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

Hyperplasia of the parathyroid glands is a central feature of familial multiple endocrine neoplasia type 1. We used cultured bovine parathyroid cells to test for mitogenic activity in plasma from patients with this disorder. Normal plasma stimulated [3H]thymidine incorporation, on the average, to the same extent as it was stimulated in a plasma-free control culture. This contrasted with the results of the tests with plasma from patients with familial multiple endocrine neoplasia type 1, in which parathyroid mitogenic activity increased 2400 percent over the control value (P less than 0.001). Plasma from these patients also stimulated the proliferation of bovine parathyroid cells in culture, whereas plasma from normal subjects inhibited it. Parathyroid mitogenic activity in plasma from the patients with familial multiple endocrine neoplasia type 1 was greater than that in plasma from patients with various other disorders, including sporadic primary hyperparathyroidism (with adenoma, hyperplasia, or cancer of the parathyroid), sporadic primary hypergastrinemia, sporadic pituitary tumor, familial hypocalciuric hypercalcemia, and multiple endocrine neoplasia type 2 (P less than 0.05). Parathyroid mitogenic activity in the plasma of patients with familial multiple endocrine neoplasia type 1 persisted for up to four years after total parathyroidectomy. The plasma also had far more mitogenic activity in cultures of parathyroid cells than did optimal concentrations of known growth factors or of any parathyroid secretagogue. This mitogenic activity had an apparent molecular weight of 50,000 to 55,000. We conclude that primary hyperparathyroidism in familial multiple endocrine neoplasia type 1 may have a humoral cause.
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PMID:Parathyroid mitogenic activity in plasma from patients with familial multiple endocrine neoplasia type 1. 287 88

Among all the radiological examination techniques, CT is today, besides scintigraphy, the method of choice as far as the detection of functional adrenal lesions is concerned. In primary aldosteronism, CT classification of the syndrome is based on the detection of an adenoma which can be reliably detected in adenoma sizes up to 8-10 mm. Thus, 70 to 80% of Conn's syndromes can be classified. In adrenal Cushing's syndrome, the distinction between adenoma and carcinoma of the adrenal gland is up to CT and can usually be easily made due to the characteristic morphology of each type of lesion. In case of a typical adrenal or juxtaadrenal tumor location, detection of a pheochromocytoma is likewise easy. In ectopic and multiple pheochromocytomas or such as occur as part of a MEN-syndrome, the situation is quite different. If lesions of the adrenal gland are found by accident in examinations otherwise indicated, the question arises whether the process is malignant or benign. In this respect, all the traditional imaging methods, including CT, involve a considerable factor of uncertainty, especially if a malignant tumor is anamnestically known and the question of metastases arises. According to recent information, MR-imaging seems to be advantageous concerning this difficult differential diagnosis.
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PMID:[Radiological diagnosis of adrenal gland diseases]. 287 94

We describe a patient who presented with sporadic pheochromocytoma and parathyroid adenoma in the absence of medullary thyroid carcinoma, which coexisted with fully developed scapular ectopic breast tissue. If not coincidental, this association might support the concept that all components of multiple endocrine neoplasia type IIA originate from embryonic ectodermal tissue, and that sporadic multiple endocrine neoplasia type IIA, as well as ectopic breast tissue, may result from a noxious event at a critical embryonic stage.
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PMID:Coexistence of sporadic multiple endocrine neoplasia and scapular ectopic breast. Coincidence or biologically associated? 287 96

We report a case of multiple endocrine neoplasia type I and hypernephroma. Parathyroid hyperplasia, adrenocortical hyperplasia, a nodular goiter, multiple lipomas, a chromophobe adenoma of the pituitary and hypernephroma had all been diagnosed previously. All but the last are features consistent with the diagnosis of multiple endocrine neoplasia type I (Wermer's syndrome). The association of multiple endocrine neoplasia type I and hypernephroma may represent a new manifestation of this pleiotropic syndrome.
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PMID:Hypernephroma associated with multiple endocrine neoplasia type I: a case report. 287 10

A case with multiple endocrine neoplasia was reported, including parathyroid adenoma, of the main cells of the gland, multiple small adenomas in the tail of pancreas, (cytologically and electron-microscopically determined as A cellular) and light-cellular adenoma of adrenal. The hyperfunction of parathyroid adenoma was manifested with hypercalcemia (3.75 mmol/l), and morphologically--with the multiple calcium metastases in lungs, kidneys and heart, established at necropsy. The cause for the death was the acutely advanced ischemic disease of myocardium, on the background of chronic pyelonephritis and renal insufficiency. The timely diagnosis of such morbid states is concluded to be important for the clinical practice and could lead to the saving of the patients by operative removal of the tumour.
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PMID:[Multiple endocrine adenomatosis manifested chiefly by hyperparathyroidism]. 287 52

A male patient with corticotropin-releasing factor (CRF) and adrenocorticotropin (ACTH)-producing syndrome is described. Soon after being referred to us the patient developed pneumonia, anaemia, oedema and respiratory distress, and died on the 24th day after admission. Autopsy and histology revealed that he had a rare type of multiple endocrine neoplasia (type 1 + paraganglioma) with a mediastinal paraganglioma, parathyroidal hyperplasia, pancreatic islet cell adenoma, duodenal multiple carcinoid tumours and adrenocortical nodular hyperplasia. It was not possible to examine the pituitary. The paraganglioma contained a large amount of immunoreactive (IR)-CRF (606 ng/g wet weight), IR-ACTH (59.4 ng/g wet weight), IR-human proopiomelanocortin n-terminal (1-76) peptide (hNT, 156.8 ng/g wet weight) and IR-beta-lipotropin (beta-LPH, 146.9 ng/g wet weight). The major IR-ACTH, beta-LPH and IR-hNT were eluted at ACTH-(1-39), beta-LPH and hNT marker positions, respectively. Big ACTH was not detected. IR-CRF eluted at the human CRF marker position on Sephadex G-75 chromatography and high performance liquid chromatography (HPLC). The IR-CRF fraction from the HPLC showed CRF bioactivity which paralleled that of synthetic human CRF in monolayer cultured rat anterior pituitary cells. Our results suggest that not only ACTH but CRF produced by the paraganglioma was responsible for the patient's Cushing's syndrome.
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PMID:Multiple endocrine neoplasia with Cushing's syndrome due to paraganglioma producing corticotropin-releasing factor and adrenocorticotropin. 287 33

Carotid body tumor is an uncommon tumor of the head and neck. The coexistence of this entity with primary hyperparathyroidism is even more unusual, with only four cases having been previously recorded. This report describes a patient with a left inferior parathyroid adenoma and a right carotid body tumor. A common neuroectodermal origin is proposed as an explanation for the simultaneous occurrence of these tumors. The fact that this may represent yet another variable expression of the multiple endocrine neoplasia syndromes emphasizes the importance of careful endocrine screening in patients with carotid body tumors.
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PMID:Carotid body tumor and hyperparathyroidism. A case report and review of the literature. 288 23

A 20-yr-old black woman presented in 1969 with headache, amenorrhea, hyperprolactinemia, hypogonadotropism, hypogonadism, and hypercalcemia due to a chromophobe adenoma. She received 5000 rads to the sella. One year later she was found to have hyperparathyroidism due to parathyroid adenoma and three and a half glands were removed. Thirteen years later she presented with 3 months of profuse watery diarrhea, hypokalemia, hypercalcemia, hyperchloremic metabolic acidosis, and a normal anion gap. A vasoactive intestinal polypeptide-producing tumor of the pancreas was found and successfully removed, after which hypercalcemia resolved. This is an unusual case of the multiple endocrine neoplasia syndrome, type 1, being associated with a vasoactive intestinal polypeptide-oma and pancreatic cholera.
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PMID:Multiple endocrine neoplasia, type 1, with pancreatic cholera. 288 44

A rise in the serum calcitonin (CT) following provocative testing has facilitated making the diagnosis of occult medullary carcinoma of the thyroid (MCT) or C cell hyperplasia (CCH) in asymptomatic children of kindred with multiple endocrine neoplasia (MEN) type IIa. Findings were reviewed for seven children varying in age from 3 to 16 years screened at our institution between 1976 and 1986. Three had elevated basal calcitonin (S-CT). Six had significant elevation of calcitonin (delta-CT) after stimulation. Total thyroidectomy was performed in all seven. Five had MCT with bilobar involvement in three. CCH was present in all five. Two patients had no gross, microscopic, or immunohistochemical evidence of MCT or CCH. One of three had an elevated S-CT. The other had a significant delta-CT. All patients have normal postoperative S-CT and delta-CT. Our experience indicates the importance of beginning stimulation tests of affected kindred at less than 3 years of age. It appears, however, that neither elevated S-CT or positive delta-CT are perfect predictors of parafollicular cell pathology. Solitary parathyroid enlargement, second thyroid malignancy, and branchial pouch anomalies may occur with MEN IIa. One patient with MCT had a focus of papillary carcinoma. One patient with primary hyperparathyroidism had a solitary enlarged parathyroid adenoma. Additional findings were the presence of nodules of ectopic thymus in close association with the thyroid gland in three patients.
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PMID:Provocative testing for occult medullary carcinoma of the thyroid: findings in seven children with multiple endocrine neoplasia type IIa. 288 76

Multiple endocrine neoplasia type II (MEN-II) syndrome is an autosomal dominant condition characterized by medullary carcinoma of the thyroid, pheochromocytoma, and parathyroid adenoma. A cytogenetic investigation was conducted on 13 MEN-II syndrome patients from four unrelated kindreds and 13 age-matched control subjects for chromosome instability and the chromosome 20 deletion reported in MEN-II syndrome. A significant increase (p less than 0.05) was found in the total number of chromatid and chromosome aberrations in MEN-II cells (12.3%) compared with control cells (6.9%) grown at 96 hours in mitomycin C (20 ng/ml, final concentration). The major difference between the two groups was in chromatid, and not chromosome, aberrations. There was no difference between MEN-II and control individuals in fragile site expression, the number of sister chromatid exchanges or cell kinetics. A blind analysis of high-resolution G-banded chromosomes was performed on blood specimens from 13 MEN-II and seven control individuals. Twelve of 13 MEN-II patients and one of seven control subjects were scored as having a 20p12.2 deletion (chi 2 = 12.6; p less than 0.001). Additional research is needed to determine if this cytogenetic finding is due to a chromosome deletion, inversion, or polymorphism.
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PMID:Cytogenetic studies of individuals from four kindreds with multiple endocrine neoplasia type II syndrome. 288 77


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