|
|
|
|
A man’s role in conception is considered to be relatively simple and straightforward, but in fact his reproductive physiology is quite complicated. It involves secretion of testosterone, communication between the pituitary gland and testes, and a highly involved process of sperm production, maturation and delivery. Disruption of this process results in nearly 7.5% to 10% of all men in the reproductive age being infertile. The manufacturing and delivery systems must function properly in order to produce large quantities of healthy sperm, which is the basis of effective conception. Therefore, when a couple is having trouble conceiving it makes sense to not only evaluate the female partner but also the male. Male infertility has been found to be the major cause of a couple’s inability to conceive in 50% of childless couples.
How is Male Infertility Defined?
Male factor infertility is defined as an abnormality in sperm production, function or delivery that impedes a couple from establishing a pregnancy.
Causes of Male Infertility
There are many causes of male infertility including: 42% varicocele, 14% obstructions, 23% idiopathic and 21% other including chromosome abnormalities, infections, undescended testes, systemic illnesses, environmental causes, social habits and sexual dysfunction.
Physical Causes
Varicocele: The most common identifiable cause of infertility in men is varicocele. Varicoceles have been recognized as a clinical problem since the 16th century. Ambrose Pare (1500-1590), the most celebrated surgeon of the Renaissance, described this vascular abnormality as containing “melancholic blood.” It was not until the late 19th century that the relationship between infertility and varicocele was first proposed by the British surgeon Barfield. Shortly thereafter, other surgeons reported an association with an “arrest of sperm secretion” and subsequent restoration of fertility following varicocele repair. Through the early 1900s reports by other surgeons continued to describe the association of infertility with varicocele. It was not until the 1950s, after a report of fertility following varicocele repair in an individual known to be azoospermic (i.e., without any sperm), however, that the concept gained support as a clinical entity among American surgeons. Research then continued with studies characterizing semen of men with varicoceles as having varying degrees of impaired sperm quality. From these studies, a pattern of low sperm count, poor motility and a predominance of abnormal sperm forms was documented. This became known as the “stress pattern” of semen.
Although not synonymous or specific for varicocele, it consistently suggests early evidence of testicular damage.
Varicocele is a condition of enlarged veins in the scrotum that interferes with temperature regulation of the testes. Several theories have been proposed to explain the deleterious effect of the varicocele on sperm quality. These include possible effects of pressure oxygen deprivation, heat injury or toxins. Despite considerable research, none of these theories have been unquestionably proven, although an elevated heat effect caused by impaired circulation appears to be the most reproducible defect. The fact that creation of a varicocele in the experimental animal can lead to poor sperm function with elevated intratesticular temperature does give support to this concept. Regardless of the mechanism of action, varicocele indisputably is a significant factor in decreasing testicular function and changing the semen quality in a large percentage of men seen for infertility. Furthermore, improvement in semen quality after varicocele correction has been repeatedly demonstrated. The resultant improvement in semen quality occurs in 50 to 70% of patients, with the most improvement seen in sperm motility rather than in sperm count. The pregnancy rate ranges from 30 to 60%, with the average pregnancy occurring 6-9 months following surgery (this is, of course, dependent on the age of the female partner and fertility factors which she may have.) Varicoceles are more common on the left than on the right for multiple anatomic reasons. They may vary in size and can be classified into 3 groups:
i) Large- easily identified by visual inspection alone
ii) Moderate- identified by palpation without bearing down
iii) Small- identified only by bearing down which increases intra-abdominal pressure, further impeding drainage and thus increasing the size of the varicocele.
It is important to remember, however, that the size of the varicocele is not related to the degree of changes in the sperm.
Obstructive azoospermia: The second major cause of infertility in men is blockages or obstructions of the male reproductive tract, meaning sperm does not reach the ejaculate, but is still being produced by the testes. This is particularly true for men with zero sperm count: azoospermia. Obstructive causes for azoospermia include:
Congenital absence of the vas deferens (CAVD): Approximately 1% of all infertile men are born with the congenital absence of the vas deferens.
Vasectomy: According to the ASRM, vasectomy has been used for family planning purposes since the 1940’s. Each year, approximately 500,000 vasectomies are performed in the US. Approximately 1 to 3 per 1,000 vasectomized men will request a reversal.
Non-obstructive azoospermia: This is an absence of sperm in the ejaculate due to a production problem, meaning they sperm are not being made. Disorders include:
Klinefelter’s Syndrome: Klinefelter’s syndrome is a genetic disorder caused by the presence of an extra X chromosome. These men usually mature late sexually and have small, firm testes and relatively low testosterone levels.
Idiopathic azoospermia
We can easily determine which of these groups an infertile male is in by performing a testicular biopsy using a microscope to minimize discomfort and complications.
Infections: The male reproductive system can be subject to acute and chronic infections. Acute infections may include: Smallpox, mumps, epididymitis (infection of the epididymis can cause scarring and blockage, inhibiting the sperm from leaving the duct), sexually transmitted diseases (chlamydia and gonorrhea), and other viral infections. Chronic infections may include: TB, leprosy, and prostatitis.
Undescended testes (cryptorchidism)
Previous surgery for inguinal hernia, scrotal, retroperitoneal, or bladder neck surgery.
Systemic illnesses especially hepatic or renal.
Environmental Causes
Injury: Examples of direct injury include: testicular or pelvic trauma, heat, or irradiation. Indirect injury may be caused by a variety of factors including the following:
Cigarette Smoking has been shown to significantly affect semen quality. Regular smoking causes a 23% decrease in sperm density (concentration) and 13% decrease in motility (when averages are taken from nine separate studies). To a lesser extent, smoking causes an increased number of morphologically abnormal sperm and toxicity to the seminal plasma (evidenced by sperm from non-smokers exhibiting significantly decreased viability when placed in the seminal plasma of smokers). Other systems affected by smoking include the hypothalamic-pituitary-gonadotropin (HPG) axis, which regulates levels of estradiol and estrone as well as the Leydig Cells of the testes, which produce testosterone and may exhibit secretory dysfunction.
Recreational Drugs: Marijuana (cannabinoid) often causes a decrease in average sperm count, motility, and normal morphology, and can affect the HPG axis,(causing decreased plasma testosterone) as well as have a direct negative effect on the Leydig Cells. Cocaine (even infrequent cocaine use) causes decreased sperm counts, motility and normal morphology. These effects can be found in men who have used cocaine in the two years preceding their initial semen analysis. There is a decreased ability of sperm to penetrate cervical mucous.
Anabolic Steroids: The use of anabolic androgenic steroids is now at almost epidemic proportions (6.6% of 12th grade males use or have used them to build muscle mass and improve athletic performance). These exogenous androgens depress testicular production of testosterone which in turn decreases intra-testicular testosterone levels and may cause severely diminished spermatogenesis or complete azoospermia. Anabolic steroids cause a persistent depression of the hypothalamus and pituitary. This may be irreversible even when the steroids are stopped.
Alcohol: Moderate alcohol use does not affect male fertility but can create problems if it becomes excessive. It then affects the HPG(hypothalamus-pituitary- gonadal) axis and is a direct gonadotoxin. In addition, excess alcohol consumption may cause associated liver dysfunction and nutritional deficiencies which are also detrimental to sperm production.
Lubricants: Most vaginal lubricants, including K-Y Jelly, Surgilube, and Lubifax are toxic to sperm and should be avoided during the fertile time of a woman's cycle. Mineral oil in small amounts has been shown to be an acceptable alternative. There are also many non-spermatotoxic lubricants available over the counter.
Hot baths and saunas: These should be avoided, as they increase the core temperature of the testes (hot showers are not a problem). This elevated temperature is known to have a negative effect on sperm production, semen quality, and fertility.
Underwear: A recent article in The Journal of Urology showed that there was no difference in either the semen analysis or the core testicular temperature between groups of men who wear boxers or briefs.
Exercise: While moderate exercise can only be helpful, it becomes problematic if it becomes excessive. As an example, long distance runners (men who run greater than 100 miles per week) may experience decreased spermatogenesis. These activities should be moderated when a sub-fertile man is attempting conception.
Anatomy and Physiology
In order to understand male infertility one must be aware of some basic anatomy and physiology. The human male reproductive system includes the hypothalamic-pituitary-testis axis in addition to the epididymis, vas deferens, seminal vesicles, prostate and urethra. Sperm production requires approximately 3 months from the beginning of mitotic divisions occurring in the complex process leading up to the formation of mature sperm for ejaculation and fertilization. This is affected by the environment within the testis. The hormonal setting of the testis must be appropriate for the testis to produce mature sperm and transport these male gametes (sperm) to the ejaculatory duct. This hormonal setting originates in the hypothalamus, which releases GnRH (gonadotropin-releasing hormone) in a pulsatile manner. This results in secretion of LH (luteinizing hormone), which travels to the pituitary via the venous portal network. FSH (follicle stimulating hormone) is also secreted as a result of GnRH pulses, but is influenced by Sertoli cells within the testis. Within the testis, LH stimulates the Leydig cell production of testosterone, which in turn stimulates spermatogenesis. Sperm assume their final shape and size in the testis, and then acquire the ability to fertilize and become motile in the epididymis. The testicles are the paired male genital organs that contain not only sperm but also cells that produce and nourish the sperm. These organs are located in a sac called the scrotum. The epididymis is a small, tubular structure attached to the testicles where sperm are stored. The vas deferens connects the epididymis to the prostate gland and is the tube through which sperm travel during ejaculation. The vas deferens is not situated by itself, but is part of a larger tissue bundle called the spermatic cord. The spermatic cord contains many blood vessels as well as the vas deferens, nerves and lymphatic channels. The veins of the spermatic cord are known as the pampiniform plexus. These veins drain blood from the testes, epididymis and the vas deferens, eventually becoming the spermatic veins that drain into the main circulation at the level of the kidneys.
|
|
|
|
