ABSTRACT
Background: Inappropriate exposure or activity of sex hormones in-utero has been postulated as a leading cause for the development of hypospadias and cryptorchidism. Anthropometric sexually dimorphic traits such as the 2nd to 4th digit ratio (2D:4D), anogenital distance (AGD) and the stretched penile length (SPL), have been associated with androgen and estrogen activity in-utero. Purpose: Evaluate anthropometric parameters in patients with hypospadias or cryptorchidism compared with healthy controls. Materials and methods: This is a case control study of male patients operated on between 2019 and 2020. Three groups were included: Hypospadias, cryptorchidism and a demographically similar control group. Anthropometric parameters 2D:4D, AGD and SPL were measured intra-operatively and compared between the groups. Results: Included in the study were 179 pediatric patients between the ages of 9-15 months (58 patients with hypospadias, 69 with cryptorchidism and 47 controls). There was no difference in AGD, 2D:4D and SPL between patients with cryptorchidism, hypospadias and controls. Conclusions: Anthropometric characteristics associated with androgen activity in utero were not different in patients with hypospadias and cryptorchidism compared with controls.
ABSTRACT
The relationship between the length of the second and fourth ring finger (2D:4D ratio) is a sexually dimorphic trait, higher in females than in males. It is established during early prenatal development under the influence of sex hormones, as demonstrated in numerous studies both in humans and in mice. The current study involves patients with congenital GH/IGF-1 deficiency, a population not yet investigated. The 2D:4D ratio was measured from hand x-rays and compared with normal hand x-rays taken from the Greulich & Pyle Atlas. The analyses of our results revealed that patients with congenital GH/IGF-1 deficiency show an identical 2D:4D ratio for both sexes, but a higher (more feminine) ratio than the normal population. These findings may be explained by a higher estrogen effect resulting from the absence of a functional GH-IGF-1 axis prenatally.
