In a patient losing salt and volume depleted, which deficiency is most likely implicated?

A patient who is losing salt and is volume depleted is most likely experiencing a deficiency in mineralocorticoids, particularly aldosterone, which is crucial for sodium retention and blood volume maintenance.

In the context of adrenal gland disorders, 21-hydroxylase deficiency is the most common cause of congenital adrenal hyperplasia. This deficiency leads to impaired synthesis of both cortisol and aldosterone, resulting in an accumulation of steroid precursors and a consequent decrease in mineralocorticoid production. The lack of aldosterone leads to sodium loss in the urine, contributing to hyponatremia (low sodium levels) and volume depletion. This condition often presents in early childhood, characterized by adrenal crisis due to insufficient aldosterone levels and the resulting inability to retain salt.

The other enzyme deficiencies listed affect adrenal steroid synthesis in different ways, but they do not primarily lead to the salt-wasting and volume depletion seen in this scenario:

• 17-hydroxylase deficiency primarily impacts sex steroid production and leads to a lack of cortisol and androgens, but aldosterone may still be produced, alleviating some of the volume depletion.

• 11-hydroxylase deficiency also leads to a form of congenital adrenal hyperplasia, with some