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Endocrine Abstracts (2018) 57 023 | DOI: 10.1530/endoabs.57.023

BES2018 BES 2018 Endogenous testosterone supports spermatogenesis even in the absence of gonadotrophins: evidence from a case report (1 abstracts)

Endogenous testosterone supports spermatogenesis even in the absence of gonadotrophins: evidence from a case report

L Antonio 1 , M Albersen 2 , J Billen 3 , G Maleux 4 , A Van Rompuy 5 & D Vanderschueren 1

1Department of Endocrinology, University Hospitals Leuven, Leuven, Belgium; 2Department of Urology, University Hospitals Leuven, Leuven, Belgium; 3Department of Laboratory Medicine, University Hospitals Leuven, Leuven, Belgium; 4Department of Radiology, University Hospitals Leuven, Leuven, Belgium; 5Department of Pathology, University Hospitals Leuven, Leuven, Belgium.

Background: In patients with testicular dysgenesis syndrome, reduced semen quality and testicular cancer are common. We report a case of a testicular tumour in a patient with a history of cryptorchidism and oligoasthenospermia. He had an unusual hormonal profile, which was not fully explained by the pathological findings.

Case: A 31-year-old man was referred to our tertiary care andrology unit for primary infertility with a history of bilateral orchidopexy during childhood. Testes were small (12 cc). Gynaecomastia was absent. Semen analysis repeatedly showed oligoasthenospermia (2.4 to 7.1 million/mL, 85 to 92% immotile). Gonadotropins (LH and FSH <0.1 U/L) were undetectable, but testosterone and estradiol were normal (850.7 ng/dL and 38.6 ng/L). Prolactin, other pituitary hormones, DHEAS, AFP, HCG and inhibin B were also normal. He denied using anabolic steroids. Suppressed gonadotrophins suggested a sex steroid producing testicular tumour. However, scrotal ultrasound only showed diffuse microcalcifications and three millimetric hypolucent lesions in the left testis, but no intratesticular mass. There were no suspicious lesions nor microcalcifications in the right testis. To further investigate the possibility of increased testicular sex steroid production, selective testicular venous sampling was performed. In the left spermatic vein, testosterone and estradiol levels were very high (3744 ng/dL and 378 ng/L), with a testis-to-periphery gradient of 4.4 and 9.0 respectively. There was no gradient in the right spermatic vein. These results confirmed increased sex steroid producing in the left testis. However, histopathological examination after orchidectomy revealed a multifocal seminoma (largest diameter 3 mm) and profuse germ cell neoplasia in situ. There were neither isolated syncytiotrophoblastic cells, nor choriocarcinoma. Leydig cell hyperplasia was present without Leydig cell tumour. HCG was remeasured with three different methods, all showing very low HCG between 0.6 and 1.1 IU/L. After orchidectomy gonadotrophin levels increased (LH 24.3 U/L, FSH 10.3 U/L), with normal total testosterone and estradiol, indicating recovery of suppression of the hypothalamic-pituitary-testis axis. Sperm concentration increased (10 million/mL.)

Key messages: 1. Our case shows that endogenous testosterone may support spermatogenesis even without gonadotropins.

2. In patients with suppressed gonadotropins, normal sex steroid levels and no testicular mass, selective testicular venous sampling can be useful in identifying the site of hormonal overproduction.

3. Thus far, the pathology findings cannot explain the hormonal profile. Further investigations are therefore ongoing.

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