RESUMO

Virility and sexual pleasure have long been associated with penile size and this, in turn, has typically been linked to some anthropometric measurements, such as foot size or height, leading to various misconceptions from both men and women. Our intention is to estimate penile size parameters in Argentina and evaluate the correlation between penile size and certain anthropometric measurements. This is a cross-sectional, descriptive, multicenter, and observational study. Male patients who underwent a urological procedure were included in four hospitals located in different regions of the country. Different anthropometric measurements were obtained: height, weight, penile circumference, flaccid and stretched length, and foot length. A total of 800 patients were evaluated. Mean left foot was 26.4 cm. Mean flaccid penile length was 11.4 (95% confidence interval [CI]: 8-14) cm, and mean penile circumference was 10.1 (95% CI: 8-12) cm. Finally, mean stretched penis was 15.2 (95% CI: 11-18.5) cm. We can confirm that estimates of the average penile measurements in Argentina are flaccid penis length of 11.4 cm, penile circumference of 10.1 cm, and stretching the penis to the maximum in flaccidity of 15.2 cm. Correlations between flaccid penis length, stretched out, penile circumference, height, weight, and length of the left foot were evaluated, finding low or no correlation between those mentioned, except for flaccid and stretched length.

Assuntos

RESUMO

Clinical manifestations and the need for treatment varies according to age in males with hypogonadism. Early foetal-onset hypogonadism results in disorders of sex development (DSD) presenting with undervirilised genitalia whereas hypogonadism established later in foetal life presents with micropenis, cryptorchidism and/or micro-orchidism. After the period of neonatal activation of the gonadal axis has waned, the diagnosis of hypogonadism is challenging because androgen deficiency is not apparent until the age of puberty. Then, the differential diagnosis between constitutional delay of puberty and central hypogonadism may be difficult. During infancy and childhood, treatment is usually sought because of micropenis and/or cryptorchidism, whereas lack of pubertal development and relative short stature are the main complaints in teenagers. Testosterone therapy has been the standard, although off-label, in the vast majority of cases. However, more recently alternative therapies have been tested: aromatase inhibitors to induce the hypothalamic-pituitary-testicular axis in boys with constitutional delay of puberty and replacement with GnRH or gonadotrophins in those with central hypogonadism. Furthermore, follicle-stimulating hormone (FSH) priming prior to hCG or luteinizing hormone (LH) treatment seems effective to induce an enhanced testicular enlargement. Although the rationale for gonadotrophin or GnRH treatment is based on mimicking normal physiology, long-term results are still needed to assess their impact on adult fertility.

RESUMO

The diagnosis of male central (or hypogonadotropic) hypogonadism, typically based on low luteinizing hormone (LH) and testosterone levels, is challenging during childhood since both hormones are physiologically low from the sixth month until the onset of puberty. Conversely, follicle-stimulating hormone (FSH) and anti-Müllerian hormone (AMH), which show higher circulating levels during infancy and childhood, are not used as biomarkers for the condition. We report the case of a 7-year-old boy with a history of bilateral cryptorchidism who showed repeatedly low FSH and AMH serum levels during prepuberty. Unfortunately, the diagnosis could not be ascertained until he presented with delayed puberty at the age of 14 years. A gonadotropin-releasing hormone (GnRH) test showed impaired LH and FSH response. By then, his growth and bone mineralization were partially impaired. Gene panel sequencing identified a variant in exon 15 of FGFR1, affecting the tyrosine kinase domain of the receptor, involved in GnRH neuron migration and olfactory bulb morphogenesis. Testosterone replacement was started, which resulted in the development of secondary sexual characteristics and partial improvement of bone mineral density. This case illustrates the difficulty in making the diagnosis of central hypogonadism in boys during childhood based on classical criteria, and how serum FSH and AMH assessment may be helpful if it is suspected before the age of puberty, and confirm it using next-generation sequencing. The possibility of making an early diagnosis of central hypogonadism may be useful for a timely start of hormone replacement therapy, and to avoid delays that could affect growth and bone health as well as psychosocial adjustment.

RESUMO

Objectives: The objective of this review was to characterize the use of biomarkers of male hypogonadism in childhood and adolescence. Contents: The hypothalamic-pituitary-gonadal (HPG) axis is active during fetal life and over the first months of postnatal life. The pituitary gland secretes follicle stimulating hormone (FSH) and luteinizing hormone (LH), whereas the testes induce Leydig cells to produce testosterone and insulin-like factor 3 (INSL), and drive Sertoli cells to secrete anti-Müllerian hormone (AMH) and inhibin B. During childhood, serum levels of gonadotropins, testosterone and insulin-like 3 (INSL3) decline to undetectable levels, whereas levels of AMH and inhibin B remain high. During puberty, the production of gonadotropins, testosterone, and INSL3 is reactivated, inhibin B increases, and AMH decreases as a sign of Sertoli cell maturation. Summary and outlook: Based on our knowledge of the developmental physiology of the HPG axis, these biomarkers can be used in clinical practice to interpret the physiopathology of hypogonadism. Additionally, these markers can have diagnostic value in different forms of hypogonadism that may appear during childhood and adolescence.

RESUMO

The definition of male hypogonadism, used in adult endocrinology, is not fully applicable to paediatrics. A clear understanding of the developmental physiology of the hypothalamic-pituitary-testicular axis is essential for the comprehension of the pathogenesis of hypogonadal states in boys and for the establishment of adequate definitions and classifications in paediatric ages. This is particularly true for central hypogonadism, usually called hypogonadotropic in adults. Because childhood is a period characterised by a physiological state of low gonadotropin and testosterone production, these markers of hypogonadism, typically used in adult endocrinology, are uninformative in the child. This review is focused on the physiological importance of prepubertal Sertoli cell markers - anti-Müllerian hormone (AMH) and inhibin B - and of the intratesticular actions of follicle-stimulating hormone (FSH) and testosterone during early infancy and the first stages of pubertal development. We discuss the role of FSH in regulating the proliferation of Sertoli cells - the main determinant of prepubertal testicular volume - and the secretion of AMH and inhibin B. We also address how intratesticular testosterone concentrations have different effects on the seminiferous tubule function in early infancy and during pubertal development.

RESUMO

In early fetal development, the testis secretes - independent of pituitary gonadotropins - androgens and anti-Müllerian hormone (AMH) that are essential for male sex differentiation. In the second half of fetal life, the hypothalamic-pituitary axis gains control of testicular hormone secretion. Follicle-stimulating hormone (FSH) controls Sertoli cell proliferation, responsible for testis volume increase and AMH and inhibin B secretion, whereas luteinizing hormone (LH) regulates Leydig cell androgen and INSL3 secretion, involved in the growth and trophism of male external genitalia and in testis descent. This differential regulation of testicular function between early and late fetal periods underlies the distinct clinical presentations of fetal-onset hypogonadism in the newborn male: primary hypogonadism results in ambiguous or female genitalia when early fetal-onset, whereas it becomes clinically undistinguishable from central hypogonadism when established later in fetal life. The assessment of the hypothalamic-pituitary-gonadal axis in male has classically relied on the measurement of gonadotropin and testosterone levels in serum. These hormone levels normally decline 3-6 months after birth, thus constraining the clinical evaluation window for diagnosing male hypogonadism. The advent of new markers of gonadal function has spread this clinical window beyond the first 6 months of life. In this review, we discuss the advantages and limitations of old and new markers used for the functional assessment of the hypothalamic-pituitary-testicular axis in boys suspected of fetal-onset hypogonadism.