Postnatal Testicular Activity in Healthy Boys and Boys With Cryptorchidism

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

A Longitudinal Study of Urinary Phthalate Excretion in 58 Full-Term and 67 Preterm Infants from Birth through 14 Months

Reproduced with permission from Environmental Health PerspectivesDanish Agency for Science, Technology and Innovation (09-067180) and by Kuopio University Hospital, EVO funding, Finlan

Evaluation of vitamin D status and its correlation with gonadal function in children at mini-puberty

WOS: 000453904100014PubMed ID: 30229999Context The effects of Vitamin D on reproductive function in adults have gained interest. Studies have demonstrated some associations. Hypothalamic-pituitary-gonadal axis is activated during the first 6 months of life, called as mini-puberty. This HPG activation is important for future gonadal function. There are no data regarding the association of gonadal hormones and 25(OH)D levels at mini-puberty. Demonstration of any association would form the basis for studies that will search for the effects of 25(OH)D on gonadal hormones at mini-puberty. Objective To characterize the associations between 25(OH)D levels and gonadal hormones at mini-puberty. Design Cross-sectional cohort analysis. Patient(s) or other participant(s) A total of 180 (94 boys and 86 girls) healthy appropriate-for-gestational-age neonates were included. Main outcome measure(s) 25(OH)D, LH, FSH, total testosterone, oestradiol, AMH and inhibin B levels were measured at postnatal 30-45 days. All infants were divided into three groups including vitamin D deficiency (20 ng/mL). Correlations between vitamin D status and reproductive hormones were analysed. Result(s) Total testosterone level was higher (mean: 0.52 +/- 0.32 vs 0.26 +/- 0.2 ng/mL; P: 0.008) and inhibin B was lower in 25(OH)D deficient than sufficient girls (mean: 21.2 +/- 15.71 vs 53.25 +/- 47.25 pg/mL; P: 0.021). Conclusion(s) A modest effect of 25(OH)D was identified on total testosterone and inhibin B in girls at mini-puberty. The 25(OH)D may have an effect on gonadal function during early life. Randomized controlled trials could clarify the importance of vitamin D on gonadal hormones at mini-puberty

The androgen metabolome of preterm infants reflects fetal adrenal gland involution.

CONTEXT The human adrenal cortex changes with fetal-neonatal transition from the fetal to the adult organ, accompanied by changes in the steroid metabolome. OBJECTIVE As it is unclear how the observed developmental changes differ between preterm and full-term neonates, we investigated whether the involution of the fetal adrenals is following a fixed time course related to postmenstrual age or whether it is triggered by birth. Furthermore, the fetal and postnatal androgen metabolome of preterm infants was characterized in comparison to term babies. DESIGN Prospective, longitudinal, two centre study collecting spot urines of preterm and term infants during the first 12-18 months of life. METHODS Steroid metabolites were measured from spot urines by gas chromatography-mass spectrometry. Data relating were modelled according to established pre- and postnatal pathways. RESULTS Fetal adrenal involution occurs around term-equivalent age in preterm infants and is not triggered by premature birth. Testosterone levels are higher in preterm infants at birth and decline slower till term compared to full-term babies. Dihydrotestosterone levels and the activity of the classic androgen biosynthesis pathway are lower in premature infants as is 5α-reductase activity. No difference was found in the activity of the alternate backdoor pathway for androgen synthesis. CONCLUSIONS Human adrenal involution follows a strict timing that is not affected by premature birth. By contrast, prematurity is associated with an altered androgen metabolome after birth. Whether this reflects altered androgen biosynthesis in utero remains to be investigated