What is a common symptom of congenital adrenal hyperplasia due to 21-hydroxylase deficiency?

Congenital adrenal hyperplasia (CAH) due to 21-hydroxylase deficiency leads to an impaired synthesis of cortisol and aldosterone while causing a buildup of steroid precursors, including 17-hydroxyprogesterone. One of the significant consequences of this enzyme deficiency is the loss of aldosterone production, which is crucial for sodium reabsorption and potassium excretion in the kidneys.

As a result, individuals with this condition often experience significant salt wasting, which occurs due to the lack of aldosterone's action. This salt wasting leads to sodium loss in urine and subsequently contributes to a state of hyponatremia and hypovolemia. In response to the low blood volume and hypotension caused by the loss of salt and water, the body often attempts to maintain blood pressure leading to other hormonal imbalances and symptoms of adrenal crisis.

In contrast, conditions like hypotension and hyperkalemia can arise from the overall impact of adrenal insufficiency but are not as definitive as the characteristic salt-wasting phenomenon seen specifically in 21-hydroxylase deficiency. Lastly, feminization of males can occur due to increased androgen levels, but it is not a direct symptom of the salt-wasting aspect of this condition,