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 69-year-old female patient had been treated with glucocorticoid for eight years because of rheumatoid arthritis. She showed characteristic Cushingoid features such as central obesity, moon face, and fragility of skin and vessels. She was disabled because of spinal compression fracture and muscle weakness. The blood pressure was 186/100 mmHg and the laboratory tests revealed serum K: 2.8 mEq/l, WBC: 15, 510/mm3, total cholesterol: 310 mg/dl. These suggested that she had iatrogenic Cushing's syndrome. After discontinuation of glucocorticoid, however, the serum cortisol level remained high. This fact prompted us to conduct further examinations for Cushing's syndrome. Oral dexamethasone administration did not suppress the plasma cortisol level and a left adrenal adenoma was found on abdominal CT scan. Because of the presence of bleeding diathesis, operation for adenoma was contraindicated. Though we tried to treat her with metyrapone, trilostane or opeprim (OP'-DDD), we had to abandon specific treatment because of severe side effects such as acute adrenal dysfunction and gastrointestinal problems. Decrease in the endogenous cortisol level after metyrapone treatment caused exacerbation of symptoms of rheumatoid arthritis. This is a peculiar case in which the long-term administration of glucocorticoid for rheumatoid arthritis might have concealed Cushing's syndrome, and conversely the increased intrinsic adrenal steroid hormone might have suppressed the activity of the rheumatoid arthritis.
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PMID:[Cushing's syndrome found during long-term glucocorticoid treatment of rheumatoid arthritis in an elderly woman]. 156 Jun 10

Ten patients with adrenal cortical carcinoma were treated from 1966 to 1986. There were 7 males and 3 females. The typical clinical manifestations, marked increase of 17-ketosteroid, 17-hydroxycorticoids and DHA, and negative dexamethasone suppression test were essential for the diagnosis. Of the ten patients, eight had secretive function and their 17-ketosteroid and 17-hydroxycorticoids varied from 36.8-93 mg% and 32.5-150 mg%, respectively. DHA was measured in 5 cases with the result of 6.95-44mg%. Those without secretive functions or obvious endocrine disturbances were usually misdiagnosed as kidney tumor, splenomagaly, liver tumor or pancreatic mass. Wood had summarized that nonsecretive ACC patients commonly had fever, pain, exhaustion syndrome (emaciation, fatigue, perspiration, anorexia), mass and distant metastasis. Adrenal scan, IVU, abdominal aortic arteriography, retroperitoneal pneumography and CT were helpful in localization. The differential diagnosis between ACC and adenoma by pathology was difficult. It is generally agreed that if the mass is larger than 100 grams, capsulated, having blood or lymphatic vessel invasion, hemorrhage, necrosis and calcification or even distant metastasis, malignant tumor should be considered. Surgical removal of the tumor is the only effective treatment. For advanced or recurrent lesions, selective adrenal artery thrombosis could be used. One of the ten patients was thus treated by this facilitated subsequent surgery. Postoperative chemotherapy, such as O.P-DDD, might be used in some cases.
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PMID:[Adrenal cortical carcinoma (ACC)--report of 10 cases]. 297 73

Since the adrenal or parathyroid cancer is a clinically rare entity. We often have difficulty in its diagnosis and treatment. The adrenocortical cancer is usually classified into two categories--endocrinologically functioning or non-functioning. The incidence is not different between them. It is often found in an advanced stage as it does not show clinical manifestation before it has grown up to a large tumor. Only an effective agent for the adrenal cancer is op'-DDD so far. Recently, cisplatin, VP-16 (etoposide) and others are administered as trial use. Most of malignant pheochromocytomas are endocrinologically active and they often cause hypertension leading to death. Therefore it is important to control hypertension in malignant pheochromocytoma. Chemotherapy and irradiation are not effective for it. Recently, 131I-MIBG (metaiodobenzylguanidine) is found to be useful not only for diagnosis but also treatment of malignant pheochromocytoma. 131I-MIBG is accumulated specifically in the chromaffin cells and with helpful to find out metastatic foci. It is also used in a large amount as a specific irradiation therapy for this malignancy. Parathyroid cancer is found in approximately 3 percent of primary hyperparathyroidism. Clinically it usually reveal serum calcium level higher than 14 mg/dl, bone lesions and renal dysfunction in addition to palpable cervical tumors adhering with skin. Sometimes it is difficult to differentiate malignancy from adenoma in histology. Most cases develop local recurrences and distant metastases in due course and dies of hypercalcemia. It is very important to control hypercalcemia in inoperable cases. As both chemotherapy and radiation therapy render no effect on this malignancy. Surgery is a sole strategy for it.
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PMID:[Current therapy of endocrine organ tumors (adrenal and parathyroid glands)]. 334 84

Tow of three patients seen with malignant tumor of adrenals had very large lesions and the outcome was rapidly fatal. Excision of tumor was possible in the third case and the patient is in good health two years after operation. Clinical signs are infrequent and diagnosis of an adrenal lesion is mainly dependent on combined ultrasound-scan imaging, with confirmation by histology. Differential diagnosis is necessary between adrenal cortex adenoma and pheochromocytoma. Malignancy is suspected from signs of extratumoral invasion and a tumor weight of over 100 g. Histologic findings are not always specific. Treatment is almost exclusively surgical, complementary therapy being unnecessary in non-secreting pheochromocytoma. Attempts to treat malignant adrenal cortex masses by o,p-DDD have not improved prognosis. The chance discovery of a small tumor requires either routine excision of mass to prevent progression of certain malignant tumors, or simple surveillance, particularly after 50 years of age, since many of these tumors are benign: the decision for choice of therapy is a debatable subject.
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PMID:[Non-secreting malignant tumors of the adrenals. Apropos of 3 cases]. 383 97

We reviewed 150 findings in 58 patients (14 males and 44 females) with adrenocortical tumors (26 with adenoma and 32 with carcinoma) admitted to Vanderbilt Hospital during 28 years. In general, our findings agree with those reported by others in multi-institutional series or literature reviews. Adenomas took longer to diagnose than carcinomas. Adenomas usually caused Cushing's syndrome, but two caused virilization and three caused no endocrine syndrome. There was no difference in time required for diagnosis of carcinoma in men or women or in those with Cushing's syndrome, virilization or no endocrine syndrome. Urinary 17-hydroxycorticoid (17-OHCS) levels were similar in those with adenoma and those with carcinoma, but 17-ketosteroid (17-KS) levels were usually less than 20 mg per day in patients with adenoma and greater than 20 mg per day in patients with carcinoma. Adenomas were uniformly independent of endogenous ACTH stimulation, but frequently responded to exogenous ACTH. As with adenomas, no carcinoma demonstrated normal suppression with dexamethasone or normal response to metyrapone, but only one responded to exogenous ACTH. Some patients had no clinical Cushing's syndrome despite high levels of plasma cortisol and urine 17-OHCS. "Nonfunctional" tumors probably merely secreted insufficient steroids to cause signs and symptoms. Patients with adenoma were uniformly cured by surgical tumor resection. Occasional patients with carcinoma enjoyed long survival despite incomplete resection of their tumors, but most patients died of recurrent of metastatic carcinoma within seven years, often within a year of two. Small tumor size and benign histologic features were insufficient to predict benign clinical behavior. The adrenocorticolytic drug, o,p'DDD, offered objective remission for only an occasional patient.
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PMID:Clinical and laboratory findings and results of therapy in 58 patients with adrenocortical tumors admitted to a single medical center (1951 to 1978). 627 75

Adrenocortical tumors can be divided into two groups based on their histopathological characteristics, i.e., benign (adenoma) and malignant (carcinoma), and also classified as functioning (or hormonal) and non-functioning (or non-hormonal) tumors, depending on the presence or absence of recognizable clinical syndromes due to excessive steroids. The syndrome of functioning adrenocortical tumors includes Cushing's syndrome, primary aldosteronism and the adrenorge genital syndrome, of which a minority presents most of the specific clinical features: Cushing's syndrome; red face, typical moon face, truncal obesity, and purplisch red striae, primary aldosteronism; muscle weakness, noctural polyuria, hypertension and hypokalemia, adrenogenital syndrome; virilization or feminization, but many of them present complete clinical picture. The diagnosis of these syndromes needs to measure urinary 17-OHCS and 17-KS and plasma concentrations of cortisol, aldosterone, dehydroepiandrosterone (DHEA) and the other steroids. Dexamenthasone suppression test, various stimulation tests and the measurement of plasma ACTH are also useful for diagnosis. Usually, adrenocortical tumors can be detected preoperatively by physical examination or radiographic studies. Some are massive enough to be palpable through the abdominal wall. Some are large enough to cause displacement of the kidney, as seen intravenous urography. Most are visible by adrenal scintigraphy using 131I-iodocholesterol, computerized tomography, or adrenal arteriography. The standard treatment for adrenocortical tumors are surgical resection. Unresectable adrenocortical carcinomas may be treated with an adrenocorticolytic drug, o'p'-DDD. Metyrapone and aminoglutethimide can be also employed to inhibit the production of steroids.
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PMID:[Diagnosis and treatment of adrenocortical tumors]. 631

Clinical, biochemical, operative, and postmortem findings have established nodular adrenal hyperplasia as a clinicopathologic entity and a cause of Cushing's syndrome. The possibility exists that there is a relationship among the various forms of adrenal and pituitary diseases that lead to hyperadrenocorticism. This may include a continuous sequence from bilateral adrenal hyperplasia to micronodular and macronodular hyperplasia to a unilateral adrenocortical adenoma and even carcinoma. We report the investigation and management of six patients with Cushing's syndrome caused by bilateral nodular adrenal hyperplasia who were treated by operation at the Glasgow Royal Infirmary, Scotland from 1975 to 1979. Investigations included a variety of biochemical and radioimmunoassay tests on plasma and urine, provocative and inhibition tests, scanning (ultrasonography, computed tomography, and iodocholesterol), arteriography, and selective venous sampling. All patients underwent a bilateral adrenalectomy by the posterior approach. The adrenal glands varied in size from 4.9 to 18 gm and histology showed that they had the features of bilateral nodular adrenal hyperplasia. Five patients did well after operation; they are presently receiving replacement steroid therapy, and at a 3- to 7-year follow-up there was no evidence of Nelson's syndrome. Advances in drug therapy (medical adrenalectomy) with aminoglutethimide, metyrapone, and O,p-DDD should not at present cause a change in our surgical approach to this condition.
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PMID:Nodular adrenal hyperplasia and Cushing's syndrome. 664 5

Laparoscopic adrenalectomy has become increasingly popular because of its minimally invasive nature, but guidelines for selection of cases suitable for this surgical procedure have not been established. We report a 52-year-old woman with adrenocortical carcinoma, manifesting as Cushing's syndrome, treated with laparoscopic adrenalectomy. The tumour was removed in toto and had been histologically diagnosed as adrenocortical adenoma. However, the patient developed intra-abdominal peritoneal dissemination of carcinoma 15 months after surgery. Review of the histopathological findings of the resected adrenocortical tumour revealed that the neoplasm met five out of nine histological criteria for adrenocortical malignancy, and was diagnosed as adrenocortical carcinoma. Histopathological examination of the tumour was also consistent with adrenocortical carcinoma. The patient responded extremely well to chemotherapy, including carboplatin, etoposide and o,p'-DDD (1,1-dichlorodiphenyldichloroethane), and a subsequent CT (computed tomography) scan 12 months after the start of chemotherapy demonstrated no evidence of disease. However, the patient developed neurological impairment, including dysarthria, as a side-effect of o, p'-DDD. The patient died of aspiration pneumonia due to a decreased pharyngeal reflex. Postmortem examination revealed no foci of residual carcinoma. This case report emphasizes the importance of excluing possible adrenocortical malignancy in patients considered for laparoscopic adrenalectomy, histopathological diagnosis of adrenocortical malignancy and careful monitoring for neurotoxicity during o,p'-DDD treatment.
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PMID:A case of adrenocortical carcinoma associated with recurrence after laparoscopic surgery. 1093 Nov 7

According to current concepts, benign proliferative breast disease (BPBD) is a direct precursor of breast cancer, in a spectrum ranging from ductal hyperplasia to overtly invasive carcinoma. In this study, comparative genomic hybridization (CGH) was used to screen ductal hyperplasia and other BPBD lesions and ductal carcinoma in situ (DCIS) for common genomic abnormalities, to test the relationship between these hyperplastic and neoplastic lesions. Immunohistochemistry for cytokeratin 5/6 was used as a diagnostic adjunct to distinguish ductal hyperplasia from DCIS. A total of 42 cases of BPBD comprising ductal hyperplasia of the usual type (n=14), papilloma (n=22), tubular adenoma (n=3), and adenosis (n=3), as well as 52 cases of DCIS, were studied. All cases of BPBD consistently displayed the presence of a subpopulation of cytokeratin 5/6-expressing basal-type cells within the proliferative lesion, whereas all of the non-high-grade and most of the high-grade DCIS lesions lacked cytokeratin 5/6-positive cells. Whereas gross genomic alterations, as determined by CGH, were undetectable in BPBD, distinct genetic changes characterized all cases of DCIS, with one exception. These results confirm the usefulness of cytokeratin 5/6 immunohistology in the diagnosis of BPBD and neoplastic breast lesions and support the view that BPBD and DCIS are not closely related entities and that BPBD is not an obligate direct precursor of DCIS.
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PMID:Ductal epithelial proliferations of the breast: a biological continuum? Comparative genomic hybridization and high-molecular-weight cytokeratin expression patterns. 1247 19

Immunohistochemistry with different cytokeratin subsets has been successfully used in the differential diagnosis of various human epithelial neoplasms. Cytokeratin 5/6 antibody, which recently became commercially available, has been found useful in the diagnosis of mesothelioma. Studies have reported only infrequent staining in adenocarcinomas. We investigated the pattern of immunoreactivity for cytokeratin 5/6 in hepatobiliary and pancreatic tumors to determine its diagnostic utility in the morphologic evaluation of these neoplasms. Formalin-fixed. paraffin-embedded tissue sections from 10 hepatocellular carcinomas, seven hepatocellular adenomas, 10 cholangiocarcinomas, 10 pancreatic ductal adenocarcinomas, and 13 pancreatic neuroendocrine carcinomas were immunostained with anticytokeratin 5/6 after heat-induced antigen retrieval utilizing a modified avidin-biotin complex technique. Positive and negative controls stained appropriately. Two pathologists evaluated the slides. Strong but focal cytoplasmic immunoreactivity was observed in five of 10 pancreatic ductal adenocarcinomas and two of 10 cholangiocarcinomas. No immunoreactivity was identified in any cases of hepatocellular carcinoma (0/10), hepatocellular adenoma (0/7), or pancreatic neuroendocrine carcinoma (0/13). Additionally, occasional cytokeratin 5/6 immunoreactive benign ductal epithelial cells were seen in the background in some cases. Fifty percent of pancreatic ductal adenocarcinomas and 20% of cholangiocarcinomas are positive with anti-cytokeratin 5/6 immunostaining. For the evaluation of poorly differentiated neoplasms in the liver, immunoreactivity with cytokeratin 5/6 may help to exclude the possibility of hepatocellular carcinoma. Cytokeratin 5/6 may be helpful as a component in the panel of immunostains to differentiate between poorly differentiated neoplasms.
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PMID:Cytokeratin 5/6 immunostaining in hepatobiliary and pancreatic neoplasms. 1205 33


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