Successful testicular sperm recovery and IVF treatment in a man with Leydig cell hypoplasia
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Fetal sex differentiation of the male involves complex processes and is dependent on the androgen production from fetal Leydig cells triggered by placental human chorionic gonadotropin (hCG) [1, 2]. It is later replaced by luteinizing hormone (LH) that is secreted by the fetal pituitary gland during gestation . The hormones, such as antimullerian hormone (AMH) synthesized by Sertoli cells of the testes, testosterone produced by the Leydig cells and dihydrotestosterone, are also essential for the formation of male genitalia [4, 5, 6]. Because the action of both hCG and LH is through the luteinizing hormone/chorionic gonadotropin receptor (LHCGR), its presence and smooth function is crucial for male sex differentiation and characteristics in fetal and adult life. Any changes in the DNA or gene expression levels of LHCGR are associated with a variety of phenotypic as well as clinical symptoms and pathologies.
Human LHCGR gene is located on chromosome 2 and encodes 11 exons...
KeywordsLuteinizing Hormone Testosterone Level Leydig Cell Azoospermia Serum Testosterone Level
This study received no funding and the authors do not have any competing interests.
Conflict of interest
All authors contributed to design, acquisition, analysis, data intrepretation, and manuscript writing and declare no conflict of interest.
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