Fujimoto Takao, Suwa Tomohide, Kabe Kazuhiko, Adachi Tomoko, Nakabayashi Masao, Amamiya Teruko
Department of Pediatric Surgery, Imperial Gift Foundation, The Aiiku Maternal & Children's Medical Center, Minami-Azabu, Minato-Ku, Tokyo 106-8580, Japan.
J Pediatr Surg. 2008 Feb;43(2):358-61. doi: 10.1016/j.jpedsurg.2007.10.046.
The association of growth retardation and hypospadias is well established. Fetal testosterone secretion is under the influence of placental human chorionic gonadotropin during first 14 weeks of gestation. We hypothesized that placental insufficiency may disrupt the supply of nutrients and human chorionic gonadotropin to the fetus leading to both growth retardation and hypospadias. To validate this hypothesis, we analyzed extremely low-birth-weight male infants with or without hypospadias for fetal growth parameters.
One hundred four male newborn infants with birth body weight of less than 1500 g admitted to a neonatal intensive care unit over a 4-year period were retrospectively reviewed, recording the presence and type of hypospadias, fetal growth parameters, infant growth parameters at birth, placental weight, placental histopathology, cord information, and maternal morbidity. These data of patients with hypospadias were compared with those of controls.
Of the 104 extremely to very low-birth-weight male infants, 16 (15.3%) had hypospadias, and 10 (62.5%) of those had severe proximal hypospadias. Sixty-two controls who did not have hypospadias and whose body weight was less than 1500 g were identified. The incidence of hypospadias in full-term male birth in the hospital was 12 (0.30%) in 3959 births. Birth body weight and their SD for gestational age were lower in patients with hypospadias compared with those for controls (824 +/- 160 vs 1255 +/- 145 g). Placenta-to-fetal ratio (0.323 +/- 0.07 vs 0.229 +/- 0.03) and gestational age were significantly higher in the patients with hypospadias. Histopathologic study of the maternal placenta obtained from the patients with hypospadias revealed pronounced degenerative changes, infarction, and calcification, whereas these abnormalities were rare in controls.
The significant association between the occurrence of hypospadias and early growth retardation with higher placenta-to-fetal ratio and placental abnormalities suggest that placental dysfunction in early gestation may play an important role in the development of hypospadias.
生长发育迟缓与尿道下裂之间的关联已得到充分证实。在妊娠的前14周，胎儿睾酮的分泌受胎盘人绒毛膜促性腺激素的影响。我们推测胎盘功能不全可能会扰乱胎儿的营养物质和人绒毛膜促性腺激素供应，从而导致生长发育迟缓和尿道下裂。为了验证这一假设，我们分析了患有或未患有尿道下裂的极低出生体重男婴的胎儿生长参数。
回顾性分析了4年间入住新生儿重症监护病房的104例出生体重小于1500g的男婴，记录尿道下裂的存在情况和类型、胎儿生长参数、出生时的婴儿生长参数、胎盘重量、胎盘组织病理学、脐带信息以及母亲的发病率。将尿道下裂患者的这些数据与对照组的数据进行比较。
在这104例极低至超低出生体重男婴中，16例（15.3%）患有尿道下裂，其中10例（62.5%）患有重度近端尿道下裂。确定了62例体重小于1500g且未患有尿道下裂的对照组。该医院足月男婴尿道下裂的发病率为3959例中有12例（0.30%）。与对照组相比，尿道下裂患者的出生体重及其孕周标准差更低（824±160 vs 1255±145g）。尿道下裂患者的胎盘与胎儿重量比（0.323±0.07 vs 0.229±0.03）和孕周显著更高。对尿道下裂患者的母体胎盘进行组织病理学研究发现有明显的退行性改变、梗死和钙化，而这些异常在对照组中很少见。
尿道下裂的发生与早期生长发育迟缓以及较高的胎盘与胎儿重量比和胎盘异常之间存在显著关联，这表明妊娠早期的胎盘功能障碍可能在尿道下裂的发生中起重要作用。
