Al-Sinani Aisha, Mula-Abed Waad-Allah S, Al-Kindi Manal, Al-Kusaibi Ghariba, Al-Azkawi Hanan, Nahavandi Nahid
National Diabetes and Endocrine Centre, Royal Hospital, Muscat, Oman.
Department of Chemical Pathology, Royal Hospital, Muscat, Oman.
Oman Med J. 2015 Mar;30(2):129-34. doi: 10.5001/omj.2015.27.
This is the first case report in Oman and the Gulf region of a 17-β-hydroxysteroid dehydrogenase type 3 (17-β-HSD3) deficiency with a novel mutation in the HSD17B3 gene that has not been previously described in the medical literature. An Omani child was diagnosed with 17-β-HSD3 deficiency and was followed up for 11 years at the Pediatric Endocrinology Clinic, Royal Hospital, Oman. He presented at the age of six weeks with ambiguous genitalia, stretched penile and bilateral undescended testes. Ultrasound showed no evidence of any uterine or ovarian structures with oval shaped solid structures in both inguinal regions that were confirmed by histology to be testicular tissues with immature seminiferous tubules only. The diagnosis was made by demonstrating low serum testosterone and high androstenedione, estrone, and androstenedione:testosterone ratio. Karyotyping confirmed 46,XY and the infant was raised as male. Testosterone injections (25mg once monthly) were given at two and six months and then three months before his surgeries at five and seven years of age when he underwent multiple operations for orchidopexy and hypospadias correction. At the age of 10 years he developed bilateral gynecomastia (stage 4). Laboratory investigations showed raised follicle-stimulating hormone, luteinizing hormone, androstenedione, and estrone with low-normal testosterone and low androstendiol glucurunide. Testosterone injections (50mg once monthly for six months) were given that resulted in significant reduction in his gynecomastia. Molecular analysis revealed a previously unreported homozygous variant in exon eight of the HSD17B3 gene (NM_000197.1:c.576G>A.Trp192*). This variant creates a premature stop codon, which is very likely to result in a truncated protein or loss of protein production. This is the first report in the medical literature of this novel HSD17B3 gene mutation. A literature review was conducted to identify the previous studies related to this disorder.
这是阿曼及海湾地区首例关于17-β-羟类固醇脱氢酶3型(17-β-HSD3)缺乏症的病例报告,该病例中HSD17B3基因存在一种医学文献中此前未描述过的新突变。一名阿曼儿童被诊断为17-β-HSD3缺乏症,并在阿曼皇家医院儿科内分泌诊所接受了11年的随访。他六周大时出现生殖器模糊、阴茎拉长和双侧睾丸未降。超声检查未发现任何子宫或卵巢结构的迹象,双侧腹股沟区有椭圆形实性结构,组织学检查证实为仅含有未成熟生精小管的睾丸组织。通过检测血清睾酮水平低、雄烯二酮、雌酮水平高以及雄烯二酮:睾酮比值高做出诊断。染色体核型分析证实为46,XY,该婴儿按男性抚养。在两岁和六岁时每月注射一次睾酮(25毫克),然后在五岁和七岁接受多次睾丸固定术和尿道下裂矫正手术前三个月也进行了注射。10岁时他出现双侧乳腺增生(4期)。实验室检查显示促卵泡激素、促黄体生成素、雄烯二酮和雌酮水平升高,睾酮水平略低于正常,雄烯二醇葡萄糖醛酸苷水平低。给予每月一次50毫克的睾酮注射(共六个月),乳腺增生明显减轻。分子分析显示HSD17B3基因外显子8存在一个此前未报道的纯合变异(NM_000197.1:c.576G>A.Trp192*)。该变异产生一个过早的终止密码子,很可能导致蛋白质截短或无法产生蛋白质。这是医学文献中关于这种新的HSD17B3基因突变的首例报告。我们进行了文献综述以确定此前与该疾病相关的研究。