Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0001430 (adenoma)
 21,222 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

From 1982 to 1992, 33 patients underwent adrenalectomy for disease of the adrenal gland: 18 patients with adrenal cortex adenoma or hyperplasia (Cushing's syndrome n = 11, Conn's syndrome n = 6, adrenogenital syndrome n = 1), 3 with pituitary-dependent Cushing's disease, 7 with pheochromocytoma (malignant n = 1), 2 with a metastasis of lung cancer and 1 with cystic adrenal necrosis. Multiple endocrine neoplasia existed in four cases. Various preoperative symptoms were noted, including complaints typical of the respective syndromes and general abdominal symptoms. Other patients were symptom-free with incidental findings. An intercostal approach was used in 30 cases, a transabdominal approach in 3 cases. In 6 cases bilateral and in 27 cases unilateral adrenalectomy was performed. In two cases additional nephrectomy became necessary because of extensive adhesions. Intraoperatively, one patient suffered a blood pressure crisis. 31 patients are still alive and symptom-free after a mean follow-up of 5.4 years (range 1-11 years). Two patients have died (one with benign pheochromocytoma and one with a metastasis of lung cancer). Detailed preoperative hormone analysis and adequate preoperative medication substantially lowers the risk involved in adrenal surgery. However, the indications for surgical treatment of hormonally inactive, symptom-free adrenal tumors that are found incidentally remain controversial, and surgery should perhaps be restricted to large tumors.
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PMID:[Surgical interventions of the adrenal gland. Diagnosis and results of treatment]. 781 48

Between July 89 and June 92, 70 patients with primary hyperparathyroidism underwent adenomectomy by unilateral incision under local anesthesia (Ul/LA), without exploration of the remaining glands. The procedure was carried out with intraoperative monitoring of urinary cyclic AMP (n = 35), Calcemia was measured 6-monthly for one year in every patient. 62 (88.6%) patients were cured after Ul/LA, whereas 5 patients required conversion to bilateral cervicotomy under general anesthesia because of abnormal hormonal levels, thus giving an overall success rate of 97% (67/70). The reasons for treatment failure of Ul/LA included misleading conclusions of cervical ultrasonography (n = 5), agitation of the patient (n = 1) and deep localization of the adenoma (n = 1). When cervical ultrasonography is suggestive of a parathyroid adenoma in expert hands, the probability of a second localization or associated hyperplasia is very low, so that adenomectomy by Ul/LA can be attempted safely, provided that the serum level of intact parathyroid hormone returns to normal values within one hour following resection. In our experience, parathyroidectomy by Ul/LA should not be considered in case of non conclusive ultrasonography, familial history pf hyperparathyroidism of MEN-I, ultrasonic evidence of several enlarged glands or associated thyroid nodule requiring simultaneous treatment.
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PMID:[Surgery of primary hyperparathyroidism by unilateral approach under local anesthesia and intraoperative determination of PTH 1-84]. 785 82

1. In 1991 we described a familial variety of primary hyperaldosteronism which was not glucocorticoid-suppressible and was associated with adenoma formation, and called it familial hyperaldosteronism type II (FH-II) in order to distinguish it from the glucocorticoid-suppressible variety described in 1966, familial hyperaldosteronism type I (FH-I). 2. In 1992 the genetic basis of FH-I was clarified by description of a hybrid gene. 3. Primary aldosteronism due to bilateral adrenocortical hyperplasia or to aldosterone-producing tumour can be part of the multiple endocrine neoplasia type I syndrome (MEN I), in which loss of heterozygosity has been described on chromosome 11q13. Loss of heterozygosity at the MEN I locus was found in five of 26 aldosterone-producing tumours from our series (by Japanese collaborators). These included two with adrenal cancer and two with FH-II. 4. We recently described an association of aldosterone responsiveness of aldosterone-producing adenomas with renin gene restriction fragment length polymorphisms, suggesting a possible role for renin genotype and intra-adrenal renin gene expression in the development and biochemical expression of some aldosterone-producing tumours. 5. We found abnormal karyotypes in 13 of 32 benign aldosterone-producing adenomas.
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PMID:Genetics of primary aldosteronism. 788 85

We describe a familial occurrence of primary hyperparathyroidism. The proband is a 60-year-old woman who had a parathyroid adenoma. Her older sister had a parathyroid adenoma with cementifying jaw fibroma and her younger sister died of parathyroid adenocarcinoma with pulmonary metastasis at the age of 38. We have not yet obtained evidence for other endocrine disorders suggesting multiple endocrine neoplasia (MEN) in this pedigree. The proband is complicated with Wilms' tumor. It is now widely accepted that respective predisposed genes of MEN type 1 and Wilms' tumor, and PTH gene are located on chromosome 11. The manifestation observed in this case may be related to mutational abnormalities on chromosome 11.
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PMID:Familial primary hyperparathyroidism complicated with Wilms' tumor. 791 71

In a series of 135 cases of primary hyperparathyroidism encountered in PUMC Hospital. Unilateral exploration was performed in 55 cases including 49 cases single adenoma, 1 double adenomas, 3 cases hyperplasia, 2 carcinoma and one MEN-I case. All the 3 cases of hyperplasia and 1 double adenomas were reoperations. There was only one case failed due to misguided by imaging diagnosis. The overall success rate of unilateral exploration was 98%. The reason of unilateral exploration is that about 80%-85% cases of hyperparathyroidism were caused by single adenoma. For single adenoma, unilateral exploration is enough and reasonable. The authors considered that once the diagnosis was made and preoperative localization has positive findings in experienced surgeon's hand the successful rate was very high, 2% of failure is acceptable. Technique point was discussed for unilateral exploration.
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PMID:[Experiences of unilateral exploration of parathyroid adenoma]. 791 36

Technetium-99m sestamibi is known to localize in primary malignant and metastatic tumors. Specifically, brain, breast, thyroid, parathyroid, lung, and kidney tumors have been imaged. The Verner Morrison syndrome, which is caused by excessive vasoactive intestinal peptide (VIP), consists of watery diarrhea, hypokalemia, and achlorhydria. This condition is rarely associated with multiple endocrine neoplasia. The authors present a case of multiple endocrine neoplasia type I with visualization of a pancreatic VIPoma and parathyroid adenoma with Tc-99m MIBI.
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PMID:Tc-99m sestamibi imaging of a pancreatic VIPoma and parathyroid adenoma in a patient with multiple type I endocrine neoplasia. 791 44

Primary hyperparathyroidism is being increasingly recognized because of the widespread availability of biological screening, thus explaining that one third of the patients are nowadays asymptomatic at diagnosis. Initially based on the hypercalcemia-hypophosphoremia syndrome, its diagnosis is now depending upon biological measurements of AMPc, intact (1-84) parathyroid hormone and dynamic tests such as the oral calcium-loading test. A controversial issue is the use of sophisticated imaging methods (ultrasonography, computed tomography, thallium-technetium scanning, magnetic resonance imaging and more infrequently venous catheterization with blood sampling) to localize the abnormal parathyroid glands, which are clearly inferior to surgery with a 95% success rate. The lesions include single adenoma in 80%, multiple adenomas in 5%, cancer in 1% and hyperplasia in 14% of the cases. Moreover, among the majority of seemingly sporadic hyperparathyroidism, about 10% of the cases appear to be part of a multiple endocrine neoplasia which is frequently misdiagnosed or lately recognized. The questions remain (as to) whether the surgical strategy should be revisited and whether intraoperative histopathological examination of the removed abnormal gland is still needed to ensure excellence in the management of hyperparathyroidism. However, since its initial description in the early 80s, the concept of unilateral cervical exploration directed by an accurate localization study and intraoperative measurements of intact hormone could become in the future the standard approach for surgical treatment in more than half of the patients.
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PMID:[What is new in surgery for primary hyperparathyroidism?]. 793 46

Since 1981 to 1993, 7 cases of primary para-hyperthyroidism with hypercalcemic crisis were encountered in PUMC Hospital. One earliest case went to emergency clinic for treatment but patient died within 24 hours in the clinic with no definite diagnosis. Autopsy proved to be single large parathyroid adenoma. 6 cases had blood Calcium level over 15 mg%, equivalent Ca++ level over 1.87 mmol/L. One case died because of unproved diagnosis. The rest 5 cases had parathyroid hormone (PTH) determined or positive findings by imaging diagnosis. Emergency operation has been performed with success, although 1 case need reoperation due to multiple endocrine neoplasm I (MEN-I). The authors emphasis that the application of large quantity infusion, diuretics and calcitonin are necessary pre-operation to reducing operation risk and smoothing postoperation recovery. Pathological diagnosis proved 4 cases were adenoma, one case corresponds to MEN-I. The authors concluded that the emergency operation is safe and effective after proper preoperative preparation, but must be done promptly without delay.
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PMID:[Emergency operation for treatment of hyper calcemic crisis due to primary hyperparathyroidism]. 803 81

The clinical evolution of type I multiple endocrine neoplasia (MEN I) was studied in 45 patients among a consecutive series of 172 with Zollinger-Ellison syndrome (ZES). These 172 patients were seen in our hospital between 1959 and 1989. Diarrhea was half as frequent in ZES-MEN I as in sporadic ZES cases. At diagnosis, mean basal acid output and serum gastrin levels in MEN I patients (28.8 +/- 6.6 mmol/h and 587 +/- 487 pg/ml, respectively) were not different from those observed in the others with sporadic ZES. Laparotomy was performed in all 36 patients with no diffuse liver involvement to attempt the removal of gastrinomas. Twenty-nine patients had adenomas, located in the pancreas in 21, in the duodenal wall in 3, and in both in 5. Adenomas were multiple in 23 cases (78%). No tumor was found in seven patients. Twenty-nine of the 36 operated patients were tumor-free after surgery; 7 died in the postoperative period between 1959 and 1970. Median follow-up of the 38 other patients was 95 months (range 17-278 months). Among the 24 patients without residual tumor at discharge (group I), biological and/or morphological evidence of a persistent or recurrent source of gastrin was obtained in 22. Among the 14 patients with residual tumor (group II), an increase in tumor size was seen in 5 after a median of 27 months (range 9-36 months), while no change occurred in 9 after 54 months (3-100 months). Actuarial survival curves were not different, either in group I versus group II patients (67 and 72% at 5-year follow-up, respectively) or in MEN I versus sporadic ZES patients. Apparently, complete resection of primary tumor did not reduce the incidence of subsequent liver metastases. In all, 21 of the 45 patients had malignant gastrinomas (47%), consisting of liver metastases in 14 (31%), metastatic lymph nodes in 11 (24%), and lung metastases in 2 (4%). Monitoring of fundic argyrophil cells disclosed hyperplasia in 13 of the 14 MEN I patients (92%), and 5 had invasive carcinoid tumors. Taken together, these results prompt us to recommend that in ZES-MEN I patients, surgery should be avoided and oxyntic mucosa regularly monitored.
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PMID:Clinical, anatomical, and evolutive features of patients with the Zollinger-Ellison syndrome combined with type I multiple endocrine neoplasia. 809 74

Although pituitary tumors arise as benign monoclonal neoplasms, genetic alterations have not readily been identified in these adenomas. We studied restriction fragment abnormalities involving the GH gene locus, and mutations in the p53 and H-, K- and N-ras genes in 22 human GH cell adenomas. Twenty two nonsecretory adenomas were also examined for p53 and ras gene mutations. Seven prolactinoma DNA samples were tested for deletions in the multiple endocrine neoplasia-1 (MEN-1) locus, as well as for rearrangements in the hst gene, a member of the fibroblast growth factor family. Pituitary adenoma tissue and lymphocytes were obtained from patients at the time of transsphenoidal surgery. In DNA from GH-cell adenomas, identical GH restriction patterns were detected in both pituitary and lymphocyte DNA in all patients and in one patient with a mixed GH-TSH cell adenoma. Using polymerase chain reaction (PCR)-single stranded conformation polymorphism analysis, no mutations were detected in exons 5, 6, 7, and 8 of the p53 gene in GH cell adenomas nor in 22 nonsecretory adenomas. Codons 12/13 and 61 of H-ras, K-ras, and N-ras genes were also intact in GH cell adenomas and in nonsecretory adenomas. Site-specific probes for chromosome 11q13 including PYGM, D11S146, and INT2 were used in 7 sporadic PRL-secreting adenomas to detect deletions of the MEN-1 locus on chromosome 11. One patient was identified with a loss of 11p, and the remaining 6 patients did not demonstrate loss of heterozygosity in the pituitary 11q13 locus, compared to lymphocyte DNA. None of these patients, demonstrated hst gene rearrangements which also maps to this locus. These results show that p53 and ras gene mutations are not common events in the pathogenesis of acromegaly and nonsecretory tumors. Although hst gene rearrangements and deletions of 11q13 are not associated with sporadic PRL-cell adenoma formation, a single patient was detected with a partial loss of chromosome 11, including the putative MEN-1 site.
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PMID:Molecular screening of pituitary adenomas for gene mutations and rearrangements. 810 Aug 31


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