Plasma aldosterone elevation due to renal sodium wasting in a boy with cystic fibrosis.
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Aldosterone↗
Biomedical subjects
K Parth
Publications and source records attributed to K Parth.
Circadian patterns of plasma cortisol, 17-hydroxyprogesterone, and testosterone in congenital adrenal hyperplasia.
In 11 children aged between 2 and 17 years with (nonsalt-losing) congenital adrenal hyperplasia (21-hydroxylase deficiency) blood was drawn at 90-minute intervals during a 24-hour period and levels of 17-hydroxyprogesterone, testosterone, and cortisol were measured. Levels of 17-ketosteroids and pregnanetriol were measured too in 24-hour urine samples. These measurements were taken under different regimens of treatment and after interruption of treatment. Cortisol level rose and fell rapidly after administered corticosteroid, and reached unphysiologically high levels. Testosterone levels showed pronounced variations but stayed in the normal range for most of the time even in untreated patients; thus testosterone provides a poor control parameter. Levels of 17-hydroxyprogesterone showed extreme fluctuations and very high peak levels in untreated patients; standard treatment with two or three daily doses of corticosteroids did not prevent a pronounced rise in its level after midnight. After the first morning dose of hydrocortisone a very steep fall was observed. The 24-hour pregnanetriol excretion correlated well with the corresponding total integrated 17-hydroxyprogesterone area. It is concluded that single 17-hydroxyprogesterone values are unlikely to give adequate information about the quality of treatment.
17-Ketosteroids↗
Hyperaldosteronism after heart surgery in children. Part II: Regulation of aldosterone secretion.
The relative importance of the various mechanisms responsible for development of postoperative hyperaldosteronism (HA) is not known. Therefore, serum sodium (NA), plasma-renin activity (PRA) and plasma cortisol (PC) were evaluated in pediatric patients with transient HA following heart surgery. PRA and PC were elevated and NA was depressed postoperatively. Plasma aldosterone (PA) was negatively correlated with NA (r = -0.77; p less than 0.001) and positively correlated with PRA (r = 0.68; p less than 0.01) but was not significantly correlated with PC. PRA and NA were significantly negatively correlated (r = 0.53; p less than 0.005). Multiple regression analysis revealed that NA had the strongest influence on PA, with PRA having a somewhat lesser but still significant influence; PC had no influence. Despite the significant negative correlation between PRA and NA, the interaction of the two variables in influencing PA was not significant (partial F-test; F = 0.12; p greater tha 0.5). It is concluded that in the postoperative state sodium depletion stimulates secretion of aldosterone not only via the angiotensin-renin system but also in a significant manner by a mechanism unrelated to the angiotensin-renin system. ACTH does not seem to play an important role in postoperative HA.
Adolescent↗
Hyperaldosteronism after heart surgery in children. Part I: Treatment with aldosterone antagonists.
The course of postoperative hyperaldosteronism and its effect on fluid and electrolyte metabolism were studied in children undergoing open and closed heart surgery. Serum sodium was transiently depressed and red cell sodium concentration remained unchanged. Serum and red cell potassium concentrations were low. Hematocrit did not change significantly during the postoperative period ruling out overhydration. Therefore, the electrolyte changes are interpreted to indicate body potassium loss. That hyperaldosteronism caused potassium loss is suggested by an inverse relationship between plasma aldosterone and red cell potassium concentration. No significant differences were observed between patients undergoing open and those undergoing closed heart surgery. An additional, alternately selected group of patients undergoing open heart surgery was treated with aldosterone antagonists beginning 48 hours before surgery. Treatment did not change the course or extent of hyperaldosteronism. Specifically, potassium loss was not diminished and there was no difference in urine volume postoperatively. We conclude that aldosterone antagonists in the dosage used had no effect on the course of postoperative hyperaldosteronism.
Adolescent↗
[The effect of aldosterone antagonists in juvenile heart surgery].
In children with congenital heart disease duration and extent of hyperaldosteronism and the influence of spironolactone after surgery with a heart-lung-machine, were evaluated by direct measurement of plasma aldosterone levels. Secondary hyperaldosteronism as seen in 11 patients without spironolactone-therapy after surgery did not persist very long. 14 children receiving spironolactone immediately after surgery showed an onset of drug efficacy at a period when plasma aldosterone in the group without spironolactone had begun to fall. As a practical consequence, spironolactone treatment should be initiated a few days prior to surgery in order to achieve full efficacy on the day of surgery.
Adolescent↗
Congenital adrenal hyperplasia: simultaneous determination of plasma aldosterone and 17-hydroxyprogesterone.
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17-Ketosteroids↗
[Endocrinological aspects of ketotic hypoglycemia and adrenal calcification (author's transl)].
Case report on a 2 6/12 years old girl with bilateral adrenal calcifications and ketotic hypoglycemia. Adrenal function tests showed a normal response of the adrenal cortex but signs of adrenal medullary insufficiency. Urinary adrenaline in samples before and after insulin did not increase significantly and plasma adrenaline was undetectable during hypoglycemia. We suggest, that the absence of adrenaline, caused by perinatal adrenal hemorrhagia, is one of the possible pathogenetic keys of ketotic hypoglycemia and examinations on this disease should always include the search for adrenal calcifications.
Acidosis↗
[Transient hypoaldosteronism. A case report].
We observed a 2-week old boy who developed a typical salt-losing syndrome. Urinary 17-ketosteroid excretion of 2.4 mg per day lead us to the diagnosis of congenital adrenal hyperplasia and the usual treatment with hydrocortisone, DOCA and NcCl orally was started. The 6-months old child will tolerate a reduction and subsequent withdrawal of hydrocortisone. Mineralcorticoid and NaCl treatment, however, is to be continued. Further studies clearly showed that in the 8 and 9-month-old child cortisol production could very well be stimulated by synthetic ACTH, but the base line plasma aldosterone was exceedingly low and stimulation by ACTH and salt depletion was impossible. Instant cortisol as well as aldosterone stimulation occurs not until the child is 14 months old. There is valid evidence for a defect in aldosterone biosynthesis, which may be caused by 18-hydroxylation or 18-dehydrogenation deficiency.
Adrenocortical Hyperfunction↗
Determination of plasma aldosterone in children by thin layer chromatography and radioimmunoassay.
An accurate and relatively simple radioimmunoassay for the determination of aldosterone concentration in peripheral plasma has been developed, 0.5-2.0 ml plasma with added [1,2-3H]aldosterone is extracted with dichloromethane. Purification of the extract is achieved by thin later chromatography in the system benzene-acetone 1:1. Recovery of [1,2-3H] aldosterone is 58 +/- 6 (SD)%. Bound and free fractions are separated by dextran-coated charcoal. The intra-assay reproducibility is 8.8% and the inter-assay reproducibility varies from 11.4-16.1%. The sensitivity of the assay for a 5 ml plasma sample can be put at 0.2 ng/100 ml. Normal values determined in 52 healthy children of different age groups are presented. Furthermore the aldosterone stimulating effect of low sodium diet (17 children), severe and prolonged vomiting (19 children) and synthetic ACTH (10 children) has been studied by our modified method.
Adolescent↗
[Serum levels of LH and FSH in patients with adreno-genital syndrome (AGS) (author's transl)].
Serum levels of LH, FSH, testosterone and 17beta-estradiol were estimated by radioimmunoassay in 13 children suffering from AGS. Hormone levels were determined during and after substitution therapy and were compared with values registered in normal subjects. After therapy was stopped a statistically significant rise of testosterone and 17beta-estradiol was observed, but no changes in the serum levels of LH and FSH was noted. The discrepancies between the two observations are discussed.
Adrenal Hyperplasia, Congenital↗
[Metabolic alkalosis and secondary hyperaldosteronism in cystic fibrosis (author's transl)].
The prolonged use of a salt restricted infant formula (1.9 mEq Na/kg/day and 1,4 mEq C1/kg/day) in a child with undiagnosed cystic fibrosis led to a life threatening metabolic disturbance. The main features were hypochloraemic alkalosis due to massive loss of electrolytes in the sweat. Urinary electrolyte excretion, however, had been lowered to a minimum due to aldosteron induced reabsorption. Plasma aldosterone levels were initially high, but returned to normal after addition of salt to the feeds. Prior to admission a sweat test had been negative. The patient clearly demonstrates the unique metabolic feature of cystic fibrosis of the ability to retain electrolytes in the tubulus and at the same time the inability of the sweat glands to reabsorb sodium and chloride. Contrary to present experience severe prolonged salt restriction is believed to be able to diminish sweat electrolytes to subpathological values.
Aldosterone↗
[Plasma aldosterone in childhood].
According to a radioimmunological method modified in our laboratory we determined plasma aldosterone levels under standardized conditions in children of different age from 2 weeks to 14 years, in women undergoing uncomplicated vaginal delivery, and in the cord blood of the corresponding newborn babies. Furthermore, the effect of different stimulating factors (ACTH, salt restriction, severe vomiting, fever) in children was studied. In mothers and cord blood we found 68.6 +/- 39.3 ng/100 ml and 75.5 +/- 37.4 ng/100 ml, respectively. In the first two years of life there is a decrease in plasma aldosterone levels to the relatively constant concentration at the age of 2 to 14 years (7.3 +/- 4.7 ng/100 ml). The age groups 2 weeks to 1 year, 1 to 2 years and 2 to 14 years all show significant differences. A correlation of age (first two years of life) and plasma aldosterone level could be shown (correlation coefficient -0.50 according to Pearson). The stimulation results are comparable with literature data concerning adults. The mechanism of stimulation by vomiting and fever is discussed.
Adolescent↗
[The clinical value of the cortisol secretion rate determination in paediatric endocrinology (author's transl)].
The cortisol secretion rate was determined in 18 children according to a modified and simplified method. In 7 cases the determination was repeated after stimulation with synthetic ACTH. 12 of these children suffered from diseases which may affect glucocorticoidsteroid production and the remaining 6 children served as normal controls. In some cases the plasma 11-hydrocorticoid level and urinary excretion of 17-ketogenic steroids were additionally determined. Differences in adrenal function were noted in 2 patients with congenital adrenal hyperplasia (one of the salt-losing type, the other nonsalt-losing type) and 5 patients with adrenal insufficiency. A normal cortisol secretion rate was found in 3 children with diverse disturbances of carbohydrate metabolism, as well as in a child with subtotal adrenalectomy. The clinical value of the determination of the cortisol secretion rate is discussed and was found to be a more reliable indicator of glucocorticoid activity than other parameters.
11-Hydroxycorticosteroids↗
[Latent adrenal gland insufficiency in ketonemic vomiting].
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Adrenal Glands↗