[Acid phosphatase activity in the regenerating skin of rats under conditions of adrenalectomy and hyperfunction of the adrenals].
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OBJECTIVE: Primary aldosteronism is the most common endocrine form of secondary hypertension, but no single test or imaging method always identifies it. Identification of a unilateral overproduction of aldosterone due to Conn's adenoma or unilateral hyperplasia is of utmost importance to the surgeon. MATERIALS AND METHODS: We reviewed our experience with primary aldosteronism in 46 consecutive patients who had undergone adrenalectomy at the Surgical Pathology Institute, University of Padua since 1993. All the patients underwent a CT scan. Adrenal venous sampling was performed in those patients with negative or equivocal findings on imaging studies. RESULTS: Computed tomography was non-contributory in 12 patients and frankly misleading in 2 patients, demonstrating a probable mass lesion in the contralateral but not in the ipsilateral adrenal. Eighteen patients had selective venous sampling that was successful in altering the management of 14 cases. Eleven patients who biochemically had an adrenal adenoma, had normal/equivocal CT, while the remaining 3 had bilateral or contralateral adrenal masses. Venous sampling localized aldosterone secretion and an adenoma, less than 1 cm in diameter, was removed, curing their hypertension. Eleven patients were treated by open adrenalectomy and 35 by the lateral transperitoneal laparoscopic approach. Histological examination revealed 45 Conn's adenomas, of which 13 had a diameter of less than 1 cm (range 0.3-0.8), and 1 case of nodular hyperplasia. CONCLUSIONS: Patients who have equivocal or unexpected CT findings should proceed to hormonal localization. Adrenal venous sampling is essential in patients with equivocal CT scans to avoid unnecessary and inappropriate adrenalectomy.
BACKGROUND: Patients with endogenous hypercortisolism are thought to be at high risk for adrenalectomy and may experience significant postoperative surgical mortality/morbidity. METHODS: From 1981 through 1991, 91 patients underwent adrenal resection for endogenous hypercortisolism. Causes were adrenal-dependent Cushing's syndrome (50%), pituitary-dependent Cushing's syndrome (27%), and an ectopic adrenocorticotropic hormone-secreting tumor (23%). Causes of adrenal-dependent Cushing's syndrome were adrenocortical adenoma (72%), bilateral nodular hyperplasia (20%), and adrenocortical carcinoma (8%). Comparative mean length of hospitalization for patients undergoing unilateral anterior versus posterior approach was 8 versus 6 days, and bilateral anterior versus posterior was 11 versus 6 days. RESULTS: Operative mortality was 2.6%. Only one patient had a wound infection, and no patient had either a venous thrombosis or a pulmonary embolism. Delayed wound healing occurred in three patients. CONCLUSIONS: (1) Adrenal surgery can be performed today with low morbidity/mortality. (2) Although there is an effect of hypercortisolism on wound healing, infection, diabetes, hypertension, coronary artery disease, and pulmonary embolism, it was possible to perform adrenalectomy surgically with acceptable morbidity and mortality. (3) These results may serve as a standard against which laparoscopic adrenalectomy may be compared.
A dog was presented with a 2 year history of polyuria and polydipsia due to pituitary-dependent hyperadrenocorticism. A low-dose dexamethasone suppression test and measurement of plasma ACTH concentration confirmed the diagnosis. Treatment was instituted with mitotane at 44 mg/kg/day and then 88 mg/kg/d without complete resolution of signs. The dog collapsed with signs consistent with liver disease and was euthanased. Necropsy revealed a phaeochromocytoma of the left adrenal medulla with extensive metastases to the liver. A chromophobe adenoma of the pars intermedia of the pituitary was found.
Urinary free 11-hydroxycorticosteroid/creatinine ratios were determined in early morning urine samples from 113 females (age range 20-45 years) and 65 males (age range 22-45 years). Basal values in normal subjects fluctuated between 5 and 55 mumol/mol creatinine. In four patients in whom Cushing's syndrome was diagnosed, urinary free 11-hydroxycorticosteroid/creatinine ratios were greater than 85 mumol/mol creatinine. Administration of dexamethasone (0.5 mg/q.i.d.) to nine normal laboratory staff for two days resulted in a suppression of the urinary free 11-hydroxycorticosteroid/creatinine ratio to less than 50% of the mean basal value in all cases. This degree of suppression did not occur in two cases of Cushing's syndrome due to adrenal tumours.
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 i.m. 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.
OBJECTIVE: To describe the clinicopathologic characteristics of dogs with hyperadrenocorticism and concurrent pituitary and adrenal tumors. DESIGN: Retrospective study. ANIMALS: 17 client-owned dogs. PROCEDURE: Signalment, response to treatment, and results of CBC, serum biochemical analysis, urinalysis, endocrine testing, and histologic examinations were obtained from medical records of dogs with hyperadrenocorticism and concurrent adrenal and chromophobe pituitary tumors. RESULTS: On the basis of results of adrenal function tests and histologic examination of tissue specimens collected during surgery and necropsy, concurrent pituitary and adrenal tumors were identified in 17 of approximately 1,500 dogs with hyperadrenocorticism. Twelve were neutered females, 5 were males (3 sexually intact, 2 neutered); and median age was 12 years (range, 7 to 16 years). Hyperadrenocorticism had been diagnosed by use of low-dose dexamethasone suppression tests and ACTH stimulation tests. During high-dose dexamethasone suppression testing of 16 dogs, serum cortisol concentrations remained high in 11 dogs but decreased in 5 dogs. Plasma concentrations of endogenous ACTH were either high or within the higher limits of the reference range (12/16 dogs), within the lower limits of the reference range (2/16), or low (2/16). Adrenal lesions identified by histologic examination included unilateral cortical adenoma with contralateral hyperplasia (10/17), bilateral cortical adenomas (4/17), and unilateral carcinoma with contralateral hyperplasia (3/17). Pituitary lesions included a chromophobe microadenoma (12/17), macroadenoma (4/17), and carcinoma (1/17). CLINICAL IMPLICATIONS: Pituitary and adrenal tumors can coexist in dogs with hyperadrenocorticism, resulting in a confusing mixture of test results that may complicate diagnosis and treatment of hyperadrenocorticism.
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In a man of 48 who had suffered for a long time from a high arterial blood pressure, the autopsy revealed corticosteroma of the left and diffuse-nodular hyperplasia of the right adrenal glands. Both adrenals also had tumours of the sympathetic nervous system considered to be a gangliocytoneurilemmoma (angliocytic neurilemmoma) on the left and gangliocytoma on the right. The combination of morphological lesions, clinical data and laboratory examinations permit to state a combination of hypercorticism and hypercatecholaminemia.
OBJECTIVE: To evaluate low- and high-dose dexamethasone suppression tests for differentiating pituitary dependent hyperadrenocorticism (PDH) from adrenal tumor hyperadrenocorticism (ATH) in dogs. DESIGN: Prospective study. ANIMALS: 181 dogs with PDH and 35 dogs with ATH. PROCEDURE: Plasma cortisol concentrations from dogs with naturally developing hyperadrenocorticism were evaluated before, and 4 and 8 hours after administration of standard low- and high-doses of dexamethasone (0.01 mg/kg of body weight, i.v., and 0.1 mg/kg, i.v.; respectively). RESULTS: In response to the low-dose test, all but 3 dogs had an 8-hours post-dexamethasone plasma cortisol concentration that was consistent with a diagnosis of hyperadrenocorticism, that is, > or = 1.4 micrograms/dl. Criteria used to distinguish PDH from ATH in response to low-dose dexamethasone included a 4-hour post-dexamethasone plasma cortisol concentration < 50% of the basal value or < 1.4 micrograms/dl, or an 8-hours post-dexamethasone plasma cortisol concentration < 50% of the basal concentration. Criteria used to distinguish PDH from ATH in response to high-dose dexamethasone included 4- or 8-hour post-dexamethasone plasma cortisol concentrations < 50% of the basal concentration or < 1.4 micrograms/dl. In response to the low-dose test, 111 dogs met criteria for suppression (each had PDH). In response to the high-dose test, 137 dogs met criteria for suppression (2 had ATH, 135 had PDH). Twenty-six dogs with PDH (12%) had indications of adrenal suppression in response to high-dose but not low-dose testing. CLINICAL IMPLICATIONS: Low-dose dexamethasone test has value as a discrimination test to distinguish dogs with PDH from those with ATH. The high-dose test need only be considered in dogs with hyperadrenocorticism that do not have adrenal suppression in response to the low-dose test.
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