Sukumar Suja, Uppula Pavan, Kumar Santosh, Bhansali Anil
Department of Endocrinology, Postgraduate Institute of Medical Education and Research, Chandigarh, India.
Department of Endocrinology, Jawaharlal Institute of Postgraduate Medical Education and Research, Puducherry, India.
BMJ Case Rep. 2017 May 9;2017:bcr-2016-219082. doi: 10.1136/bcr-2016-219082.
Development of gonadal and phenotypic sex during embryogenesis invariably corresponds to the genotypic sex. However, some disorders of sex development are associated with discordance between the chromosomal, gonadal or phenotypic sex which include complete androgen insensitivity syndrome, 46XY complete gonadal dysgenesis (Swyer syndrome) and, rarely, congenital adrenal hyperplasia due to CYP 17A1 (17α-hydroxylase) deficiency. The enzyme CYP17A1 includes 17α-hydroxylase and 17,20-lyase which are required for the synthesis of cortisol and sex steroids, respectively. The consequent cortisol deficiency results in a compensatory increase in adrenocorticotropic hormone (ACTH) drive, which stimulates the production of deoxycorticosterone and corticosterone leading to hypertension and hypokalaemia. Concurrent lack of sex steroids results in sexual infantilism without ambiguity. Both the genotypic males and females present during adolescence with a female phenotype, sexual infantilism and hypertension depending on the severity of the enzyme deficiency. We describe a case of CYP17A1 deficiency in a phenotypic female with 46XY karyotype who presented with sexual infantilism but without hypertension.
胚胎发育过程中性腺和表型性别的发育始终与基因型性别相对应。然而,一些性发育障碍与染色体、性腺或表型性别之间的不一致有关,其中包括完全雄激素不敏感综合征、46XY完全性腺发育不全(斯维尔综合征),以及罕见的因CYP 17A1(17α-羟化酶)缺乏导致的先天性肾上腺皮质增生症。CYP17A1酶包括17α-羟化酶和17,20-裂解酶,分别是合成皮质醇和性类固醇所必需的。随之而来的皮质醇缺乏会导致促肾上腺皮质激素(ACTH)驱动的代偿性增加,从而刺激脱氧皮质酮和皮质酮的产生,导致高血压和低钾血症。同时缺乏性类固醇会导致无歧义的性幼稚状态。根据酶缺乏的严重程度,青春期的基因型男性和女性均表现为女性表型、性幼稚状态和高血压。我们描述了一例具有46XY核型的表型女性CYP17A1缺乏症患者,该患者表现为性幼稚状态但无高血压。