Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0001430 (adenoma)
 21,222 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Normal subjects, normal-renin hypertensive patients, and low-renin hypertensive patients were evaluated by intravenous saline infusion and with a fludrocortisone acetate (Florinef) protocol to clarify diagnostic criteria for primary aldosteronism that are recommended for the saline infusion protocol. The patients consumed a 200 mEq sodium, 70 mEq potassium diet for 6 days, and on the last 3 days received Florinef 0.5 mg orally twice daily. On Days 3 and 6, urinary aldosterone and tetrahydroaldosterone excretions were determined, and on Days 4 and 7 plasma aldosterone (PA) was determined at 0600 after overnight recumbency and at 0800 after 2 hours of walking. Although the level of normal PA suppression by saline infusion has been commonly defined as 10 ng/dl, a value of 5 ng/dl was originally recommended. In 20 normal subjects and 45 normal-renin hypertensive patients, we found that the PA was almost always suppressed below 5 ng/dl. In 18 of 75 low-renin patients including five with aldosterone-producing adenoma (APA), the PA was never suppressed below 10 ng/dl; thus, these 18 patients had classical primary aldosteronism by generally accepted criteria. The Florinef protocol was performed in eight of these 18 patients and was abnormal in all. An abnormal Florinef protocol was also found in seven of 15 patients studied with PA suppression after saline infusion to between 5 and 10 ng/dl, but in only one of 24 patients studied with PA suppression below 5 ng/dl. Additional studies in the subgroup with abnormal results from the Florinef protocol indicated that none of these patients had evidence of APA, so they had nontumorous primary aldosteronism (NTPA).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Further evaluation of saline infusion for the diagnosis of primary aldosteronism. 638 37

Hypertension and hypokalemia were found in a 60-yr-old woman suffering from primary hyperparathyroidism. Laboratory investigations in this patient disclosed 1) elevated levels of plasma aldosterone (PA) which could not be suppressed by a high sodium diet alone or in combination with fludrocortisone (Florinef); 2) a decline of the elevated PA levels after 4 h of ambulation; and 3) low PRA which was unresponsive to stimulation by a low sodium diet coupled with diuretic-induced volume depletion and 4 h of ambulation. These findings were consistent with the diagnosis of primary hyperaldosteronism. Extirpation of a parathyroid adenoma reduced the patient's serum calcium level to normal, and subsequently, a normalization of her blood pressure, serum electrolytes, PA, and PRA were observed. On the basis of these data is is suggested that in this case hyperaldosteronism may have been caused directly or indirectly by primary hyperparathyroidism.
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PMID:Primary hyperparathyroidism: possible cause of primary hyperaldosteronism in a 60-year-old woman. 699 17