In our studies, the CUMD was measured from the underside of clitoral glans to the center of the urinary meatus, and the clitoral glans was no included. The mean CUMD (23.0 ± 4.5, min-max: 11.9–34.4 mm) in our sample was basically consistent with Bonaparte’s sample (2.3 ± 0.1 cm) in an early literature [25], but was obviously shorter than ones (28.5 ± 7.1mm, min-max: 16-45mm; 3.17 ± 0.98cm, min-max: 1-6cm), recently reported by Lloyd et al and Krissi et al respectively [27, 28]. The difference may be based on race or ethnicity.
The distance from clitoris to urethral orifice (CUMD), as one of genital dimensions of normal women, or as a possible factor associated with sexual function was studied [25, 28–30]. Moreover, the CUMD is a part of perineum. The embryogenesis and development of perineum is androgen mediated as evidenced by the larger anogenital distance (AGD) observed in men compared with women [1, 2, 13]. The CUMD is hopeful as a biomarker of prenatal androgen exposure, and probably equivalent to well-defined AGD-AC or AGD-AF. However, CUMD was weakly associated with AGD-AC in our primary analysis of all subjects, to be no statistical significance, although the correlation between AGD-AC and AGD-AF was up to medium, corresponding to the result reported elsewhere [31].
Androgen exposure during the MPW determines the maximum “potential” adult size of AGD, but secondary changes in AGD in adults may also have occurred, while the androgen-estrogen balance has been altered (eg, obesity, pregnancy, aging, and late-onset hypogonadism) [1–3, 24, 32]. Our data in further studies clearly demonstrated that the AGD-AC and AGD-AF of adult women, particularly the former, were lengthened with obesity. Meanwhile, the CUMD was not affected with increase or decrease of body weight. Exclusion of obesity, the CUMD was significantly correlated with AGD-AC, it implied that the CUMD, very likely same as AGD-AC, was affected by fetal androgen. Furthermore, the CUMD could be a marker of prenatal androgen exposure without influence of body weight. This was the advantage of CUMD indicator, compared to AGD-AC/AGD-AF indicators which were frequently used in the studies of possible role of prenatal androgen exposure. For an example, several recent studies demonstrated that AGD-AC/AGD-AF in adult patients with PCOS were longer than control, implying that extreme prenatal androgen exposure contributes to PCOS [18, 19]. Assessment of AGD-AC/AGD-AF was suggested as a diagnostic tool in PCOS [33]. But the PCOS patients usually have metabolic problems and obesity symptoms [34], therefore, eliminating the influence of obesity should be emphasized. We proposed that the CUMD measurement had better be included in the studies as a clinical or toxicological marker for fetal androgen action and risk for reproductive disorders.
The ratio between the second and fourth digit is associated with the estimated ratio of prenatal testosterone relative to prenatal estradiol, and the digits development is also androgen/estrogen mediated [35]. But the sexual dimorphic growth of digits from birth to adulthood could be due to postnatal or pubertal factors, rather than solely being the result of fetal androgen exposure [1]. Therefore, it is not surprised that the correlations between the CUMD and digit ratios in our studies were no significant meaning.
Taking into account the limitations of present study, the following points have to be pointed out. The sample is small, and the populations in our study were not healthy subjects who were randomly selected, they were patients suffered from various gynecological or psychosomatic diseases, although the admission and exclusion criteria were strictly enforced. Whereas, the body fat distribution (such as measuring the circumference of chest, waist and hip) was not studied, the lower abdominal or gluteal-femoral obesity might have a stronger impact on the AGD-AC/AGD-AF.