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PubMed1976

[Effect of ethyl ether of p-chlorphenoxyisobutyric acid on the glucocorticoid function of the adrenal cortex of guinea pigs].

In administration to quinea pigs of ethyl-p-chlorophenoxyisobutyrate daily in a dose of 0.2 g/kg per os for 15-26 days decreased the 17-OHCS concentration in the peripheral blood plasma. A fall of the urinary excretion of individual 17-OHCS occurred chiefly at the expense of free unchanged cortisol, tetrahydrocortisol and tetrahydro-11-desoxycortisol. The zona fasciculate displays the abundance of the sudanophilic material. A test with ACTH demonstrated that the present functional reserves of the adrenal cortex failed to change under the effect of the preparation. The content of NEFA decreased in the blood serum; as to cholesterol level - it reamined unchanged. Possible mechanisms of the action of the preparation and prospects of its use for the treatment of hypercorticism are discussed.

17-Hydroxycorticosteroids↗
PubMed1990

Problems associated with medical therapy of canine hyperadrenocorticism.

The cause of hyperadrenocorticism determines treatment. Pituitary-dependent hyperadrenocorticism (PDH) can be treated surgically with bilateral adrenalectomy or hypophysectomy, or it can be managed medically with the adrenocorticolytic agent o,p'DDD or the cortisol synthesis inhibitor ketoconazole. Unilateral adrenocortical tumors should be surgically removed because of metastatic potential, although medical therapy has been used with some success. Regardless of the treatment method chosen, canine Cushing's syndrome cannot be treated easily, inexpensively, or without close monitoring and follow-up.

Adrenal Cortex Neoplasms↗
PubMed1990

Comparison of two low-dose dexamethasone suppression protocols as screening and discrimination tests in dogs with hyperadrenocorticism.

Two low-dose dexamethasone suppression test protocols were evaluated in 18 dogs with hyperadrenocorticism (14 dogs with pituitary-dependent hyperadrenocorticism [PDH] and 4 dogs with adrenocortical tumor) and in 5 healthy control dogs. Blood was obtained immediately before and 2, 4, 6, and 8 hours after IV administration of either 0.01 mg of dexamethasone sodium phosphate/kg of body weight or 0.015 mg of dexamethasone polyethylene glycol/kg. At 8 hours after dexamethasone administration, 18 of 18 (100%) dogs with hyperadrenocorticism given the sodium phosphate preparation and 16 of 18 (89%) affected dogs given the polyethylene glycol preparation failed to have suppression of plasma cortisol concentration (less than 1.4 micrograms/dl). Plasma cortisol concentration was suppressed to less than 1.4 micrograms/dl at 2, 4, and/or 6 hours after administration of either dexamethasone preparation in 5 of 14 dogs with PDH and to less than 50% of baseline cortisol concentration in 10 of 14 dogs with PDH. Suppression, as identified by these 2 criteria, was not observed at 2, 4, 6, or 8 hours after administration of either dexamethasone preparation in dogs with adrenocortical tumor. For both protocols, the 8-hour plasma cortisol concentration was suppressed to less than 1.4 micrograms/dl and to less than 50% of baseline in the 5 control dogs. Both protocols were comparable for use as screening tests in establishing a diagnosis of hyperadrenocorticism. Suppression of plasma cortisol concentration to less than 50% of baseline (or less than 1.4 micrograms/dl) during the test was consistent with diagnosis of PDH. Failure to have such suppression, however, was observed in dogs with PDH as well as in those with adrenocortical tumor.

Adrenal Cortex Function Tests↗
PubMedDate not supplied

[Clinical value of radionuclide imaging in the diagnosis of the adrenal cortex lesions].

Results of using radioisotopic visualization of the adrenal glands together with the hormonal profile determination ACTH, renin, aldosterone, cortisol) for the diagnosis of the adrenal gland affections are presented. Parameters of the scintigraphic appearance of the affected adrenal cortex were developed to distinguish six types of scintigraphic patterns of the adrenal gland, which were the most frequent. Clinical analysis of the results of the examination of patients indicated Conn's disease in 24 patients (it was verified during the operation), 12 had unilateral corticosteroma of the adrenal gland, 8 suffered from residual adrenal gland tissue, and 2 had metastases of malignant tumours of the adrenal glands. Accumulation of radiopharmaceutical preparations into the corpus luteum was revealed in one case.

19-Iodocholesterol↗
PubMed1990

Plasma cortisol response to ketoconazole administration in dogs with hyperadrenocorticism.

The effect of orally administered ketoconazole on plasma cortisol concentration in dogs with hyperadrenocorticism was evaluated. Every 30 minutes from 0800 hours through 1600 hours and again at 1800 hours, 2000 hours, and 0800 hours the following morning, 15 clinically normal dogs and 49 dogs with hyperadrenocorticism had plasma samples obtained and analyzed for cortisol concentration. The mean (+/- SD) plasma cortisol concentration for the initial 8-hour testing period was highest in 18 dogs with adrenocortical tumor (5.3 +/- 1.6 micrograms/dl), lowest in 15 control dogs (1.3 +/- 0.5 micrograms/dl), and intermediate in 31 dogs with pituitary-dependent hyperadrenocorticism (PDH; 3.4 +/- 1.2 micrograms/dl). Results in each of the 2 groups of dogs with hyperadrenocorticism were significantly (P less than 0.05) different from results in control dogs, but not from each other. The same cortisol secretory experiment was performed, using 8 dogs with hyperadrenocorticism (5 with PDH; 3 with adrenocortical tumor) before and after administration at 0800 hours of 15 mg of ketoconazole/kg of body weight. Significant (P less than 0.05) decrease in the 8-hour mean plasma cortisol concentration (0.9 +/- 0.2 microgram/dl) was observed, with return to baseline plasma cortisol concentration 24 hours later. Twenty dogs with hyperadrenocorticism (11 with PDH, 9 with adrenocortical tumor) were treated with ketoconazole at a dosage of 15 mg/kg given every 12 hours for a half month to 12 months. The disease in 2 dogs with PDH failed to respond to treatment, but 18 dogs had complete resolution of clinical signs of hyperadrenocorticism and significant (P less than 0.05) reduction in plasma cortisol responsiveness to exogenous adrenocorticotropin (ACTH).(ABSTRACT TRUNCATED AT 250 WORDS)

Adenoma↗
PubMedDate not supplied

[Similarity and differences of the pathogenesis of Itsenko-Cushing syndrome variants].

Proceeding from a study of the results of the investigation of 152 patients with Icenko-Cushing's syndrome the authors have arrived at the conclusion that hyperplasia, clear cell adenoma of monomorphous structure, dark cell and mixed adenomas of polymorphous structure, cancer of the adrenal cortex are different stages of a common pathological process. Such formation of morphological changes in the adrenal gland is one of the ways of development of Icenko-Cushing's syndrome. To confirm the proposed concept of the pathogenesis of this disease the authors provide some evidence of hyperplasia or the normal structure of nontumorous adrenocortical tissue in adenoma and cancer, of the absence of difference in a rise of the mean ACTH level in the blood in hyperplasia and different adrenocortical tumors. An increase in ACTH production in most of the patients should be regarded as one of the primary factors of the above morphological changes. The absence of suppression of 17-oxycorticosteroid excretion with urine in a test with 8 mg of dexamethasone in most of the patients with dark cell and mixed adenoma of polymorphous structure and adrenocortical cancer suggests a possibility of the development of certain autonomy of these neoplasms.

17-Hydroxycorticosteroids↗
PubMed1988

Diagnostic value of alkaline phosphatase isoenzyme separation by affinity electrophoresis in the dog.

Affinity electrophoresis, using wheat germ lectin, was used to separate the alkaline phosphatase isoenzymes in the sera of 150 dogs with alkaline phosphatase values greater than or equal to 150 IU/L. The method provided clearer separation of the liver, bone and steroid-induced alkaline phosphatase isoenzymes commonly observed in canine serum, compared to conventional cellulose acetate electrophoresis. The dogs were divided into four patient groups determined by previous corticosteroid treatment, evidence of elevated endogenous corticosteroid levels, age and alanine aminotransferase values. The isoenzyme pattern of each patient was qualitatively assessed. The isoenzyme pattern most frequently observed was greater than 50% steroid induced alkaline phosphatase, which was present in 76 of 150 dogs. This pattern was observed in 18 of 22 dogs receiving corticosteroid therapy, two of three dogs with hyperadrenocorticism, and in dogs with a variety of other diagnoses. The majority of immature dogs (12 of 20) had an isoenzyme pattern consisting of greater than 50% bone. The majority of dogs with active hepatocellular injury (16 of 27) had greater than 50% liver isoenzyme. The isoenzyme pattern was not specific for certain diseases, therefore the diagnostic usefulness is limited. However the isoenzyme result is useful in some cases to determine which further diagnostic tests are indicated, and to determine the source of alkaline phosphatase elevation.

Adrenal Cortex Hormones↗
PubMed1986

[Severe hypertrophic cardiomyopathy associated with an adrenocortical adenoma].

A case of severe asymmetrical hypertrophic cardiomyopathy occurring in a 11 month-old infant presenting with adrenocortical adenoma is reported. Cardiac involvement, as shown by echocardiography, recovered after complete excision of the tumor. Despite few published cases, the etiology of the associated cardiomyopathy is discussed.

Adenoma↗
PubMed1986

Use of x-ray-computed tomography as an aid in localization of adrenal masses in the dog.

Four dogs with clinical evidence of hyperadrenocorticism were evaluated by use of x-ray-computed tomography (CT). Adrenal masses were identified accurately and localized. Unilateral adrenal masses were diagnosed accurately in dogs 1, 2, and 3 and were removed surgically via a paracostal retroperitoneal approach to the adrenal gland. Using CT and IV contrast medium, the adrenal mass in dog 3 also was accurately diagnosed as being highly vascular. The histopathologic diagnosis was adrenal adenoma in dogs 1, 2, and 3. In dog 4, the CT-roentgen diagnosis was asymmetric bilateral adrenal enlargement. Necropsy examination of dog 4 indicated moderate enlargement of the left adrenal gland and severe enlargement of the right adrenal gland. Results of microscopic examination indicated chronic inflammation of the left adrenal gland and adenocarcinoma of the right adrenal gland. Use of CT facilitated localization of adrenal masses and fulfilled the needs of a localizing technique. A unilateral mass can be removed surgically via a limited exposure, retroperitoneal incision on the affected side of the animal instead of removal via abdominal laparotomy, which is more invasive. Advantages of CT can reduce the needs of other imaging modalities for the localization of adrenal masses.

Adrenal Cortex Neoplasms↗
PubMedDate not supplied

[Interrelation of sex hormone-binding globulin and the androgen-estrogen balance in patients with hypercorticism].

The concentration of testosterone and estradiol in the blood plasma and the binding capacity of testosterone-estradiol binding globulin (TEBG) were studied in 30 women and 6 men with Icenko-Cushing's disease in the active phase and in 24 women with hormonally active adrenal tumors. In hypercorticism against a background of unchanged of lowered concentration of plasma estradiol there was a decrease in the concentration of testosterone and an increase in the testosterone-estradiol binding capacity (TEBC) in men and an increase in the concentration of testosterone and a decrease in TEBC in women. The authors have assumed that the testosterone/TEBC ratio reflects more accurately change in the dynamics of androgens than isolated concentrations of testosterone and TEBG, and recommended its determination for the assessment of the body androgenic saturation in disturbed function of the adrenal or sex glands.

Adolescent↗