Cases reported "Hyperaldosteronism"

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1/6. Licorice-induced pseudoaldosteronism.

    Licorice ingestion as a cause of pseudoaldosteronism is discussed. The mechanism whereby licorice, when consumed in large quantities, exhibits the physiologic properties of aldosterone, is reviewed. A case report of a 51-year-old male hospitalized with hypertension and hypokalemia is presented with reports of laboratory findings which lead to the diagnosis of pseudoaldosteronism.
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2/6. A case of pseudoaldosteronism, accompanied with hypocalcemia and exaggerated ACTH response.

    glycyrrhizic acid (GA) inhibits the activity of 11beta-hydroxysteroid dehydrogenase type 2 in the kidney, with the resulting increase in intrarenal cortisol concentration leading to hypertension and suppression of the renin-aldosterone system. In this paper we describe an interesting case of pseudoaldosteronism, associated with hypocalcemia and an exaggerated ACTH response. A 72-year-old woman was referred to our department for further evaluation of hypokalemia and hypocalcemia. The patient had been taking GA (150 mg/day) for the previous year for treatment of liver damage. plasma renin activity and aldosterone concentration were both within lower normal limits. Urinary excretion of potassium and calcium was within the upper limit of the normal range and increased with administration of supplements. plasma ACTH levels increased markedly in response to an intravenous injection of CRH. Cessation of GA and the potassium and calcium supplements on admission, led to a gradual normalization of serum potassium and calcium levels and blood pressure. The hypocalcaemia in our patient was related to decreased tubular reabsorption of calcium as a consequence of renal corticoid excess. It is possible that an increase in the number of CRH receptors in the pituitary following GA treatment caused the exaggerated ACTH response in association with pseudoaldosteronism. The existence of hypocalcemia and an exaggerated ACTH response should be observed carefully when managing pseudoaldosteronism.
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3/6. A case of pseudoaldosteronism induced by glycyrrhizin.

    A 55-year-old man was referred to us for evaluation of hypertension and hypokalemia. He had been administered glycyrrhizin from one year before admission for the treatment of chronic hepatitis. On admission, his blood pressure was 230/105 mmHg; serum potassium, 2.4 mEq/l; the plasma aldosterone concentration (PAC) and plasma renin activity (PRA) were undetectable. His blood pressure, potassium, PRA and PAC returned to normal within about 4 weeks after discontinuation of the glycyrrhizin. Re-administration of glycyrrhizin caused increases in PRA and PAC. His urinary cortisol excretion was increased and urinary cortisone excretion decreased, while his serum cortisol level remained unchanged. Supplementation of dexamethasone led to a decrease in blood pressure, and increased levels of serum potassium, PRA, and PAC. These results suggest that increased renal cortisol as a result of decreased conversion to cortisone might play an important role in the development of pseudoaldosteronism as well as in its own mineralocorticoid activity.
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4/6. Prolonged pseudoaldosteronism induced by glycyrrhizin.

    We describe the natural recovery from the aggravated hypertension, hypokalemia and suppression of the renin-aldosterone axis after the glycyrrhizin discontinuation in two mild hypertensive women aged 71 and 68 years, who had been administered 273 to 546 mg glycyrrhizin daily for 1.5 and 6 months, respectively, for the treatment of liver disease. About one month after the glycyrrhizin discontinuation, acceleration of hypertension, hypokalemia and suppression of the renin-aldosterone system still continued in both patients. At this stage, sodium restriction resulted in the normalization of blood pressure with weight loss and the subsequent sodium repletion produced a rapid increase in blood pressure to hypertensive levels observed before sodium restriction, with weight gain. plasma renin activity and plasma aldosterone were low and did not respond to sodium restriction. Inappropriately excessive amounts of potassium were also excreted in the presence of hypokalemia. About one and a half months later, the improvements of aggravated hypertension, hypokalemia and suppressed renin-aldosterone system gradually occurred in both patients. sodium restriction performed about three months later in case 2 no longer produced the changes in blood pressure and body weight. plasma renin activity and plasma aldosterone responded subnormally to sodium restriction. These results demonstrate that both patients had a prolongation of the syndrome resembling primary aldosteronism except the low plasma aldosterone level about one month after the glycyrrhizin discontinuation. The possible mechanisms by which this prolongation was caused are discussed.
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5/6. A case of pseudoaldosteronism due to addiction of Jintan, a mouth refresher popular among Japanese.

    A 50-year-old man with hypertension showed hypokalemia, hyporesponsive low reninemia, and low levels of aldosterone in the plasma and urine. plasma DOC and corticosterone level, adrenal scintigram, and phlebogram were within normal limits. hypertension and hypokalemia were correctable by spironolactone. It was revealed that he had been ingesting Jintan granules in large doses, corresponding to 150-220 mg of glycyrrhizic acid per day for 10 years. Upon cessation of Jintan ingestion, blood pressure and serum potassium level were normalized after 40 days. Metabolic alkalosis, hypervolemia, hyporesponsive low reninemia, and the low levels of plasma and urine aldosterone were also improved. Thus, the present case of pseudoaldosteronism was attributed to Jintan, and raises a caution to excessive Jintan ingestion.
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6/6. An autopsy case of licorice-induced hypokalemic rhabdomyolysis associated with acute renal failure: special reference to profound calcium deposition in skeletal and cardiac muscle.

    A 78-year-old man was hospitalized because of muscular weakness and acute renal failure. He had been taking glycyrrhizin (280 mg/day) for the last 7 years. hypertension was noted in his history. serum potassium was 1.9 mEq/l with metabolic alkalosis. There was hyporeninemic hypoaldosteronism. serum enzymes, including GOT, LDH and CPK were markedly elevated. In addition, serum myoglobin was as high as 46 micrograms/ml with massive myoglobinuria. oliguria occurred and blood urea nitrogen and serum creatinine rapidly elevated from 20.9 to 87 mg/dl and from 1.3 to 6.7 mg/dl, respectively. Profound calcium deposition was found in the damaged skeletal muscles, including the quadriceps femoris, axillar, neck, and cardiac muscles. These results indicate that licorice-induced pseudoaldosteronism produces hypokalemic rhabdomyolysis, resulting in acute renal failure and profound deposition of calcium into the damaged skeletal and cardiac muscles.
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