Perspectives in Pediatric Pathology, Chapter 18. Hypogonadotropic Hypogonadisms. Pediatric and Pubertal Presentations

Nistal, Manuel; Paniagua, Ricardo; González‐Peramato, Pilar; Reyes‐Múgica, Miguel

doi:10.2350/16-04-1810-pb.1

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“…In the first case, a testicular interstitium in which Leydig cells and their precursors are absent or are undetectable (Figure 7) is worth noting. In the second case, in which patients have a low GnRH, they present pulsatile secretions of FSH and LH that ensure maturation of isolated Leydig cells and then some secretion of testosterone allowing for testicular development that is closer to that of a pubertal testis [33,34].…”

Section: Delayed Puberty Associated With Chronic Illnessmentioning

confidence: 99%

Morphological Bases of Human Leydig Cell Dysfunction

Miguel¹,

González‐Peramato²,

Nistal³

2018

Advances in Testosterone Action

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In this chapter, we describe the histophysiology of human Leydig cells, their cytological characteristics, their differentiation processes, and the physiopathological processes occurring at various times throughout life. We first focus on the normal development of fetal Leydig cells as well as the pathologies of fetal Leydig cells that can affect numbers or hyperplasic processes (e.g., hypogonadotropic hypogonadism, cryptorchidism, congenital Leydig cell hyperplasia secondary to diabetes, and isoimmunization). Next, we explain the changes occurring at puberty with the onset and differentiation of adult Leydig cells and the pathophysiology of delayed puberty. We then describe the histophysiology of adult Leydig cells and the most frequent pathologies (e.g., hypogonadotropic hypogonadism, testicular dysgenesia, mild androgen insensitivity syndrome, 5-α-reductase defect, and Klinefelter syndrome). Finally, we discuss the morphological changes of these cells in the elderly.

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Section: Delayed Puberty Associated With Chronic Illnessmentioning

confidence: 99%