Chlormadinone acetate as a possible effective agent for congenital adrenal hyperplasia to suppress elevated ACTH and antagonize masculinization

Endocr J. 1995 Aug;42(4):505-8. doi: 10.1507/endocrj.42.505.

Abstract

We report two cases of congenital adrenal hyperplasia (CAH) in which administration of chlormadinone acetate (CMA), a substituted progestational agent for prostatic disease, suppressed ACTH hypersecretion and lowered plasma testosterone levels. Case 1 was 83-year-old male with advanced prostatic carcinoma and CAH due to 21-hydroxylase deficiency. His plasma testosterone did not decrease in spite of a bilateral orchiectomy. Case 2 was 40-year-old female with CAH due to 21-hydroxylase deficiency suffering from virilization after the cessation of cortisol supplement therapy because of her breast carcinoma. In these two cases, oral administration of CMA at a daily dose of 75-100 mg suppressed ACTH and cortisol to subnormal levels and reduced testosterone levels. With the suppressive effect on ACTH excess and antiandrogenic action, CMA may be suitable for patients with CAH suffering from symptoms due to overproduced ACTH or adrenal androgen.

Publication types

  • Case Reports

MeSH terms

  • Administration, Oral
  • Adrenal Hyperplasia, Congenital / complications
  • Adrenal Hyperplasia, Congenital / drug therapy*
  • Adrenal Hyperplasia, Congenital / metabolism
  • Adrenocorticotropic Hormone / drug effects
  • Adrenocorticotropic Hormone / metabolism*
  • Adult
  • Aged
  • Aged, 80 and over
  • Chlormadinone Acetate / therapeutic use*
  • Female
  • Humans
  • Male
  • Progesterone Congeners / therapeutic use*
  • Virilism / etiology
  • Virilism / metabolism
  • Virilism / prevention & control*

Substances

  • Progesterone Congeners
  • Chlormadinone Acetate
  • Adrenocorticotropic Hormone