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

In a prospective study of 37 patients who had unilateral adrenalectomy for an aldosterone-producing adenoma, five of 33 (15%) were symptomatically hypotensive after at least 1 year, and eight of 29 (28%) who were observed 3, 6, 12, 18 and 24 months after the operation showed 2-year blood pressures below the fifth percentile for age- and sex-matched controls. Postoperatively, plasma aldosterone was lower, and plasma renin activity higher than in controls, these differences being more marked in the hypotensive group. Pre-operatively elevated atrial natriuretic factor fell to levels lower than in controls. These serial changes in volume-regulatory hormones are consistent with chronic hypovolaemia, due to relative hypoaldosteronism. Plasma cortisol was lower 6 months after the operation and plasma adrenaline levels fell by half. A reduced adrenocortical (aldosterone and cortisol) and adrenomedullary (adrenaline) secretory mass may play a role in the hypotension observed after unilateral adrenalectomy.
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PMID:Reduced adrenal secretory mass after unilateral adrenalectomy for aldosterone-producing adenoma may explain unexpected incidence of hypotension. 269 27

A 37-year-old woman presented with hyperaldosteronism, suppressed renin levels, and a left adrenal mass on CT scanning. Selective adrenal venous sampling indicated a marked rise of the aldosterone level in the right adrenal vein, while the level in the left vein was low. On laparotomy, an aldosterone producing adenoma (APA) of 12x10x5 mm in size was found in the right adrenal gland and was resected, while the left mass was left in situ. The post-operative course showed normalization of both the clinical and biochemical features of primary aldosteronism, with no sign of recurrence or of enlargement of the remaining adrenal mass in 2.5 years of follow up, suggesting the possible coexistence of a "non-functioning" tumor. This case demonstrates the importance of adrenal venous sampling for the localization of APA particularly since the presence of the APA may be masked by a visualized but unrelated adrenal mass.
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PMID:Possible association of aldosterone producing adenoma and non-functioning adrenal tumor. 272 41

1. Serial observations of blood pressure after unilateral adrenalectomy for aldosterone-producing adenoma revealed an incidence of hypotension (systolic BP less than fifth percentile for age- and sex-matched normal population) of 27% at 2 years, more than 5 times that predicted. 2. Serial observations of volume regulatory hormones showed significantly raised mean levels of plasma renin activity consistent with hypovolaemia. Significantly reduced mean aldosterone levels despite significantly raised mean plasma renin activity levels may reflect reduced responsiveness of the remaining adrenal. 3. Reduction of significantly elevated preoperative ANP levels to significantly reduced levels postoperatively is also in keeping with postoperative hypovolaemia. 4. A 50% reduction in plasma adrenaline after unilateral adrenalectomy might contribute to reduced noradrenergic activity (prejunctional beta-receptor) and reduced blood pressure, but plasma noradrenaline did not fall significantly postoperatively. 5. Postoperative levels of renin, aldosterone, adrenaline and noradrenaline were not significantly different between those who did, and those who did not, become hypotensive.
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PMID:Unexpected incidence of low blood pressure 2 years after unilateral adrenalectomy for primary aldosteronism. 274 20

One must consider the 17-DOS as a biosynthetic pathway with multiple regulatory factors. ACTH is its dominant regulator but in the absence of ACTH and in conditions where plasma renin activity is increased, this biosynthetic pathway maintains its sensitivity to exogenous ACTH. Suppression of the renin system delays the general recovery of aldosterone after the removal of an aldosterone producing adenoma but not of the 17-DOS: a pattern also showed after the removal of a DOC-producing adenoma. In addition to the possible role of the renin system there remain inexplicable situations in its regulation that cannot be explained by ACTH and renin. Our studies suggest that a non-renin, non-ACTH factor may influence the basal production of these steroids, and by its reduction, permits deviation of steroid substrate to cortisol production. This sequence may be operative in the "stress syndrome". Finally, one of the more interesting phenomenonologic patients who has been observed is a young male who has the biochemical findings and clinical signs of DOC excess with hypertension, hyperplasia, suppression of aldosterone and the RAS, and normal cortisol levels. All the 17-DOS are elevated and both adrenal veins have high concentrations. He represents excessive stimulation of this pathway by putative 17-deoxy regulator excess. The renin system is suppressed and ACTH levels are normal. Treatment with suppressive doses of glucocorticoid hormones diminishes the elevated 17-DOS and cortisol and ameliorates blood pressure. In summary, there seems to occur in clinical disorders and contrived experimental settings, suggestions that a non-renin, non-ACTH factor can regulate the 17-DOS, absence can explain some of the unusual conditions described (Fig. 1). The 17-DOS, while a vestigial pathway, may still cause disease, and provide clues to central organization of the adreno-cortical response to injury, stress, and disease.
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PMID:The regulation of the 17-deoxy steroids in man. 275 48

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

1. A subgroup of patients with aldosterone-producing adenoma (APA) have been identified who lack many of the biochemical features regarded as characteristic of APA and used to distinguish APA from bilateral adrenal hyperplasia. 2. In these patients, aldosterone is responsive to infused angiotensin II (angiotensin-responsive APA), which explains their uncharacteristic responses to upright posture, saline infusion and fludrocortisone acetate administration. 3. The angiotensin-responsiveness of these patients may derive from the contralateral adrenal gland, since renin levels are less completely suppressed in angiotensin-responsive APA than in angiotensin-unresponsive APA. 4. However, while the excretion of 18-oxo-cortisol was consistently increased in angiotensin-unresponsive APA, it was normal in angiotensin-responsive APA, consistent with biochemical and biosynthetic distinctiveness residing in the tumours. 5. Angiotensin-responsive APA should always be considered as an alternative diagnosis to bilateral hyperplasia causing primary aldosteronism.
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PMID:Aldosterone-producing adenomas responsive to angiotensin pose problems in diagnosis. 282 5

Two patients with hypermineralocorticoidism due to deoxycorticosterone (DOC) excess are described. The plasma 17-deoxysteroids of the zona fasciculata (ZF), namely DOC, corticosterone, 18-hydroxydeoxycorticosterone, and 18-hydroxycorticosterone, were elevated. Plasma androgen concentrations were normal, and plasma aldosterone and renin levels were low. One patient, who had benign adrenocortical adenoma, had normal plasma cortisol levels. The other patient, who had metastatic adrenocortical carcinoma, had low plasma cortisol, presumably due to elevated plasma corticosterone levels. While tumors producing only 17-deoxysteroids are rare, they have provided new insights into the regulation of 17-deoxysteroid secretion by the ZF. Presumptive suppression of a non-ACTH factor by adenoma-produced DOC transiently impaired the early postoperative responses to ACTH of the ZF 17-deoxysteroids of the contralateral adrenal. The dissociation of 17-deoxysteroids from cortisol in normal subjects given either dexamethasone or DOC acetate provides additional evidence for such a factor.
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PMID:Pathophysiology of deoxycorticosterone-secreting adrenal tumors. 282 55

We have identified a subgroup of patients with aldosterone-producing adenoma (APA) who are responsive to angiotensin. Thus, a fall in plasma aldosterone (PA) during saline infusion may cause confusion with low-renin essential hypertension. Responsiveness of PA to angiotensin infusion and to upright posture may cause confusion with bilateral hyperplasia. Renin levels were not as completely suppressed in this angiotensin-responsive subgroup, leading to speculation that non-tumorous adrenal glomerulosa might also be less suppressed and might respond to angiotensin. This is unlikely, since angiotensin infusion soon after removal of the adenoma produced aldosterone levels of less than 10% of those achieved preoperatively. A biosynthetic peculiarity of the tumours is more likely, since urinary 18-oxo-cortisol levels were normal in this subgroup (as in bilateral hyperplasia) and raised in the more typical angiotensin-unresponsive subgroup (as in glucocorticoid-suppressible hyperaldosteronism). Since angiotensin-responsive tumours respond just as well to surgery as angiotensin-unresponsive tumours, it is important not to misdiagnose this subgroup as bilateral hyperplasia or low-renin essential hypertension.
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PMID:Angiotensin-responsive aldosterone-producing adenoma masquerades as idiopathic hyperaldosteronism (IHA: adrenal hyperplasia) or low-renin essential hypertension. 283 71

The effects of ovine corticotropin releasing factor (o-CRF) on plasma aldosterone, 18-OH-corticosterone (18-OHB), plasma adrenocorticotropin (ACTH) and cortisol were determined in eight patients with primary aldosteronism, six with aldosterone-producing adenoma (APA) and two with idiopathic hyperaldosteronism (IHA). The results were compared with those in six normal subjects and eleven patients with essential hypertension (EHT, 5 with low renin and 6 with normal renin). In patients with APA, the peak plasma aldosterone and 18-OHB responses to 100 micrograms iv of o-CRF (226% and 113% increase from baseline, respectively) were greater than those in EHT and normal subjects. The net integrated aldosterone and 18-OHB responses (840 +/- 156, and 419 +/- 121 ng/dl.hr, respectively) were also significantly greater (p less than 0.01) in APA than those in normals and EHT. In two patients with IHA, both the peak and net integrated aldosterone response were smaller than those in APA, in spite of nearly identical plasma ACTH and cortisol responses. These results suggest that augmented responses of mineralocorticoids to o-CRF may be characteristic of aldosteronism due to APA, mediated by CRF-induced ACTH, and possibly other proopiomelanocortin (POMC)-derived peptides.
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PMID:Effects of corticotropin-releasing factor (CRF) on aldosterone and 18-hydroxycorticosterone in essential hypertension and primary aldosteronism. 283 82

Endogenous opioids have been suggested to play a pathogenetic role in idiopathic hyperaldosteronism (IHA). To investigate this issue, the opiate antagonist naloxone was administered to 8 normals and 14 patients with primary aldosteronism, 6 with an aldosterone-producing adenoma (APA) and 8 with IHA. In normals, APA, and IHA, naloxone caused a significant increase in plasma cortisol and no change in ACTH, renin activity (PRA), and aldosterone levels. All subjects were retested after dexamethasone 2 mg. ACTH and cortisol were reduced and PRA was unchanged without modifications after naloxone. Baseline aldosterone was unaltered in all. While normals and APA failed to show any aldosterone response to naloxone under dexamethasone, IHA patients demonstrated a significant decrease. beta-Endorphin concentrations were in the normal range before and after dexamethasone. In normals as well as in APA and IHA, naloxone may act directly on the adrenal cortex increasing zona fasciculata responsiveness to physiological levels of ACTH. The decrease of aldosterone induced by naloxone in IHA under dexamethasone may be due to an intra-adrenal opioid control of zona glomerulosa in this disorder.
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PMID:Effect of naloxone on the adrenal cortex in primary aldosteronism. 283 6


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