What is one result of 21 beta hydroxylase deficiency?

21 beta-hydroxylase deficiency is a genetic disorder that affects steroid biosynthesis in the adrenal glands, specifically impairing the conversion of progesterone to 11-deoxycorticosterone and 17-hydroxyprogesterone to 11-deoxycortisol in the pathway leading to cortisol and aldosterone production.

As a result of this enzymatic block, the production of both cortisol and aldosterone decreases significantly. When cortisol levels drop, there is a compensatory increase in adrenocorticotropic hormone (ACTH) due to the lack of negative feedback on the pituitary gland. This increase in ACTH can stimulate the adrenal glands to produce more adrenal androgens, leading to their accumulation, which is characteristic of the condition.

This hormonal imbalance is a classic presentation in conditions such as congenital adrenal hyperplasia (CAH), where the deficiency leads to a variety of clinical manifestations, including ambiguous genitalia in females and precocious puberty in males.

In summary, the deficiency results in decreased cortisol and aldosterone levels, which directly reflects the inability to properly synthesize these crucial hormones. Hence, the statement about decreased cortisol and aldosterone accurately describes one of the primary effects of 21 beta-hydroxylase deficiency.