Division of Diabetes, Metabolism and Endocrinology, Showa University Fujigaoka Hospital, Kanagawa 227-8501, Japan.
Department of Pediatrics, Keio University School of Medicine, Tokyo 160-8582, Japan.
Endocr J. 2022 Jul 28;69(7):831-838. doi: 10.1507/endocrj.EJ21-0779. Epub 2022 Mar 2.
Congenital hypogonadotropic hypogonadism (CHH) is a rare disorder that causes gonadotropin-releasing hormone (GnRH) deficiency and sexual immaturity. CHH may accompany an abnormal sense of smell (Kallmann syndrome, KS) or no such manifestation (normosmic-CHH). This unusual combination of manifestations is explained by the fact that GnRH neurons originate in the olfactory placode and migrate to the forebrain during embryogenesis. We describe the case of a 31-year-old man with normosmic-CHH, who also had obesity, type 2 diabetes and intellectual disability. He was noticed to have sexual immaturity (small testes with no pubic hair) at age 20 years, when diabetic ketoacidosis developed. Basal and GnRH-stimulated levels of LH (1.0→12.0 IU/L) and FSH (1.9→6.1 IU/L) were detectable but low. The results of the T&T olfactometer and the Alinamin test were definitely normal, with an anatomically normal olfactory system on MRI. Sequencing of 22 CHH-related genes was performed, and compound heterozygous PROKR2 variants were identified: one was a previously known loss-of-function variant (p.Trp178Ser) and the other was a nonsense variant (p.Trp212*). Through a literature review, we found 22 patients (including our patient) with CHH due to biallelic PROKR2 variants, which led us to recognize that most of the patients (86%) were diagnosed with KS. Clinical observations in this study indicate that, even though they have CHH, biallelic PROKR2 variant carriers may have a normal olfactory system as well as presumably normal migration of GnRH neurons. This suggests that the PROK2-PROKR2 pathway affects the function of GnRH neurons after their migration.
先天性低促性腺激素性性腺功能减退症(CHH)是一种罕见的疾病,导致促性腺激素释放激素(GnRH)缺乏和性不成熟。CHH 可能伴有嗅觉异常(卡尔曼综合征,KS)或无此类表现(正常嗅觉-CHH)。这种不寻常的表现组合可以用 GnRH 神经元起源于嗅基板并在胚胎发生期间迁移到前脑这一事实来解释。我们描述了一例 31 岁的正常嗅觉-CHH 男性,他还患有肥胖症、2 型糖尿病和智力障碍。他在 20 岁时因糖尿病酮症酸中毒而出现性不成熟(睾丸小,无阴毛)。基础和 GnRH 刺激 LH(1.0→12.0 IU/L)和 FSH(1.9→6.1 IU/L)水平可检测到,但水平较低。T&T 嗅敏度计和 Alinamin 测试的结果肯定正常,MRI 显示嗅觉系统解剖结构正常。对 22 个 CHH 相关基因进行测序,发现 PROKR2 基因存在复合杂合变异:一个是先前已知的失活变异(p.Trp178Ser),另一个是无义变异(p.Trp212*)。通过文献复习,我们发现 22 例(包括本病例)CHH 患者因 PROKR2 基因的双等位基因突变所致,这使我们认识到大多数患者(86%)诊断为 KS。本研究的临床观察表明,即使存在 CHH,PROKR2 基因双等位变异携带者也可能具有正常的嗅觉系统以及推测正常的 GnRH 神经元迁移。这表明 PROK2-PROKR2 途径在 GnRH 神经元迁移后影响其功能。