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Adrenocortical function in idiopathic haemochromatosis
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Abstract.
In idiopathic haemochromatosis, excessive iron deposits include adrenal cortex, and mainly the zona glomerulosa. In this view, we measured basal and poststimulative values of plasma cortisol, aldosterone and renin activity (RA) in two groups of patients: 1) 9 normal-salt repleted subjects (NSR) who were subjected to iv ACTH and furosemide tests, 2) 10 patients who were subjected to chronic salt depletion (CSD), to iv ACTH and furosemide tests. The results were compared with two groups of 7 healthy volunteers (NSR and CSD). In the patients, basal cortisol values were either normal or increased in cases of poorly controlled diabetes (21 ± 2.1 μg/100 ml, P < 0.01) and cortisol increase after ACTH injection was normal (to 43.3 ± 4.3 μg/100ml). In the 9 NSR patients, basal aldosterone (7.75 ± 1.5 ng/100 ml) and RA (1.55 ± 0.27 ng/ml/h) values were normal; aldosterone and RA rose after furosemide injection: these increases were similar in these patients (respectively to: 13.5 ± 2.2 ng/100 ml and 4.3 ± 0.6 ng/ml/h) and in the 7 NSR controls. In the 10 CSD patients, basal aldosterone and RA values were always increased (26.5 ± 3.2 ng/100 ml and 8.5 ± 2.3 ng/ml/h) as much as in the 7 CSD controls. After ACTH administration, aldosterone values (26.1 ± 4 in NSR patients, 54 ± 8 ng/100 ml in CSD patients) were the same as in the two control groups. This study suggests that there is no adrenocortical deficiency in idiopathic haemochromatosis, in spite of excessive iron deposits in the adrenal cortex.
Oxford University Press (OUP)
Title: Adrenocortical function in idiopathic haemochromatosis
Description:
Abstract.
In idiopathic haemochromatosis, excessive iron deposits include adrenal cortex, and mainly the zona glomerulosa.
In this view, we measured basal and poststimulative values of plasma cortisol, aldosterone and renin activity (RA) in two groups of patients: 1) 9 normal-salt repleted subjects (NSR) who were subjected to iv ACTH and furosemide tests, 2) 10 patients who were subjected to chronic salt depletion (CSD), to iv ACTH and furosemide tests.
The results were compared with two groups of 7 healthy volunteers (NSR and CSD).
In the patients, basal cortisol values were either normal or increased in cases of poorly controlled diabetes (21 ± 2.
1 μg/100 ml, P < 0.
01) and cortisol increase after ACTH injection was normal (to 43.
3 ± 4.
3 μg/100ml).
In the 9 NSR patients, basal aldosterone (7.
75 ± 1.
5 ng/100 ml) and RA (1.
55 ± 0.
27 ng/ml/h) values were normal; aldosterone and RA rose after furosemide injection: these increases were similar in these patients (respectively to: 13.
5 ± 2.
2 ng/100 ml and 4.
3 ± 0.
6 ng/ml/h) and in the 7 NSR controls.
In the 10 CSD patients, basal aldosterone and RA values were always increased (26.
5 ± 3.
2 ng/100 ml and 8.
5 ± 2.
3 ng/ml/h) as much as in the 7 CSD controls.
After ACTH administration, aldosterone values (26.
1 ± 4 in NSR patients, 54 ± 8 ng/100 ml in CSD patients) were the same as in the two control groups.
This study suggests that there is no adrenocortical deficiency in idiopathic haemochromatosis, in spite of excessive iron deposits in the adrenal cortex.
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