What is 17-Hydroxyprogesterone?

A precursor to the steroid hormone cortisol, 17-hydroxyprogesterone (17-OHP) is derived from cholesterol in the adrenal glands. The production of cortisol is important for the digestion of proteins, fats, and sugars, and plays an important role in the regulation of blood pressure and the immune system [1].

While not an active steroid hormone, 17-OHP levels in the bloodstream are used as a test for congenital adrenal hyperplasia (CAH). Approximately 90% of all CAH cases are caused by a deficiency in the enzyme 21-hydroxylase, which is needed to convert 17-OHP into cortisol [1].

17-Hydroxyprogesterone and Congenital Adrenal Hyperplasia

Normal adrenal gland function converts cholesterol into cortisol through various chemical reactions through the use of many enzymes. The lack of a particular enzyme in this formation pathway will result in the buildup of precursor materials that are unable to be converted into the next product. The enzyme 21-hydroxylase is imperative to turn 17-OHP into its near-final form of cortisol [1, 2].

Low levels of cortisol in the body promote the release of ACTH (adrenocorticotropic hormone), which signals the adrenal glands to produce more hormones. ACTH release also causes the adrenal glands to grow, which medically is referred to as hyperplasia. This signaling, in turn, produces more cortisol precursors in addition to other adrenal gland secretions, such as androgens, i.e., so-called male-sex hormones [2, 3].

The lack of any enzyme that blocks the pathways of cortisol, or any other hormone produced by the adrenal gland is referred to as congenital adrenal hyperplasia (CAH). About 90-95% of all CAH diagnoses are due to a deficiency or complete lack of the enzyme 21-hydroxylase. Defective 21-hydroxylase enzymes will, therefore, cause the buildup of 17-OHP in the bloodstream [2, 3, 4]. 

The Genetics of CAH

The 21-hydroxylase enzyme is encoded by the gene CYP21A2. Mutations in this gene are often the cause of CAH. The disorder is inherited in an autosomal recessive manner; both parents must pass on a copy of a mutated gene for the disorder to manifest [2, 13].

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