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IEMbase 0119: CYP21A2-related 21-hydroxylase deficiency

Scope

Field Value
IEMbase ID 119
Nosology 24.2.01.01
Gene CYP21A2
External IDs OMIM:201910; ORPHA:418
Generated mapping MAPPED, high confidence
Candidate DisMech targets Congenital_Adrenal_Hyperplasia.yaml; subtype targets include Classic 21-OHD, Salt-Wasting 21-OHD, Simple-Virilizing 21-OHD, and Nonclassic 21-OHD
Review date 2026-07-07

IEMbase phenotype signal

IEMbase represents this as CYP21A2-related 21-hydroxylase deficiency, with alternate labels congenital adrenal hyperplasia and CAH. Treatability is marked unknown.

The characteristic biochemical rows are increased ACTH, hyperkalemia, increased renin, hyponatremia, increased 17-OH-progesterone in plasma and urine, decreased aldosterone, increased androgens, increased androstenedione, increased DHEAS, increased urinary progesterone, and increased testosterone. Clinical rows include accelerated growth, decreased fertility, testicular adrenal rest tumors, and virilization. Hydrocortisone is listed as treatment.

DisMech phenotype coverage

Congenital_Adrenal_Hyperplasia.yaml is strongly centered on CYP21A2-related CAH. It includes classic, salt-wasting, simple-virilizing, and nonclassic 21-hydroxylase deficiency subtypes; a CYP21A2 21-hydroxylase deficiency mechanism; cortisol and aldosterone deficiency; ACTH-driven adrenal hyperplasia and androgen excess; prenatal/postnatal hyperandrogenism; and biochemical testing centered on elevated 17-hydroxyprogesterone.

The phenotype section covers adrenal insufficiency, salt-wasting electrolyte crisis, ambiguous genitalia/46,XX virilization, hirsutism, irregular menstruation, infertility, hypertension, osteoporosis/osteopenia, short stature, testicular adrenal rest tumors, and abnormal glucose homeostasis. Treatments include glucocorticoid replacement, mineralocorticoid replacement, crinecerfont adjunct therapy, and investigational CYP21A2 gene therapy.

Concordance and completeness

Judgement: correct mapping with strong local coverage.

DisMech is more complete for subtype structure, mechanism, long-term phenotypes, and treatment landscape. IEMbase contributes finer biochemical resolution beyond the local elevated 17-hydroxyprogesterone and reduced cortisol rows: ACTH, renin, aldosterone, sodium, potassium, and specific androgen species are all useful future curation targets. The clinical overlap is good for virilization, fertility impairment, and testicular adrenal rest tumors; accelerated growth is partly represented indirectly through short stature/androgen excess but could be made more explicit.

Curation actions

  • Keep Congenital_Adrenal_Hyperplasia.yaml as the canonical target, with subtype resolution to the appropriate 21-OHD clinical form when needed.
  • Consider adding biochemical rows for ACTH, renin, aldosterone, sodium, potassium, androstenedione, DHEAS, testosterone, and urinary 17-OH-progesterone/progesterone.
  • Review accelerated growth as a possible explicit childhood phenotype in CYP21A2-related CAH.