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)

A 50-year-old man presented with a rapidly growing mass in the area of the right lacrimal gland. An initial erroneous histopathologic diagnosis of a pleomorphic adenoma made on a small-incisional biopsy was later corrected to a malignant rhabdoid tumor when a wide local excision of the tumor was performed. The tumor was composed predominantly of dyscohesive, globoid, and eosinophilic cells, which frequently contained cytoplasmic inclusions. These were demonstrated to be composed of whorls of intermediate vimentin filaments. The tumor cells expressed epithelial membrane antigen as well as cytokeratin. Ultrastructurally, they displayed intercellular junctions and interrupted segments of linear basement membrane material. These findings, together with the development of the lesion within the parenchyma of the lacrimal gland, are suggestive of an epithelial origin. The patient was treated with radical surgery and adjunctive radiotherapy and chemotherapy, which are the recommended treatment modalities for this highly malignant tumor.
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PMID:Adult extrarenal rhabdoid tumor of the lacrimal gland. 137 74

Ten children and a 22-y old women with tuberous sclerosis were studied. All children were epileptic but only 8 had skin lesions (white spots, sebaceous adenoma), 4 had rhabdomyoma of the heart and 4 children had astrocytoma of the retina; only in 4 children was the entire triad of tuberous sclerosis seen. The young woman with a hemorrhage of an angiolipoma of the kidney had no other symptoms of tuberous sclerosis. All patients had pathologic CT and MRT findings; 4 different types of lesion were seen in MRT. In order to elucidate human genetic aspects and to demonstrate the underlying disease all children with epileptic disorders and also all patients without the full triad of symptoms should be examined by MRT.
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PMID:[Tuberous sclerosis: broadening of the diagnosis using MR tomography and computed tomography]. 146 58

Magnetic Resonance Imaging (MRT) was performed in 36 consecutive patients with hyperparathyroidism. MR tomograms of 31 patients were evaluated and compared with the results of operation and histology (n = 29). In the remaining 5 patients MR examination was not completed, due to claustrophobia or motion artefacts. MR examinations were performed in 2 superconductive magnets (0.5 and 1.5 Tesla). A surface coil with following spinecho sequences was used: SE: TR/TE: 550-700/15-30; 2000/22-100. All patients were subjected to additional sonography. Out of 28 parathyroid adenomas 25 were identified on MR tomograms (sensitivity: 73%, specificity: 90%). However, only 2 out of 6 hyperplastic parathyroid glands were localized on MR tomograms. Lesions missed on MR tomograms measured 15 mm and less in diameter. It is characteristic that parathyroid adenomas showed isointense MR signal to the thyroid (SE 550/30 and hyperintense MR signal to fat (SE 2000/100). Different signal intensities of the adenomas were observed in 25% of the cases. MR imaging is a valuable diagnostic method for preoperative localisation of parathyroid adenomas. We think that MR imaging should be performed when sonography and subtraction scintigraphy are not able to identify a suspected adenoma in the same location.
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PMID:[Magnetic resonance tomography as a localization method in hyperparathyroidism]. 304 9

In order to establish diagnostic criteria, colour-coded duplex sonography was performed on 40 patients who had a total of 43 operatively confirmed thyroid lesions which were scintigraphically "cold" (28 adenomas, 8 carcinomas, 4 cases of thyroiditis and 3 cysts). 32 of these patients also had MRT with T2- and T1-weighted images before and after injection of Gd-DTPA (0.1 mmol/kg). Adenomatous nodules and adenomas showed a peripheral vascular halo on colour-coded duplex sonography with a sensitivity of 96% and a specificity of 93%. Malignant lesions showed marked central vascularisation and on B-images irregular marginal structures. Adenomas and adenomatous nodules showed hyperintense areas on T1-weighted unenhanced MR images and/or homogeneous uptake in the lesion (sensitivity 100%, specificity 77%). Malignant lesions typically showed an irregular margin with increased contrast uptake on MRT. If sonography and colour-coded duplex sonography is unable to classify a lesion with any degree of assurance then MRT with Gd-DTPA enhancement should be performed.
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PMID:[The color-coded duplex sonography and contrast-enhanced magnetic resonance tomography of scintigraphically cold thyroid nodules]. 830 88

In 10 patients with hypophyseal Cushing microadenomas, selective bilateral sampling from the inferior petrosal sinuses was performed and the effect of stimulation by iv TRH and CRF was compared. On the side of the microadenoma. ACTH concentration rose from 650 +/- 242 pg/ml to 2712 +/- 843 pg/ml following injection of CRF and 2025 +/- 242 pg/ml after TRH. Contralateral values were 165 +/- 79 pg/ml, 490 +/- 200 pg/ml and 165 +/- 72 pg/ml respectively. Prolactin concentration on the side of the adenoma was 98 +/- 49 ng/ml before stimulation, 236 +/- 62 ng/ml after CRF and 747 +/- 168 ng/ml after TRH. Contralateral concentration was 22 +/- 10 ng/ml, 64 +/- 19 ng/ml respectively. Sampling localised all adenomas correctly, whereas contrast-enhanced MRT diagnosed only four adenomas.
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PMID:[Selective blood sampling from the sinus petrosus inferior: a comparison of CRF and TRH stimulation]. 838 Oct 39

230 patients with arterial hypertension of adrenal origin were treated. 205 of them underwent adrenalectomy with surrounding paranephral fat. There were no lethal outcomes. Endogenic adrenocorticism was diagnosed in 134 patients. Cushing's syndrom was in 96 patients, Cushing's disease--in 34, ACTH-ectopic syndrome--in 2, adrenocortical cancer--in 2. Primary hyperaldosteronism was diagnosed in 42 cases: idiopathic hyperaldosteronism in 23 patients, aldosteronproducing adenoma (Conn's syndrome)--in 19. Tumors of chromaffine tissue were defected in 30 patients. All the patients underwent complex examination (hormonal profile, US, CT, MRT, angiography if it was necessary). Symptomatic arterial hypertension of adrenal origin was diagnosed during one year in 10% patients only because of absence of typical clinical picture. Use of complex examination has permitted to make a correct topical diagnosis and to choose optimum treatment policy in all the cases.
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PMID:[Diagnosis and surgical treatment of arterial hypertension of adrenal origin]. 1121 Mar 11

Primary hyperaldosteroneism (PHA) is one of the main causes of secondary arterial hypertension (AH). Medical histories of 62 patients with PHA were analyzed. aldosterone-produced adenoma (APA) was diagnosed in 37 (59.7%) patients (all of them were operated), idiopathic hyperaldosteroneism (IHA)--in 25 (40.3%) patients, 11 of them were operated. Complex clinical and instrumental examination (hormonal analysis, USI, CT, MRT, in difficult cases in 35 patients--selective phlebography with blood sampling) was carried out in all the patients. Clinical picture in the majority patients with PHA was unclear. Hypokaliemia is not obligatory symptom of PHA. AH is often the only symptom of PHA, therefore all the patients with AH require complex laboratory examination including repeated detection of potassium blood level, examination of serum aldosterone concentration and renin activity, diurnal urinary excretion of aldosterone. In difficult differential diagnosis between APA and IHA it is necessary to perform selective phlebography with blood sampling from inferior cava and adrenal veins with obligatory detection of aldosterone and hydrocortisone concentration. Diagnostic and curative algorithm are developed. Surgical treatment is indicated for patients with APA, and also for ones with IHA who had functionally dominant adrenal gland (based on selective blood sampling analysis) and resistant for drug therapy AH.
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PMID:[Diagnosis and surgical treatment of primary hyperaldosteronism]. 1238 Jan 79

Carcinoma of the biliary tree are rare tumours of the gastrointestinal tract with a rising incidence during the last years. Biliary neoplasms are classified into intra- and extrahepatic cholangiocarcinoma (Klatskin tumour, middle and distal extrahepatic tumours), gallbladder cancer, and ampullary carcinoma. Transformation of normal into malignant bile duct tissue requires a chain of consecutive gene mutations, similar to the adenoma-dysplasia-carcinoma-sequence in colon cancer. Abdominal ultrasound, combined non-invasive magnetic resonance cholangiography/tomography (MRC/MRT), and facultatively endoscopic retrograde cholangiography (ERC) for unclear diagnosis, represent the gold standard for primary diagnosis. For ampullary carcinoma, endosonography and endoscopic biopsy are the diagnostic tools of choice. Cure is attainable only by formal curative radical surgical resection. Increasing surgical radicality within the last years enabled clearly improved 5-year survival rates. In contrast, there has been no clinical benefit for adjuvant and neoadjuvant therapies. For palliation, bile duct stenting and photodynamic therapy are established methods. Radio- and chemotherapy should be reserved for clinical studies. New therapeutic approaches include brachytherapy, the use of modern chemotherapeutics, COX-2- and tyrosine kinase-receptor-inhibitors.
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PMID:[Current diagnostics and therapy for carcinomas of the biliary tree and gallbladder]. 1587 Oct 71

Nodular regenerative hyperplasia (NRH) is characterized by a non-cirrhotic micronodular transformation of the liver parenchyma. It is based on the obliteration of small portal veins. Macroregenerative nodules (MRN) develop in areas of favourable blood flow in otherwise hypoperfused liver tissue. Hypoperfusion is caused by obliteration of liver veins and/or large portal veins with the subsequent atrophy or extinction of parenchyma. The hyperperfused and sometimes rapidly growing MRN might simulate a malignant tumor in CT and MRT. Morphologically, MRN resemble FNH. In contrast to hepatocellular adenoma, they show a more or less nodular architecture with fibrous septa and ductular structures. NRH and cases of MRN without cirrhosis can indicate an extrahepatic/systemic disease causing altered liver perfusion. MRN in liver cirrhosis must be differentiated from dysplastic nodules and highly differentiated hepatocellular carcinoma by cytological and microarchitectural criteria. Focal nodular hyperplasia (FNH) can imitate liver cirrhosis, steatohepatitis, cholangitis or chronic hepatitis, if biopsy material does not include normal perilesional liver tissue. Telangiectatic FNH might resemble classic hepatocellular adenoma. Neoductular structures and septation argue for this rare subtype of FNH. Neoductular transformation of hypoperfused liver parenchyma might imitate cholangioma or cholangiocarcinoma.
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PMID:[Nodular lesions of liver parenchyma caused by pathological vascularisation/perfusion]. 1677 11

Primary hyperaldosteronism is the most common secondary form of hypertension. Diagnosis of this entity is recommended in hypokalemic hypertension, in therapy-resistant hypertension (at least three 3 drugs and RR > 140/90 mmHg), and in adrenal incidentalomas (= incidentally discovered adrenal tumors). For screening, the ratio between plasma aldosterone (PAC) and plasma renin concentration (PRC) should be measured. In the assessment of PAC/PRC ratio, the discontinuation of some antihypertensive medication and assay-specific cutoff values must be noticed. After a positive screening test, saline infusion test should be done as confirmatory test. In contraindications/impracticability of this test, 24-h urine collection for aldosterone-18-glucuronide under high-sodium diet can be used as alternative confirmatory test. After confirmation of primary hyperaldosteronism, differential diagnosis between aldosterone-producing adenoma and idiopathic hyperaldosteronism has to be done. For this approach, adrenal CT or MRT, posture test and adrenal vein catheterization as gold standard test are available. Whereas therapy of aldosterone-producing adenoma is surgery, idiopathic hyperaldosteronism is to be treated medically by spironolactone.
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PMID:[Diagnosis of primary hyperaldosteronism]. 1722 47


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