement with loss of the normal shape and parenchymal structure. The contralateral adrenal gland could be imaged in all dogs with unilateral tumors. Based on size, shape, and parenchymal structure, the contralateral adrenal gland was similar to adrenal glands of normal dogs. The results of this study show that: 1) both adrenal glands should be imaged routinely in dogs with hyperadrenocorticism; 2) bilateral adrenocortical tumors seem to be more frequent than previously assumed; 3) one normal adrenal gland does not exclude the existence of a contralateral FAT; and 4) the functional atrophy of the contralateral adrenal gland in dogs with FAT may not be apparent ultrasonographically.

Adrenal Cortex Neoplasms↗
PubMedDate not supplied

Iatrogenic hyperadrenocorticism in 28 dogs.

Twenty-eight dogs with iatrogenic hyperadrenocorticism were studied. The most common clinical signs were cutaneous lesions (27/28), polydipsia (21/28), polyuria (19/28), and lethargy (16/28). The most predominant findings on biochemical profile were elevated alkaline phosphatase (ALP, 15/28) and alanine transferase (ALT, 14/28); hypercholesterolemia (14/28); elevated aspartate transferase (AST, 12/28); and elevated triglycerides (12/18). Baseline cortisol levels of all 28 dogs were at the lower end of the reference range and exhibited suppressed or no response to adrenocorticotropic hormone (ACTH) stimulation. The mean time for each dog to show initial improvement of clinical signs after corticosteroid withdrawal was six weeks, with another mean time of 12 weeks to demonstrate complete remission.

Adrenal Cortex↗
PubMedDate not supplied

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.

Adenocarcinoma↗