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Query: UMLS:C0001430 (adenoma)
 21,222 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Fifteen unselected children and adolescents with Cushing's disease were treated by transsphenoidal exploration and microadenomectomy. In only three patients was radiographic examination of the sella turcica, including computed tomography, useful in indicating the presence and location of a pituitary microadenoma. Transsphenoidal microadenomectomy corrected hypercortisolism in 14 of the 15 patients; no adenoma was detected in one patient, and one required a second operation six months after the first because of incomplete removal of the adenoma. All 14 lost weight and cushingoid stigmata and had normal or catch-up growth (if epiphyses were not fused) and progression of puberty. In one patient, a recurrence was successfully treated by repeat microadenomectomy six years after the first procedure. The low morbidity and failure rate of the procedure, the low recurrence rate, the rapid amelioration of signs of hypercortisolism, and the preservation of pituitary function in the present study support transsphenoidal microadenomectomy as a low-risk approach to the initial treatment of Cushing's disease in childhood and adolescence.
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PMID:Treatment of Cushing's disease in childhood and adolescence by transsphenoidal microadenomectomy. 632 87

In an attempt to clarify the pathogenesis of hyperprolactinemia associated with Cushing's disease, PRL secretion was evaluated in 42 patients with hyperadrenocorticism (Cushing's disease, 26; and adrenocortical adenoma, 16) and in 10 patients with Nelson's syndrome. Mild hyperprolactinemia was found in 6 patients with Cushing's disease (23%) and in 5 patients with Nelson's syndrome (50%). In contrast, basal plasma levels of PRL were normal in all of the patients with Cushing's syndrome secondary to adrenocortical adenoma. Injection of TRH unequivocally induced PRL release; however, the responses were blunted in patients with Cushing's disease and in those with Nelson's syndrome who had hyperprolactinemia. Short term administration of dexamethasone, on the other hand, failed to alter PRL secretion in these patients. In 5 patients with Cushing's disease, plasma levels of PRL were reevaluated when they developed a typical clinical picture of Nelson's syndrome after bilateral adrenalectomy. Four patients had a definite increase in PRL levels. Immunohistochemistry of pituitary adenomas surgically removed from 7 patients with Cushing's disease or Nelson's syndrome demonstrated, in 4 of them, the presence of PRL-containing cells as well as ACTH-containing cells. Two of these patients had hyperprolactinemia, which was corrected by the removal of pituitary tumors. These results suggest that hyperprolactinemia is not a fortuitous occurrence in patients with Cushing's disease and could be explained by the concomitant production and secretion of PRL from corticotroph adenomas.
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PMID:Hyperprolactinemia in Cushing's disease and Nelson's syndrome. 632 16

Plasma lipoproteins, triglyceride turnover, and lipolytic enzymes were measured in 11 women with Cushing's syndrome. The studies were repeated 3 and 12 months after surgical treatment. Eleven healthy women of similar age and relative body weight served as controls. Before treatment the mean values of total cholesterol and triglyceride, of very low-density lipoprotein (VLDL) triglyceride and cholesterol, low density lipoprotein triglyceride and cholesterol, and high density lipoprotein cholesterol were all significantly increased in the patients with Cushing's syndrome. The triglyceride levels were only moderately elevated, the highest values being found in patients with adrenocortical adenoma. The production rate of VLDL triglyceride was higher in patients (13.2 mg/h . kg) than in controls (9.5 mg/h . kg, P less than 0.05), whereas the fractional catabolic rate of VLDL triglyceride was not significantly different. Consistent with the latter finding, the lipoprotein lipase activities of adipose tissue, skeletal muscle, and postheparin plasma were similar in patients and controls. The postheparin plasma hepatic lipase activity of the patients was at the lower end of the normal range. All lipid and lipoprotein abnormalities were completely abolished after successful surgery. It is concluded that endogenous hypercortisolism stimulates the hepatic production of VLDL particles. The effect is probably based on multifactorial mechanisms. In the presence of unchanged removal this leads to elevated levels of VLDL, low density lipoprotein, and high density lipoprotein.
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PMID:Plasma lipoproteins, lipolytic enzymes, and very low density lipoprotein triglyceride turnover in Cushing's syndrome. 634 67

Clinical, biochemical, operative, and postmortem findings have established nodular adrenal hyperplasia as a clinicopathologic entity and a cause of Cushing's syndrome. The possibility exists that there is a relationship among the various forms of adrenal and pituitary diseases that lead to hyperadrenocorticism. This may include a continuous sequence from bilateral adrenal hyperplasia to micronodular and macronodular hyperplasia to a unilateral adrenocortical adenoma and even carcinoma. We report the investigation and management of six patients with Cushing's syndrome caused by bilateral nodular adrenal hyperplasia who were treated by operation at the Glasgow Royal Infirmary, Scotland from 1975 to 1979. Investigations included a variety of biochemical and radioimmunoassay tests on plasma and urine, provocative and inhibition tests, scanning (ultrasonography, computed tomography, and iodocholesterol), arteriography, and selective venous sampling. All patients underwent a bilateral adrenalectomy by the posterior approach. The adrenal glands varied in size from 4.9 to 18 gm and histology showed that they had the features of bilateral nodular adrenal hyperplasia. Five patients did well after operation; they are presently receiving replacement steroid therapy, and at a 3- to 7-year follow-up there was no evidence of Nelson's syndrome. Advances in drug therapy (medical adrenalectomy) with aminoglutethimide, metyrapone, and O,p-DDD should not at present cause a change in our surgical approach to this condition.
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PMID:Nodular adrenal hyperplasia and Cushing's syndrome. 664 5

The case of a young boy bearing a pituitary PRL secreting adenoma (20-30,000 ng/ml) with the unusual association of clinical and endocrinological features of Cushing's disease successfully treated with bromocriptine is described. Brain computed tomography evidenced a huge pituitary adenoma leading to visual field defects and raised intracranial pressure. Due to the very large size of the tumor, which rendered the complete neurosurgical removal unlikely, medical treatment with bromocriptine (10 mg/day) was started. Follow-up for more than six months demonstrated an impressive reduction of tumor size, the lowering of prolactin levels into the normal range, the normalization of visual field, and the regression of both clinical and biochemical signs of hypercortisolism.
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PMID:Cushing's disease and marked hyperprolactinemia in a patient with a pituitary macroadenoma: effectiveness of bromocriptine treatment. 671 96

Surgical experience with adrenal disease from 1970 to 1979 was reviewed in 315 patients. The pathologic conditions that were encountered were hypercortisolism (74 patients), hyperaldosteronism (46 patients), adrenocortical carcinoma (35 patients), pheochromocytoma (77 patients), and nonfunctioning adenoma (47 patients). In addition, 5 patients with metastatic lesions, 14 with cysts, and 4 with myelolipoma were surgically treated. The accuracy of localizing adrenal lesions increased from about 50 percent to almost 100 percent during the decade studied. The increase was due mainly to the introduction of computerized tomography, the most important advance in the management of adrenal disease. The present study shows that adrenal surgery can be performed with low morbidity and mortality. Operative deaths were confined to patients with malignant disease or increased secretion of cortisol or catecholamines. Only patients with adrenocortical carcinoma (2 year survival probability, 34 percent) or hypercortisolism due to cortical hyperplasia (5 year survival probability, 76 percent) had significantly decreased survival.
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PMID:Adrenal surgery: trends during the seventies. 713 60

Scintigraphy was used in 66 patients with biochemically demonstrated hyperactivity of the adrenal cortex in order to determine the nature and site of the lesions. In cases of hypercortisolism, uptake was bilateral in 12 patients with Cushing's disease, unilateral in 7 patients with malignant or non-malignant tumours, and absent in 3 cases of large malignant tumours. In cases of hyperaldosteronism, scintigraphy performed during dexamethasone-induced ACTH suppression showed distinctly asymmetrical uptake in 13 patients with Conn's adenoma (confirmed by surgery as being on the good uptake side in 10 patients), symmetrical in 20 patients with biochemical findings indicating bilaterality, and intermediate in 9 patients. There was no false positive diagnosis of tumour. Scintigraphy appears to be of considerable value for locating adrenocortical lesions, especially small tumours.
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PMID:[Adrenocortical scintigraphy with 131I-19-iodocholesterol. Indications and results in 66 cases of hypercortisolism and hyperaldosteronism (author's transl)]. 722 Mar 32

We are presenting a series of 23 patients with Cushing disease selected from a larger study in which the ectopic production of ACTH (paraneoplastic or tumoral), adrenal adenoma or carcinoma were discarded. Sixteen were female and seven male. Diagnosis was fundamentally realized by clinical manifestations derived from hypercortisolism (obesity, muscular atrophy, diabetes, osteoporosis or polyglubulia). The polytomography demonstrated a deformed sella in 19 patients. Endocrine exams showed an alteration in rhythm of Cortisol and elevated levels of urinary metabolites. Others exams, Liddle Test, Metopirona Test, or stimulation of exogenic ACTH did not always permit diagnosis of pituitary adenoma. Plasmatic dosage of ACTH is the best test although results did not always agree with clinical manifestations. In each case we performed clinical treatment in preparation for surgery and later selective removal of adenoma or total pituitary ablation by transphenoidal approach. Of 21 patients, we found an adenoma during surgery in 15; the other 6 on whom we performed a total hypophysectomy, the pathological study showed an adenoma in 5 and a hyperemic gland with thick capillaries in 1. Another type of treatment was used on 2 due to their age. Nine patients were given post-operative radiotherapy. We conclude that microsurgery by transphenoidal approach offers the best possibilities for patients with Cushing disease.
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PMID:[Surgical treatment in Cushing's disease (authors' translation)]. 731 90

An unusual of bilateral adrenal benign adenoma with Cushing's syndrome is reported. Nine months after bilateral adrenalectomy, no more sign of hyperadrenocorticism was present. An adenoma was found in each gland with adjacent tissue atrophic. Physiopathology is not clear even if suppression test by dexamethasone and stimulation test by lysin-vasopressin are compatible with a central origin.
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PMID:[Cushing's syndrome caused by a bilateral adrenal adenoma (author's transl)]. 746 40

Outcome of and complications associated with bilateral adrenalectomy in 8 cats with pituitary-dependent hyperadrenocorticism and bilateral adrenocortical hyperplasia and outcome of and complications associated with unilateral adrenalectomy in 2 cats with adrenocortical tumor (adrenocortical adenoma, 1 cat; adrenocortical carcinoma, 1 cat) and unilateral adrenomegaly were determined. Glucocorticoids were administered to all cats at the time of surgery, and mineralocorticoids were administered to the 8 cats that underwent bilateral adrenalectomy. A ventral midline celiotomy was performed in all cats. Intraoperative complications did not develop in any cat. Postoperative complications developed in all cats and included abnormal serum electrolyte concentrations (n = 8), skin lacerations (n = 5), pancreatitis (n = 3), hypoglycemia (n = 2), pneumonia (n = 1), and venous thrombosis (n = 1). Three cats died within 5 weeks after surgery of complications associated with sepsis (n = 2) or thromboembolism (n = 1). Clinical signs and physical abnormalities caused by hyperadrenocorticism resolved in the remaining 7 cats 2 to 4 months after adrenalectomy. Insulin treatment was discontinued in 4 of 6 cats with diabetes mellitus. Median survival time for these 7 cats was 12 months (range, 3 to > 30 months). Two cats died of acute adrenocortical insufficiency 3 and 6 months after bilateral adrenalectomy, 2 cats were euthanatized because of chronic renal failure 3 and 12 months after bilateral (n = 1) or unilateral (n = 1) adrenalectomy, and 2 cats were alive 9 and 14 months after bilateral adrenalectomy. In the remaining cat, clinical signs recurred 10 months after the cat had undergone unilateral adrenalectomy.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Adrenalectomy for treatment of hyperadrenocorticism in cats: 10 cases (1988-1992). 755 48


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