[Scintigraphy using iodine-131-labeled 19-iodocholesterol in the study of adrenal pathology].
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The technical choice in imaging the adrenal gland will depend on several factors discussed in the review. CT and MRI are achieving increasingly high accuracy in the investigation of patients suspected to present adrenal pathology. Scintigraphy evaluates functional patterns of both adrenal cortex and medulla, depending on the radiopharmaceutical that is used. Non invasive characterization of adrenal lesions is very important in cases of incidental discovery of adrenal masses. This review concentrates on new techniques for evaluating the incidentally discovered adrenal masses and differentiating between adrenal adenomas and metastases.
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Hypertension in endocrine disorders (Cushing's syndrome, Conn's syndrome, Pheochromocytoma) is frequently accompanied by a confusing clinical symptomatology. The underlying pathology is a cortical hyperplasia or a tumor of the adrenal cortex or medulla. The differentiation from other causes of hypertension is primarily based upon laboratory findings (plasma and urinary concentration of cortico-steroids, Renin, Angiotensin and catecholamines as well as their derivates). The preoperative tumor localization by urography, arteriography and adrenal venography as well as the visualization of glandular hypertrophy by adrenal venography is of fundamental importance with regard to treatment of these disorders.
The anatomopathological and clinical features of 131 cases subjected to adrenalectomy for metastasis of breast cancer, hypercortico-adrenalism and pheochromocytoma are described. The results of surgical management are analysed.
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The influence of long-term administration of dexamethasone on pharmacodynamic activity and biotransformation of salicylamide and hexobarbital, including their absorption, distribution and excretion, were studied. Activities of the following enzymes were also determined: beta-glucuronidase (E.C.3.2.1.31), uridinediphosphoglucose dehydrogenase (E.C.1.1.1.22), uridinediphosphoglucuronyl transferase (E.C.2.4.1.17), uridinediphosphoglucuronic pyrophosphatase (E.C.3.6.1.9), and hexobarbital oxidase.
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A very rare case of echinococcal cyst of the adrenal gland is reported. Other organs were free of echinococcal cysts. Treatment consisted of surgical removal of the adrenal cyst through a subcostal incision.
Pathological changes usually occur independently in the adrenal cortex and medulla because of their distinct embryonic origins, and changes involving both the cortex and medulla are rare. We report 4 cases of corticomedullary mixed pathological changes adrenal glands. CT scanning of the adrenal glands showed unilateral abnormalities in all the 4 cases, 3 of which were diagnosed as aldosteronism and the other pheochromocytoma before surgery. Unilateral adrenalectomy was performed in the 4 patients 3 being cured and discharged. The other 1 had recurrence 18 months postoperatively with suspected pathological changes on the other side. Subsequent pathological examination confirmed the suspicion in both the cortex and medulla of the other adrenal gland. In cases with clinical presentations as simultaneous onset of aldosteronism and catecholamine responses, pathological changes in both the cortex and medulla of the adrenal glands should be considered. Perioperative management of such cases should be the same as that in cases of catecholamine responses, and the diagnosis relies on histopathological examination.
Recent progress in trials of regeneration and gene therapy in endocrine organs, especially in adrenal glands has been reviewed. Gene therapies using adenovirus have been most frequently tested in vivo and in vitro, aiming at improvement of steroidogenesis and suppression of adrenal tumor growth. Although the effects were temporal, promising results have been obtained. Interestingly, adrenocortical tissue was shown to be formed by transplantation of adrenocortical cells and to replace the adrenal functions of adrenalectomized animals. Engineered ES cells stably expressing Ad4BP/SF-1 were shown to be directed toward steroidogenic lineage, suggesting a future possibility of regeneration of adrenal cells.
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We report a case of Cushing's syndrome due to ACTH-independent macro-nodular adrenal hyperplasia (AIMAH). The patient, a 51-year-old man, had been suffering from poorly controlled arterial hypertension for the previous 6 years and he complained of progressive weight gain, gynecomastia and impotence. Physical examination revealed classic cushingoid features. Endocrine basal assessment showed increased urinary free cortisol (264-600 micrograms/24 hr). Urinary steroid profile showed an increase of total 17-hydroxycorticosteroids (17-OHCS: 23 mg/24 hr), with a threefold increase of tetrahydrocortisol (THF:9.66 mg/24 hr) and of tetrahydrocorticosterone (THB: 1.35 mg/24 hr). Tetrahydrodesossicortisol was only slightly elevated (THS:0.67 mg/24 hr) and tetrahydrodesossicorticosterone was at the inferior limit of the normal range (THDOC: 0.03 mg/24 hr). Total 17-ketosteroids were decreased (17-KS: 3 mg/24 hr). Plasma cortisol level was elevated and without circadian rhythm (26-29 micrograms/dl in the morning, 26-28 micrograms/dl at 24:00 h). DHEAs and free testosterone levels were significantly reduced (106 ng/dl and 3.9 pg/ml respectively). ACTH was undetectable and unresponsive to CRH. Both dexamethasone and octreotide failed to suppress plasma cortisol levels. Abdomen computed tomography scan demonstrated bilaterally enlarged multinodular adrenal glands. Cerebral magnetic resonance revealed no alteration of the pituitary gland. The patient underwent bilateral adrenalectomy. On macroscopic examination, adrenal glands were occupied by multiple yellow nodules and their compressive weight was 190 g, with left adrenal heavier than the right one (120 g and 70 g respectively). Histologically, nodular lesions were predominantly composed of large clear cells, with small foci of "hybrid" cells and adipose tissue metaplasia. Reticularis zone was atrophic. In the immediate post-operatory course pulmonary embolism occurred, despite prophylaxis with low molecular weight heparin. After having recovered from this complication, the patient showed progressive regression of cushingoid status. The findings of increased THF/THS and THB/THDOC ratios were in agreement with a relative hyperfunction of 11-beta-hydroxylase "in vivo", which might have contributed to the hypercortisolism, in addition to the marked increase of secernent adrenal mass.
Endocrine (adrenal) hypertension (primary aldosteronism, hypercortisolism and pheochromocytoma) had been considered for a long time as a rare cause of arterial hypertension. However, recent studies have shown a frequent incidence of primary aldosteronism among hypertensive subjects and therefore it is necessary to exclude primary aldosteronism in all subjects with severe hypertension. On the contrary, pheochromocytoma and hypercortisolism may be often overlooked in patients with incidentally found adrenal tumor and thus they can cause unexpected per- and postoperative complications.
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