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PubMed1994

Analysis of adrenocortical hyperplasia by computed tomography in patients with Cushing's Disease, idiopathic hyperaldosteronism and adrenogenital syndrome.

We assessed the usefulness and reliability of computed tomography (CT scan) in evaluating adrenal hyperplasia in 38 patients, including 14 with Cushing's disease, 17 with idiopathic hyperaldosteronism (IHA), and 7 with the adrenogenital syndrome (AGS). Eighty-two normal subjects were also examined. We analyzed the shape of the adrenal gland and quantitated its thickness, width and length. Visual inspection revealed V-shaped right adrenal glands in 100% of patients with Cushing's disease, 94% of patients with IHA, 100% of patients with AGS and in 41% of the normal subjects. Triangular left adrenal glands were observed in 100% of patients with Cushing's disease, 82% of patients with IHA, 67% of patients with AGS and in 12% of the normal subjects. Quantitative analysis showed that the right adrenal gland was significantly thicker and longer in patients with Cushing's disease, IHA and in those with AGS than in normal subjects. The right adrenal gland was significantly wider in the patients with Cushing's disease and AGS than in control subjects. The left adrenal gland was significantly wider and longer in patients with Cushing's disease and AGS than in the normal controls. Analysis of individual data indicated that the upper limit of normal for thickness of the right adrenal was 7 mm. Therefore, adrenal hyperplasia was strongly suggested when the right adrenal gland was more than 7 mm thick. Our findings suggest that the CT scan is useful and reliable in diagnosing adrenal hyperplasia.

Adrenal Cortex↗
PubMed1988

A case of glucocorticoid-suppressible hyperaldosteronism with aldosterone producing adenoma.

A 34-yr-old woman with hypertension (142/102 mmHg), hypokalemia, high plasma and urinary aldosterone and low plasma renin activity was studied. A left adrenal tumor and enlarged right adrenal gland were demonstrated by adrenal venography. During administration of dexamethasone (2 mg daily, for 3 weeks), urinary aldosterone excretion decreased abruptly from 22.5 to 9-11 micrograms/day, serum potassium increased and blood pressure fell to 120-130/80-90 mmHg. After left adrenalectomy, all manifestations improved with no medication. The resected adrenal gland revealed clear cell adenoma and micronodular adrenocortical hyperplasia. The patient was considered to be a rare case of glucocorticoid-suppressible hyperaldosteronism with an aldosterone-producing adenoma.

Adenoma↗
PubMed1989

Possible hyperaldosteronism and discrepancy in enzyme activity deficiency in adrenal and gonadal glands in Japanese patients with 17 alpha-hydroxylase deficiency.

We reviewed the pathophysiology of our previously reported female patient who had glucocorticoid-responsive hyperaldosteronism and was treated successfully with daily dose of dexamethasone (Dex) for 21 years. In this present study, the possibility that the patient may have 17 alpha-hydroxylase deficiency (17-OH-D) mainly in the adrenal could not be ruled out. We therefore reviewed 31 Japanese patients diagnosed as having 17-OH-D with suppressed plasma renin activity reported in Japan. Among these patients, 9 were found to have a high plasma aldosterone (Ald) concentration (PAC) (group I). Twenty-one patients had either normal or low-normal PAC and the remaining patient had low urine Ald (group II). The slight cross-reactivity of the anti-Ald-antibodies used with 17-deoxy-steroids such as progesterone, 11-deoxycorticosterone and corticosterone which were increased in both groups did not explain the increased PAC in group I. In the patients in group I and group II with high-normal basal PAC, PAC further increased after ACTH and was suppressed by Dex. PAC in 2 group I patients, however, did not respond to angiotensin-II or angiotensin-III infusion. PAC in patients in group II with low or low-normal basal PAC responded equivocally to ACTH and Dex. The basal plasma cortisol in group I was lower than in group II, and plasma cortisol level after ACTH in group I appeared to remain at a lower level than that in group II patients. Among the study subjects, 28 showed a negative correlation between basal PAC and plasma cortisol. A possible discrepancy in the deficiency of 17 alpha-hydroxylase activity in adrenal and gonadal glands was also suggested in three 17-OH-D patients. The pathophysiology of Ald secretion and discrepancy in the deficiency of the enzyme activities in both glands in 17-OH-D patients was discussed.

Adolescent↗
PubMed1982

Dexamethasone suppressible hyperaldosteronism in a child with nephrosclerosis.

A 9 year old Mexican boy presented with severe hypertension, hypokalaemia and features suggesting acute glomerulonephritis. Nephrosclerosis was present on renal biopsy. Aldosterone levels were unresponsive to variations in dietary salt intake and plasma renin activity was suppressed. Following oral dexamethasone therapy (2 mg/day), plasma aldosterone decreased to undetectable levels, serum potassium normalized and plasma renin activity gradually increased. Dexamethasone also restored the normal responsiveness of the renin-aldosterone system to postural stimuli. The patient exhibited a marked response to a single dose of ACTH with a rise in plasma aldosterone. Long-term blood pressure control and normal potassium levels have been achieved with oral prednisone therapy (5 mg/day) for a period of one year. This case of dexamethasone suppressible hyperaldosteronism (DSH) illustrates that the degree of hypertension in this syndrome may produce severe renal microvascular lesions. DSH should be considered in all children who present with low renin hypertension.

Adrenocorticotropic Hormone↗
PubMed1984

A case of primary hyperparathyroidism, primary hyperaldosteronism and Cushing's disease.

The rare association of parathyroid adenoma with primary hyperaldosteronism, occurring in each of 2 patients, was recently reported from this unit. The present communication records the subsequent development, in one of these patients, of Cushing's syndrome with an anterior pituitary adenoma. Screening for other endocrine abnormalities was negative. A literature search failed to produce any other cases of the association of these three conditions in one patient.

Adenoma↗
PubMed1984

Evidence for endogenous dopaminergic control of mineralocorticoids secretion in normal subjects and in patients with hyperaldosteronism.

The role of endogenous dopamine (DA) in the secretion of several mineralocorticoids was studied in six normal subjects, eight patients with primary aldosteronism (PA), two patients with non-familial idiopathic hyperaldosteronism (NF-IHA), and four patients with familial IHA (F-IHA). To these subjects 10 mg metoclopramide (MCP) was administered intravenously, and plasma aldosterone (Ald), 18-OH-corticosterone (18-OH-B), 18-OH-11-deoxycorticosterone (18-OH-DOC), and DOC were measured by RIA. Further, five normal subjects were studied with MCP test after pretreatment with DA infusion (5 micrograms/kg/min over 90 min). After the administration of MCP, normal subjects showed significant increases in their plasma Ald and 18-OH-B, and slight increases in plasma 18-OH-DOC and DOC. However, no significant changes were observed in plasma ACTH, cortisol, PRA, or serum K, Na or Cl. In patients with PA and NF-IHA, plasma Ald and the three precursors were increased after administration of MCP. Especially, marked increases in plasma 18-OH-DOC were seen in PA patients. In contrast, F-IHA patients showed increases in the above mineralocorticoids except 18-OH-B. Following DA infusion in normal subjects neither basal plasma Ald secretion nor the responsivenesses to MCP were modified. These results suggest that endogenous DA plays an inhibitory role in the terminal stages of mineralocorticoids production in man. However, the degrees of the dopaminergic inhibition may be different in normal subjects and the patients with mineralocorticoids excess, and among the three groups of aldosteronism mentioned above.

18-Hydroxycorticosterone↗
PubMed1979

Hyperaldosteronism in the sodium-depleted rat: mechanism of aldosterone stimulation by peritoneal dialysis with glucose solution.

Peritoneal dialysis with 5% glucose solution was carried out in dexamethasone-pretreated rats. Dialysis brought about a severe loss of sodium and a slight loss of potassium into the peritoneal fluid. This kind of sodium depletion took place without any decrease in total body-water space, thus it evoked a severe fall in plasma sodium concentration. Plasma renin activity and the serum concentration of aldosterone increased in response to dialysis. Peak values in renin activity were attained within 60 min, whereas aldosterone concentrations exhibited a continuous rise until at least 120 min. Despite the correlation of renin and aldosterone values, neither the administration of an angiotensin I converting enzyme inhibitor (SQ 20,881) nor the reduction of plasma renin activity by indomethacin could reduce hyperaldosteronism evoked by peritoneal dialysis. Therefore, it is assumed that there is no causal relationship between renin and aldosterone in this kind of acute, severe sodium depletion.

Aldosterone↗
PubMed1983

Primary hyperaldosteronism: comparison of CT, adrenal venography, and venous sampling.

Twenty-nine patients with primary hyperaldosteronism were evaluated with computed tomography (CT), adrenal venous sampling, and adrenal venography. Twenty-three patients had aldosteronomas and six had bilateral adrenocortical hyperplasia. Sixteen (70%) of the adenomas were accurately located by CT. All nodules of 1.5 cm or larger diameter and 50% of nodules 1.0-1.4 cm in diameter were demonstrated. Nodules of less than 1.0 cm in diameter generally were not detected. High-resolution CT appeared more sensitive than standard CT (75% vs. 58%). Adrenal venous sampling for aldosterone assay was the most sensitive of the three methods, localizing 22 (96%) of the 23 adenomas. Eighteen (78%) of the adenomas were identified by adrenal venography, although two patients with bilateral cortical hyperplasia were mistakenly diagnosed as having a small adenoma. No such false-positive studies were encountered with CT or adrenal venous sampling.

Adenoma↗
PubMed2000

Use of abdominal ultrasonography in the diagnosis of primary hyperaldosteronism in a cat.

A 13-year-old castrated male cat was examined because of a 2-week history of weakness, cervical ventroflexion, and dysphagia. Clinicopathologic abnormalities included hypokalemia and high serum creatine kinase activity. Abdominal ultrasonography revealed a 15-mm spherical mass in the area of the left adrenal gland. Plasma aldosterone concentration was high, and plasma renin activity was low. Findings were diagnostic of primary hyperaldosteronism. The cat responded well to intravenous and oral potassium supplementation while in the hospital. The owner declined surgery; therefore, repeated follow-up abdominal ultrasonography was recommended. The cat did well clinically with medical management alone until day 334, when it was lost to follow-up.

Adrenal Gland Neoplasms↗
PubMedDate not supplied

Clinical, biochemical and genetic features of five extended kindred's with glucocorticoid-suppressible hyperaldosteronism.

Glucocorticoid-suppressible hyperaldosteronism (GSH) is an uncommon form of dominantly inherited hypertension caused by the inheritence of a chimaeric 11 beta-hydroxylase/aldosterone synthase gene. Affected individuals appear to have an increased risk of premature morbidity and mortality from stroke, but treatment with low doses of dexamethasone can completely reverse the biochemical and clinical features. We assessed the clinical and genetic features of 5 British kindreds with GSH, the largest collection outwith the United States, and determined the location of the crossover regions in the chimaeric gene of all 5 kindreds. All of the kindreds were of celtic origin, another feature peculiar to GSH. In total 19 out of 60 individuals screened by genotyping were found to possess the chimaeric gene and sequencing of the chimaeric gene revealed that all the crossover regions were within the exon 3- exon 4 region of, in keeping with previous studies, and three kindreds possessed indistinguishable chimaeric genes.

Chimera↗
PubMed1982

The mineralocorticoid hormone pathways in hypertension with hyperaldosteronism.

Simultaneous measurement of the 0800-hr plasma concentrations of deoxycorticosterone (DOC), corticosterone (B), 18-hydroxycorticosterone (18-OHB), aldosterone, 18-hydroxydeoxycorticosterone (18-OHDOC) and cortisol (F) in four types of primary aldosteronism provides evidence for primary adrenal disease. Elevated DOC with normal F concentrations in the presence of elevated 18-OHB and aldosterone, and suppressed renin concentration suggests a primary adrenal abnormality of the zona glomerulosa (ZG). Steroid production by the zona fasciculata (ZF), F, 18-OHDOC, and most often B, is normal. These patterns exist only for primary adrenal hyperplasia, aldosterone-producing adenoma (APA), and aldosterone-producing adrenocortical carcinoma (AP-Ca). Elevated DOC levels are rarely found in patients with idiopathic hyperaldosteronism (IHA or adrenal hyperplasia) and suggest that IHA is not a primary adrenal disorder and should be excluded from the syndrome of primary aldosteronism as they have been heretofore.

18-Hydroxydesoxycorticosterone↗
PubMedDate not supplied

A case of unilateral adrenal hyperplasia: the diagnostic dilemma of hyperaldosteronism.

OBJECTIVE: To report the successful laparoscopic surgical management of a case of right unilateral adrenal hyperplasia. METHODS: We present a case of unilateral adrenal hyperplasia and review the pertinent literature. The effectiveness of surgical treatment of unilateral adrenal hyperplasia is evaluated. RESULTS: A 50-year-old man had a 7-year history of hypertension, which had been treated with antihypertensive medications. On initial assessment, he was taking long-acting diltiazem, 240 mg twice a day, and his blood pressure was 150/84 mm Hg. He was noted to have recurrent hypokalemia, low plasma renin activity, increased plasma aldosterone concentration, and high urinary aldosterone levels. Magnetic resonance imaging of the adrenal glands revealed a normal left adrenal gland and fullness of the right adrenal gland. Selective adrenal vein catheterization showed findings consistent with a right-sided adrenal gradient. Surgical removal of the right adrenal gland laparoscopically alleviated his symptoms and cured his hypertension and hypokalemia. Pathologic examination of the right adrenal gland revealed diffuse hyperplasia of the zona fasciculata and zona reticularis. Plasma aldosterone, renin, and potassium levels returned to normal postoperatively, and his blood pressure declined to 120/70 mm Hg. At 1-year follow-up, the patient remained normotensive without the need for antihypertensive agents. CONCLUSIONS: This rare type of hyperaldosteronism, known as unilateral adrenal hyperplasia, is difficult to categorize not only because it fails to typify a conventional subtype but also because it is difficult to confirm the pathologic diagnosis. Recognition of the variety of provocative, biochemical, and imaging results that may be seen in this disorder is important in making the correct diagnosis. Determining unilaterality of disease by selective adrenal vein sampling can result in a cure of hypertension and hypokalemia by surgical resection.

Adrenal Glands↗
PubMedDate not supplied

Primary hyperaldosteronism in two cats.

A condition of primary hyperaldosteronism resulting from an adrenal tumor in two cats is presented and was characterized by hypertension, hypokalemia, inappropriate kaliuresis, low normal plasma renin activity, and markedly increased serum aldosterone concentration. One of the two cats underwent a laparotomy, and in this case hypertension and hypokalemia resolved following the removal of an adrenal tumor.

Adrenal Gland Neoplasms↗
PubMed1980

Hypertension, hyperreninemia, and secondary hyperaldosteronism in systemic necrotizing vasculitis.

We studied the pathogenesis of hypertension in two patients with hepatitis-B surface antigen-positive systemic necrotizing vasculitis. Both presented with hypertension, hypokalemia, and renal potassium wasting. Plasma renin activity and urinary aldosterone levels were markedly elevated. Renal arteriograms showed widespread microaneurysms, and necrotizing vasculitis involving renal arteries was confirmed histologically. Hypertension was refractory to conventional treatment in both patients. In one patient, hypertension was easily controlled with the angiotension-converting enzyme inhibitor captopril. Diffuse renal vasculitis with secondary hyperreninemia and hyperaldosteronism appears to be an important cause of hypertension in patients with systemic necrotizing vasculitis.

Adult↗
PubMedDate not supplied

Prevalence of primary hyperaldosteronism assessed by aldosterone/renin ratio and spironolactone testing.

Recent studies have suggested that primary hyperaldosteronism may be present in more than 10% of patients with hypertension. We aimed to estimate the prevalence in unselected patients in primary care, and investigate the influence of current drug treatment upon the aldosterone/renin ratio (ARR) and its prediction of blood pressure response to spironolactone. We measured blood pressure, plasma electrolytes, renin activity and aldosterone in 846 patients with hypertension. Spironolactone 50 mg was prescribed for one month to patients with blood pressure > or = 130/85 mmHg and ARR > or = 400. The primary outcome measure was to discover the proportion of patients with plasma aldosterone > or = 400 pmol/l and ARR > or = 800 and either an adrenal adenoma on computed tomography scan or a systolic blood pressure response to spironolactone > or = 20 mmHg. Only one patient had an adenoma, and only 16 (1.8%) had both a plasma aldosterone > or = 400 pmol/l and ARR > or = 800. By contrast, 119 patients (14.1%) had an elevated ARR but normal plasma aldosterone. In 69 patients out of the 119 who received spironolactone, blood pressure fell by 26/11 mmHg. These patients were normokalaemic but had uncontrolled hypertension despite multiple drugs. The response to spironolactone was best predicted by a low plasma renin, < or = 0.5 pmol/ml/h (<10 mU/l), despite treatment with an ACE inhibitor. We concluded that adrenal adenomas are an uncommon cause of hypertension. In the absence of hypokalaemia, a low plasma renin is a sufficient and simple way of detecting spironolactone-responders among patients with resistant hypertension. Only patients with both hypokalaemia and low plasma renin, measured while the patient is off beta blockade, require measurement of aldosterone. A plasma aldosterone >400 pmol/l together with renin activity < or = 0.5 pmol/ml/h should trigger further investigations for an adrenal adenoma.

Adenoma↗
PubMed2000

[Hypertension and primary hyperaldosteronism].

Hypokalaemic hypertension or resistant hypertension justify investigation for primary hyperaldosteronism. The first step of this investigation is to exclude the ingestion of liquorice, alkalis and diuretics. The second is to make sure that the treatment is compatible with the hormonal tests and that the natriuresis and kaliuresis are normal. The diagnosis then depends on an increased plasma or urinary concentration of aldosterone with a low plasma renin activity. The adenoma of Conn is present in 2/3 of cases and surgically curable, and should be distinguished from adrenal hyperplasia which is treatable with distal diuretics. This is a diagnosis which requires computerised tomography or, when inconclusive, demonstration of unilateral secretion of aldosterone. Adrenalectomy, usually by coelioscopy, is indicated in Conn's adenoma when the patient is young and the hypertension severe or recent. Surgical abstention is strongly advised in cases of adrenal hyperplasia.

Adenoma↗
PubMed2001

[Adrenal vein catheterization in primary hyperaldosteronism: aid in surgical decision making?].

UNLABELLED: The localisation of aldosterone-producing adenomas (APA's) remains difficult. Indeed, CT scan may not detect small APA's while CT detected tumours do not necessarily produce aldosterone. OBJECTIVE: To evaluate the value of adrenal vein catheterization (AVC) for the diagnosis of APA's and also the rates of unsuccessful procedures and complications. PATIENTS: One-hundred-and-nine hypertensives with biological features of primary hyperaldosteronism were included. Plasma sodium, potassium, aldosterone and renin levels were obtained after one night in lying position. Aldosterone and renin levels were also measured after a one-hour walking period and after a sodium expansion with saline. All patients underwent a CT scan and AVC. For adrenal samples, the ratio of aldosterone to cortisol concentrations was calculated for both sides. Both ratios were divided by the opposite one and the higher was retained as an index of laterization (IL). For lack of a golden standard variable, we have taken as a working hypothesis that operated patients had an APA (n = 38) and the non operated ones bilateral hypereplasia (n = 71). RESULTS: Operated patients had a shorter history of hypertension, more frequently a left ventricular hypertrophy on ECG, and lower serum creatinine and potassium levels, along with a higher sodium level. None of these features appeared discriminant, however. Presence of a 10-mm tumour on CT scan was not significantly different between the 2 groups. Operated patients had more than a five-fold higher IL compared with that of non-operated patients. Analysis using a ROC curve showed that the value of 12 for "IL" was an acceptable operational criterium of lateralization, producing a specificity of 90%, while maintaining a sensitivity of 62%. AVC appeared most useful in case of middle-range pre-test probability of an APA being present, that is when when clinical, biological, or radiological features are not fully concordant. The rate of unsuccessful procedure and the rate of complications were low (1.8% and 3.6%, respectively). CONCLUSION: With a low iatrogenicity, AVC appears helpful in indicating surgery mostly when clinical, biological, and CT scan features are not fully concordant. A value of 12 for IL appears to allow a high specificity while retaining an acceptable sensitivity.

Adenoma↗