{'fraction_non_alphanumeric': 0.016047297297297296, 'fraction_numerical': 0.0059121621621621625, 'mean_word_length': 6.011834319526627, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Dissociation of plasma renin activity and plasma aldosterone level during dexamethasone suppression test in non-salt-losers with congenital adrenal hyperplasia due to 21-hydroxylase deficiency.

We have studied plasma renin activity, the plasma aldosterone level and urinary metabolites of glucocorticoid precursors before and during a dexamethasone suppression test in three non-salt-losers with congenital adrenal hyperplasia due to 21-hydroxylase deficiency, who had never been treated with glucocorticoid. Plasma renin activity, the plasma aldosterone level and urinary pregnanetriol excretion were found to be abnormally elevated before dexamethasone administration. After 7 days' dexamethasone administration, plasma renin activity still remained high above the normal level, while the plasma aldosterone level as well as urinary 17KS and pregnanetriol excretion were lowered to the normal ranges. Several possible mechanisms for this discordant suppression of plasma renin activity and aldosterone level were discussed and the presence of mineralocorticoid resistance, which is not related to ACTH dependent aldosterone antagonists, was suggested in the case of these patients.