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

The authors have reviewed the results of transsphenoidal surgery for pituitary adenomas done on 66 children (younger than 16 yr of age) between 1966 and 1992. Ninety-four percent (62 of 66) showed clinical evidence of pituitary hormonal hypersecretion. The most common type was the adrenocorticotropic hormone-secreting adenoma (n = 36), followed by the prolactinoma (n = 18) and the growth hormone-secreting types (n = 8). There were four cases of nonfunctioning adenomas. Adrenocorticotropic hormone-secreting tumors in children had presentations and surgical results similar to those seen in adults. Twenty-three of 33 patients with Cushing's disease had simple adenomectomy or subtotal hypophysectomy without symptomatic recurrence. Four of 10 initial treatment failures had subsequent successful surgical intervention, resulting in an overall cure rate of 78%. Postoperative hypocortisolism was suggestive of surgical success but was not absolute. Of three patients with Nelson syndrome, none were successfully treated with surgery alone and two developed invasive disease. Prolactin-secreting and growth hormone-secreting tumors in children occurred more commonly with suprasellar expansion than did their adult counterparts. Transsphenoidal surgery was capable of controlling disease in only 12% (1 of 8) of growth hormone-secreting tumors, and 67% (12 of 18) of prolactin-secreting tumors required postoperative medical therapy or radiotherapy for persistently elevated prolactin levels. Special difficulty was noted in boys with prolactinomas and in girls with primary amenorrhea. As in adults, preoperative prolactin levels correlated with ultimate surgical success rates.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Transsphenoidal surgery for pituitary adenomas in children. 817 79

Cushing's disease resulting from intrasellar corticotropin-releasing hormone (CRH)-secreting gangliocytomas is very rare, and only two such cases have been reported in the literature to date. The authors present a third case in which an adrenocorticotropic hormone-secreting pituitary adenoma was found in addition to a gangliocytoma in a 10-year-old girl with clinical and endocrinological symptoms of Cushing's disease. Computed tomographic and magnetic resonance imaging scans showed a suprasellar and parasellar tumor. A green-colored, heterogeneous tumor and a small adenoma were removed transsphenoidally. Histological examination revealed a large gangliocytoma immunoreactive for CRH and a small, mucoid cell pituitary adenoma immunoreactive for ACTH. This is the first case of such a tumor causing Cushing's disease in a child. It might exemplify induction of an ACTH-secreting pituitary adenoma by means of chronic overstimulation of CRH.
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PMID:Cushing's disease in a child caused by a corticotropin-releasing hormone-secreting intrasellar gangliocytoma associated with an adrenocorticotropic hormone-secreting pituitary adenoma. 826 95

Adrenocortical adenoma, nodular hyperplasia, or carcinoma was diagnosed in 50 ferrets. Thirty-five (70%) ferrets were female and 15 (30%) were male. The mean age at which clinical signs were first noticed was 3.4 years (range, 1 to 7 years). Clinical signs included large vulva (n = 31; 89% of females), alopecia (n = 43; 86%), pruritus (n = 20; 40%), and increased consumption of water and increased urine output (n = 4; 8%). A mass was palpated at the cranial pole of the kidney during physical examination of 17 (34%) ferrets. Ultrasonography, performed on 39 of 50 ferrets, revealed a unilateral adrenal gland mass in 19 (49%). Four ferrets were anemic, and 2 ferrets were thrombocytopenic. Baseline plasma concentrations of cortisol and corticosterone were within or below the reference range in all 17 ferrets tested, whereas baseline plasma estradiol concentrations were high in 4 of the 11 ferrets (36%) tested. AFter adrenocorticotropic hormone (ACTH) administration, only 1 ferret had a slightly exaggerated response on the basis of plasma cortisol concentrations, and all 17 had normal responses on the basis of plasma corticosterone concentrations. There was little or no increase in plasma estradiol concentrations after ACTH administration. Of the 50 ferrets, 39 were treated by adrenalectomy. Unilateral adrenalectomy was performed in 34 ferrets in which 1 adrenal gland was large, whereas subtotal bilateral adrenalectomy was performed in 5 ferrets with bilateral adrenal disease. Five ferrets died in the immediate postoperative period, and follow-up information was available for the remaining 34, 1 to 34 months after surgery.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hyperadrenocorticism associated with adrenocortical tumor or nodular hyperplasia of the adrenal gland in ferrets: 50 cases (1987-1991). 840 89

A case of adrenal tumor producing 11-deoxycorticosterone, 18-hydroxy-11-deoxycorticosterone and aldosterone is reported. A 55-year-old woman had hypertension, hypokalemia, low plasma renin activity and an adrenal tumor. The plasma level of aldosterone was normal, and the levels of 11-deoxycorticosterone and 18-hydroxy-11-deoxycorticosterone were extremely high. After the tumor removal, the plasma level of aldosterone decreased and plasma levels of 11-deoxycorticosterone and 18-hydroxy-11-deoxycorticosterone were normalized. The tumor was benign adenoma and the production of steroid hormones was under control of adrenocorticotropic hormone. The enzyme activity of 21-hydroxylation in the tumor was elevated and that of 11 beta-hydroxylation was decreased compared with the adjacent tissue.
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PMID:Adrenal tumor producing 11-deoxycorticosterone, 18-hydroxy-11-deoxycorticosterone and aldosterone. 868 Jan

Of 1,106 New World primates necropsied from the National Zoological Park (Washington, D.C.) and the Department of Comparative Pathology, Johns Hopkins University School of Medicine (Baltimore, Maryland) 22 (1.9%) animals were identified with 27 neoplasms. Of this group, nine animals (two females, seven males) had a total of 13 endocrine neoplasms. All animals were adults, with an age range of 2.7-25 years (average, 12.1 years). Seven were Callitrichidae and two were Cebidae. The adrenal gland was the most affected organ, with seven (53.8%) neoplasms, followed by the pituitary and thyroid gland with two (15.4%) cases each, and the pancreas and parathyroid gland with one tumor (7.7%) each. All neoplastic disorders were benign. Immunocytochemistry assays for growth hormone, adrenocorticotropic hormone, prolactin, follicle-stimulating hormone, luteinizing hormone, thyroid-stimulating hormone, and chromogranin A were performed on two pituitary neoplasms. Pheochromocytoma was the most frequent neoplasm, representing 5 (38.4%) of the 13 neoplasms. The remaining were thyroid cystadenoma (two, 15.4%), corticotrophic cell pituitary adenoma (two, 15.4%), adrenal ganglioneuroma (one, 7.7%), adrenal cortical adenoma (one, 7.7%), parathyroid chief-cell adenoma (one, 7.7%), and pancreatic islet-cell adenoma (one, 7.7%).
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PMID:Endocrine neoplasia in New World primates. 874 Sep 50

We performed pituitary-adrenocortical function test and analysis of plasma steroids in three cases of adrenocorticotropic hormone-independent bilateral adrenocortical macronodular hyperplasia, and examined the plasma cortisol response to meal and oral glucose in two cases. On pathological examination, nodules were mainly composed of clear cells and some nests of compact cells were observed. Immunohistochemistry of steroidogenic enzymes showed positive P-450C17 only in the compact cells and positive 3 beta-hydroxysteroid dehydrogenase only in the clear cells. These cases were similar to clinical or preclinical Cushing's syndrome due to adenoma in both pituitary-adrenocortical function and plasma steroid patterns, but different from adenoma cases in the distribution of steroidogenic enzymes.
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PMID:Three cases of clinical or preclinical Cushing's syndrome due to adrenocorticotropic hormone-independent bilateral adrenocortical macronodular hyperplasia: pituitary-adrenocortical function and immunohistochemistry. 877 67

1. In familial hyperaldosteronism type I (FH-I), expression of an adrenocorticotropic hormone (ACTH)-dependent hybrid 11 beta-hydroxylase/aldosterone synthase gene causes excessive 'hybrid steroid' (18-hydroxy- and 18-oxo-cortisol) production. In order to study the mechanism of elevated 'hybrid steroid' levels in angiotensin-unresponsive (AII-U) aldosterone-producing adenoma (APA), we compared responses of 24 h urinary 18-oxo-cortisol, aldosterone and cortisol to dexamethasone (0.5 mg q6h for 4 days) in 11 FH-I patients, 11 patients with AII-U APA, 11 patients with AII-responsive (AII-R) APA and 10 patients with bilateral adrenal hyperplasia (BAH). 2. Consistent, marked suppression (by at least 60%) of 18-oxo-cortisol levels by dexamethasone was seen in all groups except AII-U APA. Aldosterone levels were consistently suppressed to undetectable levels only in FH-I. Cortisol levels were suppressed to undetectable levels in all patients except two with AII-U APA. 3. Production of both 18-oxo-cortisol and aldosterone (and occasionally cortisol) in AII-U APA appears relatively ACTH-independent, consistent with a common mechanism involved in the formation of these two steroids from their respective precursors, which differs from that in FH-I. 4. In AII-R APA and BAH, 18-oxo-cortisol production appears markedly ACTH-dependent, but aldosterone production is not.
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PMID:Production of 18-oxo-cortisol in subtypes of primary aldosteronism. 880 May 94

A 9-year-old male Doberman Pinscher was referred to the Department of Clinical Sciences of Companion Animals, Faculty of Veterinary Medicine, Utrecht University, for polyuria/polydipsia, anorexia, and vomiting. Laboratory examination of blood and urine revealed hyperglycemia, glucosuria, and acidosis. Diabetes mellitus was diagnosed but was very resistant to subsequent insulin treatment. At the owners' request, the dog was euthanatized and a postmortem examination was performed. In addition to hepatic, pancreatic, and renal changes compatible with diabetes mellitus, an acidophilic adenoma of the adenohypophysis was found. Immunohistochemical staining for growth hormone, adrenocorticotropic hormone, and prolactin showed a strong immunolabeling for growth hormone within the cytoplasm of the tumor cells. Although growth hormone level was not measured in the plasma, our findings suggest that the diabetes mellitus in this dog was caused by excess growth hormone secreted by the pituitary neoplasm.
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PMID:Diabetes mellitus in a dog with a growth hormone-producing acidophilic adenoma of the adenohypophysis. 881 49

Somatotroph adenomas often secrete prolactin (PRL) besides growth hormone (GH) and are sometimes immunostained for other anterior pituitary hormones or their subunits, such as thyroid-stimulating hormone (TSH) beta-subunit and glycoprotein hormone alpha-subunit (alpha SU). However, somatotroph adenomas showing hypersecretion of adrenocorticotropic hormone (ACTH) are extremely rare. There have been, to our knowledge, only five published reports on somatotroph adenomas accompanied by excessive ACTH secretion. Here we report a case of intracavernously invading somatotroph macro-adenoma with high serum GH, PRL, and ACTH levels. We examined the case using immunohistochemistry (IHC), in situ hybridization (ISH), and cell culture, and confirmed GH, PRL, and ACTH, as well as alpha SU, production, and the expression of Pit-1 protein by the adenoma, which is known as a transcriptional factor for GH, PRL, and TSH, not for ACTH. Therefore, the presence of unknown transcriptional factor other than Pit-1, common to GH, PRL, and ACTH, may be speculated to be expressed in this adenoma. In our previous study, we had found plurihormonal mRNA expression, especially for ACTH, the beta-subunit of follicle-stimulating hormone and luteinizing hormone in some somatotroph adenomas, using non-radio-isotopic ISH, and suggested that these adenomas might be derived from plurihormonal primordial stem cells. Our present case is significant from the viewpoint of histogenesis of pituitary adenomas, because it further supports the cell origin of somatotroph adenomas from plurihormonal primordial stem cells, and moreover it suggests the presence of unknown transcriptional factor other than Pit-1, common to GH, PRL, and ACTH.
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PMID:A case of pituitary somatotroph adenoma with concomitant secretion of growth hormone, prolactin, and adrenocorticotropic hormone--an adenoma derived from primordial stem cell, studied by immunohistochemistry, in situ hybridization, and cell culture. 889 Sep 99

A 43-year-old woman presented with obesity and lumbago. Endocrinological examinations revealed normal plasma cortisol levels and a suppressed serum adrenocorticotropic hormone (ACTH) level. On venous sampling, markedly elevated plasma cortisol levels were observed for bilateral adrenal veins (243 and 62.3 micrograms/dl on the right and left sides, respectively). Although the computed tomogram revealed bilaterally enlarged adrenal glands, 131I-adosterol scintigram showed a strong uptake only on the right side. Right adrenalectomy successfully relieved Cushing's syndrome. Pathological diagnosis was adrenocortical adenoma, 3.5 cm in diameter. Cushing's syndrome recurred in 9 years. At that time, she underwent left subtotal adrenalectomy including a 3-cm adrenocortical adenoma. Postoperative convalescence has been uneventful with oral steroid supplementation. All 14 previously reported cases of bilateral adrenocortical adenoma (BAA) causing Cushing's syndrome as well as the present case were concurrent and dominant in females of reproductive age. This suggests that some cofactors other than ACTH, such as estrogen, contribute to the pathogenesis of BAA.
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PMID:[A case of concurrent bilateral adrenocortical adenoma causing Cushing's syndrome]. 916 55


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