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

During the period from March 1954 to June 1976, 489 cases of hepatic tumors were experienced at the Department of Surgery, National Taiwan University Hospital. The pathological classification are: Hemangioma 5; Cystic hamartoma 2; Hemangioendothelioma 2; Non-parasitic localized cyst 5; Polycystic liver 9; Tuberculoma 1; Actinomycosis 1; Hyperplasia 1; Adenoma 1; Primary liver sarcoma 2; Primary liver cancer 442; and Metastatic liver cancer 18. Of the 489 hepatic tumors, two cases were treated with excision, 148 cases with hepatic lobectomy and nine cases of polycystic liver were treated with fenestration. Benign hepatic tumors are all well up to eight years after the operation, 14 cases of primary liver cancer survived five to 17 years after hepatic lobectomy.
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PMID:Hepatic tumors, surgical treatment and its results. 20 37

Immunohistochemistry and electron microscopy allow new insights into the biology and natural history of the proliferative processes of the hypophysis. Hyperplasia can be diffuse or focal. Its function and/or growth are controlled by hypothalamic factors. Hyperplasia may precede the formation of an adenoma. Function and/or growth of adenomas is partially or completely independent of hypothalamic regulation. Adenomas are divided according to their functional activity into an endocrine active and inactive group. A further subdivision is made according to the secreted hormone. Inactive adenomas may have lost the ability to produce hormones, may secrete hormones at a very low rate, or may secrete abnormal substances.
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PMID:Pituitary adenomas. Clinico-morphologic correlations. 51 26

We examined 12 depressed tubular adenomas of the stomach pathologically and immunohistochemically in order to clarify the difference between the depressed type and the elevated type. Depressed tubular adenomas showed shallow mucosal depression and, of the 12, nine were endoscopically diagnosed as early gastric cancer. Histologically, the adenoma cells showed dysplasia in varying degree and focal adenocarcinoma occurred in two adenomas measuring over 2 cm. The mean height of the adenoma glands was 0.63 +/- 0.31 mm in the 12 depressed adenomas and 1.32 +/- 0.43 mm in 44 elevated adenomas, while the mean heights of the subjacent mucosa were 0.18 +/- 0.19 mm and 1.07 +/- 0.71 mm, respectively. Thus, depressed adenomas resulted from paucity of the mucosa subjacent to the adenoma glands and the height of the adenomatous glands was half that found in the elevated type. Goblet cells, a variety of endocrine cells and lysozyme-containing cells were found in nine, nine and eight depressed adenomas, respectively, in variable numbers. Hyperplasia of these cells was also detected in depressed adenomas showing mild or moderate dysplasia. Immunohistochemical examination revealed no difference in the phenotypic expression of adenoma cells as between the depressed and the elevated type.
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PMID:Depressed tubular adenoma of the stomach: pathological and immunohistochemical features. 198 68

A histologic and immunocytochemical study of 69 autopsy-obtained pituitaries from women who died during pregnancy, after abortion, or in the postpartum period revealed an accumulation of large chromophobic to slightly acidophilic and periodic acid-Schiff-negative pregnancy cells that were immunoreactive for prolactin but not for other pituitary hormones. This increase in the number of prolactin cells was confirmed by cell counts. Thus, pregnancy cells are capable of prolactin production. The finding of mitotic figures in such cells supports the view that they arise by multiplication from preexisting prolactin cells. With use of "mirror section" techniques, no mammosomatotrophs (cells immunoreactive for growth hormone and prolactin) were identified. Hyperplasia of prolactin cells was evident at 1 month of pregnancy and gradually disappeared within several months after delivery or abortion; the process of involution seemed to be retarded in the one lactating patient investigated. In some pituitaries, the accumulation of prolactin cells was so extensive that the hyperplastic foci resembled microadenomas. Another striking change in the pituitaries of pregnant women was appreciable reduction of immunostaining of gonadotropic cells, a process that was reversible as soon as 1 month after delivery. Among the 69 pituitaries studied, 8 noninvasive microadenomas (12%) were encountered (7 contained prolactin only and 1 was plurihormonal). Prolactin-producing adenomas were no more numerous or larger than were similar tumors encountered in nonpregnant women or normal men; thus, pregnancy neither initiates formation of pituitary adenomas nor accelerates their growth. In the pituitaries that harbored prolactin-producing adenomas, massive pregnancy cell hyperplasia was evident outside the tumor; thus, prolactin production by adenoma cells did not seem to suppress the proliferation of prolactin-containing pregnancy cells.
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PMID:The pituitary gland in pregnancy: a clinicopathologic and immunohistochemical study of 69 cases. 215 93

Multiple gastric and duodenal biopsy specimens from 102 asymptomatic patients with familial adenomatous polyposis, taken during a prospective endoscopic screening programme were examined. One hundred patients had microscopic gastroduodenal pathology, often in the absence of macroscopic lesions. Adenomas were found in 94 patients in the duodenum, in the second and third parts. Hyperplasia of villous and crypt epithelium was also seen, sometimes in the absence of adenomas: this may be a precursor of neoplastic change. In the stomach fundic gland polyps were the commonest abnormality, seen microscopically in 44 patients. Chronic antral gastritis was common in patients without fundic polyps. Gastric adenomas were present in six patients, all of whom also had duodenal adenomas. If duodenal adenomas in familial adenomatous polyposis have a similar malignant potential to those in the colorectum sequential endoscopy and biopsy are necessary to detect cancer in these patients.
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PMID:Upper gastrointestinal pathology in familial adenomatous polyposis: results from a prospective study of 102 patients. 217 Apr 64

Cushing syndrome can recur following an adrenalectomy. One of the primary causes is recurrence of adrenal carcinoma either locally or from metastases. Hyperplasia and hyperfunction of adrenal remnants may also occur if there is pituitary stimulation. We have a patient in whom recurrent Cushing syndrome developed from small nonmalignant deposits of adrenal tissue in the perirenal adipose tissue following adrenalectomy of a benign adenoma. These deposits were identifiable by computed tomography. A false-negative NP-59 iodocholesterol scan was instructive in pointing out some problems in the interpretation of this type of scan for adrenal tissue.
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PMID:Unusual cause for recurrent Cushing syndrome and its diagnosis by computed tomography and NP-59 radiocholesterol scanning. 239 18

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

MAMBNA is a new N-nitroso compound isolated from Fusarium moniliforme-inoculated corn meal. In the present studies the carcinogenicity of MAMBNA is shown by the induction of forestomach carcinomas and liver tumors in mice and rats following the gastric intubation of this compound. Among 42 mice of Kunming (KM) stock treated with MAMBNA (10-20 mg/week), 22 showed epithelial hyperplasia of the esophagus, 29 papillomas and 4 squamous carcinomas in the forestomach, and there were 6 liver adenomas and 3 hepatomas. One mouse had forestomach carcinoma and carcinoma in the liver. Most tumors developed in mice receiving the treatment for 136-317 days, with a total dose of 210-670 mg (Table 1). No tumor was found in 12 controls observed for 239-357 days. In the experiment with 29 Wistar strain rats, administration of MAMBNA (20-120 mg/week) resulted in 11 epithelial hyperplasias in the lower esophagus, 14 atypical hyperplasias and papillomas, and 11 squamous carcinomas in the forestomach. The earliest forestomach carcinoma appeared in a rat treated for 454 days, receiving 4480 mg of MAMBNA, and the other 10 carcinomas occurred in animals treated for 518-640 days. Hyperplasia of liver cells was noted in 4 rats and liver adenoma in 7 and hepatocellular carcinoma in 8. Most hepatomas developed in rats treated for 480-640 days, and 5 rats had both forestomach carcinoma and hepatoma (Table 2). In 11 untreated rats observed for 411-644 days only one forestomach papilloma was noted.
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PMID:[Forestomach carcinoma and hepatoma induced in mice and rats by N-3-methylbutyl-N-1-methylacetonylnitrosamine (MAMBNA)]. 300 54

After diagnosis of primary aldosteronism on the basis of biochemical evidence, the detection of the tumour is of crucial importance in the management of the disease. We reviewed the efficacy of CT-Scan, Iodo-Cholesterol Scintigraphy, digitalized phlebography, adrenal vein sampling for steroid measurements (AVS), and Nuclear Magnetic Resonance (NMR) in 160 hypertensive patients with primary aldosteronism. Diagnosis of Conn's adenoma (n = 96) or Adrenal Hyperplasia (n = 40) was confirmed by surgery or at least two concordant tumour localization tests. Scintigraphy gave a correct diagnosis in 53% of the 51 exams, CT-Scan in 82% of the 85 exams, and phlebography in 79% of 61 exams. Plasma Aldosterone/Cortisol ratio was 5 times higher on the side of adenoma in 55% of the 47 cases but this ratio was also present in 23% of 22 patients with adrenal hyperplasia. Each procedure exhibited few false positive and false negative cases. NMR performed in 15 patients with Conn's adenoma identified all the cases. But tumours displayed a signal close to the liver signal and identical to the normal adrenal. These results and the risk of invasive procedure (failure of catheterization of the right adrenal vein (n = 6) and adrenal haematoma (n = 2) lead us to propose a schema of exploration of patients with primary aldosteronism. The CT-Scan could be performed at the first step once the biological diagnosis confirmed. Phlebography and AVS will be performed only if tumour was less than 1 cm at the CT-Scan despite important biological abnormalities. This schema requires to be validated by a prospective evaluation.
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PMID:[Localization of primary hyperaldosteronism]. 320 1

Forty-five patients with biochemically documented primary hyperparathyroidism as part of multiple endocrine neoplasia syndrome types 1 or 2 were surgically treated from 1960 through 1980. Hyperplasia occurred in 69% of the patients, single adenoma in 27%, and double adenomas in 4%. All but two patients with hyperplasia underwent subtotal parathyroidectomy. In this group, the cure rate was 93% and the incidence of permanent postoperative hypoparathyroidism 23%. In the adenoma group, treatment included excision of the adenoma and biopsy of at least one other gland. The cure rate was 76%, with no postoperative hypoparathyroidism. Analysis of patients with persistent hyperparathyroidism suggested that failure to recognize multiple gland disease was the principal cause of postoperative hypercalcemia. In view of the high incidence of hypocalcemia after subtotal parathyroidectomy, approximately 500 mg of tissue should be cryopreserved to allow transplantation should hypocalcemia ensue postoperatively.
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PMID:Primary hyperparathyroidism in patients with multiple endocrine neoplasia syndromes. Surgical experience. 613 93


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