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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Leydig cell carcinoma of the testicle is a rare tumor with 16 well-documented cases in the medical literature. Radiotherapy and chemotherapy have not been successful in treating patients with metastatic disease. The patient described in this report had widely metastatic Leydig cell carcinoma associated with hypertension, hypokalemic alkalosis, and an elevated serum concentration of desoxycorticosterone. He experienced an objective clinical remission and disappearance of pulmonary metastases while receiving o,p'-DDD as the sole chemotherapeutic agent. This response was similar to that found in patients with adrenal cortical carcinoma. The regression of this tumor with an adrenolytic agent, in conjunction with the similar morphologic and biochemical features of these two types of tumors, provides additional evidence of the close similarity between Leydig cell carcinoma and adrenal cortical carcinoma.
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PMID:Malignant Leydig cell tumor: objective tumor response to o,p'-DDD. 722 52

For the purpose of studying the relation of diversities of basic lesion as well as clinical manifestation to hormonal abnormality in Cushing's syndrome, 12 kinds of steroid hormones was simultaneously measured in plasma by using 2 types of Sephadex LH-20 column chromatography in a total of 30 patients comprosing 28 cases of Cushing's syndrome and 2 cases of adrenocortical carcinoma which had abnormal plasma steroid hormone levels without sign or symptom of Cushing's syndrome. In the group of Cushing's syndrome were included cases of pituitary ACTH-dependent hyperplasia (Hp.), adrenocortical adenoma(Ad.), bilateral nodular hyperplasia, ectopic ACTH syndrome as well as recurrent Cushing's syndrome following subtotal adrenalectomy. Twelve steroids measured in plasma were pregnenolone(Preg)., 17-OH pregnenolone(17Preg.), progesterone(Prog.), 17-OH progesterone(17Prog.), 11-deoxycorticosterone (DOC), corticosterone(B), aldosterone(Ald.), 11-deoxycortisol(S), cortisol(F), dehydroepiandrosterone(DHA), androstendione(A-dione) and testosterone(T), including precursors (Prec.: Preg., 17-preg., Prog., 17-prog.) as well as hormones belonging to the 3 systems in the biosynthetic pathways of steroid; i.e., glucocorticoids(Glu.C.'s: S,F), mineralocorticoids(Min.C.'s: DOC, B, Ald.) and sex steroids(And.'s: DHA, A-dione, T). In addition, steroidogenesis in isolated adrenal cells obtained surgically from patients with Cushing's syndrome due to Hp. and Ad, was observed. The results were as follows: (1) In cases due to Hp., plasma levels of Glu.C's and And.'s were slightly elevated, while levels of Min.C.'s were within the normal range. On the whole, however, the 3 systems were well balanced. (2) In cases due to Ad., elevated secretion of Glu.C.'s and Min.C.'s was observed, while secretion of And.'s was depressed. Among the 3 fractions of And.'s, depression of DHA and A-dione was characteristic of Ad.. (3) Elevation of And.'s in Hp. and Min.C.'s in Ad. in addition to elevation of Glu.C.'s was in fair correlation with moderate virilism in Hp. and with hypertension and hypokalemia in Ad. respectively. (4) In vitro experiments revealed that Ad. produces not only F but all 12 steroids hormones and that increased DOC and depressed DHA secretion reflected in their plasma levels were the characteristics of Ad. in steroidogenesis. Furthermore, isolated adenoma cells were found to produce Ald. at a higher rate than normal or hyperplasia adrenal cells. This finding may suggest that an intermediate type between Cushing's syndrome and primary hyperaldosteronism can exist in cases of adenoma. (5) In ectopic ACTH syndrome, plasma levels of Glu.C.'s, Min.C.'s and And.'s were equally but more markedly elevated as compared with Hp.. The increase of B was characteristic of this disorder and, coupled with a marked increase of F, seems to be the main cause of hypokalemic alkalosis frequently associated with this syndrome. (6) Nodular hyperplasia was accompanied by elevated Min.C...
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PMID:[Plasma steroid hormones in Cushing's syndrome: their relation to cause and clinical manifestations (author's transl)]. 728 45

A 39-year-old male presented with gross hematuria and left lower abdominal discomfort. Excretory urography showed a left ureteral stone and hydronephrosis. CT scans and magnetic resonance imaging showed a solid mass at the upper pole of the left kidney. Angiography revealed a hypervascular lesion at this area. The laboratory data showed a slightly decreased serum potassium level. In the endocrinological study, the serum deoxycorticosterone (DOC) level was markedly elevated. There was, however, no evidence of hypertension. The operation was performed on November 13, 1992. The tumor was almost separated from the left kidney, but an aberrant artery which divided from the renal artery and penetrated the renal parenchyma was found. Therefore, we had to carry out en bloc removal of the tumor together with the left kidney and the ureter which contained the ureteral stone. Pathological diagnosis was adrenocortical carcinoma. After the operation, hypokalemia and the serum concentration of DOC returned to normal range. Therefore, the tumor was diagnosed as DOC producing adrenocortical carcinoma. The patient was discharged 30 days after the operation with uneventful postoperative course. He received 2.5 g of op'-DDD a day. There was no evidence of distant metastasis or local recurrence 12 months after the operation. Nineteen cases of DOC producing adrenocortical tumor have been reported in the world literature. A case and a review of the literature are herein reported.
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PMID:[Deoxycorticosterone-producing adrenocortical carcinoma--a case report]. 777 67

An 18 year old woman with congenital hemihypertrophy of her left side, presented with the rapid onset of virilism, hypertension and a cushingoid appearance. A computed tomographic examination revealed adrenal and hepatic masses. Adrenocortical carcinoma was confirmed by surgical pathology. Hemihypertrophy is linked to a variety of benign and malignant disorders that usually appear during childhood. These disorders include adrenocortical carcinoma and hepatoblastoma. We bring this case to clinical attention to increase awareness that adult patients with congenital hemihypertrophy are still at a significant risk of developing neoplasms.
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PMID:A virilized patient with congenital hemihypertrophy. 783 Nov 77

A 45-year-old man presented with gynecomastia, hypertension and a large left adrenal mass. Further evaluation revealed elevated serum concentrations of estrogen, estrone sulfate, androstenedione, dehydroepiandrosterone, dehydroepiandrosterone sulfate, deoxycorticosterone, and aldosterone and increased 24-hour urinary 17-ketosteroid and free cortisol excretion. Removal of a 10 kg adrenocortical carcinoma led to normalization of the hormone concentrations and partial resolution of the gynecomastia. There was no clinical evidence of metastases. Incubation of tumor slices demonstrated that the tumor had an active aromatase and sulfotransferase. We estimated that about half the serum estrone arose from peripheral conversion of androstenedione. Feminizing adrenocortical carcinomas are rare and this case is unusual given the lack of clinical metastases and the probable dual source of estrogen from tumor as well as from the peripheral conversion of tumor-derived androgens.
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PMID:Feminization as a result of both peripheral conversion of androgens and direct estrogen production from an adrenocortical carcinoma. 793 Mar 80

Adrenal tumors showing no clinical manifestations (incidentaloma) are frequently encountered during imaging analysis upon routine examinations. These tumors are sometimes associated with hypertension and/or diabetes mellitus (DM). We have examined six cases of incidentalomas with these symptoms in this study. All patients underwent endocrinological evaluation by measuring plasma cortisol and aldosterone levels to assess adrenocortical function. The levels of urinary 17-hydroxysteroids, 17-ketosteroids and catecholamines were also measured. Imaging analysis were performed by using 131I-adosterol scintigraphy, computed tomography and magnetic resonance imaging. Whereas one case was diagnosed as having an adrenal adenoma without the examination of a surgical specimen, other cases underwent surgical removal of the tumor, and final diagnoses were made by pathohistological examination of the tumors. Three cases were diagnosed as having adrenocortical adenomas (one was functioning and others were non-functioning) and one case was diagnosed as having a functional adrenocortical carcinoma. Adenomas were found to produce either non-functional steroids or a small amount of functional steroid hormones. The adenoma patients all suffered hypertension, whereas one of the adenoma patients and the carcinoma patient showed signs of DM. By contrast, of the six cases, one case was diagnosed as having an adrenal cyst, and one case was diagnosed with myelolipoma. Although these two cases suffered DM and hypertension, respectively, it seemed to be unlikely that these clinical symptoms were caused by the adrenal disease. Thus, the present analysis of the six incidentaloma patients suggests that once an adrenal incidentaloma patient with hypertension and/or DM is found, both endocrinological and imaging examinations are necessary to determine the indication of surgical treatment. This analysis supports the present consensus that non-functional adenomas whose sizes are 3cm or less and whose sizes do not change at any reevaluation period, as well as adrenal cysts and myelolipoma should not be surgically removed.
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PMID:[Endocrinological and imaging analyses of adrenal incidentalomas with hypertension and/or diabetes mellitus]. 800 91

Excessive secretion of aldosterone from the adrenal results in the most common form of endocrine hypertension. An understanding of the regulatory processes involved in aldosterone synthesis and release is needed to define the biomolecular mechanisms controlling excessive production of aldosterone. However, in vitro studies regarding the regulatory mechanisms of human aldosterone production have been limited because of difficulties in obtaining tissue and the subsequent isolation of aldosterone-secreting glomerulosa cells. Herein we describe an adrenocortical carcinoma cell line, NCI-H295, which provides a suitable angiotensin-II (AII)-responsive model system to investigate the acute and chronic regulation of aldosterone synthesis. The cells were characterized with regard to the effects of AII on second messenger systems, aldosterone release, and levels of aldosterone synthase (P450c18) mRNA. In the presence of lithium, AII caused a rapid, but transient, increase in the production of inositol tris- and bisphosphates, whereas a prolonged gradual accumulation of inositol monophosphate occurred. Treatment with AII resulted in a 4.5-fold increase in total inositol phosphates in a concentration-dependent manner and an increase in intracellular cytoplasmic free Ca2+. Significant increases in aldosterone (3.5-fold) were detected within 1 h of AII addition. Aldosterone release occurred in a concentration-and time-dependent manner. The type 1 AII (AT1) receptor was shown to be responsible for activation of phosphoinositidase-C, increased intracellular free Ca2+, and aldosterone production, as determined by use of the AT1 receptor antagonist DuP753. In addition, AII treatment resulted in a time-dependent increase in levels of P450c18 mRNA, as detected by RNAse protection assay. In summary, NCI-H295 cells provide a valuable model system to define mechanisms regulating human aldosterone production.
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PMID:Human NCI-H295 adrenocortical carcinoma cells: a model for angiotensin-II-responsive aldosterone secretion. 840 94

A 29-year-old woman with deoxycorticosterone (DOC)-producing adrenocortical adenoma had hypertension and hypokalemia but without Cushingoid features. Plasma renin activity and the aldosterone concentration were low, while the DOC concentration was high (6.10-10.3 ng/ml; normal range 0.03-0.33). Plasma cortisol, androgens, and estrogens as well as urinary 17-OHCS and 17-KS were within normal limits. Furosemide administration and two hours upright posture resulted in a 3-fold increase in plasma DOC, but the administration of ACTH, dexamethasone, or angiotensin III had no effect on plasma DOC. Following resection of a right adrenal tumor weighing 70 g, the hypertension and hypokalemia disappeared. DOC content in the tumor was high. On light microscopic examination, the tumor was encapsulated, composed of cells with clear cytoplasm and large nuclei and there were extensive areas of fibrosis and infiltration of lymphocytes. According to Weiss's criteria, the tumor was considered to be an adrenocortical adenoma. Immunohistochemically, P450scc, 3 beta HSD, P450C21 and P45011 beta were positive with heterogeneity of intra-tumoral expression. No immunoreactivity for P45017 alpha in this adenoma was detected. This is different from a previous report in which a relatively small number of cells in DOC-secreting adrenocortical carcinoma were positive for P45017 alpha.
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PMID:A case of deoxycorticosterone-producing adrenal adenoma. 857 86

Two cases of adrenal cortical carcinoma in the pediatric age group are reported: the first case regards a fourteen month old female patient which presented with virilization and Cushing's syndrome: the second case regards a twelve year old boy with severe hypertension. Histopathologic distinction between benign and malignant adrenal cortical neoplasms is difficult: the usual cytologic criteria of benignity and malignancy in relation to prognosis are not very helpful while tumor size and tumor invasion appear to be the more important prognostic factors. Therefore early diagnosis, which is easier in the pediatric age because of the more frequent presentation of these neoplasms with hormonal effects, is essential.
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PMID:[Adrenal cortex neoplasms in children: diagnostic and therapeutic difficulties]. 904 94

In untreated hyperadrenocorticism, clinical problems may result from metastasis of an adrenocortical carcinoma, growth of a pituitary tumor, or complications associated with sustained hypercortisolemia itself, such as hypertension, cardiovascular disease, thromboembolism, glucose intolerance, and increased susceptibility to infection. This article discusses the origin, diagnosis, and treatment of the many complications associated with hyperadrenocorticism.
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PMID:Complications and concurrent disease associated with canine hyperadrenocorticism. 907 10


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