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Query: UMLS:C0001430 (adenoma)
 21,222 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Adrenal venous sampling of blood was performed for nine patients with aldosterone-producing adenoma (APA). Measurement of adrenal venous aldosterone is useful for localization of APA but difficult, because catheterization of the right adrenal vein is not easy, and the blood is diluted by nonadrenal flow. To solve these problems, levels of aldosterone (A; ng/dl) and cortisol (C; micrograms/dl) were measured in samples from the left adrenal vein (LAV) and the inferior vena cava (IVC), and the LAV A/C and (LAV A/C)/(IVC A/C) ratios were calculated. These ratios were also obtained for 16 patients with essential hypertension. The adenoma could be localized in three of the nine cases by the measurement of aldosterone alone, but the use of a LAV A/C ratio greater than 5 x 10(-3) and a (LAV A/C)/(IVA A/C) ratio less than 1.0 as criteria separated the patients into those with a left APA, right APA, or essential hypertension. Consequently, adrenal venous sampling and the calculation of these ratios enables preoperative localization of APA with more accuracy, especially when the tumor is small or the result of CT and adrenal scintigraphy is not consistent.
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PMID:Localization of aldosterone-producing adenoma: venous sampling in primary aldosteronism. 238 50

Dexamethasone-suppression (DS) adrenal scintigraphy localizes an aldosteronoma, but with false-negative results, i.e. 2 of 19 cases in our study. Our aim was to clarify the clinical meaningfulness of this test. Adrenal iodomethyl-norcholesterol (NP-59) uptake on the adenoma side correlated with the estimated adenoma volume (n = 15, r = 0.843, P less than 0.001). Accordingly, the uptake ratio on the adenoma side to that on the opposite side depended on the adenoma volume (r = 0.683, P less than 0.01). This explains the false-negative results (uptake ratio less than 2) in two cases with small adenomas. The NP-59 uptake correlated weakly with the plasma aldosterone level (r = 0.516, P less than 0.05). This result indicates the low correlation between NP-59 uptake and the ability to secrete aldosterone. NP-59 accumulation in the surgically removed gland was analyzed by autoradiography in six cases where DS scintigraphy was done just before surgery. The density was higher in the adenoma cells than in the adjacent cortical cells in five cases, but the difference was rather small, i.e., within a 2-fold difference in four cases. In one case, almost the same density was observed in both types of cells. Thus, the laterality of NP-59 uptake primarily depends on the adenoma volume although NP-59 uptake somewhat reflects the adenoma's ability to secrete aldosterone or the adenoma cell's activity in accumulating NP-59. Care must be taken in interpreting the findings from DS scintigraphy where the adenoma is small or adrenal uptake is low.
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PMID:Iodomethylnorcholesterol uptake in an aldosteronoma shown by dexamethasone-suppression scintigraphy: relationship to adenoma size and functional activity. 240 12

Plasma concentrations of atrial natriuretic factor and some vasoactive substances were determined in 8 patients with aldosterone-producing adenoma, 10 with idiopathic adrenal hyperplasia, 10 normotensive subjects and 12 patients with essential hypertension. Plasma atrial natriuretic factor concentration in patients with aldosterone-producing adenoma was the highest among the examined groups. Adrenal surgery reduced plasma concentrations of atrial natriuretic factor and aldosterone concomitant with the elevation in urinary sodium excretion, plasma renin activity and urinary sodium-to-potassium ratio. Withdrawal of trilostane (3 beta-hydroxysteroid dehydrogenase inhibitor) in patients with idiopathic adrenal hyperplasia increased plasma concentrations of atrial natriuretic factor and aldosterone, and decreased the urinary sodium-to-potassium ratio, plasma renin activity and urinary sodium excretion. However, reduced urinary sodium excretion following trilostane treatment returned to the control level successively despite the high levels of plasma atrial natriuretic factor and aldosterone. Acute infusion of saline remarkably increased plasma atrial natriuretic factor concentration in patients with idiopathic adrenal hyperplasia and aldosterone-producing adenoma. These results suggest that a high level of atrial natriuretic factor is a characteristic feature in patients with aldosterone-producing adenoma caused chiefly by the expansion of extracellular fluid volume, and circulating atrial natriuretic factor may contribute to regulation of the sodium escape phenomenon in patients with aldosterone-producing adenoma or idiopathic adrenal hyperplasia.
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PMID:The effect of adrenal surgery on plasma atrial natriuretic factor and sodium escape phenomenon in patients with primary aldosteronism. 252 99

Cross-sectional imaging techniques have dramatically improved the diagnosis of adrenal disease. In most patients with endocrine-active adrenal disease, CT is the only imaging test needed to establish the correct diagnosis. Adrenal venography with blood sampling may provide important additional information in patients with Conn adenoma. Magnetic resonance imaging and (IMBG) scintigraphy appear to be the best imaging tests for the localization of multiple or extra-adrenal pheochromocytomas. Inactive adrenal tumors detected incidentally are a problem as for as diagnosis is concerned, since inactive adrenal adenomas have to be differentiated from carcinomas and metastases. MRI is rarely helpful in these cases. For patients with a known primary tumor, the authors recommend CT-guided biopsy. In all other cases a follow-up study often reveals that the adrenal tumor detected is benign.
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PMID:[Current developments in the radiologic diagnosis of the adrenal glands]. 264 16

Adrenal incidental tumors are masses incidentally discovered on ultrasonography or CT for other abdominal disorders. Management depends on tumor size, nature, content, and hormonal behaviour. We report on a large, nonfunctioning adrenocortical adenoma that was incidentally discovered in a 59-year-old male patient with right-sided costo-lumbar trauma.
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PMID:[Incidental adrenal tumor: non-functioning cortical adenoma]. 267 80

A 47-year-old female presented with hypertension, hypokalaemia, low plasma renin, high plasma aldosterone and was found to have a left adrenal tumour 4 cm in diameter by computerized tomography. Detailed biochemical studies showed high plasma levels of 11-deoxycorticosterone and corticosterone in addition to aldosterone and 18-hydroxycorticosterone. Basal 11-deoxycorticosterone levels were particularly high. Corticosterone, 18-hydroxycorticosterone and aldosterone concentrations were abnormally sensitive to infusions of ACTH and angiotensin II. Plasma cortisol and assays for sex hormones were normal although there was evidence that cortisol derived from the neoplasm. At operation a well-differentiated adrenocortical carcinoma weighing 50 g (56 X 30 X 36 mm) was removed. There was no evidence of metastases following surgery. Adrenal function returned to normal. Review of the literature suggests that adrenocortical carcinoma should be suspected in patients who otherwise have typical features of Conn's syndrome, but whose tumours are more than 3 cm in diameter. Measurement of steroids such as 11-deoxycorticosterone in addition to aldosterone is recommended since abnormally high values may also help to distinguish between hyperaldosteronism due to adenoma and carcinoma. Previously reported cases of isolated aldosterone production by a carcinoma cannot be substantiated.
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PMID:Hypermineralocorticoidism due to adrenal carcinoma: plasma corticosteroids and their response to ACTH and angiotensin II. 282 95

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

We describe the third report testosterone-producing, virilizing, adrenal Leydig cell adenoma, which was identified in a oophorectomized postmenopausal female patient. Light- and electron-microscopy demonstrated typical Leydig cell differentiation, including numerous intracytoplasmic and intranuclear Reinke crystals and rice-like bodies (elementary tubular inclusions). Testosterone production by the adenoma was demonstrated by the immunoperoxidase technique. We propose that adrenal Leydig cell adenomas arise as a result of ovarian gonadal stromal metaplasia associated with elevated follicle-stimulating hormone and luteinizing hormone in the postmenopausal female patient. Adrenal Leydig cell lesions must be considered in the virilized woman with elevated testosterone levels and normal levels of the adrenal androgens and their 17-ketosteroid metabolites.
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PMID:Virilizing Leydig cell adenoma of adrenal gland. 302 13

After diagnosis of primary aldosteronism on the basis of biochemical evidence, the detection of the tumour is of crucial importance in the management of the disease. We reviewed the efficacy of CT-Scan, Iodo-Cholesterol Scintigraphy, digitalized phlebography, adrenal vein sampling for steroid measurements (AVS), and Nuclear Magnetic Resonance (NMR) in 160 hypertensive patients with primary aldosteronism. Diagnosis of Conn's adenoma (n = 96) or Adrenal Hyperplasia (n = 40) was confirmed by surgery or at least two concordant tumour localization tests. Scintigraphy gave a correct diagnosis in 53% of the 51 exams, CT-Scan in 82% of the 85 exams, and phlebography in 79% of 61 exams. Plasma Aldosterone/Cortisol ratio was 5 times higher on the side of adenoma in 55% of the 47 cases but this ratio was also present in 23% of 22 patients with adrenal hyperplasia. Each procedure exhibited few false positive and false negative cases. NMR performed in 15 patients with Conn's adenoma identified all the cases. But tumours displayed a signal close to the liver signal and identical to the normal adrenal. These results and the risk of invasive procedure (failure of catheterization of the right adrenal vein (n = 6) and adrenal haematoma (n = 2) lead us to propose a schema of exploration of patients with primary aldosteronism. The CT-Scan could be performed at the first step once the biological diagnosis confirmed. Phlebography and AVS will be performed only if tumour was less than 1 cm at the CT-Scan despite important biological abnormalities. This schema requires to be validated by a prospective evaluation.
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PMID:[Localization of primary hyperaldosteronism]. 320 1

19-Nor-deoxycorticosterone is a newly recognized mineralocorticoid which has been associated with some forms of genetic, experimental, and human hypertension. To further examine this relationship, specific inhibitors of 19-nor-deoxycorticosterone biosynthesis must be developed. Since 19-hydroxylation is the pivotal step in both 19-nor-deoxycorticosterone biosynthesis and aromatization of androgens to estrogens, we evaluated an aromatase inhibitor, 4-hydroxyandrost-4-ene-3,17-dione on the inhibition of 19-hydroxylation in both rat and human adrenal mitochondria in vitro and 19-nor-deoxycorticosterone production and blood pressure in spontaneously hypertensive rats in vivo. Adrenal mitochondria from 48 male Sprague-Dawley rats and 1 patient with an aldosterone-producing adenoma were incubated in the presence of deoxycorticosterone substrate both with and without 4-hydroxyandrost-4-ene-3,17-dione. 4-Hydroxyandrost-4-ene-3,17-dione produced significant inhibition of 19-hydroxy-deoxycorticosterone production in both rat and human adrenal mitochondria, with a smaller and not significant inhibition of corticosterone and 18-hydroxy-corticosterone. 4-Hydroxyandrost-4-ene-3,17-dione given subcutaneously to spontaneously hypertensive rats lowered 19-nor-deoxycorticosterone by 69% and completely abolished hypertension compared to Wistar-Kyoto controls. These data demonstrate that 4-hydroxyandrost-4-ene-3,17-dione is a specific inhibitor of 19-hydroxylase, that it lowers 19-nor-deoxycorticosterone production and prevents hypertension in the spontaneously hypertensive rat. These studies reinforce the possible pathogenic significance of 19-nor-deoxycorticosterone in hypertension in spontaneously hypertensive rats.
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PMID:Selective 19-hydroxylase inhibition by an aromatase inhibitor, 4-hydroxyandrostenedione. 320 87


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