Literature DB >> 33819959

Two cases of 17α-hydroxylase/17,20-lyase deficiency caused by the CYP17A1 mutation.

Hae In Lee1, Ahreum Kwon1, Jung Hwan Suh1, Han Saem Choi1, Kyung Chul Song1, Hyun Wook Chae1, Ho-Seong Kim1.   

Abstract

17α-hydroxylase/17,20-lyase deficiency, caused by mutations in the cytochrome P450 family 17 subfamily A member 1 gene (CYP17A1), is an extremely rare form of congenital adrenal hyperplasia that is characterized by diverse phenotypes resulting from specific mutations. Here, we report 2 phenotypic females with 17α-hydroxylase/17,20-lyase deficiency: one with the 46,XX karyotype presenting primary amenorrhea and sexual infantilism, and the other with the 46,XY karyotype presenting a disorder of sexual development. In both cases, the serum levels of adrenocorticotropic hormone, 11-deoxycorticosterone, and gonadotropin were elevated, whereas the levels of testosterone and dehydroepiandrosterone were reduced. Next-generation sequencing revealed one patient with compound heterozygosity for p.Trp17Ter (c.51G>A) and p.His373Leu (c.1118A>T), and the other with homozygosity for p.His373Leu (c.1118A>T). This report further describes 2 cases of 17α-hydroxylase/17,20-lyase deficiency in patients who harbored a p.His373Leu substitution, commonly found in Korean individuals, and presented diverse phenotypes.

Entities:  

Keywords:  Congenital adrenal hyperplasia; High-throughput nucleotide sequencing; Mutation; Steroid 17-α-hydroxylase

Year:  2021        PMID: 33819959     DOI: 10.6065/apem.2040184.092

Source DB:  PubMed          Journal:  Ann Pediatr Endocrinol Metab        ISSN: 2287-1012


  1 in total

1.  A rare case of 17α-hydroxylase/17, 20-lyase deficiency: Clinical and genetic findings and follow-up outcomes.

Authors:  Li-Zhen Dai; Hong Ma; Jian-Fang Ke; Chen-Shi Lin; Yanling Huang; Yuan Tian; Danling Chen
Journal:  Womens Health (Lond)       Date:  2022 Jan-Dec
  1 in total

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