Azoospermia

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Azoospermia
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Semen analysis revealing no sperm cells and multiple white blood cells
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Azoospermia is the medical condition of a man whose semen contains no sperm. [1] It is associated with male infertility, but many forms are amenable to medical treatment. In humans, azoospermia affects about 1% of the male population [2] and may be seen in up to 20% of male infertility situations in Canada. [3]

Contents

In a non-pathological context, azoospermia is also the intended result of a successful vasectomy. [4]

Classification

Azoospermia can be classified into three major types as listed. [3] Many conditions listed may also cause various degrees of oligospermia rather than azoospermia. Pretesticular and testicular azoospermia are known as non-obstructive azoospermia, whereas post-testicular azoospermia is considered obstructive.

Pretesticular

Pretesticular azoospermia is characterized by inadequate stimulation of otherwise normal testicles and genital tract. Typically, follicle-stimulating hormone (FSH) levels are low (hypogonadotropic) commensurate with inadequate stimulation of the testes to produce sperm. Examples include hypopituitarism (for various causes), hyperprolactinemia, and exogenous FSH suppression by testosterone. Chemotherapy may suppress spermatogenesis. [5] Pretesticular azoospermia is seen in about 2% of azoospermia. [3] Pretesticular azoospermia is a kind of non-obstructive azoospermia.

Testicular

Testicular azoospermia means the testes are abnormal, atrophic, or absent, and sperm production severely disturbed to absent. FSH levels tend to be elevated (hypergonadotropic) as the feedback loop is interrupted (lack of feedback inhibition on FSH). The condition is seen in 49–93% of men with azoospermia. [3] Testicular failure includes absence of failure production and low production and maturation arrest during the process of spermatogenesis.

Causes for testicular failure include congenital issues such as in certain genetic conditions (e.g. Klinefelter syndrome), some cases of cryptorchidism or Sertoli cell-only syndrome as well as acquired conditions by infection (orchitis), surgery (trauma, cancer), radiation, [5] or other causes. Mast cells releasing inflammatory mediators appear to directly suppress sperm motility in a potentially reversible manner, and may be a common pathophysiological mechanism for many causes leading to inflammation. [6] Testicular azoospermia is a kind of non-obstructive azoospermia.

Generally, men with unexplained hypergonadotropic azoospermia need to undergo a chromosomal evaluation.

Post-testicular

In post-testicular azoospermia, sperm are produced but not ejaculated, a condition that affects 7–51% of azoospermic men. [3] The main cause is a physical obstruction (obstructive azoospermia) of the post-testicular genital tracts. The most common reason is a vasectomy done to induce contraceptive sterility. [7] Other obstructions can be congenital (for example, agenesis of the vas deferens as seen in certain cases of cystic fibrosis) or acquired, such as ejaculatory duct obstruction for instance by infection.

Ejaculatory disorders include retrograde ejaculation and anejaculation; in these conditions sperm are produced but not expelled.

Unknown

Idiopathic azoospermia is where there is no known cause of the condition. It may be a result of multiple risk factors, such as age and weight. For example, a review in 2013 came to the result that oligospermia and azoospermia are significantly associated with being overweight (odds ratio 1.1), obese (odds ratio 1.3) and morbidly obese (odds ratio 2.0), but the cause of this is unknown. [8] The review found no significant relation between oligospermia and being underweight. [8]

Genetics

Genetic factors can cause pretesticular, testicular, and post-testicular azoospermia (or oligospermia) and include the following situations: [9] The frequency of chromosomal abnormalities is inversely proportional to the semen count, thus males with azoospermia are at risk to have a 10–15% (other sources citing 15–20% incidence [10] ) abnormalities on karyotyping versus about <1 % in the fertile male population. [2]

Pretesticular azoospermia may be caused by congential hypopituitarism, Kallmann syndrome, Prader-Willi syndrome and other genetic conditions that lead to GnRH or gonadotropin deficiency. Testicular azoospermia is seen in Klinefelter syndrome (XXY) and the XX male syndrome. In addition, 13% of men with azoospermia have a defective spermatogenesis that is linked to defects of the Y chromosome. [9] Such defects tend to be de novo micro-deletions and affect usually the long arm of the chromosome. A section of the long arm of the Y chromosome has been termed Azoospermia Factor (AZF) at Yq11 and subdivided into AZFa, AZFb, AZFc and possibly more subsections. Defects in this area can lead to oligospermia or azoospermia, however, a tight genotype-phenotype correlation has not been achieved. [9] Spermatogenesis is defective with gene defects for the androgen receptor.[ citation needed ]

Post-testicular azoospermia can be seen with certain point mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) gene commonly associated with congenital vas deferens abnormalities.[ citation needed ]

Genetic counselling is indicated for men with genetic causes of azoospermia. In terms of reproduction, it needs to be considered if the genetic defect could be transmitted to the offspring.[ citation needed ]

BRD7

BRD7, a transcription regulatory protein, is normally highly expressed in the testis. Absent or reduced expression of BRD7 protein was observed in the testes of azoospermia patients exhibiting spermatogenesis arrest. [11] Homozygous knockout mice [BRD7(-/-)] are infertile and have higher levels of apoptosis and DNA damage in their germline cells. [11]

Gene polymorphisms

The human breast cancer susceptibility gene 2 ( BRCA2 ) is employed in DNA repair. A common single nucleotide polymorphism in BRCA2 is associated with idiopathic male infertility with azoospermia. [12]

Four genes involved in DNA double-strand break repair and chromosome synapsis (TEX11, TEX15 , MLH1 and MLH3 ) have key roles in genomic integrity, meiotic recombination and gametogenesis. Polymorphisms in these genes were tested for associations with male infertility. Single nucleotide polymorphisms in two of these genes (TEX11 and MLH3) were found to be associated with male infertility involving azoospermy or oligospermia. [13]

Diagnosis

Algorithms for the workup of the infertile male. Algorithm to be considered on initial assessment (top). Algorithm for the management of the patient presenting with azoospermia (bottom). Cln-66-04-691-g004.jpg
Algorithms for the workup of the infertile male. Algorithm to be considered on initial assessment (top). Algorithm for the management of the patient presenting with azoospermia (bottom).

Azoospermia is usually detected in the course of an infertility investigation. It is established on the basis of two semen analysis evaluations done at separate occasions (when the seminal specimen after centrifugation shows no sperm under the microscope) and requires a further work-up. [14]

The investigation includes a history, a physical examination including a thorough evaluation of the scrotum and testes, laboratory tests, and possibly imaging. History includes the general health, sexual health, past fertility, libido, and sexual activity. Past exposure to a number of agents needs to be queried including medical agents like hormone/steroid therapy, SSRIs, antibiotics, 5-ASA inhibitors (sulfasalazine), alpha-blockers, 5-alpha-reductase inhibitors, chemotherapeutic agents, pesticides, recreational drugs (marijuana, alcohol), and heat exposure of the testes. A history of surgical procedures of the genital system needs to be elicited. The family history needs to be assessed to look for genetic abnormalities. [3]

Congenital absence of the vas deferens may be detectable on physical examination and can be confirmed by a transrectal ultrasound (TRUS). If confirmed, genetic testing for cystic fibrosis is in order. Transrectal ultrasound can also assess azoospermia caused by obstruction, or anomalies related to obstruction of the ejaculatory duct, such as abnormalities within the duct itself, a median cyst of the prostate (indicating a need for cyst aspiration), or an impairment of the seminal vesicles to become enlarged or emptied. [15] Retrograde ejaculation is diagnosed by examining a post-ejaculatory urine for presence of sperm after making it alkaline and centrifuging it. [10]

Low levels of LH and FSH with low or normal testosterone levels are indicative of pretesticular problems, while high levels of gonadotropins indicate testicular problems. However, often this distinction is not clear and the differentiation between obstructive versus non-obstructive azoospermia may require a testicular biopsy. [3] On the other hand, "In azoospermic men with a normal ejaculate volume, FSH serum level greater than two times the upper limit of the normal range is reliably diagnostic of dysfunctional spermatogenesis and, when found, a diagnostic testicular biopsy is usually unnecessary, although no consensus exists in this matter." [14] [16] [17] Extremely high levels of FSH (>45 ID/mL) have been correlated with successful microdissection testicular sperm extraction. [18]

Serum inhibin-B weakly indicates presence of sperm cells in the testes, raising chances for successfully achieving pregnancy through testicular sperm extraction (TESE), although the association is not very substantial, having a sensitivity of 0.65 (95% confidence interval [CI]: 0.56–0.74) and a specificity of 0.83 (CI: 0.64–0.93) for prediction the presence of sperm in the testes in non-obstructive azoospermia. [19]

Seminal plasma proteins TEX101 and ECM1 were recently proposed for the differential diagnosis of azoospermia forms and subtypes, and for prediction of TESE outcome. [20] [21] Mount Sinai Hospital, Canada started clinical trial to test this hypothesis in 2016. [22]

Primary hypopituitarism may be linked to a genetic cause. So a genetic evaluation may be done for men with azoospermia as a result. [2] Azoospermic men with testicular failure are advised to undergo karyotype and Y-micro-deletion testing. [23] [9] [14]

Treatment

Pre- and post-testicular azoospermia are frequently correctible, while testicular azoospermia is usually permanent. [2] In the former the cause of the azoospermia needs to be considered and it opens up possibilities to manage this situation directly. Thus men with azoospermia due to hyperprolactinemia may resume sperm production after treatment of hyperprolactinemia or men whose sperm production is suppressed by exogenous androgens are expected to produce sperm after cessation of androgen intake. In situations where the testes are normal but unstimulated, gonadotropin therapy can be expected to induce sperm production.

A major advancement in recent years has been the introduction of IVF with ICSI which allows successful fertilization even with immature sperm or sperm obtained directly from testicular tissue. IVF-ICSI allows for pregnancy in couples where the man has irreversible testicular azoospermia as long as it is possible to recover sperm material from the testes. Thus men with non-mosaic Klinefelter's syndrome have fathered children using IVF-ICSI. [24] Pregnancies have been achieved in situations where azoospermia was associated with cryptorchism and sperm where obtained by testicular sperm extraction (TESE). [25]

In men with post-testicular azoospermia, different approaches are available. For obstructive azoospermia, IVF-ICSI or surgery can be used and individual factors are considered for the choice of treatment. [7] Medication may be helpful for retrograde ejaculation.

See also

Related Research Articles

<span class="mw-page-title-main">Intracytoplasmic sperm injection</span> In vitro fertilization procedure

Intracytoplasmic sperm injection is an in vitro fertilization (IVF) procedure in which a single sperm cell is injected directly into the cytoplasm of an egg. This technique is used in order to prepare the gametes for the obtention of embryos that may be transferred to a maternal uterus. With this method, the acrosome reaction is skipped.

<span class="mw-page-title-main">Spermatogenesis</span> Production of sperm

Spermatogenesis is the process by which haploid spermatozoa develop from germ cells in the seminiferous tubules of the testicle. This process starts with the mitotic division of the stem cells located close to the basement membrane of the tubules. These cells are called spermatogonial stem cells. The mitotic division of these produces two types of cells. Type A cells replenish the stem cells, and type B cells differentiate into primary spermatocytes. The primary spermatocyte divides meiotically into two secondary spermatocytes; each secondary spermatocyte divides into two equal haploid spermatids by Meiosis II. The spermatids are transformed into spermatozoa (sperm) by the process of spermiogenesis. These develop into mature spermatozoa, also known as sperm cells. Thus, the primary spermatocyte gives rise to two cells, the secondary spermatocytes, and the two secondary spermatocytes by their subdivision produce four spermatozoa and four haploid cells.

Kallmann syndrome (KS) is a genetic disorder that prevents a person from starting or fully completing puberty. Kallmann syndrome is a form of a group of conditions termed hypogonadotropic hypogonadism. To distinguish it from other forms of hypogonadotropic hypogonadism, Kallmann syndrome has the additional symptom of a total lack of sense of smell (anosmia) or a reduced sense of smell. If left untreated, people will have poorly defined secondary sexual characteristics, show signs of hypogonadism, almost invariably are infertile and are at increased risk of developing osteoporosis. A range of other physical symptoms affecting the face, hands and skeletal system can also occur.

Terms oligospermia, oligozoospermia, and low sperm count refer to semen with a low concentration of sperm and is a common finding in male infertility. Often semen with a decreased sperm concentration may also show significant abnormalities in sperm morphology and motility. There has been interest in replacing the descriptive terms used in semen analysis with more quantitative information.

Y chromosome microdeletion(YCM) is a family of genetic disorders caused by missing genes in the Y chromosome. Many men with YCM exhibit no symptoms and lead normal lives. It is present in a significant number of men with reduced fertility. Reduced sperm production varies from oligozoospermia, significant lack of sperm, or azoospermia, complete lack of sperm.

Hypospermia is a condition in which a man has an unusually low ejaculate volume, less than 1.5 mL. It is the opposite of hyperspermia, which is a semen volume of more than 5.5 mL. It should not be confused with oligospermia, which means low sperm count. Normal ejaculate when a man is not drained from prior sex and is suitably aroused is around 1.5–6 mL, although this varies greatly with mood, physical condition, and sexual activity. Of this, around 1% by volume is sperm cells. The U.S.-based National Institutes of Health defines hypospermia as a semen volume lower than 2 mL on at least two semen analyses.

Male infertility refers to a sexually mature male's inability to impregnate a fertile female. In humans it accounts for 40–50% of infertility. It affects approximately 7% of all men. Male infertility is commonly due to deficiencies in the semen, and semen quality is used as a surrogate measure of male fecundity. More recently, advance sperm analyses that examine intracellular sperm components are being developed.

<span class="mw-page-title-main">XX male syndrome</span> Congenital condition where an individual with a 46,XX karyotype has male characteristics

XX male syndrome, also known as de la Chapelle syndrome, is a rare congenital intersex condition in which an individual with a 46,XX karyotype has phenotypically male characteristics that can vary among cases. Synonyms include 46,XX testicular difference of sex development, 46,XX sex reversal, nonsyndromic 46,XX testicular DSD, and XX sex reversal.

Spermatogenesis arrest is known as the interruption of germinal cells of specific cellular type, which elicits an altered spermatozoa formation. Spermatogenic arrest is usually due to genetic factors resulting in irreversible azoospermia. However some cases may be consecutive to hormonal, thermic, or toxic factors and may be reversible either spontaneously or after a specific treatment. Spermatogenic arrest results in either oligospermia or azoospermia in men. It is quite a difficult condition to proactively diagnose as it tends to affect those who have normal testicular volumes; a diagnosis can be made however through a testicular biopsy.

<span class="mw-page-title-main">Testicular sperm extraction</span> Surgical procedure

Testicular sperm extraction (TESE) is a surgical procedure in which a small portion of tissue is removed from the testicle and any viable sperm cells from that tissue are extracted for use in further procedures, most commonly intracytoplasmic sperm injection (ICSI) as part of in vitro fertilisation (IVF). TESE is often recommended to patients who cannot produce sperm by ejaculation due to azoospermia.

Azoospermia factor (AZF) is one of several proteins or their genes, which are coded from the AZF region on the human male Y chromosome. Deletions in this region are associated with inability to produce sperm. Subregions within the AZF region are AZFa, AZFb and AZFc. AZF microdeletions are one of the major causes of male infertility for azoospermia and severe oligozoospermia males. AZF is the term used by the HUGO Gene Nomenclature Committee.

<span class="mw-page-title-main">Sertoli cell-only syndrome</span> Medical condition

Sertoli cell-only syndrome (SCOS), also known as germ cell aplasia, is defined by azoospermia where the testicular seminiferous tubules are lined solely with sertoli cells. Sertoli cells contribute to the formation of the blood-testis barrier and aid in sperm generation. These cells respond to follicle-stimulating hormone, which is secreted by the hypothalamus and aids in spermatogenesis.

<span class="mw-page-title-main">DAZ2</span> Protein-coding gene in the species Homo sapiens

Deleted in azoospermia protein 2 is a protein that in humans is encoded by the DAZ2 gene.

<span class="mw-page-title-main">Klinefelter syndrome</span> Human chromosomal condition

Klinefelter syndrome (KS), also known as 47,XXY, predominantly found in men, is an aneuploid genetic condition where the recipient has an additional copy of the X chromosome. The primary features are infertility and small, poorly functioning testicles. These symptoms are often noticed only at puberty, although this is one of the most common chromosomal disorders, occurring in one to two per 1,000 live births. It is named after American endocrinologist Harry Klinefelter, who identified the condition in the 1940s.

<span class="mw-page-title-main">Activin and inhibin</span> Regulators of feedback on FSH-production

Activin and inhibin are two closely related protein complexes that have almost directly opposite biological effects. Identified in 1986, activin enhances FSH biosynthesis and secretion, and participates in the regulation of the menstrual cycle. Many other functions have been found to be exerted by activin, including roles in cell proliferation, differentiation, apoptosis, metabolism, homeostasis, immune response, wound repair, and endocrine function. Conversely, inhibin downregulates FSH synthesis and inhibits FSH secretion. The existence of inhibin was hypothesized as early as 1916; however, it was not demonstrated to exist until Neena Schwartz and Cornelia Channing's work in the mid-1970s, after which both proteins were molecularly characterized ten years later.

FNA mapping is an application of fine-needle aspiration (FNA) to the testis for the diagnosis of male infertility. FNA cytology has been used to examine pathological human tissue from various organs for over 100 years. As an alternative to open testicular biopsy for the last 40 years, FNA mapping has helped to characterize states of human male infertility due to defective spermatogenesis. Although recognized as a reliable, and informative technique, testis FNA has not been widely used in U.S. to evaluate male infertility. Recently, however, testicular FNA has gained popularity as both a diagnostic and therapeutic tool for the management of clinical male infertility for several reasons:

  1. The testis is an ideal organ for evaluation by FNA because of its uniform cellularity and easy accessibility.
  2. The trend toward minimally invasive procedures and cost-containment views FNA favorably compared to surgical testis biopsy.
  3. The realization that the specific histologic abnormality observed on testis biopsy has no definite correlation to either the etiology of infertility or to the ability to find sperm for assisted reproduction.
  4. Assisted reproduction has undergone dramatic advances such that testis sperm are routinely used for biological pregnancies, thus fueling the development of novel FNA techniques to both locate and procure sperm.
<span class="mw-page-title-main">Paul J. Turek</span>

Dr. Paul J Turek is an American physician and surgeon, men's reproductive health specialist, and businessman. Turek is a recent recipient of a National Institutes of Health (NIH) grant for research designed to help infertile men become fathers using stem cells.

Hypergonadotropic hypogonadism (HH), also known as primary or peripheral/gonadal hypogonadism or primary gonadal failure, is a condition which is characterized by hypogonadism which is due to an impaired response of the gonads to the gonadotropins, follicle-stimulating hormone (FSH) and luteinizing hormone (LH), and in turn a lack of sex steroid production. As compensation and the lack of negative feedback, gonadotropin levels are elevated. Individuals with HH have an intact and functioning hypothalamus and pituitary glands so they are still able to produce FSH and LH. HH may present as either congenital or acquired, but the majority of cases are of the former nature. HH can be treated with hormone replacement therapy.

XXXYdisease is a genetic condition characterized by a sex chromosome aneuploidy, where individuals have two extra X chromosomes. People in most cases have two sex chromosomes: an X and a Y or two X chromosomes. The presence of one Y chromosome with a functioning SRY gene causes the expression of genes that determine maleness. Because of this, XXXY syndrome only affects males. The additional two X chromosomes in males with XXXY syndrome causes them to have 48 chromosomes, instead of the typical 46. XXXY syndrome is therefore often referred to as 48,XXXY. There is a wide variety of symptoms associated with this syndrome, including cognitive and behavioral problems, taurodontism, and infertility. This syndrome is usually inherited via a new mutation in one of the parents' gametes, as those affected by it are usually infertile. It is estimated that XXXY affects one in every 50,000 male births.

Cryopreservation of testicular tissue is an experimental method being used to preserve fertility in pre-pubescent males, or males who cannot produce sperm, to allow them the option of having biological children.

References

  1. ↑ Berookhim, BM; Schlegel, PN (February 2014). "Azoospermia due to spermatogenic failure". The Urologic Clinics of North America. 41 (1): 97–113. doi:10.1016/j.ucl.2013.08.004. PMID   24286770.
  2. 1 2 3 4 Male Infertility Best Practice Policy Committee of the American Urological Association; Practice Committee of the American Society for Reproductive Medicine (2001). Infertility: Report on Evaluation of the Azoospermic Male (PDF). American Urological Association; American Society for Reproductive Medicine. ISBN   978-0-9649702-8-1. Archived (PDF) from the original on 2018-03-26. Retrieved 2010-06-14.{{cite book}}: |author1= has generic name (help)
  3. 1 2 3 4 5 6 7 Jarvi, K; Lo, K; Fischer, A; Grantmyre, J; Zini, A; Chow, V; Mak, V (2010). "CUA Guideline: The workup of azoospermic males". Canadian Urological Association Journal. 4 (3): 163–7. doi:10.5489/cuaj.10050. PMC   2874589 . PMID   20514278.
  4. ↑ Barone, Mark A.; Irsula, Belinda; Chen-Mok, Mario; Sokal, David C.; the Investigator study group (2004-07-19). "Effectiveness of vasectomy using cautery". BMC Urology. 4 (1): 10. doi: 10.1186/1471-2490-4-10 . ISSN   1471-2490. PMC   503392 . PMID   15260885.
  5. 1 2 Dohle, Gert R (2010). "Male infertility in cancer patients: Review of the literature". International Journal of Urology. 17 (4): 327–331. doi: 10.1111/j.1442-2042.2010.02484.x . PMID   20202000.
  6. ↑ Menzies, F. M.; Shepherd, M. C.; Nibbs, R. J.; Nelson, S. M. (2010). "The role of mast cells and their mediators in reproduction, pregnancy and labour". Human Reproduction Update. 17 (3): 383–396. doi: 10.1093/humupd/dmq053 . PMID   20959350.
  7. 1 2 Practice Committee of ASRM, August 2008. "The management of infertility due to obstructive azzospermia" (PDF). Archived (PDF) from the original on March 4, 2016. Retrieved June 14, 2010.{{cite web}}: CS1 maint: numeric names: authors list (link)
  8. 1 2 Sermondade, N.; Faure, C.; Fezeu, L.; et al. (2012). "BMI in relation to sperm count: An updated systematic review and collaborative meta-analysis". Human Reproduction Update. 19 (3): 221–231. doi:10.1093/humupd/dms050. PMC   3621293 . PMID   23242914.
  9. 1 2 3 4 Poongothai, J; Gopenath, TS; Manonayaki, S (2009). "Genetics of human male infertility". Singapore Medical Journal. 50 (4): 336–47. PMID   19421675.
  10. 1 2 Padubidri; Daftary (2011). Shaw's Textbook of Gynaecology, 15e. p. 205. ISBN   978-81-312-2548-6
  11. 1 2 Wang H, Zhao R, Guo C, Jiang S, Yang J, Xu Y, Liu Y, Fan L, Xiong W, Ma J, Peng S, Zeng Z, Zhou Y, Li X, Li Z, Li X, Schmitt DC, Tan M, Li G, Zhou M (2016). "Knockout of BRD7 results in impaired spermatogenesis and male infertility". Sci Rep. 6: 21776. Bibcode:2016NatSR...621776W. doi:10.1038/srep21776. PMC   4754950 . PMID   26878912.
  12. ↑ Zhoucun A, Zhang S, Yang Y, Ma Y, Zhang W, Lin L (2006). "The common variant N372H in BRCA2 gene may be associated with idiopathic male infertility with azoospermia or severe oligozoospermia". Eur. J. Obstet. Gynecol. Reprod. Biol. 124 (1): 61–4. doi:10.1016/j.ejogrb.2005.09.001. PMID   16257105.
  13. ↑ Zhang X, Ding M, Ding X, Li T, Chen H (2015). "Six polymorphisms in genes involved in DNA double-strand break repair and chromosome synapsis: association with male infertility". Syst Biol Reprod Med. 61 (4): 187–93. doi: 10.3109/19396368.2015.1027014 . PMID   26086992.
  14. 1 2 3 Esteves SC, Miyaoka R, Agarwal A. An update on the clinical assessment of the infertile male. Clinics (Sao Paulo). [corrected]. 2011;66(4):691–700.
  15. ↑ Lotti, F.; Maggi, M. (2014). "Ultrasound of the male genital tract in relation to male reproductive health" (PDF). Human Reproduction Update. 21 (1): 56–83. doi: 10.1093/humupd/dmu042 . ISSN   1355-4786. PMID   25038770.
  16. ↑ Fertil Steril. 2008;90(5 Suppl):S74-7.
  17. ↑ Coburn, M., Wheeler, T., and Lipshultz, L.I. Testicular biopsy. Its use and limitations. Urol Clin North Am. 1987; 14: 551–561.
  18. ↑ Ramasamy R, Lin K, Gosden LV, Rosenwaks Z, Palermo GD, Schlegel PN. High serum FSH levels in men with nonobstructive azoospermia does not affect success of microdissection testicular sperm extraction. Fertil Steril. 2009;92(2):590-3.
  19. ↑ Toulis, K. A.; Iliadou, P. K.; Venetis, C. A.; Tsametis, C.; Tarlatzis, B. C.; Papadimas, I.; Goulis, D. G. (2010). "Inhibin B and anti-Mullerian hormone as markers of persistent spermatogenesis in men with non-obstructive azoospermia: a meta-analysis of diagnostic accuracy studies". Human Reproduction Update. 16 (6): 713–724. doi: 10.1093/humupd/dmq024 . PMID   20601364.
  20. ↑ Drabovich, A. P.; Dimitromanolakis, A.; Saraon, P.; Soosaipillai, A.; Batruch, I.; Mullen, B.; Jarvi, K.; Diamandis, E.P. (2013). "Differential Diagnosis of Azoospermia with Proteomic Biomarkers ECM1 and TEX101 Quantified in Seminal Plasma". Science Translational Medicine. 5 (212): 212ra160. doi:10.1126/scitranslmed.3006260. PMID   24259048. S2CID   13541504.
  21. ↑ Korbakis, D.; Schiza, C.; Brinc, D.; Soosaipillai, A.; Karakosta, T.D.; Légaré, C.; Sullivan, R.; Mullen, B.; Jarvi, K.; Diamandis, E.P.; Drabovich, A.P. (2017). "Preclinical evaluation of a TEX101 protein ELISA test for the differential diagnosis of male infertility". BMC Medicine. 15 (1): 60. doi: 10.1186/s12916-017-0817-5 . PMC   5363040 . PMID   28330469.
  22. ↑ "Use of Semen TEX101 to Improve Sperm Retrieval Rates for Men With Non-obstructive Azoospermia". March 8, 2019. Archived from the original on April 13, 2017. Retrieved April 13, 2017– via clinicaltrials.gov.
  23. ↑ Schlegel, PN (2004). "Causes of azoospermia and their management". Reproduction, Fertility, and Development. 16 (5): 561–72. doi:10.1071/RD03087. PMID   15367371.
  24. ↑ Fullerton, G.; Hamilton, M.; Maheshwari, A. (2010). "Should non-mosaic Klinefelter syndrome men be labelled as infertile in 2009?". Human Reproduction. 25 (3): 588–597. doi: 10.1093/humrep/dep431 . PMID   20085911.
  25. ↑ Haimov-Kochman, R.; Prus, D.; Farchat, M.; Bdolah, Y.; Hurwitz, A. (2010). "Reproductive outcome of men with azoospermia due to cryptorchidism using assisted techniques". International Journal of Andrology. 33 (1): e139–e143. doi: 10.1111/j.1365-2605.2009.00977.x . PMID   19622071.
-spermia,
Further information: Testicular infertility factors
Aspermia—lack of semen; anejaculation
Asthenozoospermia—sperm motility below lower reference limit
Azoospermia—absence of sperm in the ejaculate
Hyperspermia—semen volume above upper reference limit
Hypospermia—semen volume below lower reference limit
Oligospermia—total sperm count below lower reference limit
Necrospermia—absence of living sperm in the ejaculate
Teratospermia—fraction of normally formed sperm below lower reference limit
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