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Biomedical subjects

E Arteaga

Publications and source records attributed to E Arteaga.

At least 91 records · Page 5Linked to original sources
PubMed1985

Use of the saline infusion test to diagnose the cause of primary aldosteronism.

Angiotensin II has a major effect on mineralocorticoid hormone synthesis in patients with idiopathic hyperaldosteronism; it has little or no effect in those with an aldosterone-producing adenoma. To determine if this difference could be of use in clinically separating these two forms of primary aldosteronism, saline infusion tests were performed in 20 patients--14 with surgically proved aldosterone-producing adenoma and six with idiopathic hyperaldosteronism. With the patients receiving a balanced diet containing 120 meq of sodium, 1,250 ml of isotonic saline was infused intravenously between 8 A.M. and 10 A.M. after overnight recumbency. Plasma samples were obtained immediately before and after the infusion. Plasma cortisol level decreased appropriately in both groups, but plasma renin concentration decreased only in those patients with idiopathic hyperaldosteronism (p less than 0.05). Aldosterone and 18-hydroxycorticosterone levels decreased in both groups. To account for the circadian variation in adrenocorticotropin levels during the course of saline infusion, 18-hydroxycorticosterone/cortisol and aldosterone/cortisol ratios were examined. Both ratios increased in every patient with aldosterone-producing adenoma (p less than 0.01 and p less than 0.001, respectively), but these ratios remained unchanged or decreased in the patients with idiopathic hyperaldosteronism. This divergent variation in ratios after saline infusion allows for the differentiation of patients with an aldosterone-producing adenoma from those with idiopathic hyperaldosteronism. In patients with primary aldosteronism, an 18-hydroxycorticosterone/cortisol ratio of less than 3.0 or an aldosterone/cortisol ratio of less than 2.2 after saline infusion is diagnostic of idiopathic hyperaldosteronism.

18-Hydroxycorticosterone↗
PubMed1985

Congenital 11 beta-hydroxysteroid dehydrogenase deficiency associated with juvenile hypertension: corticosteroid metabolite profiles of four patients and their families.

Four children with 11 beta-hydroxysteroid dehydrogenase deficiency are described. All patients had severe hypertension, hypokalaemia, and low plasma aldosterone and renin activities. Two of the patients were siblings and two were unrelated. The most noticeable biochemical feature of these individuals was the extremely low excretion of cortisol metabolites containing an 11-carbonyl group compared to the excretion of the 11 beta-hydroxyl containing metabolites. Although this condition is readily diagnosed in affected individuals by urinary steroid analysis, carriers of the defect do not differ from normal in their urinary steroids. Both parents of the affected siblings had normal 11-oxo-steroid/11 beta-hydroxysteroid ratios under baseline conditions and the lesions could not be revealed by ACTH administration.

11-beta-Hydroxysteroid Dehydrogenases↗
PubMed1984

Aldosterone-producing adrenocortical carcinoma. Preoperative recognition and course in three cases.

Three patients with primary aldosteronism due to adrenocortical carcinoma were studied, two with hyperaldosteronism alone and one also with hypercortisolism; in the later stages all three had hypersecretion of glucocorticoid and androgenic hormones. Although clinical presentations were similar to those of patients with benign adenoma, all had significantly higher concentrations of deoxycorticosterone and aldosterone and more profound hypokalemia. Stimulation with adrenocorticotropin in two patients showed a good cortisol response but no aldosterone response. The circadian rhythm for cortisol was normal but absent for aldosterone and deoxycorticosterone. Sequential 24-hour circadian studies in one patient showed that as the disease progressed, corticosterone and finally cortisol lost their circadian rhythms. Treatment with spironolactone, mitotane, or aminoglutethimide had transient clinical effects. The patients died 2 to 13 years later.

Adrenal Cortex Neoplasms↗
PubMed1983

Increased excretion of kallikrein during dexamethasone administration in normal man on low and normal salt intake.

The effect of dexamethasone administration for 3 days on urinary kallikrein excretion was studied in 12 normal men with normal sodium intake (n = 6) or low sodium intake (n = 6). Urinary excretion of sodium, potassium, 17-hydroxycorticosteroids, aldosterone and water was also measured in all subjects. Dexamethasone administration was associated with a significant increase in urinary kallikrein excretion (F3, 30 = 6.9; P less than 0.001) regardless of sodium intake. No significant correlation could be established between the increase in urinary kallikrein excretion and changes in urinary sodium, potassium, 17-hydroxycorticosteroids, aldosterone or water. These results suggest that dexamethasone can exert a direct action on the renal kallikrein-kinin system.

17-Hydroxycorticosteroids↗
PubMed1983

Effect of the combination of dexamethasone and sodium ipodate on serum thyroid hormones in Graves' disease.

To investigate the effect of the combination of dexamethasone (Dex) and sodium ipodate (SI) on hyperthyroidism, we studied 24 patients with typical Graves' disease, divided into four groups of six persons each. Three groups (Study I) were studied acutely (24 h) to determine the effects of Dex (5 mg every 12 h intramuscularly), SI (one oral dose of 3 g) and both drugs at the same doses, upon T4, T3, and rT3 at 0900 h before therapy was started and 24 h later. The group on Dex and that on SI had a similar T3 decrement of 25.9 +/- 4.0% and 35.8 +/- 5.0%, respectively, (P less than 0.05), whereas the effect of both drugs combined was greater (64.2 +/- 3.6%; P less than 0.01, Dex, and P less than 0.01, SI, respectively). The increment of rT3 was markedly greater in those patients on SI than in those on Dex (561.3 +/- 149.2% and 58.9 +/- 11%, respectively, P less than 0.025). A fourth group (Study II) was studied for seven days while receiving both Dex (1 mg orally three times per day) and SI (500 mg orally three times per day). Both T4 (from 18.8 +/- 1.1 to 13.1 +/- 1.1 micrograms/dl, P less than 0.02) and T3 (from 593 +/- 41 to 136.3 +/- 12.7 ng/dl, P less than 0.001) decreased at day 8. The initial brisk increment of rT3 at 24 h (808 +/- 149%, P less than 0.005) then diminished concomitantly with the fall of its precursor, T4.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗