Abstract
BackgroundAn increase in cryptorchidism has been reported in many countries. One mechanism could be low fetal testosterone production possibly secondary to altered placental human chorionic gonadotrophin (hCG) release. Our Objective was to compare hCG values from maternal blood between boys with cryptorchidism and normal boys.MethodsTotal hCG and α-fetoprotein (AFP) values [12–16 weeks of gestation; from the double test for Down syndrome screening) were compared between cases of cryptorchidism and normal control boys who were matched for maternal age, maternal smoking, gestational age at time of hCG measurement (±1 day), birth weight and birth term. Measurements were performed in a single laboratory; values were expressed as absolute values (KU/L) and multiples of the median (MoM). Boys whose mothers had had a complicated pregnancy were excluded. Groups were compared using the Student’s t test. Log transformation was used to normalize hCG, MoM hCG, AFP and MoM AFP distribution, and values were expressed as geometric means (-1, + 1 tolerance factor).ResultsTotal hCG and MoM hCG levels were significantly lower in the 51 boys with cryptorchidism compared to 306 controls (21.4 (12.3; 37) KU/L vs 27.7 (15.9; 47.9) KU/L and 0.8 (0.5; 1.2) MoM vs 1.0 (0.6; 1.6) MoM, respectively, p < 0.01). By contrast, AFP and MoM AFP levels were similar between groups.ConclusionThis study showed a link between low maternal serum hCG levels and cryptorchidism in boys from uncomplicated pregnancy, while normal AFP levels indicated a normal fetoplacental unit. Whether these abnormalities were due to endogenous or exogenous factors remains to be determined.
Highlights
An increase in cryptorchidism has been reported in many countries
The cases were compared with healthy boys born during the same time period in the Department of Obstetrics of Angers University Hospital, whose mothers had had blood collected at the University Hospital of Angers for double test screening (Down syndrome screening), and whose neonatal records reported no genital abnormalities: 306 controls babies were matched for maternal age (±0.5 yrs), maternal smoking, gestational age at time of human chorionic gonadotrophin (hCG) measurement (±1 day), birth weight (±100 g), and week of gestation at birth ( ±1 wk) (i.e. 1 case per 6−8 controls)
Total hCG and multiples of the median (MoM) hCG levels were significantly lower in the 51 boys with cryptorchidism compared to 306 controls (21.4 (12.3; 37) KU/L vs 27.7 (15.9; 47.9) KU/L and 0.8 (0.5; 1.2) MoM vs 1.0 (0.6; 1.6) MoM, respectively, Table 1 Characteristics of cases with cryptorchidism and their matched controls
Summary
One mechanism could be low fetal testosterone production possibly secondary to altered placental human chorionic gonadotrophin (hCG) release. Several studies have reported an unexplained increase in congenital malformations of the male reproductive tract, such as hypospadias and cryptorchidism [1]. Definitive proof of a physiological link between estrogen exposure and abnormal male differentiation is elusive, estrogens have been shown to inhibit placental gonadotropin releasing hormone (GnRH) [9], a key hormone stimulating hCG production [10]. All these studies suggest that abnormal placental hCG production could play a key role in disorders of sex differentation
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