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Congenital cryptorchidism undescended testis is one of the most common congenital urogenital malformations in boys. Prevalence of cryptorchidism at birth among boys born with normal birth weight ranges from 1. Cryptorchidism is associated with a risk of low semen quality and an increased risk of testicular germ cell tumors.

Testicular hormones, androgens and insulin-like peptide 3 INSL3have an essential role in the process of testicular descent from intra-abdominal position into the scrotum in fetal life. This explains the increased prevalence of cryptorchidism among boys with diseases or syndromes associated with congenitally decreased secretion or action of androgens, such as patients with congenital hypogonadism and partial androgen insensitivity syndrome. There is evidence to support that cryptorchidism is associated with decreased testicular hormone production later in life.

It has been shown that cryptorchidism impairs long-term Sertoli cell function, but may also affect Leydig cells. Germ cell loss taking place in the cryptorchid testis is proportional to the duration of the condition, and therefore early orchiopexy to bring the testis into the scrotum is the standard treatment. However, the evidence for benefits of early orchiopexy for testicular endocrine function is controversial.

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The hormonal treatments using human chorionic gonadotropin hCG or gonadotropin-releasing hormone GnRH to induce testicular descent have low success rates, and therefore they are not recommended by the current guidelines for management of cryptorchidism.

However, more research is needed to assess the effects of hormonal treatments during infancy on future male reproductive health.

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Cryptorchidism undescended testis, maldescendus testis is a condition in which one or both testes fail to descend into the bottom of the scrotum 1. Instead, the testis is found at a location along the normal route of testicular descent, and it may have an intra-abdominal, inguinal, suprascrotal, or high scrotal position.

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Congenital cryptorchidism is one of the most common congenital malformations in boys. Its prevalence at birth among boys with birth weight more than 2, g has been reported to range from 1.

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The prevalence at the age of 3 months and 1 year is 0. Cryptorchidism is associated with a future risk of poor semen quality and increased incidence of testicular germ cell tumors TGCT 45. The risk of TGCT is increased 2—5-fold when compared to the general population 56. Notably, early treatment of cryptorchidism does not ificantly Pussy dating in Cuesta Del Rato the risk of TGCT later in life 78. These findings support the testicular dysgenesis syndrome TDS hypothesis, which suggests that cryptorchidism and TGCT have a common origin in fetal life 9 There is evidence to support that cryptorchidism is associated with decreased testicular hormone concentrations.

On the other hand, congenital hypogonadism may have cryptorchidism as one of the manifestations. The classical definition of hypogonadism is testicular dysfunction associated with androgen deficiency However, Rey et al. In this article, we will review the literature from human studies focusing on the associations between congenital cryptorchidism and reproductive hormone levels. We conducted a Pubmed search between March and October with no publication date limit.

Full texts of the relevant articles were obtained. Reference lists of these articles were also checked to identify additional studies. We classified the studies according to different periods of life—birth, mini-puberty, prepuberty, puberty, and adulthood. Normal position of the testis is inside the scrotum, where the center of the testis is at or below the border between the upper and lower half of the scrotum Retractile testis is a testis that can be pulled to the bottom of the scrotum and does not return up immediately after release.

A High scrotal position means that a testis is at the upper part of the scrotum. Some testes at the high scrotal position can be drawn to the middle or the bottom of the scrotum, but immediately after release they return to the original position, which distinguishes them from retractile testes.

Suprascrotal position is the area above the scrotum.

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The testis may also be close to the external inguinal ring. The testis at the inguinal position stays inside the inguinal canal, which is sometimes difficult to palpate, but can be visible with ultrasonography Retractile testes and testes with scrotal position are considered normal. In rare cases, the testis is located outside the normal path of the testicular descent, and is called ectopic testis. In this case, the testis can be located at, for instance, perineal, femoral, or pubopenile area, or at a crossed scrotal position. When a testis is non-palpable, it probably has an inguinal, abdominal, or ectopic location, or it has vanished 14 — See Figure 1 for the illustration of different testicular positions.

Figure 1. Testicular locations. Normally, both testes locate at the bottom of the scrotum. In cryptorchidism, one or both testes do not stay at the normal position, but anywhere along the normal path of testicular descent as illustrated in the figure. According to the literature they start to secrete androgens during gestational weeks GW 8—10, and the highest levels of these hormones are measured around GW 16 17 — Dihydrotestosterone DHT converted from testosterone by 5-alpha reductase mostly in peripheral tissues, is crucial for the differentiation of male external genitalia and prostate during GW 8—12 17 — Androgen secretion in fetal Leydig cells is stimulated by human chorionic gonadotropin hCG from the placenta during the first trimester of pregnancy and later by luteinizing hormone LH from the anterior pituitary gland of the developing fetus 19 Placental hCG also regulates the secretion of INSL3, which is a peptide hormone of insulin-related gene family 22and essential for the transabdominal phase of testicular descent The gonadotropin levels reach their peaks at midgestation and subsequently decrease toward the time of delivery 21 The gonadotropin levels decline steadily toward the time of delivery For a comprehensive overview of reproductive hormone production during pregnancy, see Scott et al.

Gonadotropin and testosterone levels start to rise again about 1 week after birth and peak at the age of 1—3 months, a period also known as mini-puberty 30 During this period, there is an increased proliferation of Leydig cells 33Sertoli cells 34and germ cells The post-natal surge of gonadotropins is also associated with accelerated penile growth 36testicular descent 37increased prostatic activity 38and male sex-typed behavior at 14 months Mini-puberty is also associated with an increase in testicular volume and inhibin B levels, reflecting the growing of Sertoli cells 40 — Furthermore, it has also been shown that the transformation of gonocytes into type A-dark Ad spermatogonia, i.

Interestingly, the testosterone surge stimulated by increased gonadotropin levels during mini-puberty has also been suggested to have a role in this process as one study showed that cryptorchid boys who received hCG treatment before orchiopexy ended up having a higher of Ad spermatogonia than boys who underwent the operation without receiving hCG However, the role of androgen in this process is still unclear, and animal studies do not provide a strong support for it Notably, however, the timing of germ cell development is different between Pussy dating in Cuesta Del Rato and man, and the from mouse work cannot be directly extrapolated to human After 6—9 months of age, LH and testosterone levels decrease rapidly to very low or undetectable levels, while the decline in FSH level is also substantial but remains detectable.

Plasma levels for all these hormones remain low for the rest of the Pussy dating in Cuesta Del Rato and until the time of puberty, which is characterized by reactivation of the hypothalamic-pituitary-testicular HPT axis, and its sustained function continuing throughout adulthood 47 The inhibin B level at 3 months of age is even higher than in adulthood.

After 15 months of age, the inhibin B level decreases, however it is still detectable throughout childhood 30474851 AMH level is still high after the age of 6 months, reflecting the functional immaturity of Sertoli cells Interestingly, its function in postnatal males is still unclear.

AMH secretion continues until the start of puberty, demarcating functional maturation of Sertoli cells 56 Inhibin B suppresses FSH secretion from the anterior pituitary gland Interestingly, in childhood inhibin B is secreted solely by Sertoli cells. It is detected at all ages in males FSH is a moderate inducer of AMH production, whereas testosterone is a potent inhibitor of its synthesis AMH level is high in the fetus, remains rather stable until birth, and is elevated during mini-puberty 6061 due to FSH surge.

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Although testosterone level is also high at this time, lack of androgen receptor AR expression renders Sertoli cells unresponsive to the inhibitory effect of testosterone During prepuberty, Sertoli cells continue producing high levels of AMH, even without FSH stimulation, because there is no strong inhibitory effect on AMH production by testosterone which is nearly absent Sertoli cells start to express AR in the prepubertal testis When boys enter puberty, the increased testosterone production causes high intratesticular testosterone levels, which strongly inhibit AMH production and overcome the stimulatory effect of FSH 55hence resulting in a low AMH level.

This effect persists until adulthood Therefore, serum AMH is a biomarker of immature Sertoli cell function during prepuberty In humans, the presence of androgen receptors in Sertoli cells is necessary for the downregulation of AMH expression However, the downregulation of AMH expression in mouse Sertoli cells does not require androgen action Mice with a selective ablation of androgen receptor in Sertoli cells SCARKO mice or androgen receptor knockout ARKO mice with an ubiquitous ablation of androgen receptor display a strong downregulation of AMH expression during the first weeks after birth and early puberty Notably, in men with congenital hypogonadotropic hypogonadism CHHAMH levels remain high after puberty due to the lack of testosterone effect FSH stimulates the secretion of inhibin B from Sertoli cells Both FSH and high intratesticular testosterone promote spermatogenesis.

INSL3, unlike testosterone, is not prone to the acute fluctuations of the HPG axis activity 67 because it is dependent on the long-term trophic effect of LH 68and its levels thus reflect the of Leydig cells and their differentiation status FSH and inhibin B are recognized as markers of Sertoli cell Pussy dating in Cuesta Del Rato and spermatogenesis 6669 The correlation between FSH and inhibin B levels varies according to age, suggesting that the canonical negative feedback regulation does not apply at every stage of development.

The relationship between serum FSH and inhibin B levels during infancy is not clear, but the negative association is likely established already at this age 4051 However, during early puberty, a positive association between FSH and inhibin B levels is found.

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In contrast, a negative association is observed during late puberty 72and it continues into adulthood A negative correlation is also observed in men with hood history of cryptorchidism Testicular descent in male fetuses is a complex process.

Normal function of the HPT axis and androgen secretion and action are crucial for normal testicular descent The physiology of testicular descent has been extensively reviewed elsewhere 2346 Here, we describe this process only briefly. Bipotential gon are formed during weeks 4—6 of embryonic development They Pussy dating in Cuesta Del Rato located on the dorsal wall of the body cavity.

The primordial germ cells migrate from the extraembryonic mesoderm to the gon via the hindgut Subsequently, the differentiation of male gon is initiated by the expression of Sex determining region of the Y-chromosome SRY gene, first resulting in specification of Sertoli cells and followed by Leydig cell differentiation The somatic cells of the gonadal primordium start to differentiate into pre-Sertoli cells at approximately GW 7—8 19 Subsequently, Sertoli cells proliferate, aggregate around the primitive germ cells and start tubulogenesis, i.

About 1 week after the Sertoli cells have been specified, Leydig cell differentiation is initiated in primitive interstitial cells of mesonephric origin. There is some evidence that this process might be controlled by the paracrine influences of AMH During the second trimester of pregnancy, Sertoli cells proliferate rapidly, and the of germ cells and Leydig cells also increases—adding to the volume of the testis The developing testis is anchored by two structures—the cranial suspensory ligament attaching the upper pole of the testis to the diaphragm and the genitoinguinal ligament gubernaculum anchoring the testis to the future inguinal area via the epididymis 77 Testicular descent from the abdomen to the scrotum is a complex process that is divided into two phases— transabdominal phase and inguinoscrotal phase 23 ,

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