Cases reported • Hyperaldosteronism; Aldosteronism

1/42. Clinics in diagnostic imaging (39). Conn's syndrome due to adrenocortical adenoma (Conn's tumour).

A 33-year-old man presenting with muscle weakness and hypertension was found to have hypokalaemia and metabolic alkalosis. Computed tomography (CT) showed an adrenal mass. Conn's syndrome due to an adrenocortical adenoma was confirmed at surgery. hypertension-related adrenal disorders such as Cushing's syndrome, carcinoma and phaeochromocytoma are discussed. CT is currently the single most useful imaging method for identifying adrenal masses.

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2/42. Coexistence of atherosclerotic renal artery stenosis with primary hyperaldosteronism.

The discovery of two forms of secondary hypertension in the same patient is unusual and suggests similar pathophysiological mechanisms, a predisposition to one type in the presence of the other or a chance occurrence. We describe two patients with renal artery stenosis who after successful correction of the stenotic lesions were discovered to have primary hyperaldosteronism associated with bilateral adrenal hyperplasia. Initially prior to revascularisation of the renal artery stenosis, the diagnosis of primary hyperaldosteronism was not evident. Both patients were subjected to further diagnostic evaluation after the appearance of hypokalaemia in one patient and continued resistant hypertension in both patients. The addition of spironolactone therapy reduced blood pressure impressively in both patients. Clinicians should be aware of the possibility that these two forms of secondary hypertension may be present in the same patient and that optimal blood pressure control requires diagnostic assessment and intervention for both disorders.

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3/42. Renal calculi in primary hyperaldosteronism.

Increased urinary calcium (Ca++) excretion and the presence of negative Ca++ balance is well documented in primary hyperaldosteronism. However, renal calculi as a major manifestation of this disorder is not previously described. This report describes probably the first patient who presented with renal calculi in association with primary hyperaldosteronism. We believe that primary hyperaldosteronism was a major pathogenetic factor in formation of renal calculi since increased urinary excretion of Ca++ and uric acid noted at the onset declined following short-term spironolactone administration and remission from renal calculi has persisted following initial nephrolithotomy and continued spironolactone therapy which also corrected hypertension and hyperkalemia, a hallmark of this disorder.

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4/42. Three patients with adrenal tumors having been treated simply for diabetes mellitus.

Three patients with functional adrenal tumors, Cushing's syndrome, primary aldosteronism and pheochromocytoma, who underwent adrenalectomy and were subsequently cured, were studied. All these patients had been treated for diabetes for several years before the diagnosis of adrenal tumors. In each case the state of diabetes before and after surgery, including parameters of insulin secretion and insulin resistance, was compared to demonstrate how the adrenal disorder influenced the nature of diabetes. In the case of Cushing's syndrome the hypercortisolemia caused insulin resistance in the peripheral tissues. In the case of primary aldosteronism, excessive production of aldosterone diminished insulin secretion possibly through hypokalemia. pheochromocytoma affected both insulin secretion and insulin sensitivity through hypersecretion of catecholamines. In all these patients the adrenal tumors were found in clinical contexts other than management of diabetes itself. By careful retrospective review of these three patients' history, several important points that might have drawn the physician's attention to the underlying adrenal disorders were pointed out. These included past history of acute myocardial infarction with onset at unexpectedly young age in the case of Cushing's syndrome and unexpectedly high insulin resistance for the patient's body mass index in the case of pheochromocytoma.

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5/42. Conn's syndrome and bilateral renal artery stenosis in the presence of multiple renal arteries.

We report the case of a 42-year-old male who was admitted to our hospital after an acute hypertensive crisis despite four-way anti-hypertensive therapy. The renal scintigraphy, the excretory urogram and the biochemical profile performed two years before were unremarkable, except for slightly elevated serum creatinine and plasma aldosterone, in presence of normal aldosterone/renin ratio. The renal arterial angiography that was performed despite a second unremarkable scintigraphy revealed high-grade bilateral arterial stenosis in the presence of multiple renal arteries. Following dilatation of the left stenosis, the aldosterone/renin ratio was pathologic. Recumbent and orthostatic aldosterone values were 830 pg/ml and 1824 pg/ml, respectively, and recumbent and orthostatic renin values were 0.82 and 1.21 ng angiotensin i/ml/h, respectively. The abdominal computed tomography performed to investigate a possible concomitant Conn's syndrome resulted in the detection of a left adrenal tumor. After resection of the lesion, plasma-aldosterone levels normalized and a pronounced rise in serum potassium levels was observed. Following angioplasty of the right renal artery stenosis, blood pressure could easily be managed with combined beta and calcium channel blocker therapy. Particularly in cases of bilateral (but also in the presence of unilateral) renal artery stenosis in association with Conn's syndrome, all the available screening methods for these disorders can fail. In cases of poor response to combination hypertensive therapies, renal arteriography and a fludrocortisone-suppression test should be performed in order to rule out both renal arterial stenosis and Conn's syndrome, even in the absence of clinical and biochemical findings suspicious for either disorder.

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6/42. 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.

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7/42. Anterior ischemic optic neuropathy associated with idiopathic aldosteronism and hypertension.

A 49-year-old man suffered from bilateral anterior ischemic optic neuropathy almost simultaneously, and was diagnosed with idiopathic aldosteronism associated with hypertension. Because this patient had multiple organ disorders, multiple cerebral infarctions, and a mild loss of renal function, it was important to treat his primary disease.

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8/42. Severe hypomagnesaemia-induced hypocalcaemia in a patient with Gitelman's syndrome.

Gitelman's syndrome (GS) is characterized by hyperreninaemic hyperaldosteronism, hypokalaemia, metabolic alkalosis, hypomagnesaemia and hypocalciuria and is due to a defect of the Na-Cl cotransporter at the distal tubule, which may appear in a sporadic or in a familial form. It is an autosomal recessive disorder associated with normal or reduced blood pressure. We report a case of severe hypomagnesaemia-induced hypocalcaemia in a 39-year-old Caucasian woman with GS. The patient had impaired parathormone (PTH) responsiveness to peripheral stimuli, as proved by the marked PTH increase and normalization of plasma calcium levels after acute and chronic administration of magnesium salts. Secondary normotensive hyperreninaemic hyperaldosteronism with hypokalaemia and metabolic alkalosis was also present. Normal plasma renin activity (PRA) and aldosterone levels were restored by administration of an inhibitor of prostaglandin synthesis. The electrolyte imbalance was successfully corrected with chronic treatment with magnesium and potassium salts. Genetic analysis identified a compound heterozygous mutation in the Na-Cl cotransporter gene (NCCT), confirming the diagnosis of GS. The striking feature of this case of GS was impaired PTH responsiveness to peripheral stimuli determined by hypomagnesaemia and the resulting severe hypocalcaemia, which had not previously been described in this syndrome.

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9/42. Unilateral adrenal hyperplasia causing primary aldosteronism: limitations of I-131 norcholesterol scanning.

Primary aldosteronism is a disorder that is commonly considered in patients referred to the hypertension clinic. The ease of measuring the random aldosterone-to-renin ratio in conjunction with an elevated serum aldosterone level has led to an increased screening for this disorder. Typically, patients undergo a confirmatory test after a positive screening test. However, once primary aldosteronism is confirmed, subtype delineation is critical to decide on the optimal treatment. We report a patient with resistant hypertension and primary aldosteronism with a normal computed tomographic scan of the adrenal glands, a left-sided uptake on adrenal scintigraphy, and a right-sided lateralization of aldosterone after adrenal vein sampling. A repeat adrenal vein sampling confirmed the aldosterone lateralization to the right adrenal gland, which was then removed laparoscopically. The patient had a good clinical and biochemical response, and unilateral adrenal hyperplasia was discovered at histology. Excessive reliance on adrenal scintigraphy without adrenal vein sampling may lead to serious errors in patient management.

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10/42. Adrenal cortical diseases: international case conference.

Six pathologists from japan and the United Kingdom evaluated four different cases of adrenocortical disorders independently. These adrenocortical disorders included an adrenal tumor in a 45-yr-old female without any endocrine abnormalities, bilateral adrenocortical lesions in a 55-yr-old female with cushing syndrome, an adrenocortical mass in a 44-yr-old man with hypertension, and an adrenocortical lesion in a 62-yr-old female with chronic hypertension for 30 yr. In this article, we provide a clinical summary, macroscopic and histologic findings, and histologic diagnosis of these four adrenocortical cases.

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