Cases reported "Hypokalemia"

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1/131. Saline-resistant metabolic alkalosis, severe hypokalemia and hypertension in a 74-year-old woman.

    The case of a 74-year-old woman with past history of hypertension and cerebrovascular accident admitted with pneumonia, dehydration, hypernatremia and severe hypokalemic alkalosis is presented. After correction of the hypertonic dehydration, the hypokalemia and alkalosis persisted in spite of aggressive potassium supplementation and the patient became hypertensive. Mineralocorticoid excess was suspected and excluded after extensive endocrinological testing. The use of aldactone failed to revert the abnormalities. triamterene administration corrected the electrolytes and acid base aberrations, and dramatically improved the blood pressure control. This clinical picture is compatible with the diagnosis of Liddle's syndrome. Our patient exemplifies the unique occurrence of hypokalemic metabolic alkalosis in association with volume contraction at the start of the hospitalization and volume expansion later on her course.
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2/131. Low doses of liquorice can induce hypertension encephalopathy.

    Prolonged ingestion of liquorice is a well-known cause of hypertension due to hypermineralocorticoidism. We describe 2 cases of hypertension encephalopathy (in addition to the classical symptoms of hypertension, hypokalemia and suppression of the renin-aldosterone system) which resulted in pseudohyperaldosteronism syndrome due to the regular daily intake of low doses of liquorice. Glycyrrhizic acid, a component of liquorice, produces both hypermineralocorticism and the onset of encephalopathy through the inhibition of 11beta-hydroxysteroid dehydrogenase. hypertension encephalopathy due to the daily intake of low doses of liquorice, however, has not been previously documented. It is proposed that some people could be susceptible to low doses of glycyrrhizic acid because of a 11beta-hydroxysteroid dehydrogenase deficiency.
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3/131. Liddle's syndrome: a report in a middle-aged woman.

    A 54-year-old woman with diabetes mellitus was hospitalized with generalized edema and weakness. She was also found to have hypertension, hypokalemia and metabolic alkalosis. Detailed examination showed subnormal plasma renin activity and plasma aldosterone concentration. Adrenal CT scanning revealed no adrenal tumor. A successful treatment with amiloride established the diagnosis of Liddle's syndrome for the patient. Liddle's syndrome, a rare hereditary disease usually found in young patients, should be considered in the differential diagnosis of hypertension even in elderly individuals.
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4/131. Hypokalemic thyrotoxic paralysis: a rare cause of tetraparesis with acute onset in Europeans.

    We describe a 21-year-old Italian male affected by hypokalemic tetraparesis with acute onset. In the emergency ward, the patient was agitated, with tachycardia (140/min) and systolic hypertension (180/70 mm Hg). He was not able to flex the lower extremities against a light resistance and furthermore, he was hypotonic and without tendon reflexes. One hour later he developed strength deficit of the upper extremities as well. Biochemical analyses revealed severe hypopotassemia (2.1 meg/l). After administration of 140 meq potassium phosphate, the patient began to improve, and 12 h after the onset he was able to walk normally. Successive investigations documented an undiagnosed case of Graves' disease. Thyrotoxic hypokalemic paralysis has been observed almost only in Asians, however, with this case and others reported, we believe that it should be considered as a cause of muscular paralysis also in Caucasians.
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5/131. nephrocalcinosis and renal cysts associated with apparent mineralocorticoid excess syndrome.

    Apparent mineralocorticoid excess (AME) syndrome is a rare inherited disorder caused by 11beta-hydroxysteroid dehydrogenase (11-HSD 2) isozyme deficiency in the kidney. This enzyme is responsible for oxidizing cortisol to its inactive metabolite cortisone. An elevated tetrahydrocortisol (THF) and allotetrahydrocortisol (aTHF) to tetrahydrocortisone (THE) ratio in the urine is pathognomonic of AME syndrome. Clinical features include hypertension, hypokalemia, alkalosis, reduced plasma renin activity (PRA), low aldosterone levels, and occasionally nephrocalcinosis. Here we describe a 13-year-old boy who presented with severe hypertension, hypokalemia, low PRA and aldosterone levels, and elevated THF plus aTHF/THE ratio in the urine consistent with a diagnosis of AME syndrome. On ultrasound examination, he had severe nephrocalcinosis, and bilateral renal cysts. Renal cysts have not been previously reported in AME syndrome. The development of nephrocalcinosis and renal cysts may be associated with chronic long-standing hypokalemia. An early diagnosis and treatment of AME syndrome could help to prevent these sequelae, and to preserve renal function.
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6/131. Polymorphic ventricular tachycardia due to renal artery stenosis--a case report.

    Atherosclerotic renal artery disease is common among patients with hypertension over the age 50 years who are resistant to medical treatment. In this case report, the authors present a 55-year-old woman with unilateral renal artery stenosis with a history of cardiac arrest. QT prolongation and evident hypokalemia were the main clinical findings of the patient. The patient also had an episode of polymorphic ventricular tachycardia during hospitalization that degenerated into ventricular fibrillation. After successful balloon dilation of the stenotic renal artery, the patient stayed normotensive and normokalemic without medication, and no arrhythmia was observed during the 6-month follow-up period.
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ranking = 0.2
keywords = hypertension
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7/131. Two sporadic cases of Liddle's syndrome caused by De novo ENaC mutations.

    Liddle's syndrome is a rare form of hereditary hypertension caused by mutations of the epithelial sodium (Na( )) channel (ENaC). Analysis of the diseased pedigrees indicates an autosomal dominant inheritance, and the identified mutations are heterozygotes of gain-of-function mutations. However, sporadic cases of Liddle's syndrome have been reported in the literature, including one recently reported case caused by a de novo mutation of ENaC. We identified two patients with Liddle's syndrome who did not have family histories of hypertension. sequence analysis showed a mutation in each case (P616L in betaENaC and W576X in gammaENaC), both confirmed to be de novo mutations. These data indicate that Liddle's syndrome should be considered even in patients without a family history of hypertension.
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8/131. Approach to the patient with hypertension, unexplained hypokalemia, and metabolic alkalosis.

    We present a patient with hypertension and hypokalemia secondary to an aldosterone-producing adenoma that was renin responsive (APARR). We discussed the sequential approach to the diagnosis of the different subtypes of primary aldosteronism and confirmed the presence of an APARR. The most common cause of primary aldosteronism is an aldosteronoma; functionally, these adenomas respond poorly to angiotensin ii but show a brisk response to adrenocorticotropin hormone. They have a pattern of aldosterone level that declines in parallel with cortisol levels. Our patient had an APARR, with an increase of aldosterone in the upright posture. The unusual physiologic response, incidence, and clinical characteristics of APARR are reviewed.
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keywords = hypertension
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9/131. Intermittent hyperaldosteronism in a child due to an adrenal adenoma.

    aldosterone producing adenoma (APA) is a rare but potentially curable form of paediatric hypertension. We report a case of APA in a 9-year-old boy, suspected due to persistent hypokalaemia. Neither BP nor initial laboratory investigations disclosed the diagnosis and the presence of an APA was suggested by functional tests and radiological findings. Histologically, a cortical tumour was found associated with a marked medullary hyperplasia of both chromaffin and ganglion cells. CONCLUSION: This case reinforces the need for further investigations in patients with misleading clinical and laboratory data.
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10/131. hypokalemia, metabolic alkalosis, and hypertension: Cushing's syndrome in a patient with metastatic prostate adenocarcinoma.

    Ectopic adrenocorticotropic hormone (ACTH) and/or corticotropin-releasing hormone (CRH) are associated with a growing list of tumors. We report a 69-year-old white man with a history of high-grade prostate carcinoma and widely metastatic adenocarcinoma who presented with metabolic alkalosis, hypokalemia, and hypertension secondary to ectopic ACTH and CRH secretion. Laboratory values were consistent with hypokalemia and metabolic alkalosis. Markedly elevated serum cortisol (135 microg/dL), ACTH (1,387 pg/dL), CRH (69 pg/dL), and urine free cortisol (16,276 microg/24 h) levels were found. Chest computed tomographic (CT) scan showed small noncalcified parenchymal densities; however, bronchoscopy and bronchoalveolar lavage washings were unremarkable for a neoplastic process. Abdominal CT scan and magnetic resonance imaging showed multiple small liver lesions and multiple thoracic and lumbar intensities consistent with diffuse metastatic disease. Histological analysis of a biopsy specimen from the thoracic spine showed an undifferentiated adenocarcinoma consistent with a prostate primary tumor. The severe metabolic alkalosis secondary to glucocorticoid-induced excessive mineralocorticoid activity was treated with potassium supplements, spironolactone, and ketoconazole. In this case report, we describe an unusual tumor associated with ectopic ACTH and CRH production and the pharmacodynamic relationship of plasma cortisol levels and urinary cortisol excretion with ketoconazole treatment.
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keywords = hypertension
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