Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P50583 (asymmetrical)
 12,197 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Adrenal scintigraphy with 131I-19-iodo-cholesterol was performed in 13 hypertensive patients with biochemical disturbances suggesting an aldosterone-producing adenoma. The actual presence of an adenoma was subsequently confirmed in all cases. An asymmetrical tracer uptake (lateralization) was seen in 7 patients and in 6 of these the adenoma was located in the adrenal with the higher uptake. In one patient a large necrotic tumour was not visualized and a faint contralateral accumulation was wrongly taken to represent a tumour. In 6 patients the scintigram was non-lateralizing. In these highly selected patients a lateralizing scintigram had a high diagnostic specificity and at present adrenal scintigraphy should be the method of first choice in the preoperative side prediction. However, the sensitivity is low: a non-lateralizing scintigram does not exclude the presence of an aldosterone-producing adenoma.
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PMID:Adrenal scintigraphy in primary aldosteronism caused by an aldosterone producing adenoma. 720 37

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

Occult aspects of tumor proliferation are likely recorded genetically as their microsatellite (MS) loci become polymorphic. However, MS mutations generated by division may also be eliminated with death as noncoding MS loci lack selective value. Therefore, highly polymorphic MS loci cannot exist unless mutation rates are high, or unless mutation losses are inherently minimized. Mutations accumulate differently when cell fates are determined intrinsically before or extrinsically after division. Stem cell (asymmetrical division as in intestinal crypts) and random (asymmetrical and symmetrical division) proliferation, respectively, represent simulated cell fates determined before or after division. Whereas mutations regardless of selection systematically persist once inherited with stem cell proliferation, mutations are eliminated by the symmetrical losses of both daughter cells with random proliferation. Therefore, greater genetic diversity or MS variance accumulate with stem cell compared with random proliferation. MS loci in normal murine intestinal mucosa and xenografts of cancer cell lines accumulated mutations, respectively, consistent with stem cell and random proliferation. Tumors from patients with hereditary nonpolyposis colorectal cancer (HNPCC) demonstrated polymorphic MS loci. Overall, three of five adenomas and one of six cancers exhibited high MS variances. Assuming mutation rates are not significantly greater in adenomas than in cancers, these studies suggest the stem cell proliferation and hierarchy of normal intestines persists in many HNPCC adenomas and some cancers. An adenoma stem cell architecture can explain the complex polymorphic MS loci observed in HNPCC adenomas and account for many adenoma features. In contrast, cancers may lose intrinsic control of cell fate. These studies illustrate a feasible phylogenetic approach to unravel and describe occult aspects of human tumor proliferation. The switch from predominantly stem cell to random proliferation may be a critical and defining characteristic of malignancy.
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PMID:Tracing cell fates in human colorectal tumors from somatic microsatellite mutations: evidence of adenomas with stem cell architecture. 977 50

The primitive hyperparathyroidism (PHPT) constitutes still cause of discussion both from the diagnostic point of view and from the therapeutic one although surgical successes are generally reported. Between the most important problems there is the increase of the HPT asymptomatic or oligosymptomatic patients with the decisional difficulties in the timing of the surgical treatment and the difficult framing of the HLP disease associated with MEA and the relating surgical failures. Besides some authors support an unilateral dissection of the neck in patients with adenoma diseases diagnosed before the intervention against the traditional address of a bilateral exploration. Our experience is based on 31 patients subjected to intervention of parathyroidectomy for primitive HPT: 26 carriers of adenomas, of which 1 double, and 5 of diffused hyperplasia. We have effected 25 simple parathyroidectomy for adenoma, 1 resection of three parathyroid glands for double adenoma, 2 subtotal parathyroidectomy (7/8) for diffused hyperplasia. 2 patients had new surgical treatment for persistent hypercalcemia, and they were respectively carriers: 1 of a second ectopic adenoma and 1 of asymmetrical hyperplasia; 2 patients finally, operated in other hospitals had a second exploration and they were affected from MLP. In 26 patients we had very good results, in 2 persistence of hypercalcemia (patients who had a second look) and 3 hypocalcemia.
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PMID:[The surgical treatment of primary hyperparathyroidism: clinical experience]. 1080 73

Ectopic pituitary adenomas (EPAs) are rare and their association with orthotopic corticotroph hyperplasia has not been published. The case of a 30-year-old woman with clinical and biochemical evidence of Cushing disease (CD) is reported. A magnetic resonance image obtained preoperatively revealed asymmetrical inhomogeneity of the pituitary gland, which was suggestive of localized adenoma. It also showed what was thought to be a small sphenoid polyp. Postoperatively the latter lesion was found to be an ectopic corticotroph adenoma. The pituitary gland, which was free from any tumor, exhibited diffuse unilateral corticotroph hyperplasia. Clinical, radiological, laboratory, and histopathological findings are presented. A review of the literature and a discussion of possible causes of this unique association between the ectopic corticotroph adenoma and the pituitary hyperplasia are provided.
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PMID:Juxtaposition of an ectopic corticotroph adenoma of the sphenoid sinus with orthotopic intrasellar corticotroph hyperplasia in a patient with Cushing disease. Case report. 1269 18

A 12-year-old crossbred dog (case 1) and a 12-year-old Shetland sheepdog (case 2) were presented with a history of lameness and distal limb swelling. Physical examination revealed joint effusions and asymmetrical swellings of the extremities. In case 1, a diagnosis of arthritis and cellulitis was made on fine-needle aspiration biopsy of the synovium and subcutis. In case 2, bone biopsies and synovial aspirates diagnosed osteomyelitis and arthritis. A diagnosis of pancreatic disease was made on the findings of marked elevations of serum lipase concentrations and ultrasonographic identification of pancreatic masses in both cases. Both the cases were non-responsive to symptomatic management and were subsequently euthanased. Postmortem examination confirmed the diagnosis of panniculitis, arthritis and osteomyelitis in both cases. A pancreatic exocrine adenoma was identified in case 1 and a pancreatic adenocarcinoma with widespread metastases in case 2. To the authors' knowledge the association of panniculitis, polyarthritis and osteomyelitis with pancreatic disorders has not been reported previously in canine clinical cases.
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PMID:Panniculitis, polyarthritis and osteomyelitis associated with pancreatic neoplasia in two dogs. 1684 78

Sessile serrated adenoma (SSA) is a newly characterized type of the large bowel adenoma. It arises in hyperplastic polyp (HP) and represents a precursor lesion of colorectal carcinoma with microsatellite instability. SSAs differ from common HPs by abnormal proliferation of the crypt epithelium and by nuclear atypia. We examined 15 SSAs from 15 patients. The age range was 25-80 years (average 60 years). Six patients were females and 9 were males. For comparison, we examined 10 conventional tubular adenomas and 10 common HPs with vesicular cells. The sites of SSAs were as follows: 8 in rectum, 4 in rectosigmoid colon, 1 in transverse colon, 1 next to mucinous carcinoma of ascending colon, 1 in anastomosis after resection of the transverse colon adenocarcinoma. The diameter of the lesions ranged from 5 to 12 mm. Histologically, SSAs showed asymmetrical proliferation of the epithelium, irregular shape of the crypts with their branching and some crypt dilatations especially in the basal parts of the crypts. Cellular atypia (dysplasia) was usually low. In 5 cases the nuclei were focally stratified and localized in the lower part of the cells. High-grade dysplasia was found only in SSA adjacent to mucinous adenocarcinoma. Immunohistochemically, SSAs showed secretion of gastrointestinal mucin expressing MUC2 and MUC5A. Both MUC2 and MUC5A were also positive in mucinous carcinoma. In previous studies these expressions were considered specific for serrated type of carcinogenesis. However, our study found positivity of MUC2 and MUC5A also in conventional adenomas. Expression of p53 in SSAs was minimal. SSAs have malignant potential comparable with conventional adenomas and for this reason they must be distinguished from HPs.
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PMID:Sessile serrated adenomas of the large bowel. Clinicopathologic and immunohistochemical study including comparison with common hyperplastic polyps and adenomas. 1695 61

Two professional musicians, a 55-year-old clarinet player and a 58-year-old trumpet player, presented to the surgical outpatient clinic with a Warthin's tumour and a pleomorphic adenoma in the deep lobe of the parotid gland, respectively. The several branches of the facial nerve form the virtual plane between the superficial and deep lobes of the parotid gland. Due to the localisation of this nerve, parotid surgery entails a significant risk of neurapraxia of the facial nerve branches. Before the operation, both patients were informed carefully about both the necessity and the risks of surgical excision of parotid tumours. Even slight damage to the facial nerve during parotidectomy could have severe implications for their careers. Both underwent subtotal parotidectomy. Postoperatively, there was clinically a temporary minor marginal branch dysfunction in one patient. Pre- and postoperative electromyography did not indicate asymmetrical function of the facial muscles. A few weeks after the operations, both musicians could resume playing; subtotal parotidectomy can apparently be safely performed in players of wind instruments.
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PMID:[Subtotal parotidectomy for a parotid gland tumour in two players of wind instruments, with preservation of facial nerve function]. 1737 97

While a germline activating mutation of the luteinizing hormone receptor (LHR) gene is known to cause autonomous production of testosterone from testicular Leydig cells in male-limited precocious puberty, only a few studies have addressed the role of somatic LHR mutation in testicular pathology. The authors report a case of a 6-year-old boy who developed secondary sex characteristics including facial acne, enlarging genitalia, and aggressive behavior, for which serial biochemical evaluation confirmed the status of peripheral precocious puberty. Examination revealed asymmetrical testicular volume, following which a left testicular tumor was detected through ultrasonography. A left orchiectomy was performed, and histopathology revealed a well-circumscribed Leydig cell tumor Molecular study of the exon 11 of the LHR gene revealed a missense mutation at the nucleotide position 1,732, leading to a substitution of histidine for aspartic acid at codon 578. Interestingly, the substitution was consistent with all previously reported LHR alteration in pediatric Leydig cell adenoma, but which had never before been reported in male-limited precocious puberty, suggesting that the mutation is a molecular signature of the adenoma.
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PMID:Peripheral precocious puberty in a male caused by Leydig cell adenoma harboring a somatic mutation of the LHR gene: report of a case. 2087 84

Ectopic adrenal cortical neoplasms are extremely rare; few involve the central nervous system (CNS). We report a 17-month-old girl with spinal adrenal cortical neoplasms. She was unable to crawl or stand and was irritable at night. Her appearance was asymmetrical; the right side of her face and her lower right leg were enlarged. In addition, she manifested hyperplasia of the thymus, fibrous hyperplasia of the bladder, and hamartoma in the liver. However, all abnormalities were asymptomatic. Magnetic resonance imaging (MRI) revealed well-circumscribed masses within the dura mater at the T12-L1 and L3-L4 level. Histology disclosed that the lesions were composed of sheets and nests of round and polygonal cells with mostly round regular nuclei; eosinophilic to clear cytoplasm was abundant. Immunohistochemically, the tumor cells were strongly positive for inhibin-alpha, positive for synaptophysin and vimentin, and negative for GFAP, EMA, S-100, NSA, and chromogranin A. In addition, the nuclei stained positive for steroidogenic factor 1 (Ad4BP/SF-1), which is involved in adrenal steroidogenesis. This case confirms the occurrence of adrenocortical adenoma in the CNS. We suggest that this tumor should be considered in the differential diagnosis of CNS tumors.
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PMID:Ectopic adrenal cortical adenoma in the spinal region: case report and review of the literature. 2104 15


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