Endocrine Abstracts

Introduction

Infertility associated with hypergonadotropism is usually an unpromising condition related to acheiving fertilization. We describe the patient presented as oligoasthenoteratozoospermia (OAT syndrome), with laboratory primary hypergonadotropic hypogonadism but normal male fenotype, including typical male hair dustribution.

Case description

male, born 41 year ago, presented when he was 29 year old, as infertility with oligozoospespermia of sperm count of 0.2–0.4×0⁶/semen volume, total motility of 14%, testosteron without Clomifen stimulation 9–11.5 nmol/l, FSH 11.8–18 mIU/ml, LH 6.8–9.1 mIU/ml, regularly on Profertil^® therapy. When he was 35 year old he gave his consent for gonadotropin supression therapy with testosteron depo preparation od 125 mg im per 2 weeks. After 4 months od such a therapy his FSH was 2.1 and LH 0.1 mIU/ml, and as expected azoospermia. We discontinued testosteron therapy and after 1 year he came with FSH 11.4 mIU/ml, sperm count of 36.5×10⁶/semen volume. After that time he has intermitently been on Clomifen and Profertil therapy, and sperm parameters more or less in normal ranges. His testosteron values has been in low values, when without Clomofen stimulation. In 2019 year for the first time we measured several times dihitrotestosteron levels which was always in normal ranges 454–785 ng/ml (referent 250–990) while testosteron was low 5.68–10.19 nmol/l.

Discussion

The aim of this case report is to emphasize the constelation of low testosteron levels and normal dihidrotestosteron in patient with normal male habitus but initialy with OAT syndroma. Although at the moment we have not been maesured precursors of testosteron and dihidrotestosteron we are in thinking about the so called ’’backdoor’’ pathway of androgen synthesis, until this time described only in animals and considered in human male development.