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Male Infertility

Approximately 15% of couples attempting their first pregnancy meet with failure. Most authorities define these patients as primarily infertile if they have been unable to achieve a pregnancy after one year of unprotected intercourse. Conception normally is achieved within twelve months in 80-85% of couples who use no contraceptive measures, and persons presenting after this time should therefore be regarded as possibly infertile and should be evaluated. Data available over the past twenty years reveal that in approximately 30% of cases pathology is found in the man alone, and in another 20% both the man and woman are abnormal. Therefore, the male factor is at least partly responsible in about 50% of infertile couples.

Important issues related to the evaluation of the male factor include the most appropriate time for the male evaluation, the most efficient format for a comprehensive male exam, and definition of rationale and effective medical and surgical regimens in the treatment of these disorders. It is extremely important in the evaluation of infertility to consider the couple as a unit in evaluation and treatment and to proceed in a parallel investigative manner until a problem is uncovered. It has been shown that the longer a couple remains sub fertile, the worse their chance for an effective cure. Many couples experience significant apprehension and anxiety after only a few months of failure to conceive. Unduly prolonged unprotected intercourse should not be advocated before a workup of the man is instituted. Initial screening of the man should be considered whenever the patient presents with the chief complaint of infertility. This initial evaluation should be rapid, non-invasive and cost effective. Of interest is the fact that pregnancy rates of up to 50% have been reported when only the woman has been investigated and treated even when the man was found to have moderately severe abnormalities of semen quality.


Causes generally can be divided into pretesticular, testicular, and posttesticular.

Pretesticular Causes of Infertility

Pretesticular causes of infertility include congenital or acquired diseases of the hypothalamus, pituitary, or peripheral organs that alter the hypothalamic-pituitary axis.


Disorders of the hypothalamus lead to hypogonadotropic hypogonadism. If GnRH is not secreted, the pituitary does not release LH and FSH. Ideally, patients respond to replacement with exogenous GnRH or HCG, an LH analogue, although this does not always occur.

  • Idiopathic hypogonaotropic hypogonadism
  • A failure of GnRH secretion without any discernible underlying cause may be observed alone (isolated) or as part of Kallmann syndrome, which is associated with midline defects such as anosmia, cleft lip and cleft palate, deafness, cryptorchidism, and color blindness. Kallmann syndrome has been described in both familial (X-linked and autosomal) and sporadic forms, and its incidence is estimated as 1 case per 10,000-60,000 births.
  • A failure of GnRH neurons to migrate to the proper location in the hypothalamus has been implicated. Patients generally have long arms and legs due to a delayed closure of the epiphyseal plates, delayed puberty, and atrophic testis. Testosterone therapy may allow patients to achieve normal height but does not improve spermatogenesis. Exogenous testosterone should never be administered in an attempt to boost sperm production because it actually decreases intratesticular testosterone levels owing to feedback inhibition of GnRH release.
  • Pulsatile GnRH and HCG have been used but result in only 20% achieving complete spermatogenesis.
  • Adding recombinant human FSH to HCG has been shown to be effective in achieving spermatogenesis in most patients.
  • Select patients with adult-onset idiopathic hypogonadotropic hypogonadism may respond to clomiphene citrate therapy.
  • Prader-Willi syndrome: Patients have characteristic obesity, mental retardation, small hands and feet, and hypogonadotropic hypogonadism due to a GnRH deficiency. Prader-Willi syndrome is caused by a disorder of genomic imprinting with deletions of paternally derived chromosome arm 15q11-13.
  • Laurence-Moon-Biedl syndrome: Patients with this syndrome have retinitis pigmentosa and polydactyly. Infertility is due to hypogonadotropic hypogonadism.
  • Other conditions: Various other lesions and diseases, such as CNS tumors, temporal lobe seizures, and many drugs (eg, dopamine antagonists) may interrupt the hypothalamic-pituitary axis at the hypothalamus.


Both pituitary insufficiency and pituitary excess cause infertility. Pituitary failure may be congenital or acquired. Acquired causes include tumor, infarction, radiation, infection, or granulomatous disease. Nonfunctional pituitary tumors may compress the pituitary stalk or the gonadotropic cells, interrupting the proper chain of signals leading to pituitary failure. In contrast, functional pituitary tumors may lead to unregulated gonadotropin release or prolactin excess, interrupting the proper signaling.


  • A prolactin-secreting adenoma is the most common functional pituitary tumor. Prolactin stimulates breast development and lactation; therefore, patients with infertility due to a prolactinoma may have gynecomastia and galactorrhea. In addition, loss of peripheral visual fields bilaterally may be due to compression of the optic chiasm by the growing pituitary tumor.
  • A prolactin level of more than 150 mcg/L suggests a pituitary adenoma, while levels greater than 300 mcg/L are nearly diagnostic. Patients should undergo an MRI or CT scan of the sella turcica for diagnostic purposes to determine whether a microprolactinoma or a macroprolactinoma is present.
  • Bromocriptine, a dopamine agonist, is used to suppress prolactin levels and is the therapy of choice for microprolactinomas. Cabergoline is also a treatment option. Some men respond with an increase in testosterone levels; many also recover normal sperm counts. Transsphenoidal resection of a microprolactinoma is 80-90% successful, but as many as 17% recur. Surgical therapy of a macroprolactinoma is rarely curative, although this should be considered in patients with visual-field defects or those who do not tolerate bromocriptine.
  • Isolated LH deficiency (fertile eunuch): In these patients, LH levels are decreased while FSH levels are within the reference range. Patients have eunuchoidal body habitus, large testis, and a low ejaculatory volume. The treatment of choice is exogenous HCG.
  • Isolated FSH deficiency: This is a very rare cause of infertility. Patients present with oligospermia but have LH levels within the reference range. Treatment is with human menopausal gonadotropin (HMG) or exogenous FSH.
  • Thalassemia: Patients with thalassemia have ineffective erythropoiesis and undergo multiple blood transfusions. Excess iron from multiple transfusions may get deposited in the pituitary gland and the testis, causing parenchymal damage and both pituitary and testicular insufficiency. Treatment is with exogenous gonadotropins and iron-chelating therapy.
  • Cushing disease: Increased cortisol levels cause a negative feedback on the hypothalamus, decreasing GnRH release.

Peripheral Organs

The hypothalamus-pituitary axis may be interrupted by hormonally active peripheral tumors or other exogenous factors, due to cortical excess, cortical deficiency, or estrogen excess.

  • Excess cortisol may be produced by adrenal hyperplasia, adenomas, carcinoma, or lung tumors. High cortisol levels may also be seen with exogenous steroid use, such as that administered to patients with ulcerative colitis, asthma, arthritis, or organ transplant. For example, high cortisol levels are seen in patients with Cushing syndrome, which causes negative feedback on the pituitary to decrease LH release.
  • Cortical deficiency may be seen in patients with adrenal failure due to infection, infarction, or congenital adrenal hyperplasia (CAH). CAH may be due to the congenital deficiency of one of several adrenal enzymes, the most common of which is 21-hydroxylase deficiency. Because cortisol is not secreted, a lack of feedback inhibition on the pituitary gland occurs, leading to adrenocorticotropic hormone (ACTH) hypersecretion. This leads to increased androgen secretion from the adrenal gland, causing feedback inhibition of GnRH release from the hypothalamus. Patients present with short stature, precocious puberty, small testis, and occasional bilateral testicular rests. Screening tests include increased plasma 17-hydroxylase and urine 17-ketosteroids.
  • Estrogen excess may be seen in patients with Sertoli cell tumors, Leydig tumors, liver failure, or severe obesity. Estrogen causes negative feedback on the pituitary gland, inhibiting LH and FSH release.

Primary Testicular Causes of Infertility

Primary testicular problems may be chromosomal or non chromosomal in nature. While chromosomal failure is usually caused by abnormalities of the sex chromosomes, autosomal disorders are also observed.

Chromosomal Abnormalities 

An estimated 6-13% of infertile men have chromosomal abnormalities (compared with 0.6% of the general population). Patients with azoospermia or severe oligospermia are more likely to have a chromosomal abnormality (10-15%) than infertile men with sperm density within the reference range (1%). A karyotype test and a Y chromosome test for microdeletions are indicated in patients with nonobstructive azoospermia or severe oligospermia (<5 million sperm/mL), although indications are expanding.

  • Klinefelter syndrome is the most common chromosomal cause of male infertility, estimated to be present in 1 per 500-1000 male births. Classic Klinefelter syndrome has a 47, XXY karyotype and is caused by a nondisjunction during the first meiotic division, more commonly of maternal origin; mosaic forms are due to nondisjunction following fertilization. The only known risk factor for Klinefelter syndrome is advanced maternal age. Infertility is caused by primary testicular failure, and most patients are azoospermic. Hormonal analysis reveals increased gonadotropin levels, while 60% have decreased testosterone levels. Surprisingly, most patients have normal libido, erections, and orgasms, so testosterone therapy has only a limited role; exogenous testosterone may also suppress any underlying sperm production.
  • Physical examination reveals gynecomastia, small testis, and eunuchoid body habitus due to delayed puberty. In some patients, secondary sex characteristics develop normally, but they are usually completed late. These men are at a higher risk for breast cancer, leukemia, diabetes, empty sella syndrome, and pituitary tumors. Testicular histology reveals hyalinization of seminiferous tubules. Some men with Klinefelter syndrome may be able to conceive with the help of assisted reproductive techniques. Of azoospermic patients with Klinefelter syndrome, 20% show the presence of residual foci of spermatogenesis. Although the XXY pattern is observed in the spermatogonia and primary spermatocytes, many of the secondary spermatocytes and spermatids have normal patterns. The chromosomal pattern of the resultant embryos can be assessed with preimplantation genetic diagnosis.
  • XX male (sex reversal syndrome): An XX karyotype is due to a crossover of the sex-determining region (SRY) of the Y chromosome (with the testis determining factor) to either the X chromosome or an autosome. Patients are often short, with small firm testis and gynecomastia, but they have a normal-sized penis. Seminiferous tubules show sclerosis.
  • XYY male: An XYY karyotype is observed in 0.1-0.4% of newborn males. These patients are often tall and severely oligospermic or azoospermic. This pattern has been linked with aggressive behavior. Biopsy reveals maturation arrest or germ cell aplasia. Functional sperm that are present may have a normal karyotype.
  • Noonan syndrome (46, XY): Patients with Noonan syndrome, also known as male Turner syndrome, have physical characteristics similar to that of women with Turner syndrome (45, X). Features include a webbed neck, short stature, low-set ears, ptosis, shield-like chest, lymphedema of hands and feet, cardiovascular abnormalities, and cubitus valgus. Leydig cell function is impaired, and most patients are infertile due to primary testicular failure.
  • Mixed gonadal dysgenesis (45, X/46, XY): Patients have ambiguous genitalia, a testis on one side, and a streaked gonad on the other.
  • Y chromosome microdeletion syndrome: The long arm of the Y chromosome (Yq) is considered critical for fertility, especially Yq11.23 (interval 6). Macroscopic deletions of Yq11 are often observed in patients with azoospermia, although many new microdeletions have been implicated as a significant cause of infertility. These microdeletions are not observed on regular karyotype; rather, their identification requires polymerase chain reaction (PCR)–based sequence-tagged site mapping or Southern blot analysis. Three regions have been described, called azoospermic factors a, b, and c (AZFa, AZFb, AZFc). These deletions are observed in 3-19% of patients with idiopathic infertility and 6-14% of patients with oligospermia, although up to 7% of patients with other known causes of infertility may also be found to have a deletion. Patients with azoospermia or severe oligospermia seeking assisted reproductive techniques should be screened.
  • Bilateral anorchia (vanishing testis syndrome): Patients have a normal male karyotype (46, XY) but are born without testis bilaterally. The male phenotype proves that androgen was present in utero. Potential causes are unknown, but it may be related to infection, vascular disease, or bilateral testicular torsion. Karyotype shows a normal SRY gene. Patients may achieve normal virilization and adult phenotype by the administration of exogenous testosterone, but they are infertile.
  • Down syndrome: These patients have mild testicular dysfunction with varying degrees of reduction in germ cell number. LH and FSH levels are usually elevated.
  • Myotonic dystrophy: This is an autosomal dominant defect in the dystrophin gene that causes a delay in muscle relaxation after contraction. Seventy-five percent of patients have testicular atrophy and primary testicular failure due to degeneration of the seminiferous tubules. Leydig cells are normal. Histology reveals severe tubular sclerosis. No effective therapy exists.

Nonchromosomal Testicular Failure

Testicular failure that is nonchromosomal in origin may be idiopathic or acquired by gonadotoxic drugs, radiation, orchitis, trauma, or torsion.


  • A varicocele is a dilation of the veins of the pampiniform plexus of the scrotum. Although varicoceles are present in 15% of the male population, a varicocele is considered the most common correctable cause of infertility (30-35%) and the most common cause of secondary (acquired) infertility (75-85%). Varicoceles are observed more commonly on the left side than the right. Those with isolated right-sided varicoceles should be evaluated for retroperitoneal pathology.
  • Varicoceles are generally asymptomatic, and most men with varicoceles do not have infertility or testicular atrophy. However, varicoceles may lead to impaired testicular spermatogenesis and steroidogenesis, potentially due to an increased intratesticular temperature, reflux of toxic metabolites, and/or germ cell hypoxia as potential causes of these changes, and this appears to be progressive over time.
  • Varicoceles lead to an increased incidence of sperm immaturity, apoptosis, and necrosis with severe disturbances in meiotic segregation compared to fertile men without varicoceles, and these parameters generally improve after repair.
  • Patients with a grade 2-3 varicocele (visible or palpable) associated with infertility should have the varicocele repaired. After repair, 40-70% of patients have improved semen parameters, while 40% are able to achieve a pregnancy without other interventions. Those with a varicocele diagnosable only on scrotal ultrasonography will likely not benefit from repair. Adolescents with a varicocele and testicular atrophy or lack of growth should similarly undergo repair. Controversy exists regarding whether to routinely repair an adolescent varicocele not associated with testicular atrophy.
  • In those with azoospermia and a varicocele, sperm may appear after repair in up to one third, but most of these men return to an azoospermic state within a few months. If sperm appears, these men should be offered cryopreservation.


  • An estimated 3% of full-term males are born with an undescended testicle, but fewer than 1% remain undescended by age 1 year. Undescended testicle may be isolated or may be observed as part of a syndrome such as prune belly syndrome. Patients are at increased risk of infertility, even if the testicle is brought down into the scrotum, as the testicle itself may be inherently abnormal. The farther from the scrotum, and the longer duration that the testicle resides outside the scrotum, the greater the likelihood of infertility. Testicular histology typically reveals a decreased number of Leydig cells and decreased spermatogenesis. Cryptorchidism may be due to inherent defects in both testes because even men with unilateral cryptorchidism have lower than expected sperm counts.
  • Trauma: Testicular trauma is the second most common acquired cause of infertility. The testes are at risk for both thermal and physical trauma because of their exposed position.
  • Sertoli cells-only syndrome (germinal cell aplasia): Patients with germinal cell aplasia have LH and testosterone levels within the reference range but have an increased FSH level. The etiology is unknown but is probably multifactorial. Patients have with small- to normal-sized testes and azoospermia, but normal secondary sex characteristics. Histology reveals seminiferous tubules lined by Sertoli cells and a normal interstitium, although no germ cells are present.
  • Chemotherapy: Chemotherapy is toxic to actively dividing cells. In the testicle, germ cells (especially up to the preleptotene stage) are especially at risk. The agents most often associated with infertility are the alkylating agents such as cyclophosphamide. For example, treatment for Hodgkin disease has been estimated to lead to infertility in as many as 80-100% of patients.
  • Radiation therapy: While Leydig cells are relatively radioresistant because of their low rate of cell division, the Sertoli and germ cells are extremely radiosensitive. If stem cells remain viable after radiation therapy, patients may regain fertility within several years. However, some have suggested that patients should avoid conception for 6 months to 2 years after completion of radiation therapy because of the possibility of chromosomal aberrations in their sperm caused by the mutagenic properties of radiation therapy. Even with the testis shielded, radiation therapy below the diaphragm may lead to infertility due to the release of reactive oxygen free radicals.


  • The most common cause of acquired testicular failure in adults is viral orchitis, such as that caused by the mumps virus, echovirus, or group B arbovirus. Of adults with who are infected with mumps, 25% develop orchitis; two thirds of cases are unilateral, and one third are bilateral. While orchitis develops a few days after the onset of parotid gland inflammation, it may also precede it. The virus may either directly damage the seminiferous tubules or indirectly cause ischemic damage as the intense swelling leads to compression against the tough tunica albuginea. After recovery, the testicle may return to normal or may atrophy. Atrophy is observed within 1-6 months, and the degree of atrophy does not correlate with the severity of orchitis or infertility. Normal fertility is observed in three fourths of patients with unilateral mumps orchitis and in one third of patients in bilateral orchitis.
  • Granulomatous disease: Leprosy and sarcoidosis may infiltrate the testicle and lead to testicular failure.
  • Sickle cell disease: Sickling of cells within the testis leads to microinfarcts and secondary testicular failure.
  • Excessive use of alcohol, cigarettes, caffeine, and marijuana may lead to testicular failure.
  • Idiopathic causes: Despite a thorough workup, nearly 25% of men have no discernible cause for their infertility.

Posttesticular Causes of Infertility

Posttesticular causes of infertility include problems with sperm transportation through the ductal system, either congenital or acquired. Genital duct obstruction is a potentially curable cause of infertility and is observed in 7% of infertile patients. Additionally, the sperm may be unable to cross the cervical mucus or may have ultrastructural abnormalities.

Congenital blockage of the ductal system: An increased rate of duct obstruction is observed in children of mothers who were exposed to DES during pregnancy. Segmental dysplasia is defined as a vas deferens with at least 2 distinct sites of vasal obstruction.

  • Cystic fibrosis: CF is the most common genetic disorder in whites. Patients with CF nearly uniformly have CBAVD. The cystic fibrosis transmembrane regulator (CFTR) protein plays a role in mesonephric duct development during early fetal life, so these patients may also have urinary tract abnormalities. Patients may be candidates for assisted reproduction techniques after appropriate genetic screening in the partner.
  • Acquired blockage of the ductal system: Genital ducts may become obstructed secondary to infections, such as chlamydia, gonorrhea, tuberculosis, and smallpox. Young syndrome is a condition that leads to inspissation of material and subsequent blockage of the epididymis. Trauma, previous attempts at sperm aspiration, and inguinal surgery may also result in ductal blockage. Small calculi may block the ejaculatory ducts, or prostatic cysts may extrinsically block the ducts. Scrotal surgery, including vasectomy, hydrocelectomy (5-6%), and spermatocelectomy (up to 17%), may lead to epididymal injury and subsequent obstruction.
  • Antisperm antibodies: Antisperm antibodies bind to sperm, impair motility, and lead to clumping, impairing movement through the female reproductive tract and interaction with the oocyte.
  • Immotile cilia syndrome may be isolated or part of Kartagener syndrome with situs inversus. Because of a defect in the dynein arms, spokes, or microtubule doublet, cilia in the respiratory tract and in sperm do not function properly. In addition to sperm immobility, patients experience sinusitis, bronchiectasis, and respiratory infections.
  • Ejaculatory duct obstruction: Complete and partial ejaculatory duct obstruction has been implicated as a cause of 1-5% of patients with male infertility. Patients may have a normal palpable vas deferens bilaterally but show decreased ejaculate volume and hemospermia and may experience pain upon ejaculation. Etiologies include cysts (midline and eccentric), ductal calcification and stones, postinfectious, and postoperative. Transrectal ultrasonography (TRUS) may reveal enlarged seminal vesicles, but this is not universal. Seminal vesicle aspiration revealing numerous sperm or a dynamic test such as injection of indigo carmine into the seminal vesicle or ejaculatory duct may be necessary for diagnosis.
  • Anejaculation/retrograde ejaculation may be due to an open bladder neck or a lack of rhythmic contractions during ejaculation. Etiologies include diabetic neuropathy, bladder neck surgery, RPLND, transurethral prostatectomy, colon or rectal surgery, multiple sclerosis, spinal cord injury, or the use of medicines such as alpha-antagonists. Diagnosis is suggested by history, a low ejaculate volume, and the observance of 10-15 sperm per high-power field (HPF) in the postejaculatory urine.

Physical Symptoms of Male Infertility

For men, the most typical symptom of male infertility that may signal an underlying fertility problem is six months of unprotected intercourse without successful conception. Unlike many cases of female infertility, most men do not show any physical symptoms of infertility problems, but continue to have trouble getting pregnant with their partner. Nonetheless, there are some infertility symptoms that may be experienced along with difficulty getting pregnant as a result of a specific, underlying cause of infertility.

Risk Factors

A number of risk factors are linked to male infertility. They include:

  • Age. Men older than 35 may have a gradual decline in fertility.
  • Tobacco smoking. Fertility may improve when you quit smoking.
  • Alcohol use. Heavy alcohol use can lower testosterone levels, cause erectile dysfunction and decrease sperm production.
  • Being overweight — or too thin. Being at an unhealthy weight can reduce sperm count.
  • Celiac disease. A digestive disorder caused by a sensitivity to gluten, untreated celiac disease can cause male infertility. Fertility may improve after adopting a gluten-free diet.
  • Prostate infections. Past prostate or other genital infections such as mumps or a sexually transmitted disease can affect fertility.
  • Exposure to toxins. Examples include heavy metals, industrial chemicals and radioactivity.
  • Exposure to certain drugs and medications. Examples include cancer medications and anabolic steroids.
  • High temperatures. Exposing the testicles to high temperatures — such as a hot tub or sauna — can temporarily reduce fertility.
  • Previous vasectomy. Some men who’ve had a vasectomy reversed remain infertile.


Many types of male infertility aren’t preventable. However, there are a few things that you can avoid that are known causes of male infertility:

  • Don’t have a vasectomy. If there’s any possibility you’ll want to father a child in the future, opt for other forms of birth control. Even if reversed, a vasectomy may still affect fertility.
  • Avoid illicit drugs. Use of anabolic steroids, marijuana and cocaine can impair sperm production.
  • Don’t drink too much alcohol. Heavy drinking can impair fertility and sexual function. Drink no more than two drinks a day.
  • If you smoke tobacco, quit. Smoking is linked to impaired fertility.
  • Avoid exposure to heat. Steer clear of extended or regular use of hot tubs, saunas and steam baths. High temperatures are thought to temporarily impair sperm production.

Tests and Diagnosis

If you and your partner are unable to become pregnant within a reasonable time, see your doctor. Some infertile couples have more than one cause of their infertility. Your doctor will usually begin a comprehensive infertility examination on both you and your partner.

In some cases, the cause of your infertility may be unclear, or it may take a number of tests to determine the cause. Infertility tests can be expensive and may not be covered by insurance — find out what your medical plan covers ahead of time.

For a man to be fertile, the testicles must produce enough healthy sperm, and the sperm must be ejaculated effectively into the woman’s vagina. Tests for male infertility attempt to determine whether any of these processes are impaired.

General Physical Examination and Medical History

This includes examination of your genitals and questions about illnesses, disabilities and surgeries that could affect fertility. Your doctor will want to know what medications you take and your sexual habits. Your doctor may also ask about your sexual development as a boy and whether you’ve had any signs of low testosterone, such as decreased body or facial hair.

Semen Analysis

This is the most important test for the male partner. Semen is generally obtained by masturbating or by interrupting intercourse and ejaculating your semen into a clean container. A laboratory analyzes the physical characteristics of your semen, the number of sperm present and looks for any abnormalities in the shape and structure (morphology) and movement (motility) of the sperm. The lab will also check your semen for signs of problems, such as infections or blood. Often sperm counts fluctuate from one specimen to the next, so your doctor may want to evaluate a few different samples. If your sperm analysis is normal, your doctor will likely recommend thorough testing of your female partner before conducting further male infertility tests.

Depending on initial findings, your doctor may recommend additional, more specialized tests that can help identify the cause of your infertility. These can include:

Scrotal Ultrasound

Ultrasound, which uses high-frequency sound waves to produce images of structures within your body, can help your doctor look for evidence of a varicocele or obstruction of the epididymis.

Hormone Testing

Hormones produced by the pituitary and hypothalamus glands and the testicles play a key role in sexual development and sperm production. Your doctor may recommend a blood test to determine the level of testosterone and other male hormones that affect fertility. A number of infertility problems can be caused by an underlying condition that affects hormone levels.

Genetic Tests

These tests are used if your doctor suspects your fertility problems could be caused by an inherited sex chromosome abnormality. When sperm concentration is extremely low, genetic causes could be involved. A blood test can reveal whether there are subtle changes in the Y chromosome.

Testicular Biopsy

This test involves removing samples from the testicle with a needle. It may be used if your semen analysis shows no sperm at all. The results of the testicular biopsy will tell if sperm production is normal. If it is, your problem is likely caused by blockage or another problem with sperm transport.

Anti-Sperm Antibody Tests

These tests are used to check for immune cells (antibodies) that attack sperm and can affect their ability to function. You are especially likely to have anti-sperm antibodies if you’ve had vasectomy reversal.


In some cases, contrast dye is injected into each vas deferens to see whether they are blocked.

Specialized Sperm Function Tets

A number of different tests can be used to evaluate how well your sperm survive after ejaculation, how well they can penetrate the egg membrane, and whether there’s any problem attaching to the egg.


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