The di red radiuimmunoassa)• for plasma aldosll'ronc (P ,\) set up in this laboratory has hccn rc1wrtcd elscwcrc. Subjects were 115 normal full term nc,1 horns and infants. During the first

The simultaneous determination of cortisol and 17α-hydroxyprogesterone (17-OHP) was carried out on a single plasma sample (0.6 ml) by the competitive protein-binding technique after a steroid partition by water and carbon tetrachloride. This procedure was tested for sensitivity, accuracy, reproducibility and specificity. It was then applied to plasma samples obtained from 20 control subjects and 28 patients with 21-hydroxylase deficiency. The cortisol value in the control group was 9.3 μg/100 ml ± 0.7 (se). This was moderately decreased in the untreated patients (group I): 6.7 μg/100 ml ± 0.9 (se), markedly decreased in those who discontinued treatment for 3 to 15 days (group II): 1.5 μg/100 ml ± 0.3 (se) and was suppressed in the treated patients (group III). In normal children, the 17-OHP level was at the limit of sensitivity of the method. It was increased to 29 μg/100 ml ± 2.8 (se) in group I and was unchanged in group II: 26.5 μg/100 ml ± 3.4 (se). The plasma 17-OHP remained elevated in the patients who received an oral cortisol dose ≦ 20 mg/m2/ day and decreased to ≦ 3 μg/100 ml in those who were treated with a cortisol dose > 20 μg/m2/day. A 17-OHP response to ® and a 17-OHP diurnal rhythm were were observed in the untreated patients. In contrast, the patients who had temporarily stopped their treatment had no reaction. A negative correlation between the cortisol and ACTH levels appeared in groups I and II (N = 19; r = –0.66; P < 0.01) and a positive correlation was noted between the 17-OHP and urinary pregnanetriol values in all the patients (N = 33; r = 0.52; P < 0.01). The reported technique described is simple and contributes to the diagnosis of congenital adrenal hyperplasia; it can also be useful in the follow-up of treated patients.

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Plasma aldosterone and 17\g=a\-hydroxyprogesterone(17-OHP) concentrations were measured in 35 patients with congenital adrenal hyperplasia resulting from 21-hydroxylase deficiency. Ten patients had never been treated and among them were 4 salt-losing infants. Both aldosterone and 17-OHP were high in the 6 untreated non salt-losers. The values ranged respectively from 110 to 376 pg/ml and from 150 to 292 ng/ml. Results were variable in the 4 salt-losers. Three out of 5 untreated non salt-losers who were submitted to a low sodium diet, responded by doubling their aldosterone levels.When plasma 17-OHP concentrations were <30 ng/ml, the mean aldosterone level in the treated non salt-losers (n = 6) was 15.3 pg/ml \ m=+-\4.3 (se). This value was not different from the mean level found in the control children (n = 7), 18.8 pg/ml \ m=+-\ 3.2. In the treated salt-losers (n = 9), the measured aldosterone levels were xx 10 pg/ml 7 times out of 9. When the treated patients exhibited plasma 17-OHP concentrations > 30 ng/ml, the salt-losers (n = 11) were distinguished from the non salt-losers (n = 8) in that they showed a significantly lower aldosterone mean level, 24.6 pg/ml \ m=+-\4.3 against 69 pg/ml \m=+-\13.4 found in the non salt-losers. The salt-losers displayed no aldosterone increases to synthetic ACTH stimulation under treatment or at the withdrawal of treatment, while !) This study was supported by I. N.

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