Leydig Cell in Idiopathic Varicocele

Sirvent, Juan J.; Bernat, Ramona Bernat; Navarro, Miguel; Tolrá, J. Rodríguez; Guspi, R; Bosch, Ruud

doi:10.1159/000464051

Cited by 66 publications

(29 citation statements)

References 19 publications

(25 reference statements)

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“…A notable finding of all 3 studies was uniform changes to the Leydig cell populations in both testes despite most of the subjects presenting with unilateral varicocele. [42][43][44] These data further support the notion that unilateral varicoceles result in bilateral testicular effects. 40,45 A follow-up study by Weiss and colleagues 8 tested the in vitro ability of biopsied Leydig cells to produce testosterone.…”

Section: Pathophysiology Of Leydig Cell Dysfunction Human Studiessupporting

confidence: 80%

Testosterone and Varicocele

Hayden

Tanrikut

2016

Urologic Clinics of North America

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Section: Pathophysiology Of Leydig Cell Dysfunction Human Studiessupporting

confidence: 80%

Testosterone and Varicocele

Hayden

Tanrikut

2016

Urologic Clinics of North America

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“…In cases where the diagnosis of nodular LCHY was made, areas of LCT were ruled out, based on the following morphological criteria, which are usually absent in LCTs: the presence of multiple nodules, the existence of seminiferous tubules (either normal or atrophic) within the nodules, and scarce Reinke crystals in the cytoplasm of cells (Kim et al, 1985;Naughton et al, 1998). Although LCHY has been reported in association with other testicular abnormalities in adults, such as germ cell tumours (Oosterhuis et al, 2003;Nistal et al, 2006), the androgen insensitivity syndrome (Regadera et al, 1999), cryptorchidism (Gotoh et al, 1984), varicocele (Sirvent et al, 1990) and the Klinenfelter syndrome (Regadera et al, 1991), we found only a few reports of its association with LCT (Kim et al, 1985;Castle & Richardson, 1986;Hekimgil et al, 2001), and it is not clear whether LCHY may represent a precursor lesion for LCTs (Naughton et al, 1998).…”

Section: Discussionmentioning

confidence: 99%

Non‐tumoural parenchyma in Leydig cell tumours: pathogenetic considerations

et al. 2007

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Little is known about the pathogenesis of Leydig cell tumours (LCTs) of the testis. The observation of several associated dysgenetic features in the non-tumoural parenchyma and in the contralateral testes of men with testicular germ cell neoplasms has served as the basis to propose that there may be a common mechanism for different male reproductive disorders. However, the possible relationship between LCTs and other testicular lesions has not been explored. Here we describe the presence of primary lesions in the non-tumoural parenchyma of testes with LCT, from which we try to establish possible pathogenetic associations. We studied the non-tumoural parenchyma adjacent to 16 LCT specimens. Parameters as Leydig cell hyperplasia (LCHY), qualitative evaluation of the germinal epithelium and spermatogenesis, the presence of Sertoli cell-only tubules (SCOT), and the Sertoli cell nuclear morphology were consistently assessed in all cases. SCOT associated with Sertoli cell dysgenetic morphology was the most frequent finding, present in 50% of the cases. Another interesting finding was the presence of LCHY in four cases (25%). Abnormal spermatogenesis was found in 81.25% of the cases, and it consisted of lesions of the adluminal or basal compartments of seminiferous tubules. The occurrence of either dysgenetic Sertoli cells or LCHY adjacent to LCTs could represent primary anomalies, resulting from a common insult also involved in tumourigenesis. The abnormalities in spermatogenesis observed here are likely to represent consequences of either tumour compression or abnormal hormonal production. The significance of these associations merits further investigation regarding a common pathogenesis.

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“…Prior studies have demonstrated varicocele’s effect on Leydig cell dysfunction. Testicular biopsy in patients with idiopathic varicocele shows decreased tubular diameter, increased Leydig cell atrophy with vacuolization and decreased Leydig cells in testicular tissue when staining for testosterone (8). Venous pooling results in increased hypoxia, oxidative stress in seminiferous tubules and increased gonadotoxic renal and adrenal metabolites in the spermatic cord (9).…”

Section: Review Of Literaturementioning

confidence: 99%

Effects of varicocelectomy on serum testosterone

Whelan

Levine

2016

Transl. Androl. Urol.

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Varicocele is most often surgically repaired due to male infertility, however, has recently been linked to low serum testosterone. This paper serves to review the current literature regarding varicocele and its subsequent repair on serum testosterone. Twenty-eight human studies were identified with fifteen showing improved serum testosterone after repair. The majority of the studies that demonstrated improvement had preoperative testosterone levels that were low or below normal. Additionally, multiple well-designed studies with control groups not undergoing surgical repair demonstrated significant difference between groups. This improvement was less observed in studies with normal preoperative serum testosterone. A majority of these patients studied were presenting for infertility. It remains to be determined if these findings can be reproduced in men without infertility. The findings suggest that microsurgical varicocele repair can improve serum testosterone in men with low levels preoperatively in appropriately counseled men. It remains to be seen whether varicocele repair can help prevent the development of low testosterone in the future or which patients are at risk of developing low testosterone due to varicocele.

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Leydig Cell in Idiopathic Varicocele

Cited by 66 publications

References 19 publications

Testosterone and Varicocele

Testosterone and Varicocele

Non‐tumoural parenchyma in Leydig cell tumours: pathogenetic considerations

Effects of varicocelectomy on serum testosterone

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