Short-Term Hormonal Changes Following Microdissection Testicular Sperm Extraction among Men with Non-Obstructive...

Area of Science:

• Reproductive Endocrinology
• Urology
• Andrology

Background:

• Non-obstructive azoospermia (NOA) affects male fertility, with microdissection testicular sperm extraction (mTESE) being a key surgical intervention.
• Hormonal profiles are crucial for male reproductive health and can be influenced by testicular procedures.
• Understanding the impact of mTESE on hormone levels is essential for patient management and counseling.

Purpose of the Study:

• To investigate potential hormonal changes after microdissection testicular sperm extraction (mTESE) in men diagnosed with non-obstructive azoospermia (NOA).
• To identify predictors of hormonal shifts, specifically testosterone deficiency (TD), in NOA patients undergoing mTESE.

Main Methods:

• Prospective analysis of 102 NOA men undergoing mTESE, excluding those with prior hormonal therapies.
• Preoperative and 3-month postoperative serum hormone levels (total testosterone, LH, FSH, 17β-estradiol) were measured.
• Patients were categorized based on preoperative and postoperative total testosterone (tT) levels to assess for eugonadal status or development of TD.

Main Results:

• mTESE did not significantly alter short-term postoperative levels of total testosterone (tT), luteinizing hormone (LH), or follicle-stimulating hormone (FSH) compared to baseline.
• A notable 13.5% of initially eugonadal men developed testosterone deficiency (TD) by 3 months post-mTESE.
• Men who developed TD post-surgery had significantly lower baseline testicular volume and a higher prevalence of karyotype abnormalities.

Conclusions:

• Microdissection testicular sperm extraction (mTESE) does not cause significant short-term hormonal disturbances in men with non-obstructive azoospermia (NOA).
• A subset of NOA patients may develop testosterone deficiency (TD) after mTESE, highlighting the need for careful hormonal monitoring.
• Lower testicular volume and karyotype abnormalities are associated with an increased risk of developing TD after mTESE.