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PubMed1993

Estimation of urinary aldosterone using thin-layer chromatography and fluorimetry.

AIMS: To develop a fluorimetric method for the estimation of urinary aldosterone; to establish a normal range in 24 hour and overnight urine samples; and to investigate the use of overnight urines for detecting hyperaldosteronism. METHODS: Essential steps include hydrolysis of the 18 conjugate to release aldosterone and its oxidation with Benedict's solution, followed by thin-layer chromatography on silica gel and development of fluorescence on the plate with sulphuric acid. RESULTS: There was a linear correlation between the amount of aldosterone and the area under the peak on the chromatogram. The mean intra-assay and interassay coefficients of variation were 4.4% and 6.8%, respectively. The mean aldosterone excretion in 67 adults was 15.7 (SD 8.1) nmol/24 hours. The mean overnight excretion in 65 adults was 2.6 (1.4) nmol/8 hours. The method detected raised concentrations in patients with primary and secondary aldosteronism. CONCLUSIONS: This technique provides an accurate means of assaying urinary aldosterone. Overnight estimations seem to be as effective as 24 hour assays for identifying patients with hyperaldosteronism.

Adolescent↗
PubMed1998

Extreme diuretic dependence in idiopathic edema: mechanisms, prevention and therapy.

Idiopathic edema patients abusing diuretics are occasionally becoming dependent to such a degree on increasing doses of diuretics that their withdrawal results in severe cardiorespiratory failure, occasionally even pulmonary edema. Two such patients are described and 1 is investigated in depth as to the mechanism of the diuretic abuse-induced excessive tubular avidity for sodium. An extreme diuretic-induced secondary hyperaldosteronism and atrial natriuretic factor suppression, although tapering off when diuretics are stopped, results in a continuous tubular sodium hyper-reabsorption. Since the most affected patient was deprived of the benefits of converting enzyme inhibitors because of their side effects, the only way to partially overcome this condition was a generous combination of several diuretics acting at several segments of the nephron. This contrasted with a similar patient who was relatively well controlled by a converting enzyme inhibitor combined with lower dose diuretics. Diuretic abuse-induced secondary hyperaldosteronism and diuretic resistance are apparently best prevented by converting enzyme inhibitors. When nonpharmacological preventive measures fail, converting enzyme inhibitors are preferable to diuretics as the first-choice treatment of idiopathic edema patients.

Adult↗
PubMed2006

Psychological aspects of primary aldosteronism.

BACKGROUND: Except for 3 case reports of Conn's syndrome presenting as depression, psychosocial factors have not been explored in primary aldosteronism. We investigated psychological correlates in primary aldosteronism using methods that were found to be sensitive and reliable in psychosomatic research. METHOD: Ten consecutive newly diagnosed patients with primary aldosteronism were studied: 5 males/5 females; mean age (+/-SD) 45.5 +/- 6.6 years, age range 34-54 years; 4 with an aldosterone-producing adenoma and 6 with idiopathic aldosteronism; systolic/diastolic blood pressure 189 +/- 20/111 +/- 7.7 mm Hg; upright plasma aldosterone 40.0 +/- 18.3 ng/dl; upright plasma renin activity (PRA) 0.2 +/- 0.1 ng/ml/h; aldosterone/PRA ratio 229.2 +/- 191.0; serum K(+) 3.5 +/- 0.5 mmol/l. The Structured Clinical Interview for the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV) for eliciting psychiatric diagnoses, and a shortened version of the structured interview for subclinical psychological syndromes, the Diagnostic Criteria for Psychosomatic Research (DCPR), were administered. RESULTS: Seven patients (2 with aldosterone-producing adenoma and 5 with idiopathic hyperaldosteronism) received both DSM-IV and DCPR diagnoses, while 3 had neither. As to DSM-IV, generalized anxiety disorder was detected in 6 cases (in 1 it was associated with panic disorder and in 1 with major depression) and obsessive-compulsive disorder in 1. The most frequent DCPR cluster was demoralization (5 cases), while persistent somatization occurred in 2 cases (associated with demoralization in 1) and irritable mood in 1. CONCLUSIONS: The occurrence of anxiety disorders in patients with primary aldosteronism was much higher than that found in the general population and in primary care. Since an association between hyperaldosteronism and anxiety has also been suggested in previous animal studies, it seems worthwhile to gain further knowledge on clinical aspects by larger population studies.

Adult↗
PubMed1987

A renin-secreting tumor.

A 23-year-old white male was referred for hypertension resistant to triple antihypertensive treatment, with hypokalemia, hyperaldosteronism and elevated levels of circulating plasma renin activity (PRA). Renal angiography and echoscans put in evidence an avascular solid mass at the midlower level of the right kidney. Renal vein catheterization with sampling of blood from the lower branches of the right renal vein showed lateralization of renin secretion from that side. After surgical exeresis, the mass (1.0 cm) was diagnosed as a renal hemangiopericytoma on the basis of light and electron microscopy. Tumor exeresis was followed by a prompt normalization of blood pressure and plasma potassium, with a decrease in PRA and aldosterone. Two months after surgery the patient was still normotensive. Circulating levels of inactive (trypsin-activable) renin were around 60% of the total pool of plasma renin, i.e. much lower than those reported in other cases of renin-secreting tumors. After surgery, inactive and active renin fell in parallel, implying that both were secreted by the tumor. Tumoral PRA responded to postural stimulation, but was unresponsive to acute converting enzyme inhibition, suggesting that sympathetic stimuli were still operative, but the negative feedback inhibition by angiotensin II on renin secretion was lost. Acute converting enzyme inhibition by captopril dropped blood pressure; however, during long-term treatment, the drug (3 X 50 mg/day) was ineffective in terms of either blood pressure normalization or relief of secondary hyperaldosteronism. Acute calcium entry blockade by nifedipine (10 mg p.o.) caused an evident blood pressure drop.

Adult↗
PubMed1971

A decreased metabolic clearance rate of aldosterone in benign essential hypertension.

Aldosterone secretion rate, metabolic clearance rate, and/or plasma concentration were determined in 16 patients with benign, uncomplicated essential hypertension and compared with those of control subjects. The mean metabolic clearance rate of aldosterone in 10 patients was significantly (P < 0.001) lower (mean 867 liters of plasma/day per m(2) +/-270 SD) than in a group of 7 healthy subjects (mean 1480 liters/day per m(2) +/-265 SD). Secretion rates in 13 patients (including the 10 already mentioned) tended to be low (83 +/-43 vs. 109 +/-54 mug/day) and plasma concentrations tended to be high (13.6 +/-4.6 vs. 7.5 +/-4.8 ng/100 ml), but neither of these differences was statistically significant. The lower metabolic clearance rate could account for elevated plasma concentrations of aldosterone even when the secretion rate is normal or low. Measurement of secretion rate or urinary excretion only is therefore insufficient to establish the presence and/or mode of evolution of hyperaldosteronism. Failure of the aldosterone secretion to adapt fully to a decreased aldosterone metabolic clearance rate (MCR) could explain the state of relative hyperaldosteronism in patients with benign essential hypertension, even when the secretion rate and the urinary excretion rate are in the normal range.

Adaptation, Physiological↗
PubMedDate not supplied

Dopaminergic regulation of aldosterone secretion: assessment in different subtypes of primary aldosteronism and in essential hypertension.

The inhibitory effect of dopamine on aldosterone secretion was investigated in patients with different types of primary aldosteronism, six with idiopathic hyperaldosteronism (IHA) and four with dexamethasone-suppressible hyperaldosteronism (DSH), and in 10 patients with essential hypertension. The effects of 10 mg metoclopramide given intravenously, 10 mg bromocriptine given orally and 100 micrograms adrenocorticotrophic hormone given intravenously on plasma aldosterone and renin activities were investigated in all patients. Metoclopramide induced a rise in plasma aldosterone activity only in patients with IHA and not in those with DSH and essential hypertension. After bromocriptine plasma aldosterone concentrations decreased in patients with IHA only, and after adrenocorticotrophic hormone plasma aldosterone concentrations increased in patients with DSH only. Plasma renin activity was unaffected in all cases. These results provide evidence of increased endogenous dopaminergic inhibition of aldosterone secretion in IHA and of a blunted aldosterone response in both DSH and essential hypertension.

Adrenocorticotropic Hormone↗
PubMed2006

Diagnostic value of biochemical parameters in the differential diagnosis of an adrenal mass.

In patients with an adrenal mass, hormonally active tumors including pheochromocytomas as well as aldosterone- and cortisol-secreting adenomas need to be considered. Several studies have demonstrated that metanephrines, which are the metabolites of catecholamines, are reliable parameters for the diagnosis of pheochromocytoma. In patients with an adrenal mass, we found plasma metanephrines, measured by a newly available radioimmunoassay, to be highly sensitive and specific for pheochromocytomas, with a better accuracy than any other biochemical parameter. The plasma aldosterone concentration (PAC) to plasma renin activity (PRA) ratio is an established screening tool for primary hyperaldosteronism. However, determination of active renin concentration (ARC) in contrast to PRA may offer advantages in regard to processing and standardization. We found a PAC to ARC ratio of >62 in patients with PAC levels>200 ng/L to be a reliable screening method for primary hyperaldosteronism in patients with adrenal masses. The screening for hypercortisolism relies on excess urinary cortisol secretion, loss of the physiological feedback during dexamethasone challenge, and loss of the circadian rhythm. Because urinary-free cortisol may not identify subclinical Cushing's syndrome, in which hypercortisolism is still mild, the 1-mg dexamethasone suppression test has been recommended in all patients with incidentally detected masses. Alternatively, late-night cortisol levels in saliva have been found to have a high sensitivity and specificity for the diagnosis of Cushing's syndrome. In summary, in patients with an adrenal mass, hormonally active adrenal tumors can be excluded with high certainty using a few highly reliable biochemical parameters.

Adrenal Gland Neoplasms↗
PubMed2004

Comparison of the insulin action parameters from hyperinsulinemic clamps with homeostasis model assessment and QUICKI indexes in subjects with different endocrine disorders.

The aim of this study was to compare insulin sensitivity expressed by the hyperinsulinemic clamp and by the homeostasis model assessment (HOMA) and QUICKI indexes in subjects with various disorders influencing insulin action. We examined 41 type 2 diabetic patients, 20 insulinoma patients, 32 women with polycystic ovary syndrome, 16 patients with primary hyperaldosteronism, 12 patients with essential high renin hypertension, and 47 healthy subjects. The metabolic clearance rate of glucose and the insulin sensitivity index calculated from the clamps were compared with both the HOMA and QUICKI indexes. The relationship of insulin action to body mass index, serum cholesterol, and triglycerides as well as to systolic and diastolic blood pressures was also evaluated. Body mass index was very strongly associated with the insulin sensitivity index (r = -0.70; P < 0.0001) in the entire cohort of 168 subjects. Cholesterol, triglycerides, and blood pressure influenced insulin action in the healthy subjects and type 2 diabetic patients. A significant relationship was observed between the insulin sensitivity index and the HOMA or QUICKI indexes in healthy subjects (r = -0.66; P < 0.0001), type 2 diabetic patients (r = -0.68; P < 0.0001), and women with polycystic ovary syndrome (r = -0.65; P < 0.0001). We did not find any relationship between the above variables in the patients with insulinoma or primary hyperaldosteronism. The HOMA and QUICKI indexes do not offer the same information as glucose clamps in the rare cases with differently impaired peripheral or hepatic insulin action.

Adolescent↗
PubMed1976

Evidence for an unidentified ACTH-induced steroid hormone causing hypertension.

The hypothesis that hyperaldosteronism is not the sole cause of hypertension in dexamethasone-suppressible hyperaldosteronsim was tested in an 18-year-old male. After six years of little or no treatment, the hypertension and mild hyperaldosteronism were promptly decreased by a small dose of dexamethasone. During dexamethasone treatment, when aldosterone secretion was suppressed to less than normal and he was normotensive, steroids were given by constant infusion in an attempt to reproduce the hypertension of the dexamethasone-free state. Neither five days of aldosterone or 18-hydroxydesoxycorticosterone (18-OH-DOC) at 1 mg/day, nor desoxycorticosterone (DOC) at 30 mg/day caused hypertension. However, sodium retention and potassium loss was observed during aldosterone and DOC infusion. Hypertension was produced within five days during infusion with ACTH or oral metyrapone. The hypertensive effect of the latter was abolished by addition of aminoglutethimide treatment. These studies suggest that a steroid other than aldosterone, 18-OH-DOC, or DOC may be the cause of the ACTH-induced hypertension in this patient. The aminoglutethimide data suggest that the ACTH effect on blood pressure is due to a steroid, and the metyrapone studies suggest that the steroid may be an 11-desoxysteroid. Urine and blood collected under ACTH stimulation and metyrapone treatment may be a rich source from which we may characterize this hormone.

18-Hydroxydesoxycorticosterone↗
PubMed1983

Single dose captopril as a diagnostic test for primary aldosteronism.

Most diagnostic tests for primary aldosteronism use maneuvers to expand the extracellular fluid volume, thereby suppressing the renin-angiotensin system. This results in a decline in plasma aldosterone concentrations in normal subjects and essential hypertension (EH) patients, but not in patients with primary aldosteronism. Captopril blocks angiotensin II synthesis and might be used as a diagnostic test for primary aldosteronism. We have measured plasma aldosterone concentrations 2 h after the administration of 25 mg captopril in 9 normotensive subjects, 10 patients with EH, and 12 patients with primary aldosteronism while they were ingesting an unrestricted diet. The plasma aldosterone concentration decreased to less than 15 ng/dl in all normotensive subjects and in 9 of 10 patients with EH, but remained greater than 15 ng/dl in 4 of 5 patients with idiopathic hyperaldosteronism and in all patients with an aldosterone-producing adenoma. The aldosterone to renin ratio was greater than 50 in 4 of 5 patients with idiopathic hyperaldosteronism and in all adenoma patients, but less than 50 in all normotensive subjects and EH patients. A nomogram comparing the plasma aldosterone concentration with the aldosterone to renin ratio clearly separated primary aldosteronism patients from EH patients.

Adenoma↗
PubMed1984

Endogenous prostacyclin synthesis is decreased during activation of the renin-angiotensin system in man.

Prostacyclin has been implicated as a mediator of renin release, whereas angiotensin II evokes prostaglandin I2 (PGI2) release from both vascular and nonvascular tissues in vitro. The physiological significance of these observations was assessed by measurement of an index of endogenous prostacyclin biosynthesis in human volunteers during varied activation of the renin-angiotensin system secondary to manipulation of dietary sodium. Excretion of the major urinary metabolite of prostacyclin in man, 2,3-dinor-6-keto-PGF1 alpha (PGI-M), fell from 295 +/- 51 to 176 +/- 35 (+/- SEM) ng g creatinine-1 (P less than 0.01) in 10 normal subjects when sodium intake was decreased from 150 to 10 meq/day. In five patients with primary hyperaldosteronism, PGI-M fell from 199 +/- 34 ng g creatinine-1 preoperatively to 120 +/- 26 pg/mg creatinine-1 after removal of the adenoma. In such patients, the reduction in PGI-M was associated with a significant increase in PRA. Thus, in both normal subjects and patients with hyperaldosteronism, PGI-M excretion fell rather than increased with activation of the renin-angiotensin system. This suggests that systemic biosynthesis of PGI2 is unrelated to renin release and that angiotensin II is unlikely to stimulate endogenous prostacyclin biosynthesis under these conditions in man.

Adenoma↗
PubMed1984

Transitory increment in urinary free 19-nor-deoxycorticosterone after diuretic-induced renin stimulation.

19-Nor-deoxycorticosterone (19-nor-DOC) is a potent mineralocorticoid recently identified in human urine. The factors regulating 19-nor-DOC production are unknown; short term dietary sodium depletion or excess has little effect on 19-nor-DOC excretion in human subjects. This study sought to determine if more prolonged renin stimulation could increase 19-nor-DOC production. Six normal subjects were admitted to a metabolic unit. After a 5-day electrolyte balance period, hydrochlorothiazide (50 mg/day) was administered for 28 days. This treatment resulted in acute natriuresis, a more sustained hypokalemia, and secondary hyperaldosteronism lasting throughout the remainder of the study. Despite the sustained secondary hyperaldosteronism, however, urinary 19-nor-DOC extraction, measured by RIA, increased only slightly on day 3 and subsequently decreased to normal values throughout the remainder of the study (19-nor-DOC, 103 +/- 27 ng/day 0, 175 +/- 26 on day 3, 127 +/- 27 on day 28). The results of this study demonstrate only a minor and transient effect on diuretic-induced renin stimulation on 19-nor-DOC production. Therefore, the physiological regulation of 19-nor-DOC is largely independent of the renin-angiotensin system.

Adult↗
PubMed1988

Glucocorticoid-suppressible aldosteronism: a disorder of the adrenal transitional zone.

Glucocorticoid-suppressible aldosteronism (GSA) is a rare form of hyperaldosteronism in which the increased secretion of aldosterone and the elevation of blood pressure are corrected when ACTH secretion is suppressed. Two 17-hydroxylated analogs of 18-hydroxycorticosterone and aldosterone, 18-hydroxycortisol and 18-oxocortisol, which had been identified in the urine of patients with hyperaldosteronism due to an adrenal adenoma and in bullfrog adrenal tissue incubated with cortisol, are produced in greater than normal quantities in patients with GSA. The excretion of 18-hydroxycortisol and 18-oxocortisol in nine patients with GSA was 2914 +/- 923 (+/- SD) nmol/day [1108 +/- 351 micrograms/day; normal, 165 +/- 94 nmol/day (63 +/- 36 micrograms/day)] and 141 +/- 77 nmol/day [53 +/- 29 micrograms/day; normal, 3.2 +/- 2.4 nmol/day (1.2 +/- 0.9 micrograms/day)], respectively. The excretion of aldosterone 18-oxoglucuronide was 53 +/- 18 nmold/day [19.4 +/- 6.8 micrograms/day; normal, 16.9 +/- 7.5 nmol/day (6.1 +/- 2.7 micrograms/day)]. Aldosterone excretion was elevated in six patients and within the normal range in three patients. The degree of abnormality in 18-hydroxycortisol and 18-oxocortisol excretion was significantly greater than that in aldosterone. Dexamethasone administration decreased excretion of the three steroids to the normal range. ACTH administration for 3 days resulted in an exaggerated increase in the excretion of these steroids, suggesting ACTH dependence of these steroids in patients with GSA. The excessive production of these steroids, which are 17- and 18-hydroxylated, indicate that they are produced by hybrid-type cells which we have called transitional cells, which are also capable of producing aldosterone. These findings are consistent with the postulate that cytochrome P-450-corticosterone methyl oxidase fails to disappear normally in the zona glomerulosa cells as they migrate to the zona fasciculata and acquire 17-hydroxylase activity. This abnormality explains the supernormal conversion of cortisol to 18-hydroxycortisol and 18-oxocortisol and the ACTH dependence of aldosterone secretion in GSA.

Adolescent↗
PubMed1997

Somatic mutations of the angiotensin II (AT1) receptor gene are not present in aldosterone-producing adenoma.

Angiotensin II stimulates aldosterone secretion from the adrenal zona glomerulosa and mediates most of its biological effects via G protein-coupled type 1 angiotensin II receptors (AT1). A number of G protein-coupled receptors are constitutively activated as a result of somatic mutations in the gene encoding the protein. It is, therefore, possible that primary hyperaldosteronism caused by an aldosterone-producing adenoma (APA) may be the result of constitutive activation of the AT1 receptor. The 1.1-kilobase coding region (exon 5) of the AT1 receptor gene was analyzed in APA and normal adrenal tissue for the presence of mutations using single stranded conformational polymorphism and sequencing techniques. In 17 APAs, no functional mutations were found that could account for the observed pathophysiology. However, three silent polymorphisms were detected in regions encoding the second extracellular loop, the intracellular arm preceding the COOH terminal, and the 3'-untranslated region. In conclusion, somatic mutations in the coding region of the AT1 receptor gene do not appear to play a role in primary hyperaldosteronism caused by an APA.

Adenoma↗
PubMed1998

Incidentally discovered adrenal tumors: endocrine and scintigraphic correlates.

Hormonal and morphological data were investigated in 202 consecutive patients with adrenal incidentalomas (171 unilateral and 31 bilateral) in an attempt to assess subclinical hyperfunction or malignancy. In addition to the classical evaluation, scintiscan was carried out in a large number of these patients. In unilateral incidentalomas, 83% showed normal hormonal function, whereas 17% had biochemical signs of adrenal overactivity (hyperaldosteronism in 3, hypercortisolism in 17, medullary hyperfunction in 9). [75Se]Methylnorcholesterol scintigraphy depicted malignant, space-occupying lesions as decreased or absent radiotracer uptake by the mass, and cortical adenomas as increased or normal uptake. In cortical adenomas a relationship between radiocholesterol uptake and degree of functional autonomy was demonstrated. [123I]Metaiodobenzilguanidine scintiscan visualized 7 of 8 pheochromocytomas. In bilateral incidentalomas, abnormal adrenal function was more frequent, accounting for 29% of cases (hyperaldosteronism in 3, hypercortisolism in 3, adrenal insufficiency in 2, and congenital adrenal hyperplasia in 1). Malignant lesions were not scintigraphically visualized. [75Se]Methylnorcholesterol scan also provided functional information in the case of a cortisol-secreting adenoma and an aldosteronoma with a concomitant contralateral nonhypersecreting adenoma, showing the greatest uptake in the hyperfunctioning adenomas. In both unilateral and bilateral lesions, endocrine testing failed to differentiate benign from malignant tumors. Although hormonal assessment is mandatory to clarify the functional patterns, only morphofunctional examination by scintiscan seems to provide more data about the likelihood of malignancy.

17-alpha-Hydroxyprogesterone↗
PubMed1998

Diagnosis of glucocorticoid-remediable aldosteronism in primary aldosteronism: aldosterone response to dexamethasone and long polymerase chain reaction for chimeric gene.

Aldosterone suppression by dexamethasone, and high 18-hydroxycortisol and 18-oxocortisol levels are used to differentiate glucocorticoid-remediable aldosteronism (GRA) from other forms of primary aldosteronism. These methods are time consuming, expensive, and impractical for large studies. Moreover, diagnosis of GRA requires a confirmatory genetic test. We evaluated 117 patients with primary aldosteronism referred to our centers by the use of a long PCR technique to reveal the chimeric gene of GRA. In 60 of 117 patients, the response of aldosterone to dexamethasone (2 mg/day for 4 days) was also assessed. None of our patients, including 2 pairs of siblings, was positive for the chimeric gene. The results of long PCR were confirmed by Southern blotting. Despite a negative genetic test, 6 patients (1 with aldosterone-producing adenoma and 5 with idiopathic hyperaldosteronism) had plasma aldosterone suppressed by dexamethasone (i.e. < or = 2 ng/dL). Of 117 patients, 43 were identified as having aldosterone-producing adenoma and 74 as having idiopathic hyperaldosteronism. In our experience, the long PCR technique is a reliable and simple test to at least exclude GRA in patients with primary aldosteronism. A short term dexamethasone suppression test of aldosterone can be misleading in identifying GRA. The prevalence of GRA in primary aldosteronism remains to be established.

Adult↗
PubMed2000

Predictive value of preoperative tests in discriminating bilateral adrenal hyperplasia from an aldosterone-producing adrenal adenoma.

In primary hyperaldosteronism, discriminating bilateral adrenal hyperplasia (BAH) from an aldosterone-producing adenoma (APA) is important because adrenalectomy, which is usually curative in APA, is seldom effective in BAH. We analyzed the results from our most recent 7-yr series to evaluate the predictive value of preoperative noninvasive tests compared with adrenal vein sampling (AVS). Forty-eight patients with hypertensive hyperaldosteronism underwent bedside testing, computed tomography (CT) imaging, and AVS. Those in whom the results of AVS indicated APA underwent adrenalectomy. Twelve (30%) and 14 (34%) of 41 patients with APA had paradoxical falls with ambulation in plasma aldosterone concentration (PAC) and 18-hydroxycorticosterone (18-OH-B), respectively. Twenty-nine (70%) and 26 (65%) APA patients had a rise in PAC and 18-OH-B, respectively, as did all 8 BAH patients. Significant identifiers of BAH were supine PAC values less than 15 ng/dL (P: = 0.04), an increase greater than 60% (P: = 0.02) in PAC with ambulation, and supine 18-OH-B values less than 60 ng/dL (P: = 0.04). CT imaging alone was not predictive for BAH or APA. In our population, patients with a positive bedside test result (e.g. a fall in PAC and/or 18-OH-B) and a unilateral adrenal nodule on CT (10 of 41 patients) could have proceeded directly to adrenalectomy for APA. However, a positive bedside test result with a negative CT or a negative bedside test result regardless of CT findings required AVS to confirm the diagnosis and site of disease.

Adenoma↗
PubMed1975

Adrenal venography and ultrasound in the investigation of the adrenal gland: an analysis of 58 cases.

Adrenal venography has been carried out in 58 patients with the left adrenal vein being successfully catheterized in 91 per cent and the right in 77 per cent. Of the 30 patients with primary hyperaldosteronism, 11 adenomas (12-35 mm diameter) have been demonstrated at venography and two of 15 mm suspected, all of which were confirmed surgically. Aldosterone levels in the adrenal vein plasma were raised on the affected side. In the group of proved micronodular hyperplasia, two patients had surgically confirmed macronodules and venography demonstrated one of 12 mm diameter. Two adenomas of 11 mm and one macronodule of 15 mm have been demonstrated at venography in the remainder who have not had an operation. Ultrasound was carried out in 12 patients with primary hyperaldosteronism, ten of which had tumours at venography. Two adenomas measuring 30 and 31 mm were outlined by ultrasound and confirmed surgically. Seven adenomas, including one macronodule (10-25 mm in diameter) were not defined. Three intra-adrenal phaeochromocytomas (45-90 mm) and one extra-adrenal (80-85 mm) were demonstrated at arteriography, identified by ultrasound and confirmed surgically. Of the ten patients with Cushing's syndrome three had enlarged glands at venography, this was confirmed surgically. Cumulative experience from this analysis and published reports indicate that venography will demonstrate tumours of 10 mm or more in diameter and outline enlarged glands; aldosterone assays will lateralize tumours as small as 3 mm; ultrasound will outline tumours of 30 mm and selective adrenal arteriography will demonstrate tumours of 10 mm. One patient developed acute adrenal cortical insufficiency with intra-adrenal extravasation on one side and thrombosis of the central vein on the opposite side. A second case developed temporary adreno-cortical insufficiency. Published reports indicate that the risk of complication is about 1 per cent. The report includes an anatomical study of the efferent adrenal veins in 50 patients paying particular attention to the diameter, number of accessory hepatic veins, and the angle of entry and position of the right adrenal vein.

Adenoma↗