Kuiri-Hänninen Tanja, Koskenniemi Jaakko, Dunkel Leo, Toppari Jorma, Sankilampi Ulla
Department of Pediatrics, Kuopio University Hospital, Kuopio, Finland.
Research Centre for Integrative Physiology and Pharmacology, Institute of Biomedicine, University of Turku, Turku, Finland.
Front Endocrinol (Lausanne). 2019 Jul 23;10:489. doi: 10.3389/fendo.2019.00489. eCollection 2019.
Cryptorchidism, or undescended testis, is a well-known risk factor for testicular cancer and impaired semen quality in adulthood, conditions which have their origins in early fetal and postnatal life. In human pregnancy, the interplay of testicular and placental hormones as well as local regulatory factors and control by the hypothalamic-pituitary (HP) axis, lead to testicular descent by term. The normal masculine development may be disrupted by environmental factors or genetic defects and result in undescended testes. Minipuberty refers to the postnatal re-activation of the HP-testicular (T) axis after birth. During the first weeks of life, gonadotropin levels increase, followed by activation and proliferation of testicular Leydig, Sertoli and germ cells. Consequent rise in testosterone levels results in penile growth during the first months of life. Testicular size increases and testicular descent continues until three to five months of age. Insufficient HPT axis activation (e.g., hypogonadotropic hypogonadism) is often associated with undescended testis and therefore minipuberty is considered an important phase in the normal male reproductive development. Minipuberty provides a unique window of opportunity for the early evaluation of HPT axis function during early infancy. For cryptorchid boys, hormonal evaluation during minipuberty may give a hint of the underlying etiology and aid in the evaluation of the later risk of HPT axis dysfunction and impaired fertility. The aim of this review is to summarize the current knowledge of the role of minipuberty in testicular development and descent.
隐睾症，即睾丸未降，是成年期睾丸癌和精液质量受损的一个众所周知的风险因素，这些情况起源于胎儿早期和出生后阶段。在人类妊娠期间，睾丸激素和胎盘激素以及局部调节因子的相互作用，以及下丘脑 - 垂体（HP）轴的控制，导致足月时睾丸下降。正常的男性发育可能会受到环境因素或基因缺陷的干扰，从而导致睾丸未降。小青春期是指出生后HP - 睾丸（T）轴的重新激活。在生命的最初几周，促性腺激素水平升高，随后睾丸间质细胞、支持细胞和生殖细胞被激活并增殖。随后睾酮水平的升高导致出生后最初几个月阴茎生长。睾丸大小增加，睾丸下降持续到三到五个月大。HPT轴激活不足（例如，低促性腺激素性性腺功能减退）通常与睾丸未降有关，因此小青春期被认为是正常男性生殖发育的一个重要阶段。小青春期为婴儿早期HPT轴功能的早期评估提供了一个独特的机会窗口。对于隐睾症男孩，小青春期期间的激素评估可能会提示潜在病因，并有助于评估后期HPT轴功能障碍和生育能力受损的风险。本综述的目的是总结当前关于小青春期在睾丸发育和下降中作用的知识。
