What a nil sperm count means (Diagnosis & Definition)
If your semen analysis report states ‘Nil’, ‘Zero’, or ‘Azoospermia’, it indicates that no spermatozoa were detected in the semen sample examined under standard microscopy.
This is a precise laboratory observation rather than a complete biological conclusion. Men often assume that a nil count means the body is entirely incapable of producing sperm. However, clinical andrology distinguishes between the presence of sperm in the ejaculate and the biological capacity of testicular tissue to generate sperm. Understanding this distinction guides every diagnostic and therapeutic step that follows.
Two fundamental clinical principles must be established at the outset:
A single routine test does not establish a final diagnosis: Sperm production undergoes biological fluctuations, and collection or processing artifacts can occur. Standard guidelines from the American Urological Association (AUA) and European Association of Urology (EAU) require that an initial zero count be confirmed with a repeat semen analysis several weeks later. Furthermore, the laboratory must centrifuge the specimen at high speed and examine the pellet to differentiate true azoospermia from cryptozoospermia (the presence of rare, occult sperm cells that can be utilized for ICSI without surgery).
A nil sperm count is distinct from an absence of ejaculate fluid: If minimal or no fluid emerges during ejaculation, that condition is clinically categorized as aspermia or retrograde ejaculation (where fluid travels backward into the urinary bladder). In contrast, most men with azoospermia produce normal ejaculate volume, color, and consistency, because seminal fluid is primarily manufactured by the seminal vesicles and prostate gland, independent of testicular sperm.
According to global epidemiological studies published by the World Health Organization (WHO), azoospermia affects approximately 1% of all men and roughly 10% to 15% of men evaluated for infertility. Receiving this report is understandably disorienting, but it marks the start of a structured clinical evaluation rather than the definitive conclusion of your family planning options.
Can a man with zero sperm have a biological child?
For many couples, yes, biological fatherhood is achievable. However, the realistic feasibility depends directly on identifying whether the absence of sperm results from a physical blockage or an underlying impairment in testicular production.
In obstructive azoospermia, testicular sperm production is generally normal, but an anatomical obstruction prevents sperm from exiting into the ejaculate. In these cases, viable sperm can be retrieved directly from the epididymis or testicle in the vast majority of patients.
In non-obstructive azoospermia, testicular sperm manufacturing is significantly compromised or patchy. Even in this group, modern reproductive microsurgery (micro-TESE) successfully identifies focal islands of active sperm production in approximately 40% to 50% of men, enabling biological conception when paired with Intracytoplasmic Sperm Injection (ICSI).
Navigating an azoospermia diagnosis requires transparent, evidence-based guidance. The following sections outline the established medical diagnostics, surgical success parameters, and assisted reproductive pathways defined by global andrology consensus.
Obstructive vs. non-obstructive azoospermia: Types & key differences
Clinical management begins by identifying whether the condition is obstructive or non-obstructive:
1. Obstructive Azoospermia (OA): In this category, spermatogenesis within the testicular seminiferous tubules is preserved. However, physical blockage along the reproductive tract prevents sperm from reaching the ejaculate. Common etiologies include previous elective vasectomy, severe genitourinary infections (such as chlamydial epididymitis or gonorrhea), iatrogenic injury during pediatric hernia repair, surgical trauma, or Congenital Bilateral Absence of the Vas Deferens (CBAVD). CBAVD is strongly linked to mutations in the Cystic Fibrosis Transmembrane Conductance Regulator (CFTR) gene. For men with obstructive azoospermia, the prognosis for biological fatherhood is favorable, as outpatient percutaneous or open retrieval procedures (such as PESA or TESA) reliably recover viable sperm with high success rates (typically 90% to 98% in uncomplicated cases).
2. Non-Obstructive Azoospermia (NOA): In this category, the reproductive ducts are open, but the testicles have intrinsic difficulty generating mature spermatozoa. Recognized causes include chromosomal anomalies, Y-chromosome microdeletions, history of undescended testicles (cryptorchidism), testicular torsion, past exposure to gonadotoxic chemotherapy or radiotherapy, severe mumps orchitis, hypogonadotropic hypogonadism, or unexplained (idiopathic) testicular failure. Although non-obstructive azoospermia presents a greater clinical challenge, spermatogenesis is often heterogeneous rather than uniformly absent. Even in small or damaged testicles, isolated microscopic tubules often harbor active sperm production (focal spermatogenesis) that can be targeted under high-magnification microsurgery.
| Clinical Feature | Obstructive Azoospermia (OA) | Non-Obstructive Azoospermia (NOA) | Diagnostic Significance |
| Sperm Production | Preserved within the testicles | Severely reduced, patchy, or absent | Determines surgical retrieval strategy |
| Underlying Cause | Physical blockage (vasectomy, infection, hernia surgery, CBAVD) | Primary testicular failure, genetic deletions, cryptorchidism, chemotherapy | Differentiates treatment feasibility |
| Hormone Levels (FSH/LH) | Normal FSH and LH levels | Typically elevated FSH and LH; normal to low Testosterone | High FSH indicates testicular strain but does not rule out retrieval |
| Primary Treatment | Simple surgical retrieval (PESA/TESA) or microsurgical reconstruction | Micro-TESE (microdissection) paired with ICSI | 90% – 98% retrieval in OA; ~40% – 50% retrieval in NOA |
The essential diagnostic tests before any surgical decision
A structured diagnostic workup is essential before planning any surgical intervention. Proper testing differentiates obstructive from non-obstructive etiology, establishes realistic prognosis, and prevents unwarranted invasive procedures.
Centrifuged Semen Analysis (Repeat Confirmation): Performed following 2 to 7 days of sexual abstinence. Centrifugation of the specimen at 3000g for 15 minutes allows microscopic inspection of the pellet to confirm true azoospermia versus severe cryptozoospermia, where isolated viable sperm can be cryopreserved.
Physical & Andrological Examination: A specialist palpates testicular volume (using an orchidometer) and consistency, checks for epididymal fullness or induration, assesses the bilateral presence of the vas deferens, and evaluates for clinical varicoceles.
Endocrine Hormone Profile (FSH, LH, Total Testosterone, Prolactin, Inhibin B): Measures the hypothalamic-pituitary-gonadal regulatory loop. Clinical interpretation: Serum FSH reflects pituitary feedback. In men with NOA, FSH is often elevated due to impaired negative feedback from diminished Sertoli cell Inhibin B production. However, American Urological Association (AUA) and ESHRE guidelines note that FSH elevation alone does not reliably predict the absence of retrievable focal sperm. Therefore, elevated FSH should not be used as a standalone contraindication to surgical exploration.
High-Resolution Scrotal & Transrectal Ultrasound (TRUS): Evaluates testicular parenchymal texture, detects subclinical varicoceles, and identifies anatomical abnormalities such as ejaculatory duct cysts, midline prostatic cysts, or seminal vesicle agenesis.
Genetic Testing (Karyotyping & Y-Chromosome Microdeletions): Mandatory for all men with non-obstructive azoospermia or severe oligozoospermia (<5 million/mL) prior to surgical exploration.
Genetic Evaluation Details: Genetic testing includes two distinct investigations: a peripheral blood karyotype analysis (identifying structural or numerical chromosomal variations such as Klinefelter syndrome, 47,XXY) and Y-chromosome microdeletion testing using multiplex PCR. The microdeletion panel screens for submicroscopic deletions in the Azoospermia Factor (AZF) regions of the Y chromosome, designated AZFa, AZFb, and AZFc.
In a comprehensive analysis of 1,591 men published in Fertility and Sterility (Stahl et al., Cornell Medical Center), Y microdeletions were identified in 10.4% of azoospermic men. The specific AZF region involved provides definitive prognostic information:
Complete AZFa or AZFb Deletions: These regions encode genes critical for early germ cell proliferation and meiosis. In peer-reviewed clinical series, sperm retrieval rates in men with complete AZFa or AZFb deletions approach zero. Consequently, international guidelines consider complete AZFa or AZFb deletions a clinical contraindication to surgical exploration, sparing couples futile surgical interventions.
AZFc Microdeletions: The surgical outlook is significantly different. In the Stahl et al. cohort, men with isolated AZFc deletions achieved a 71.4% surgical sperm retrieval rate via micro-TESE, compared to 48.8% in men with idiopathic non-obstructive azoospermia. Furthermore, clinical pregnancy rates following ICSI reached 66.7% in couples where sperm was retrieved. An AZFc deletion confirms a genetic etiology, but represents a favorable clinical scenario for microsurgical retrieval.
Genetic Counseling & Inheritance: Because AZF deletions reside on the Y chromosome, any male offspring conceived via ICSI will obligatorily inherit the identical deletion and will likely experience subfertility in adulthood. Female offspring do not inherit the Y chromosome. Couples are advised to complete professional genetic counseling to discuss inheritance patterns prior to treatment.
CBAVD and CFTR Partner Screening: When physical examination or imaging indicates Congenital Bilateral Absence of the Vas Deferens (CBAVD), CFTR gene sequencing is indicated. Importantly, clinical guidelines mandate that the female partner must also be screened for CFTR carrier status before proceeding with ICSI, to evaluate the risk of having a child affected by cystic fibrosis.
Legal & Regulatory Context in India: Karyotyping and Y-microdeletion tests evaluate biological gametogenesis and male subfertility etiologies. These clinical tests comply strictly with India’s Pre-Conception and Pre-Natal Diagnostic Techniques (PCPNDT) Act, which strictly prohibits prenatal sex determination.
Can azoospermia be treated with medicine, ayurveda or diet? (The Medical Truth)
Given the widespread marketing of alternative remedies, patients frequently ask whether medical therapy, herbal supplements, or dietary modifications can restore sperm production. Evidence-based andrology provides clear guidance on what medical therapy can achieve and where its limitations lie:
For Obstructive Azoospermia: No oral medication, dietary regimen, or alternative supplement can dissolve mechanical fibrous scars or rebuild absent anatomical structures like the vas deferens. Obstructive conditions require either microsurgical reconstruction (such as vasoepididymostomy or vasovasostomy) or direct surgical sperm retrieval.
For Non-Obstructive Azoospermia: There are no approved commercial tonics, herbal extracts, or over-the-counter fertility supplements proven to initiate spermatogenesis in primary testicular failure. While specific endocrine conditions respond well to targeted medical protocols, non-specific alternative therapies frequently lead to treatment delays without clinical benefit. Proven medical approaches include:
Targeted Gonadotropin Therapy for Hypogonadotropic Hypogonadism: In men whose pituitary gland fails to secrete adequate FSH and LH (secondary hypogonadism), medical replacement with human chorionic gonadotropin (hCG) and human menopausal gonadotropin (hMG) or recombinant FSH can effectively induce spermatogenesis, often restoring sperm to the ejaculate over 6 to 12 months.
Cessation of Exogenous Testosterone and Anabolic Steroids: Exogenous androgen administration suppresses pituitary LH and FSH release via negative feedback, resulting in secondary azoospermia. This condition is often reversible, but recovery is not instantaneous. Spermatogenesis typically requires 6 to 12 months or longer to recover after stopping exogenous androgens. In men with prolonged steroid exposure, medical management with SERMs (clomiphene citrate) or hCG under andrological supervision may be required to accelerate hypothalamic-pituitary recovery.
Eliminating Gonadotoxic Exposures: Discontinuing gonadotoxic medications (under physician guidance), avoiding chronic testicular hyperthermia, and stopping tobacco use help preserve baseline testicular microcirculation.
Timely Referral for Surgical Retrieval: When endocrine etiologies are excluded, proceeding with evidence-based microsurgical sperm retrieval avoids the prolonged psychological and financial burden of unverified commercial remedies.
Surgical sperm retrieval: PESA, TESA, TESE & micro-TESE success rates
When sperm is absent in the ejaculate, reproductive urologists can harvest sperm directly from the epididymis or testicular parenchyma. The surgical approach is determined by whether the etiology is obstructive or non-obstructive:
PESA (Percutaneous Epididymal Sperm Aspiration): A minimally invasive outpatient procedure performed under local anesthesia. A fine needle is inserted through the scrotum into the caput of the epididymis to aspirate fluid containing stored sperm. It is a primary retrieval method for obstructive azoospermia.
TESA (Testicular Sperm Aspiration): A needle aspiration performed under local anesthesia, inserting a needle directly into the testis to obtain seminiferous tubules. Widely used for obstructive cases and as a diagnostic biopsy technique.
Conventional TESE (Testicular Sperm Extraction): An open surgical biopsy where small incisions are made in the tunica albuginea to excise random samples of testicular tissue. Suitable for obstructive cases where aspiration fails, but limited in non-obstructive azoospermia due to sampling error.
Micro-TESE (Microdissection TESE): The surgical gold standard for Non-Obstructive Azoospermia. Performed under general anesthesia using high-magnification operating microscopes (15x to 25x). The surgeon bivalves the testis and systematically searches for larger, opaque seminiferous tubules that are more likely to contain active spermatogenesis, while preserving microvascular architecture.
| Technique | Tissue Target | Invasiveness & Anesthesia | Primary Indication | Typical Sperm Retrieval Rate |
| PESA | Epididymis | Percutaneous fine needle; Local anesthesia | Obstructive Azoospermia (OA) | 90% – 98% in OA (AUA Guidelines) |
| TESA | Testicle | Needle aspiration biopsy; Local anesthesia | Obstructive Azoospermia / Selected Biopsy | 85% – 95% in OA; Limited in NOA |
| Conventional TESE | Testicle | Small open biopsy; Local or sedation | Obstructive or Selected NOA | 35% – 45% in NOA (Deruyver et al.) |
| Micro-TESE | Testicle (Under Operating Microscope) | Microsurgical open exploration; General anesthesia | Non-Obstructive Azoospermia (NOA) | 45% – 55% in NOA (Corona et al., Bernie et al.) |
Sperm Retrieval Evidence in Non-Obstructive Azoospermia: In a comprehensive meta-analysis of 117 studies by Corona et al. (Human Reproduction Update 2019), the pooled surgical sperm retrieval rate in men with non-obstructive azoospermia was 47%. This demonstrates that nearly half of men with primary testicular impairment have retrievable gametes when evaluated microsurgically.
Micro-TESE vs Conventional TESE: Systematic reviews and meta-analyses by Deruyver et al. (2014) and Bernie et al. (2015) indicate that micro-TESE provides superior or comparable overall retrieval rates (~46% to 52%) with distinct advantages in challenging histological subtypes such as Sertoli-Cell-Only (SCO) pattern. Furthermore, optical magnification minimizes devascularization and testicular parenchymal loss compared to blind multi-biopsy approaches.
What happens after sperm is retrieved: ICSI & pregnancy rates
Surgically extracted testicular spermatozoa cannot be utilized for intrauterine insemination (IUI) or standard IVF. Testicular sperm are present in low numbers and lack progressive motility acquired during transit through the epididymis.
Consequently, retrieved sperm is paired with Intracytoplasmic Sperm Injection (ICSI). Under an inverted microscope, an embryologist immobilizes a single morphologically viable spermatozoon and microinjects it directly into the cytoplasm of a mature MII oocyte obtained from the female partner.
This treatment is coordinated between both partners. The male partner undergoes surgical sperm retrieval (with the option of immediate fertilization or cryopreservation), while the female partner undergoes controlled ovarian stimulation and ultrasound-guided egg retrieval.
Clinical Outcome Data: In the meta-analysis by Corona et al. (2019), among couples where testicular sperm was successfully retrieved and paired with ICSI, the pooled clinical pregnancy rate was approximately 29% per cycle, and the cumulative live birth rate was approximately 24% per cycle.
Clinical Perspective: In non-obstructive azoospermia, sperm is retrieved in approximately 45% to 50% of surgical explorations. Among that group, roughly one in four ICSI cycles culminates in a live birth. While not universally successful, these outcomes represent a meaningful clinical pathway for couples who previously had no biological reproductive options.
What happens if no sperm is found? (Realistic next steps & options)
Transparent clinical care requires discussing the reality that surgical exploration does not identify sperm in approximately 50% of non-obstructive cases.
When an exhaustive microdissection procedure performed by an experienced andrologist yields no viable sperm, the outcome is emotionally difficult. Acknowledging this possibility and planning clinical next steps helps couples navigate the diagnosis with clarity.
Recommended steps following an unsuccessful retrieval:
Histopathological Review: A formal biopsy specimen taken during the procedure is evaluated by a specialized pathologist. The histological pattern (Hypospermatogenesis, Maturation Arrest, or complete Sertoli-Cell-Only Syndrome) provides definitive biological understanding and diagnostic closure regarding testicular architecture.
Allowing Adequate Decision Time: There is rarely a medical necessity to make immediate decisions about subsequent family building pathways. Taking time to process the emotional impact allows couples to evaluate options collaboratively.
Third-Party Reproduction (Donor Sperm): Using certified donor sperm through IUI or IVF/ICSI enables the couple to experience pregnancy and childbirth, maintaining maternal biological lineage. In India, donor gamete treatments are strictly regulated under the Assisted Reproductive Technology (ART) Act, ensuring mandatory genetic screening, infectious disease testing, and confidentiality.
Adoption: Adoption represents an established, legally protected pathway to parenthood that many couples pursue.
Ferty9 provides dedicated reproductive counseling and psychological support services to help couples navigate severe male factor diagnoses with dignity and mutual understanding.
If you are reading this for your husband: Support, communication & next steps
In clinical practice, a significant proportion of initial information seeking regarding male infertility is initiated by female partners.
Cultural factors often lead men to associate semen parameters with virility, masculinity, or sexual competence. Receiving a nil sperm report can trigger substantial distress, self-blame, and social withdrawal.
Practical approaches to support your partner:
Differentiate Cellular Biology from Masculinity: Azoospermia is a localized cellular or anatomical condition involving microscopic ducts or tubule kinetics. It has no bearing on masculinity, sexual function, hormonal vigor, or personal character.
Focus on Diagnostics Before Surgery: Men frequently fear that an andrology consultation leads immediately to surgery. Reassure your partner that initial evaluation focuses on non-invasive diagnostics: clinical history, physical examination, endocrine blood panels, and genetic testing.
Adopt a Shared Perspective: Framing evaluation as a joint investigation (‘Let us determine which clinical category this is’) fosters partnership, whereas framing it around individual deficit (‘We must fix your issue’) can increase emotional withdrawal.
Prioritize Comprehensive Genetic Workup: Ensure karyotype and Y-microdeletion testing are completed prior to agreeing to any operative procedure. This ensures surgical decisions are based on established clinical indications.
Common patient myths vs. clinical realities in male infertility
Misinformation surrounding male subfertility often causes unwarranted anxiety. The following table contrasts common patient misconceptions with clinical andrological evidence:
| Common Patient Myth | Clinical Reality | Medical Science & Evidence |
| Myth 1: ‘A nil sperm count means a man is completely sterile and cannot father children.’ | Reality: Zero sperm in the ejaculate does not equate to zero sperm in testicular tissue. Obstructive cases and approximately 40% to 50% of non-obstructive cases yield viable sperm. | Evidence: Clinical meta-analyses (Corona et al. 2019) document a pooled 47% surgical retrieval rate in non-obstructive azoospermia. |
| Myth 2: ‘Elevated FSH levels indicate surgical sperm retrieval will definitely fail.’ | Reality: High FSH reflects reduced negative feedback from testicular tubules, but does not reliably predict whether focal sperm-producing islands exist. | Evidence: Systematic reviews and AUA guidelines confirm that surgical retrieval rates cannot be predicted by baseline serum FSH alone. |
| Myth 3: ‘Ayurvedic powders, homeopathy, or diet can cure a nil sperm count.’ | Reality: No dietary change or alternative remedy has been demonstrated to reopen blocked reproductive ducts or restore primary testicular failure. | Evidence: Apart from medical gonadotropin therapy for hypogonadotropic hypogonadism, clinical guidelines caution against delays caused by unverified therapies. |
| Myth 4: ‘Azoospermia means a man cannot produce normal semen fluid.’ | Reality: Semen volume is primarily produced by the seminal vesicles and prostate. Azoospermic men have normal ejaculate volume and appearance. | Evidence: Absence of fluid is termed aspermia, a distinct condition usually related to retrograde ejaculation or autonomic neurological dysfunction. |
| Myth 5: ‘Micro-TESE is guaranteed to find sperm in every patient.’ | Reality: While micro-TESE is the most sensitive retrieval technique, successful sperm harvesting occurs in approximately 45% to 55% of cases. | Evidence: Genetic deletions (complete AZFa/AZFb) and diffuse Sertoli-cell-only histology carry retrieval rates approaching zero. |
| Need Expert Guidance on a Nil Sperm Count Report? A semen analysis report reading ‘Nil’ requires specialized andrological evaluation. At Ferty9 Fertility Center, our senior andrologists, urologists, and reproductive microsurgeons provide comprehensive male fertility assessments, advanced centrifuged semen testing, genetic screening, and precision Micro-TESE procedures with complete privacy and clinical rigor. Schedule a confidential consultation with an andrology specialist at your nearest Ferty9 clinic today. |
Frequently asked questions
What does ‘Nil’ mean on a semen analysis report?
In diagnostic andrology, ‘Nil’ indicates that no spermatozoa were observed in the examined semen specimen. Standard clinical protocols require confirmation with a second sample that is centrifuged at high speed to detect any occult sperm cells before establishing a diagnosis of azoospermia.
Is azoospermia permanent, or can it be reversed?
Reversibility depends strictly on etiology. Obstructive azoospermia caused by vasectomy or focal blockages can often be surgically reconnected. Azoospermia triggered by exogenous testosterone or anabolic steroid use is often reversible, though recovery may take 6 to 12 months or longer. Primary testicular failure is permanent, but focal sperm can still be retrieved surgically in roughly 40% to 50% of cases.
Is azoospermia a genetic condition?
In a notable subset of men, yes. Chromosomal variations (such as Klinefelter syndrome, 47,XXY) and Y-chromosome microdeletions (AZFa, AZFb, AZFc) represent established genetic causes. Karyotyping and Y-microdeletion testing are standard diagnostic requirements for non-obstructive azoospermia.
If I have azoospermia, will my biological son inherit it?
If the etiology is a Y-chromosome microdeletion (such as AZFc) and sperm is successfully retrieved to conceive a male child via ICSI, that boy will inherit the identical Y-chromosome microdeletion and will likely experience subfertility in adulthood. Female children do not inherit Y-chromosome deletions. Genetic counseling is advised prior to treatment.
What is the difference between azoospermia and oligospermia?
Azoospermia denotes a complete absence of measurable spermatozoa in the ejaculate. Oligospermia indicates that sperm are present, but at a concentration below the World Health Organization reference limit (fewer than 15 million sperm per milliliter).
What is the difference between azoospermia and aspermia?
Azoospermia refers to normal ejaculate fluid volume containing zero spermatozoa. Aspermia refers to the complete absence of ejaculate fluid, typically caused by retrograde ejaculation or autonomic neurological injury.
Can a varicocele cause azoospermia?
Severe bilateral varicoceles can impair testicular thermoregulation and venous drainage, contributing to testicular dysfunction. In carefully selected men with non-obstructive azoospermia and clinical varicoceles, microsurgical varicocelectomy results in the reappearance of sperm in the ejaculate in roughly 20% to 30% of cases (primarily hypospermatogenesis), though assisted reproduction is usually still required.
Can azoospermia resolve or cure itself naturally?
True primary testicular failure does not resolve spontaneously. However, if temporary spermatogenic arrest occurred due to acute high fever, viral illness, severe heat exposure, or anabolic steroid use, sperm parameters may gradually rebound over 6 to 12 months following removal of the offending trigger.
What are the chances of finding sperm during a Micro-TESE procedure?
In specialized reproductive microsurgery centers, sperm is successfully identified in approximately 45% to 55% of men with non-obstructive azoospermia. The exact probability depends on testicular histology and genetic microdeletion status.
How much does azoospermia testing and treatment cost in India?
Comprehensive diagnostic evaluation (centrifuged semen analysis, endocrine hormone panel, scrotal Doppler ultrasound, and genetic karyotyping/Y-microdeletion testing) generally ranges from Rs 6,000 to Rs 15,000 depending on the specific genetic assays used. Surgical sperm retrieval (TESA, PESA, or Micro-TESE) paired with ICSI varies based on clinical complexity. Contact Ferty9 for itemized, transparent pricing across our centers.
Verified medical & scientific references
All scientific studies cited in this clinical guide are peer-reviewed and indexed in the National Library of Medicine (PubMed). Live URLs are provided below for editorial verification and immediate web linking:
1. Corona G, Minhas S, Giwercman A, Bettocchi C, Dinkelman-Smit M, Dohle G, et al. “Sperm recovery and ICSI outcomes in men with non-obstructive azoospermia: a systematic review and meta-analysis.” Human Reproduction Update. 2019;25(6):733-757. PMID: 31665451.
https://academic.oup.com/humupd/article/25/6/733/5609422
2. Stahl PJ, Masson P, Mielnik A, Marean MB, Schlegel PN, Paduch DA. “A decade of experience emphasizes that testing for Y microdeletions is essential in American men with azoospermia and severe oligozoospermia.” Fertility and Sterility. 2010;94(5):1753-1756. PMID: 19896650.
https://pubmed.ncbi.nlm.nih.gov/19896650
3. Goncalves C, Cunha M, Rocha E, Fernandes S, Silva J, Ferraz L, et al. “Y-chromosome microdeletions in nonobstructive azoospermia and severe oligozoospermia.” Asian Journal of Andrology. 2017;19(3):338-345. PMID: 26908064.
4. Deruyver Y, Vanderschueren D, Van der Aa F. “Outcome of microdissection TESE compared with conventional TESE in non-obstructive azoospermia: a systematic review.” Andrology. 2014;2(1):20-24. PMID: 24193894.
https://onlinelibrary.wiley.com/doi/10.1111/j.2047-2927.2013.00148.x
5. Bernie AM, Mata DA, Ramasamy R, Schlegel PN. “Comparison of microdissection testicular sperm extraction, conventional testicular sperm extraction, and testicular sperm aspiration for nonobstructive azoospermia: a systematic review and meta-analysis.” Fertility and Sterility. 2015;104(5):1099-1103.e1-3. PMID: 26493120.
https://www.fertstert.org/article/S0015-0282(15)01647-7/fulltext
No need to worry, your data is 100% safe with us!