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Results for “ADRENAL GLAND HYPERFUNCTION”

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Cushing syndrome, sexual precocity, and polyostotic fibrous dysplasia (Albright syndrome) in infancy.

The sexual precocity of polyostotic fibrous dysplasia is occasionally accompanied by other endocrine disorders, but in only two previous instances has Cushing syndrome been reported. The history of a 6-month-old girl is presented, in whom this syndrome was complicated by congenital Cushings syndrome. Although endocrinopathies of polyostotic fibrous dysplasia have usually been ascribed to a central (hypothalamic) origin, the findings in this patient suggest autonomous hyperfunction of the peripheral endocrine glands, with the Cushing syndrome caused by hyperplastic nodules in the adrenal glands and the precocity by luteinized follicular cysts of the ovary.

Adrenal Glands↗

Adrenal myelolipoma.

A myelolipoma of the adrenal gland is reported. Diagnostic features include (1) hyperlucent mass on intravenous pyelography with renal displacement, (2) an avascular mass on arteriography and venography, (3) solid tissue mass on B-mode ultrasonography, and (4) no clinical or chemical evidence of adrenal hyperfunction.

Adrenal Gland Neoplasms↗

[Reaction of the adrenal glands to laser puncture during combined effects of ionizing radiation].

In experiments in mature female guinea pigs it was shown that a combination of external X-radiation (12.9 mC/kg) and incorporated 131I (6.5 mCi/kg) induced morphohistochemical changes in the adrenals at remote times (6 months) which indicate the state of the organ functional tension. Laser biostimulation in these conditions promotes a transition of the process of cell hyperfunctioning to the depletion and functional deficiency.

Adrenal Glands↗

Coexistence of pituitary adrenocorticotropin-dependent Cushing's syndrome with a solitary adrenal adenoma.

A 45-yr-old woman presented with a 2-hr history of Cushing's syndrome. Baseline cortisol and ACTH levels were elevated and lacked a normal circadian rhythm. Dynamic testing of her pituitary-adrenal function revealed positive responses to metyrapone and synthetic ACTH and suppression with high doses of dexamethasone. The finding of asymmetrical adrenal uptake of 6-[131I]methyl-19-nor-cholesterol and a tumor image in the right adrenal on venography led to the preoperative diagnosis of pituitary ACTH-dependent adrenal hyperfunction coexisting with a right adrenal adenoma. Surgical resection of the right adrenal demonstrated a solitary 39-g nodule, 4 cm in diameter. There were no additional nodules present in the surrounding cortex. When incubated in vitro, both the adenoma and the surrounding tissue were functional and responsive to ACTH. This was in contrast to the lack of response to ACTH in vitro of similar tissues removed from two other patients with ACTH-independent adrenal adenomas. We suggest that this case represents a transition between pituitary ACTH-dependent bilateral adrenocortical hyperfunction and solitary adrenal adenoma.

Adenoma↗

Scintigraphic patterns of adrenocortical carcinoma: morpho-functional correlates.

OBJECTIVE: Adrenocortical scintigraphy has demonstrated clinical utility in the morpho-functional characterization of adrenal tumors. The aim of this study was to identify possible relationships between the scintigraphic pattern and endocrine and/or morphological data in a series of adrenocortical carcinomas. DESIGN AND METHODS: Twenty-one patients with adrenocortical carcinoma (11 nonfunctioning and 10 hormone-secreting) were investigated with 75Se-methyl-nor-cholesterol scintigraphy. Clinical, hormonal, radiological, and pathological data were analyzed. RESULTS: The adrenal mass showed no radiocholesterol uptake in 18 cases (11 nonfunctioning and 7 functioning lesions). Contralateral normal adrenal gland was visualized in all patients with nonfunctioning tumors, whereas classic bilateral nonvisualization was observed in the 7 cases with hyperfunctioning masses. Three patients with cortisol-producing carcinomas showed radiotracer uptake by the mass, without visualization of the contralateral gland. At histology, the tumors were shown to be undifferentiated adrenocortical carcinomas; they had an aggressive clinical behavior. CONCLUSIONS: Radiocholesterol scintigraphy has an important role in diagnosing adrenocortical carcinomas, which typically are not visualized. However, 30% of hypersecreting adrenocortical carcinomas show an atypical increased tracer uptake, not predictive of the biochemical and histological features of the tumor.

Adolescent↗

Results of clinical examinations, laboratory tests, and ultrasonography in dogs with pituitary-dependent hyperadrenocorticism treated with trilostane.

OBJECTIVE: To determine the efficacy of trilostane, a 3beta-hydroxysteroid dehydrogenase inhibitor, in dogs with pituitary-dependent hyperadrenocorticism (PDH). ANIMALS: 11 dogs with PDH. PROCEDURE: The initial dose of trilostane was 30 mg, PO, q 24 h for dogs that weighed < 5 kg and 60 mg, PO, q 24 h for dogs that weighed > or = 5 kg. A CBC count, serum biochemical analyses, urinalysis, ACTH stimulation test, and ultrasonographic evaluation of the adrenal glands were performed in each dog 1, 3 to 4, 6 to 7, 12 to 16, and 24 to 28 weeks after initiation of treatment. RESULTS: All dogs responded well to treatment. All had reductions in polyuria-polydipsia and panting and an increase in activity. Polyphagia decreased in 9 of 10 dogs, and 9 of 11 dogs had improvement of coat quality and skin condition. Concentration of cortisol after ACTH stimulation significantly decreased by 1 week after initiation of treatment. After treatment for 6 months, clinical signs resolved in 9 dogs. In the other 2 dogs, marked clinical improvement was reported for 1 dog, and moderate improvement was reported in the other dog. Ultrasonographically, there was a considerable change in the parenchyma and an increase in size of the adrenal glands. Adverse effects consisted of 1 dog with transient lethargy and 1 dog with anorexia. CONCLUSIONS AND CLINICAL RELEVANCE: Trilostane is an efficacious and safe medication for treatment of dogs with PDH. Additional studies in a larger group of dogs and characterization of progressive changes in adrenal glands are needed.

Adrenocortical Hyperfunction↗

Experimental studies on perinatal development of adrenal and thyroid glands in the rat.

In the rat, as regards the adrenal gland, (1) during the fetal period, the adrenal cortex first begins to develop autonomically, (2) subsequently, the cortex comes under the control of the hypophysis, (3) later, the hypophysial-adrenal system comes under hypothalamic regulation, (4) after birth, the adrenal gland becomes shrunken temporarily, accompanied by an abrupt rise and a subsequent decline of the plasma corticosterone concentrations (PCC) just before and after birth. The rise and decline of PCC is probably responsible for the temporary hiatus of the hypothalamic-hypophysial activity, and (5) a preventive therapy of the abrupt rise of PCC allows the adrenal gland to escape neonatal shrinkage. As to the thyroid gland, (1) the initial formation of thyroid follicles is independent of thyroid-stimulating hormone (TSH), (2) follicles, once developed, are capable of responding to TSH, (3) the fetal hypophysial-thyroid function is independent of the hypothalamic regulation, (4) the early neonatal thyroid gland does not seem to undergo hyperfunctioning, and (5) hypothalamic regulation of the thyroid gland seems to begin 5 or more days after birth.

Adrenal Cortex↗