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Introduction Primary adrenal tumors account for < 2% and about 0.2% of canine and feline neoplasia, respectively. 1 Adrenalectomy has been associated with an overall favorable long-term outcome regardless of the benign or malignant nature of
invasion occurs in approximately 25% of adrenal tumors in dogs and has been seen in 4 of 21 cases of histologically confirmed functional adrenal neoplasia in cats. 9,11,12,26 At this time, in agreement with the conclusions of Jiménez Peléez et al, 23
Introduction Adrenalectomy is the treatment of choice for adrenal tumors in canines. 1 – 4 Surgical treatment of unilateral adrenal gland tumors has been well described in the veterinary literature, and unilateral laparoscopic adrenalectomy
To the author's knowledge, sparse information regarding surgical techniques for removal of adrenal tumor thrombi that extend within the vena cava distal to the diaphragm in dogs has been published. Several reports 1–4 mention extensive adrenal tumor
of canine adrenal tumor cells, human H295R adrenocortical carcinoma cells were used to investigate the effect of lignans and melatonin on adrenocortical function. The H295R cells are capable of producing mineralocorticoids, corticosteroids, androgens
hormones. 13,18,19 Medical treatment does not appear to have a clinically important effect on the size of the developing adrenal tumor. Surgical treatment, on the other hand, offers the potential for a complete cure, although it does not prevent the
associated with anesthesia and surgical removal of an adrenocortical tumor commonly encountered in dogs with NOH. Each of the 9 ATH dogs successfully underwent adrenal tumor extirpation 8 to 10 weeks after beginning trilostane treatment. The goal of treatment
Abstract
Objective—To evaluate adrenal sex hormone concentrations in response to ACTH stimulation in healthy dogs, dogs with adrenal tumors, and dogs with pituitary- dependent hyperadrenocorticism (PDH).
Design—Prospective study.
Animals—11 healthy control dogs, 9 dogs with adrenal-dependent hyperadrenocorticism (adenocarcinoma [ACA] or other tumor); 11 dogs with PDH, and 6 dogs with noncortisol-secreting adrenal tumors (ATs).
Procedure—Hyperadrenocorticism was diagnosed on the basis of clinical signs; physical examination findings; and results of ACTH stimulation test, low-dose dexamethasone suppression test, or both. Dogs with noncortisol-secreting ATs did not have hyperadrenocorticism but had ultrasonographic evidence of an AT. Concentrations of cortisol, androstenedione, estradiol, progesterone, testosterone, and 17-hydroxyprogesterone were measured before and 1 hour after IM administration of 0.25 mg of synthetic ACTH.
Results—All dogs with ACA, 10 dogs with PDH, and 4 dogs with ATs had 1 or more sex hormone concentrations greater than the reference range after ACTH stimulation. The absolute difference for progesterone, 17-hydroxyprogesterone, and testosterone concentrations (value obtained after ACTH administration minus value obtained before ACTH administration) was significantly greater for dogs with ACA, compared with the other 3 groups. The absolute difference for androstenedione was significantly greater for dogs with ACA, compared with dogs with AT and healthy control dogs.
Conclusions and Clinical Relevance—Dogs with ACA secrete increased concentrations of adrenal sex hormones, compared with dogs with PDH, noncortisol-secreting ATs, and healthy dogs. Dogs with noncortisol-secreting ATs also have increased concentrations of sex hormones. There is great interdog variability in sex hormone concentrations in dogs with ACA after stimulation with ACTH. (J Am Vet Med Assoc 2005;226:556–561)
Abstract
Objective—To evaluate the clinical and endocrine responses of ferrets with adrenocortical disease (ACD) to treatment with a slow-release implant of deslorelin acetate.
Animals—15 ferrets with ACD.
Procedure—Ferrets were treated SC with a single slow-release, 3-mg implant of deslorelin acetate. Plasma estradiol, androstenedione, and 17-hydroxyprogesterone concentrations were measured before and after treatment and at relapse of clinical signs; at that time, the adrenal glands were grossly or ultrasonographically measured and affected glands that were surgically removed were examined histologically.
Results—Compared with findings before deslorelin treatment, vulvar swelling, pruritus, sexual behaviors, and aggression were significantly decreased or eliminated within 14 days of implantation; hair regrowth was evident 4 to 6 weeks after treatment. Within 1 month of treatment, plasma hormone concentrations significantly decreased and remained decreased until clinical relapse. Mean time to recurrence of clinical signs was 13.7 ± 3.5 months (range, 8.5 to 20.5 months). In 5 ferrets, large palpable tumors developed within 2 months of clinical relapse; 3 of these ferrets were euthanatized because of adrenal gland tumor metastasis to the liver or tumor necrosis.
Conclusions and Clinical Relevance—In ferrets with ACD, a slow-release deslorelin implant appears promising as a treatment to temporarily eliminate clinical signs and decrease plasma steroid hormone concentrations. Deslorelin may not decrease adrenal tumor growth in some treated ferrets. Deslorelin implants may be useful in the long-term management of hormone-induced sequelae in ferrets with ACD and in treatment of animals that are considered at surgical or anesthetic risk. (Am J Vet Res 2005;66:910–914)
Abstract
Objective—To determine testing protocols used by board-certified internists and dermatologists for diagnosis of hyperadrenocorticism (HAC) in dogs.
Design—Survey.
Study Population—Board-certified internists and dermatologists.
Procedure—A questionnaire was mailed to 501 specialists to gather information pertaining to diagnosis of HAC.
Results—206 surveys were returned. Only 26% of respondents indicated they would screen a dog for HAC if the dog had only a few laboratory abnormalities consistent with HAC and no clinical signs consistent with the disease; 31% indicated they would not, and 43% indicated they would sometimes. Overall, 55% of respondents indicated they preferred to use the lowdose dexamethasone suppression test for routine screening of dogs suspected to have HAC. However, many respondents indicated they would use a different screening test than usual in particular circumstances. Sixty-eight percent of respondents indicated they would perform a second screening test for confirmation if results of an initial screening test were positive but there were few clinical or laboratory abnormalities consistent with HAC. Most respondents used some sort of test to differentiate pituitary-dependent HAC from HAC secondary to an adrenal tumor (AT), but no 1 test was clearly preferred. Ultrasonography was commonly used, whereas computed tomography and magnetic resonance imaging were not, even if available.
Conclusions and Clinical Relevance—Results suggest that the low-dose dexamethasone suppression test is the test most commonly used to screen dogs for HAC but that other tests may be used in certain circumstances. A variety of tests were used to differentiate pituitary-dependent HAC from HAC secondary to an AT. (J Am Vet Med Assoc 2002;220:1643–1649)
