Lee Hae In, Kwon Ahreum, Suh Jung Hwan, Choi Han Saem, Song Kyung Chul, Chae Hyun Wook, Kim Ho-Seong
Department of Pediatrics, Severance Children's Hospital, Endocrine Research Institute, Yonsei University College of Medicine, Seoul, Korea.
Ann Pediatr Endocrinol Metab. 2021 Mar;26(1):66-70. doi: 10.6065/apem.2040184.092. Epub 2021 Mar 31.
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.
17α-羟化酶/17,20-裂解酶缺乏症由细胞色素P450家族17亚家族A成员1基因(CYP17A1)突变引起,是先天性肾上腺皮质增生症的一种极其罕见的形式,其特征是特定突变导致多种表型。在此,我们报告2例17α-羟化酶/17,20-裂解酶缺乏症的表型女性患者:1例核型为46,XX,表现为原发性闭经和性幼稚症,另1例核型为46,XY,表现为性发育障碍。在这两例病例中,促肾上腺皮质激素、11-脱氧皮质酮和促性腺激素的血清水平均升高,而睾酮和脱氢表雄酮水平降低。二代测序显示,1例患者为p.Trp17Ter(c.51G>A)和p.His373Leu(c.1118A>T)的复合杂合子,另1例为p.His373Leu(c.1118A>T)的纯合子。本报告进一步描述了2例17α-羟化酶/17,20-裂解酶缺乏症患者,他们携带常见于韩国人的p.His373Leu替代突变,并表现出多种表型。