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The efficacy of L-Deprenyl in dogs with pituitary-dependent hyperadrenocorticism.

Ten dogs with pituitary-dependent hyperadrenocorticism (PDH) received 2 mg/kg of L-Deprenyl once daily for 6 months. Monthly patient assessment consisted of evaluation of the owner's daily observation protocol, a standardized owner questionnaire, physical examination, CBC, biochemical profile, determination of the urine cortisol/creatinine ratio (UC/C), low-dose dexamethasone suppression (LDDS) test, corticotropin releasing hormone (CRH) test, and adrenal ultrasonography. At the beginning and the end of the study, an adrenocorticotropic hormone (ACTH) stimulation test and computed tomography also were performed. Two dogs developed neurologic signs and 2 dogs developed acute pancreatitis. An increase in activity, decrease in polyphagia, and decrease in panting were reported by 6, 4, and 2 owners, respectively. Seven owners believed that water intake decreased, but this was confirmed in only 3 dogs. Water intake increased in 2 dogs and remained unchanged in 5 dogs. The condition of the hair coat and skin improved in 2 dogs, worsened in 3, and remained unchanged in 5. Urine specific gravity, urine osmolality, ACTH test results, UC/C, and adrenal gland size did not change significantly throughout the study. In 4 of 8 dogs, LDDS was abnormal at the start of the study but normal at the end of the study, and in 2 dogs, the opposite occurred. Marked individual variation was noted in the CRH test, with a tendency for smaller increases in ACTH toward the end of the study. A marked increase in hypophyseal tumor size occured in 4 dogs. Treatment with L-Deprenyl resulted in improvement, deterioration, and stagnation of clinical signs in 2, 4, and 4 dogs, respectively. The results of this study indicate that L-Deprenyl cannot be recommended as the sole treatment for canine PDH.

Adrenal Glands↗

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↗

[The place of adrenal angiography (phlebography and arteriography) in the diagnostic stepwise program in arterial hypertension].

Arteriographical and phlebographical methods are distinctly suited for the diagnostics of the adrenal glands in the stop program of the combat against hypertension. Hypervascular tumours of the adrenal medulla, especially phaeochromocytomata may be established arteriographically relatively certainly. Avascular processes of the adrenal cortex, however, are better to be diagnosed by the selective phlebography of the adrenal glands. The phlebography is also suited for the planimetric determination of the size. The following uncorrected normal values were established: on the left m1 = 10.58 +/- 1.17 cm2, on the right m2 = 6.95 +/- 1.39 cm2. The mean value of normal couples of adrenal glands is M = 18.17 +/- 1.96 cm2. The left adrenal gland is statistically significantly larger than the right one (p greater than 0.001). In 214 patients altogether 44 selective arteriographies and 276 selective phlebographies of the adrenal glands were performed. As angiographical basis examination of all patients was at first performed an abdominal aortography or an angiography of the kidneys. The phlebographical diagnostics was successful on the left in 98.7% and on the right in 90.4% of the cases. 72 patients had pathological processes of the adrenal glands, out of them 20 times a solitary adenoma of the adrenal glands was present. 38 patients had a one- or double-sided hyperplasia, and 4 patients had a phaeochromocytoma. In 10 other cases more infrequent changes were found.

Adenoma↗

Concurrent pituitary and adrenal tumors in dogs with hyperadrenocorticism: 17 cases (1978-1995).

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.

Adenoma↗

[Value of retropneumoperitoneum in the exploration of Cushing's syndrome. 155 cases].

The study is based upon 155 cases of Cushing's syndrome and shows the diagnostic value ognosis of the suprarenal lesion responsible was possible. Bilateral suprarenal hyperplasia was always recognised with accuracy. Pneumoretroperituneum is the technique of choice for the surveillance of the therapeutic effects of synthetic anti-cortisols (especially O.P.'D.D.D.).

Adenoma↗

Effect of combination of stresses on myocardial metabolism.

The effect of hypoxia, exercise, and thermal stress on myocardial metabolism have been widely investigated, but little attention has been paid to studying the effects of a combination of these stress. The influence of hypoxia as modified by physical exertion (swimming) and cold stress was therefore studied. The parameters investigated included myocardial glycogen and noradrenaline, serum free fatty acid, adrenal ascorbic acid, and adrenal weight. It was observed that maximal stress was produced when hypoxia was combined with physical exertion. No suppression of cold-induced lipolysis by hypoxia was observed, in contrast to previously reported observations. Maximal depletion of cardiac blycogen and cardiac noradrenaline was noted in hypoxic exercise. Adrenal overactivity was not found to be related to any particular stress but was seen to be proportional to the severity of the stress applied.

Adrenal Glands↗

Cushing's syndrome.

Sixteen cases of verified Cushing's syndrome, and twelve cases of probable Cushing's syndrome were reviewed and data on them were compared with various reports on Cushing's syndrome in the literature. The diagnosis hinges upon a high index of suspicion, and one or several of the major criteria may be lacking. Ultimate establishment of correct diagnosis should be based largely on the clinical features, although stimulation and suppression tests may help to confirm a clinical diagnosis. In well-established clinical cases, with borderline laboratory confirmation, exploration may be justified, especially if tests fail to identify a specific cause. In cases of adrenal cortical tumor, all pathological tissue should be removed if possible, with great care to support and stimulate the remaining atrophic adrenal gland during and following operation. In cases of bilateral adrenal cortical hyperplasia, the problem is one of how much to remove. At present most investigators advocate radical subtotal resection, leaving less than 10 per cent of one side.

Adrenal Cortex Neoplasms↗

[Cushing's syndrome due to bilateral adrenal macronodular hyperplasia. From ACTH-dependent hypercortisolism to ACTH-independent hypercortisolism].

A 35 year old female with Cushing's syndrome and bilateral adrenal macronodular hyperplasia, in whom a change from ACTH dependency to autonomy was observed, is presented. The diagnosis of Cushing's syndrome was based on the failure of suppression of urinary ketogenic steroids (17 KCS) and free cortisol (uF) with the administration of 2 mg of dexamethasone daily for 2 days. CT scan of the abdomen showed adrenal bilateral multinodular hyperplasia and the sellar CT scan was normal. Initially 8 mg for 2 days of dexamethasone suppressed 17 KCS and uF; however, a few months later this effect was lost as well as the effect of endogenous ACTH on cortisol. Bilateral adrenalectomy was carried out, prior to attainment of normal cortisol levels with Ketoconazole. The adrenal glands has multiple nodules and they weighed 10 and 21 grams. Her postoperative plasmatic cortisol levels were imperceptible. Physiopathologic mechanisms involved in bilateral macronodular adrenal hyperplasia are reviewed.

Adrenal Glands↗