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The pituitary-gonadal axis in cryptorchid infants and children
J C Job1, J E Toublanc, J L Chaussain
1Hôpital Saint Vincent de Paul, Paris, France.
Insights
Cryptorchidism in infants and children is linked to luteinizing hormone (LH) deficiency and lower testosterone levels. Antigonadotropin cell antibodies (AGCA) were found in over 50% of patients, suggesting an autoimmune component.
Area of Science:
- Pediatric Endocrinology
- Reproductive Endocrinology
- Immunology
Background:
- Cryptorchidism, or undescended testes, is a common congenital condition in infants.
- Hormonal imbalances, including luteinizing hormone (LH) and testosterone deficiencies, are suspected in cryptorchidism.
- The role of antigonadotropin cell antibodies (AGCA) in the pathogenesis of cryptorchidism is not well understood.
Purpose of the Study:
- To investigate LH and testosterone levels in infants and children with cryptorchidism.
- To explore the correlation between hormonal levels and the presence of AGCA.
- To evaluate the effectiveness of hormonal treatments in cryptorchidism.
Main Methods:
- Measurement of LH and testosterone levels via LH-Releasing Hormone (LH-RH) and human chorionic gonadotropin (hCG) stimulation tests.
- Immunofluorescence assay to detect AGCA in pituitary cells.
- Comparison of hormonal levels between cryptorchid patients and controls at different ages and pubertal stages.
Main Results:
- Infants with permanent cryptorchidism showed diminished LH peaks and significantly lower postnatal testosterone surges compared to controls.
- In children, reduced LH and testosterone levels were observed at specific pubertal stages (P1, P2).
- AGCA were detected in over 50% of patients, independent of age or endocrinological data.
Conclusions:
- A primary LH deficiency may play a role in cryptorchidism, evidenced by diminished LH and secondary testosterone deficiencies.
- The presence of AGCA suggests a potential autoimmune contribution to cryptorchidism.
- Hormonal treatments like hCG and GnRH showed limited success, particularly in younger children.
Abstract:
We have attempted to document in cryptorchid children that there is an LH deficiency and a secondary deficiency of testosterone. We have shown a diminished LH peak after LH-RH in cryptorchid versus normal infants (P less than 0.05). The postnatal surge of testosterone is significantly low (P less than 0.001) in permanent cryptorchids versus infants with secondary testicular descent, whose levels are similar to those in controls. In permanent cryptorchids during the same period (0-4 months), LH and testosterone levels were significantly lower (P less than 0.01 and P less than 0.05 respectively) than in infants with secondary descent, and the levels of testosterone and LH were correlated in both populations. In children, a low basal level of LH was observed at pubertal stage P2, and LH peak after LH-RH was significantly reduced at stages P1 and P2 (P less than 0.01 and P less than 0.05 respectively). The post-stimulatory levels of testosterone after hCG were reduced at the same stages (P less than 0.01, P less than 0,05), and the two levels were correlated (P less than 0.01). No differences are seen for LH and testosterone afterwards. It has been possible to show by immunofluorescence on pituitary cells the occurrence of antigonadotropin cell antibodies (AGCA) in more than 50% of our patients, with no relation to age and no correlations between endocrinological data and the presence or absence of AGCA. The relatively low success rate of hCG treatment, mainly in young children, and of GnRH irrespective of the regimen of treatment, does not exclude the role of primary LH deficiency in cryptorchidism.