ESPE Abstracts (2019) 92 P3-238

ESPE2019 Poster Category 3 Sex Differentiation, Gonads and Gynaecology or Sex Endocrinology (32 abstracts)

Bilateral Testicular Atrophy and Normal Inhibin B level: A Paradoxal Clinical Finding For A Rare Biochemical Cause !

Leïla ESSADDAM 1,2 , Marie PIKETTY 3 , Wafa KALLALI 1,2 , Rahma GUEDRI 1,2 , Laura GONZALEZ 3 , Nadia MATTOUSSI 1,2 , Michel POLAK 3 & Saayda BEN BECHER 1,2


1Children Hospital Bechir Hamza of Tunis, Tunis, Tunisia. 2Université de Tunis El Manar, Tunis, Tunisia. 3Hôpital Necker, Paris, France


Background: Testicular atrophy is a rare complication following inguinal hernia repair particularly in children<2 years and those with an undescended testis at highest risk> with an undescended testis. Inhibin B is secreted from the testis as a product of Sertoli cells, and has been suggested as a good marker for spermatogenesis. Its value is expected to be very low in children with bilateral testicular atrophy

Case Report: A 7-year-old child underwent surgery at 6 years for undescendent testis. Intraoperative exploration shows two very small testis: the right one was fixed in the scrotum, the left one was left was fixed in the pubis. On examination, we found a normal penis of 6 cm and 2 non palpable testes. Karyotype: 46,XY. Hormonal balance shows: normal FSH and LH levels, low levels of testosterone < 0,025 ng/mL before and after HCG test, AMH < 0,01 ng/mL and surprisingly a normal level of inhibine B: 113 ng/mL controlled at 139 ng/mL. We seek first for an extragonadal production of Inhibine B but AFP and B HCG were normal. We though seek for the ELISA assay technique (of Beckman Coulter) and blood samples were adressed for a dosage using the less common ELISA technique of Anshlabs. Inhibin B was then found to be undetectable (<4,6 pg/mL). Fertility is thus found to be compromised. The child will receive a testosterone replacement therapy when aged 12 in addition to bilateral testicular prothesis.

Discussion: Heterophilic antibodies are present in a significant proportion of the population, and are likely to give a false-increased result in sandwich assays (such as the inhibin assay). They are thought to be produced following immunization with animal proteins (mouse, rabbit, goat, sheep etc.). In particular, a vaccine produced on rabbit cells had been the cause of false TSH results in the 1980s. This interference can be found nowadays in 1 serum/10 000.

Conclusion: Hormonal assays are often the diagnostic pivot in pediatric endocrinology. Being aware of biochemical causes of paradoxal hormonal dosages can be a key to avoid unecessary additional explorations.

Volume 92

58th Annual ESPE

Vienna, Austria
19 Sep 2019 - 21 Sep 2019

European Society for Paediatric Endocrinology 

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