Cases reported "Hyperaldosteronism"

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11/83. 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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12/83. Idiopathic intracranial hypertension with primary aldosteronism: report of 2 cases.

    Although unconfirmed, the syndrome idiopathic intracranial hypertension (IIH), commonly seen in overweight 20- to 50-year-old women, has been proposed to have its origins in an endocrine-based disturbance of electrolytes. Herein we report on 2 women with IIH and primary aldosteronism (PAL). aged 57 and 55 (patients 1 and 2), each had a longstanding history of mild-to-moderate arterial hypertension, recurrent hypokalemia, and headaches. They were found to have IIH at ages 51 and 45. PAL was diagnosed at ages 57 and 35, respectively, due to proven left adrenal adenoma in patient 1; and presumptive adrenal nodular hyperplasia in patient 2. This is the first report to appear in the English medical literature that describes an association between IIH and PAL. It raises the prospect that in some cases of IIH associated with arterial hypertension, an autonomous production of aldosterone should be considered.
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13/83. adenomatoid tumor of the adrenal gland with micronodular adrenal cortical hyperplasia.

    We report a case of an adenomatoid tumor (AT) of an adrenal gland with micronodular adrenal cortical hyperplasia (ACH). A 51-year-old man was found to have newly developed hypertension with clinical evidence of primary aldosteronism. A computerized tomogram of the abdomen revealed a solitary mass in the right adrenal gland. He underwent a right adrenalectomy for a presumptive clinical diagnosis of a solitary aldosterone-producing adrenal cortical adenoma. On histopathologic examination, the adrenal gland demonstrated an AT, diagnosed by the characteristic histological features, immunohistochemical stain results, and electron microscopic findings. The surrounding adrenal cortex showed multiple small hyperplastic cortical nodules. After the adrenalectomy, the patient's blood pressure normalized. Primary AT of the adrenal gland coexisting with micronodular ACH associated with hypertension has not been previously reported.
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14/83. Cardiomyopathy in an adult with Bartter's syndrome and hypokalemia. Hemodynamic, angiographic and metabolic studies.

    A case of an adult with Bartter's syndrome (hyperplasia of the juxtaglomerular complex with hyperaldosteronism and hypokalemic alkalosis) is described; the patient had the unusual manifestation of cardiomyopathy, probably secondary to severe hypokalemia. Results of metabolic studies and kidney biopsy were consistent with Bartter's syndrome; angiographic and hemodynamic findings were abnormal. The cardiomyopathy was confirmed at autopsy after the patient's sudden death. Conclusions from this case are that severe hypokalemia can pose a serious threat both immediately in the form of dangerous arrhythmias and in the long term in the form of cardiomyopathy.
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keywords = hyperplasia
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15/83. Hypertension, hypokalemia, hyporeninemia and severe target organ damage.

    A 51-year-old woman with a 20-year history of severe hypertension and target organ damage had nondiuretic hypokalemia, kaluresis, suppressed plasma renin activity and elevated urinary excretion of aldosterone. Renal arteriography demonstrated unilateral renal artery stenosis secondary to fibromuscular hyperplasia. blood pressure responded only minimally to almost all antihypertensive agents. spironolactone, 300 to 400 mg/d, produced distinct improvement in blood pressure, which was maintained for 13 months.
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keywords = hyperplasia
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16/83. Primary hyperparathyroidism associatiated with aldosterone-producing adrenocortical adenoma and breast cancer: relation to MEN1 gene.

    A rare case of primary hyperparathyroidism associated with primary aldosteronism and breast cancer is reported. A 44-year-old woman was admitted to our hospital to undergo surgical removal of breast cancer. She had hypertension with low serum potassium, and slightly but significantly elevated serum calcium levels. Further studies demonstrated an enlarged left superior parathyroid gland and a left aldosterone-producing adrenocortical adenoma. blood pressure was controlled with spironolactone and nifedipine, and left mastectomy was done for breast cancer. The pathological diagnosis was scirrhous breast carcinoma. Although the postoperative course was uneventful, her serum calcium gradually and progressively rose to higher levels. Left superior parathyroidectomy and left adrenalectomy were then performed simultaneously. The pathological diagnoses of the resected parathyroid gland and adrenal gland were parathyroid chief cell adenoma and adrenocortical adenoma with hyperplasia of zona glomerulosa, respectively. To clarify if the occurence of these tumors may be related to MEN1 gene mutations, we analyzed MEN1 gene in this patient, and found a loss of heterozygosity of the MEN1 locus in the parathyroid adenoma and breast cancer. Thus, we conclude that an alteration of the MEN1 gene and/or another tumor suppressor gene located at the MEN1 locus on chromosome 11q13 may be responsible for the development of parathyroid adenoma and breast cancer in our patient suggesting that the clinical spectrum of MEN1 might include breast cancer. In addition, serum calcium should be interpreted with caution in primary aldosteronism, because hypercalcemia may be masked in the presence of aldosterone excess.
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keywords = hyperplasia
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17/83. Concurrence of primary aldosteronism and renal artery stenosis.

    1. An unusual clinical case is described in which renal artery stenosis (RAS) was found to coexist with adrenocortical hyperplasia, resulting in hypertension. 2. Partial relief of the hypertension was achieved by correction of RAS, and then further relief by extirpation of one adrenal gland affected by unilateral hyperplasia, in interventions 8 months apart. 3. Biochemical features typical of primary hyperaldosteronism were observed both before and after RAS repair but were not present after unilateral adrenalectomy. 4. The association of these two lesions could have occurred by chance, through genetic linkage, or by progression from RAS to tertiary aldosteronism.
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keywords = hyperplasia
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18/83. Bartter's syndrome--case report.

    A 26-year-old female with Bartter's syndrome associated with Graves' disease is reported. This patient had a history of Graves' disease from the age of 22 and anti-thyroid drug (methimazole) had been administered for 2 years. Thyroid function returned to normal but general fatigue and polyuria continued. hypokalemia was diagnosed at 25 years of age and she was referred to our hospital for evaluation. blood pressure was normal and laboratory data revealed normal thyroid function, hypokalemic alkalosis, high plasma renin activity and high plasma aldosterone concentration. She showed normal pressor sensitivity to norepinephrine infusion, grossly diminished pressor sensitivity to exogenous angiotensin ii infusion compared with the normal. A renal biopsy specimen showed juxtaglomerular cell hyperplasia. Electron microscopy confirmed lacis cell (agranular cell) proliferation.
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ranking = 0.2
keywords = hyperplasia
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19/83. A case with primary aldosteronism due to unilateral multiple adrenocortical micronodules.

    A 46-year-old male with long-term treatment-resistant hypertension and past history of cerebral hemorrhage was found to have suppressed plasma renin activity (PRA) and normal plasma aldosterone concentration (PAC) with aldosterone/renin ratio of 25.3. furosemide plus upright test did not stimulate PRA, but computed tomography scan of the abdomen revealed no abnormal lesions in either adrenal gland. Selective adrenal venous sampling (SAVS) showed that PAC in the left and the right adrenal vein were 1000 ng/dl and 230 ng/dl, respectively, which increased to 1500 ng/dl and 620 ng/dl, respectively, after ACTH stimulation. diagnosis of primary aldosteronism due to hypersecretion of aldosterone from the left adrenal gland was made, and laparoscopic left adrenalectomy was performed. Pathological examination of the 'apparently normal' adrenal tissue resected revealed the presence of poorly encapsulated multiple adrenocortical micronodules which showed positive immunoreactivity for 3beta-hydroxysteroid dehydrogenase by immunohistochemical study, but negative immunoreactivity in the hyperplastic zona glomerulosa consistent with paradoxical hyperplasia associated with primary aldosteronism. Postoperatively, PRA was normalized and his high blood pressure was well controlled with lower doses of antihypertensive drugs than those used before surgery. The clinicopathological features of our case are consistent with the diagnosis of unilateral multiple adrenocortical micronodules (UMN), a new subset of primary aldosteronism, in which SAVS proved to be a useful diagnostic tool for its localization.
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ranking = 0.2
keywords = hyperplasia
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20/83. A case of primary aldosteronism due to unilateral adrenal hyperplasia.

    The case of a patient with primary aldosteronism due to unilateral adrenal hyperplasia (UAH) is reported. A 43-year-old man with an 8-year history of hypertension presented at our institution with hypokalemia, increased plasma aldosterone concentration (PAC), and suppressed plasma renin activity (PRA). An abdominal CT scan showed almost normal adrenal glands with slight enlargement in the left gland. 131I-Norcholesterol adrenal scintigraphy under dexamethasone suppression showed bilaterally decreased uptake. To rule out idiopathic hyperaldosteronism, an adrenal vein sampling before and after ACTH stimulation was performed and a left-sided lateralization of PAC was observed. A left adrenalectomy was performed, and the patient had a good clinical and biochemical response. Micronodular hyperplasia was discovered in the adrenal gland histologically, and in the immunohistochemical analysis, positive staining for 3beta-hydroxysteroid dehydrogenase in micronodular lesions confirmed the diagnosis of UAH. Although UAH is a rare subset of primary aldosteronism, it is surgically correctable as a unilateral autonomous aldosterone-producing lesion. Careful investigations, including bilateral adrenal vein sampling, should be performed for the diagnosis.
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ranking = 1.2
keywords = hyperplasia
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