Our Treatments


Book : A to Z Infertility


A to Z Infertility : Hope for Infertile Couples

How to get Pregnant : Online Book for Infertile Couples


Dr. Papolu Rama Devi, MD
Dr. Rama’s Institute for Fertility, Hyderabad, India.

Contents of the Book

Read this Book online free


The optimal method for semen collection is masturbation.

Traditionally, the suggested optimal period for abstinence prior to giving a semen specimen for analysis has been 2-5 days. Recent literature suggests that this period is possibly 5-10days. Volume and count increase steadily with duration of abstinence, while other parameters, including motility, morphology (Kruger’s strict criteria) and hypo osmotic swelling test, do not alter significantly. Only sperm acrosin content decrease almost two fold after 5 days of abstinence. Even for asthenozoospermia men, an increase in progressive motility after 5 days has been reported. After recurrent analysis & data collected from various studies & sources it has been generalized that optimal period of abstinence be 3- 5 days for obtaining a viable pregnancy through assisted techniques.


There is an associated impairment of male reproductive functions in patients with human immune deficiency virus infection, particularly in those with more advanced stages of the disease. This might be due to a direct effect of the virus, an HIV related malignancy, opportunistic infections or toxic side effects of therapeutic agents for such infections. Advanced stages of the disease (AIDS related complex characterized by persistent lymphadenopathy and fever plus weight loss) are associated with a loss level of testosterone and lower testosterone/ estrogen ratio. The mechanism which causes these low androgen levels is controversial, since some patients show low gonadotropins while others are hypergonadotropic. Semen analysis shows only slight variation of sperm quality, mainly reduced sperm motility, which could be related to impairment of epididymal sperm maturation following testosterone reduction. Late stages of the disease are associated with testicular atrophy. HIV positive asymptomatic patients have no significant hormonal or semen abnormalities.

Studies are there, which show that these men can father children through the modified wash technique through IUI or IVF/ET /ICSI procedure wherein the risk of transmission of the infection to the spouse or the child is reduced.


Acrosin is released from the acrosome of spermatozoa as a consequence of the acrosome reaction. Acrosin is a serine proteinase enzyme associated with acrosome of the spermatozoon. It is present on the inner acrosomal membrane of spermatozoa in the form of the inactive pro-acrosin. Activation of pro-acrosin during the acrosome reaction is thought to ease the binding to and the penetration of the sperm through the zona pellucida. Suspicion about deficiency of acrosin should be raised if there is no sperm binding to the zona pellucida or if no fertilization is achieved with in vitro fertilization (IVF).


An irreversible event associated with the final phase of capacitation. The acrosome is a membrane bound organelle that develops from the Golgi apparatus during the spermatid phase of spermatogenesis. It covers the anterior 50-70% of the sperm head. The acrosome reaction involves fusion of the sperm plasma membrane with the outer acrosomal membrane, thereby releasing the acrosomal contents as vesicles and exposing the inner acrosomal membrane. It is an essential part of sperm zona binding. In vitro acrosomal reaction prevents fertilization. Testing of acrosomal reaction can possibly serve as a tool, providing additional information about the fertilizing capacity of a semen sample.


Laboratory assessment of this process is essential in the case of fertilization failure. As the human acrosomal cap is too small to be visualized directly with phase contrast microscopy, indirect methods have to be applied:

  1. Staining techniques (e.g. triple stain);
  2. Indirect immunofluorescence with monoclonal antibodies;
  3. Direct immunofluorescence with fluorescein labeled lectins (these reagents bind to acrosome associated antigens); and
  4. Electron microscopy

Acrosome reacted spermatozoa show either no acrosomal labeling or an equatorial band. The predictive value of measuring the acrosome reaction is not known. The development of a bioassay which correlates the fertilizing potential of a capacitated sperm population to the inducibility of the acrosome reaction by ionophore challenge (ARIC).


In males activin enhances spermatogenesis.A glycoprotein hormone which is produced in one heterodimer form, activin AB (βA and (βB), and in two homodimer forms, activin A(βA and βA) and activin B (βB and βB). It is secreted by the Leydig cells and possibly by Sertoli cells and stimulates follicle stimulating hormone (FSH) secretion.


The process when spermatozoa are bound to each other by antibodies. Normally the spermatozoa are motile, and only a few other cells and debris are seen. In the case of agglutination there is decreased motility and the involvement of other round cells and the amount of debris is minimal. Patterns of agglutination include head to head, tail to tail and head to tail agglutination. This is known to affect fertilization potential of the sperm. Many doctors recommend 1 gram of Vit C per day for infertile men particularly those diagnosed with sperm agglutination.


Clumping of usually dead spermatozoa, mixed with a substantial amount of other cells and debris. Small aggregates are found in almost every semen specimen, large clumps are abnormal.


With increasing age there is a significant decrease in sperm motility and increase in sperm density. Other parameters such as morphology, ejaculatory volume and zona free hamster penetration test show less impressive changes. Research shows that low sperm motility is affected by DNA fragmentation with increased age.

Semen of men of older age differs from younger men, probably because of significant longer periods of abstinence. Male age is a significant factor contributing to a decreased likelihood in intrauterine insemination treatment. In general, sexual activity decreases with age, possible due to age related decline in testosterone levels which goes along with progressively increasing gonadotropin levels. Erectile dysfunction is a major contributory factor: being 2% at age 40, and 50% at age 75. Estradiol, androstenedione and dehrdroepiandrosterone levels decrease significantly with age though men continue to produce sperm all their age. Aging does affect the quality of sperm. Therefore older men are most likely pass on any mutation in the genes to their progenies. There is a highly significant age related increase in structural chromosomal abnormalities in spermatozoa: from 2.8% at 20 to 13.6 % at 45 years and above. This is reflected in an increased risk for subsequent major birth defects, rising from 0.2/1000 below 30 to around 4/1000 above age 40. Most studies do not show any correlation between paternal age and down’s syndrome. The percentage of X or Y bearing sperm is not related to age.

The aging male syndrome is characterized by a number of symptoms like

Loss of libido
Decrease in the levels of male hormone testosterone, erectile dysfunction, and other physical symptoms like bone loss, hair loss, weight loss, memory problems musucle loss, low stamina and increased urination.


Early fetal testicular degeneration between 60 and 69 days after conception is associated with minimal Wolffian development, preserved Mullerian ducts and ambiguous external genitalia. Levels of luteinizing hormone (LH) and follicle stimulating hormone (FSH) are high. The chromosomal structure is 46 XY.


Alcohol (methanol, ethanol, propanol) inhibits the zinc-dependent conversion of vitamin A to bioactive retinol in the testis. Testicular biopsies in alcohol abusers show decreased maturation of the germinal epithelium. Alcohol inhibits testosterone synthesis directly, an action independent of the effect on the liver. In addition, the metabolic clearance rate of testosterone is increased. The hypothalamic-pituitary axis is impaired as well, since low testosterone is not associated with appropriate luteinzing hormone(LH) elevation. Literature generally reports no or moderate alterations in fertility in alcohol users, although postcoital tests show better results in non alcohol users.

Alcohol is bad for fertility. Too much of alcohol can affect the quality of sperm and it can damage the sex drive.

Mechanism of how alcohol impairs male fertility

  1. In large amount, alcohol becomes a toxic substance that would destroy healthy cells that would produce sperm cells. Atropy of men’s testicles can also be caused by too much alcohol. Most alcohol men usually have very low levels of sexual urge due to a disease known as gynaecomastia caused by alcohol in take.
  2. Medical tests have found that changes in the make up of the testicles can lower the T serum in the sperm thatcan lead to infertility.Alcohol consumptioncan effectively cause the structure of testicle to change, thereby lowering the T serum component of sperm resulting to infertility.
  3. Alcohol can effectively decrease the ability of sperm count. It can also mutilate the normal shapes and sizes of the sperm. Too much alcohol in the system would tend to make sperm have abnormal shapes and even without tails. This actually is the reason why many alcoholics cannot hope to have children because their sperm have been damaged by continuous alcohol intake
  4. Morphology is also highly affected .Either a man is fertile because he has good sperm morphology which would meanthe density is good & the sizes & forms of the sperms are normal.


A term used for all types of spermatozoa with bizarre forms or with multiple defects, not fitting in any of the main categories of abnormal morphology. Otherwise normal semen analysis may include amorphous spermatozoa.


Androgen-binding protein (ABP) is a glycoprotein (beta-globulin) produced by the Sertoli cells in the seminiferous tubules of the testis that binds specifically to testosterone (T), dihydrotestosterone (DHT), and 17-beta-estradiol.

By binding to T and DHT these hormones are made less lipophilic and become concentrated within the luminal fluid of the seminiferous tubules. The higher levels of these hormones enable spermatogenesis in the seminiferous tubules and sperm maturation in the epididymis.

ABP has the same amino acid sequence as sex hormone-binding globulin (SHBG); the difference is the site of production and the addition of different sugar moieties. ABP contains 403 amino acids resulting in a molecular weight of 44,533. Its gene is located on chromosome 17.

ABP’s production is regulated under influence of FSH on Sertoli cell, enhanced by insulin, retinol, and testosterone.Its presence enables the very high intratesticular androgen levels necessary for adequate spermatogenesis.

ABP has a strong similarity with testosterone estradiol binding globulin (TEBG); differences are mainly found in the carbohydrate content.


Now used to denote failure of any of the mechanisms involved in the response of target cells to androgens. Since androgens are essential for normal male sexual development, failure of this mechanism to occur will result in anomalous male differentiation. Patients affected with the androgen insensitivity syndrome can present from one extreme side of the spectrum as a phenotypical female to the other end presenting as mildly undervirilized but potentially fertile male. Originally, only one end of the spectrum was described, the testicular feminization syndrome: a form of congenital insensitivity to androgen, caused by an X-linked recessive disorder resulting in 46 XY males with female phenotype, lacking both developed Wolffian and Mullerian ducts. The diagnostic criterion for all forms is the finding of elevated luteinzing hormone and testosterone concentration in the absence of virilization.

The following categories can be distinguished in individuals with androgen insensitivity:

  1. Absence of androgen receptor binding;
  2. Reduced androgen receptor binding;
  3. Normal binding to abnormal androgen receptor; and
  4. Normal androgen receptor binding but abnormal postreceptor mechanisms.

The phenotypical expression of the syndrome is variable and cannot be related to the type of abnormality in the receptor. This suggests that genetic determinants other than the coding sequence of the androgen receptor will alter the phenotype.

Variations produced by androgen insensitivity

Although many distinct mutations have been discovered, the spectrum of clinical manifestations has been divided into six phenotypes, which roughly correspond to increasing amounts of androgen effect due to increasing tissue responsiveness. It should be emphasized that some affected persons will have features that fall between the phenotypes described.

1. Complete AIS (CAIS): completely female body except no uterus, fallopian tubes or ovaries; testes in the abdomen; minimal androgenic(pubic or axillary) hair at puberty.
2. Partial or incomplete AIS (PAIS): male or female body, with slightly virilized genitalia or micropenis; testes in the abdomen; sparse to normal androgenic hair.
3. Reifenstein syndrome: obviously ambiguous genitalia; small testes may be in abdomen or scrotum; sparse to normal androgenic hair; gynecomastia at puberty.
4. Infertile male syndrome: normal male genitalia internally and externally; normal male body or possible female androgyny, normal virilization and androgenic hair; reduced sperm production; reduced fertility or infertility.
5. Undervirilized fertile male syndrome: male internal and external genitalia with micropenis; testes in scrotum; normal androgenic hair; sperm count and fertility normal or reduced.
6. X-linked spinal and bulbar muscular atrophy: normal or nearly normal male body and fertility; exaggerated adolescent gynecomastia; adult onset degenerative muscle disease.


Testosterone has many biological effects in the male. The action of testosterone can be exerted in different ways .

  1. Passive diffusion into a tissue and binding to androgen receptor.
  2. Passive diffusion into a tissue, conversion to dihydrotestosterone and binding to androgen recerptor
  3. Passive diffusion into a tissue, aromatization to estradiol and binding to estrogen receptor.

Effect in tissue independent of androgen or estrogen receptor.

The action of testosterone


Stimulation of body growth, nitrogen retention, muscular development.

Maturation of secondary sexual characteristics

Accessory sexual organs (penis, aprostate, scrotum, seminal vesicle) growth of larynx and vocal cords male hair growth


Facilitates libido and potency

Protein synthesis (stimulation or suppression)

Liver, kidney, salivary gland


Interaction with FSH on Sertoli cell, stimulation of spermatogenesis


Stimulation of erythropoietin


Prevention of bone loss


Assertive, aggressive


The primary indication is as substitution for sexual dysfunction in hypo-androgenic states, not for treatment of infertility. It has no role in patients with secondary hypogonadism, where fertility is usually achieved by gonadotropin releasing hormone (GnRH) or human menopausal gonadotropin/human chorinic gonadotropin (hMG/hCG). There is no evidence that low dose androgen therapy is effective in idiopathic oligoasthenospermia. Like wise high dose testosterone rebound therapy is no longer being used for the same reason. In addition, a small number of patients treated with high dose androgens have persistently decreased sperm density secondary to the treatment and even cases of permanent azoospermia have been reported.


Anejaculation, as its name implies, is a condition characterized by the absence of ejaculation. The causes can be psychological and physical. Psychological anejaculation is usually anorgasmic i.e. unaccompanied by orgasm. This again, can be situational or total. Situational anejaculation means that a man can ejaculate in some situations but not in others. For instance, a man may be able to ejaculate and attain orgasm with one partner but not with another. This usually occurs when there is a psychological conflict or a relationship difficulty with one partner. Or he may be able to ejaculate quite normally during masturbation but not during intercourse. It can also occur in stressful situations, as when a man is asked to collect a sample of semen in the laboratory for infertility treatment. In total anejaculation, the man is never able to ejaculate when awake. Deep-rooted psychological conflicts are usually the cause. Such men, however, usually have normal nocturnal (night) sleep emissions.

Physical (organic) anejaculation, which includes retrograde ejaculation (vide supra), can occur due to neurogenic and obstructive causes. Many of the neurogenic causes are similar to those outlined earlier.Failure to obtain ejaculation that is forceful expulsion of the semen from the posterior urethra. Anejaculation can occur as a result of spinal cord injury, retroperitoneal surgery, diabetes mellitus or multiple sclerosis. Treatment nowadays consists of rectal probe electro-ejaculation or penile vibratory stimulation.


Absence of one of both testes. Late fetal testicular regression after 140 days postconception is associated with male phenotype, but no testes are present. Often called the vanishing testis syndrome. Levels of luteinzing hormone and follicle stimulating hormone are high. The chromosomal sex is 46 XY.


The impact of the effects of antibiotics on infertility is perhaps greater than generally assumed. It is well documented that antibiotics like nitrofurantoin and gentamycin can lead to spermatogenic arrest at the spermatocyte level. Although the use of antibiotics has increased greatly in the last decades, direct measurement of the effects on male fertility has many confounding factors. The potentially negative effects of antibiotics on human fertility can be categorized .

For the antibiotics as categorized below, so far only animal data are suggestive for possible negative effects on spermatogenesis and /or semen parameters.

The potential negative effects of antibiotics on male fertility


Effects in human



Reversible reduction of sperm count spermatogenic arrest at primary spermatocyte level



Impaired count and motility



Cessation of meiosis at primary seprmatocyte level



Impaired count, motility



Strong negative effect on motility



Impaired count, motility and morphology


Co- Trimoxazole

Impaired count, motility and morphology


The potential negative effects of antibiotics on spermatogenesis and sperm parameters


Animal data

Class / comment


Spermatogenic arrest



Decreased motility



Decreased motility


Penicillin G

Spermatogenic arrest



Decreased fertilizing capacity



Decreased motility



Decreased motility

Inhibit DNA gyrase –so far, no adverse effects reported

The use of antibiotics in men with an infertility problem, or even without such, should be balanced against the possible negative effects on semen quality of a specific antibiotic. The use of tetracycline with its strong effect on sperm motility, for example, seems to be only justified after thorough evaluation.


Antioxidants are substances that may protect your cells against the effects of free radicals. Free radicals are molecules produced when your body breaks down food, or by environmental exposures like tobacco smoke and radiation. Free radicals can damage cells, and may play a role in diseases, cancer etc..
Antioxidant substances include

  • Beta-carotene
  • Lutein
  • Lycopene
  • Selenium
  • Vitamin A
  • Vitamin C
  • Vitamin E

Antioxidants are found in many foods. These include fruits and vegetables, nuts, grains, and some meats, poultry and fish.

Oxygen radicals are involved in the initiation of peroxidative damage to the sperm plasma membrane. On the other hand, superoxide anions and hydrogen peroxide also participate in the induction of biological key events such as hyperactivated motility and acrosome reaction. Thus human spermatozoa appear to use reactive oxygen species for different physiological purposes. Anti oxidants like vitamin C, vitamin E, tourine, hypotaurine and glutathione can possibly protect against negative effects on sperm quality and against oxidative DNA damage, especially under circumstances of oxidative stress such as is the case in laboratory handling of semen samples with poor quality spermatozoa or leukocytes. The negative effects of smoking may also be attributed to oxidative stress, especially in heavy smokers or alcohol consumers etc.


Antisperm antibodies are one immune factor which could be involved in infertility. Antisperm antibodies are cells that fight against normal, healthy sperm. If one has antisperm antibodies, instead of seeing sperm as natural cells, our immune system fights against the sperm and destroys them. This prevents from producing any viable sperm. Though still to be proven, there is evidence that antibodies against sperm can result in male infertility.

Antisperm antibodies can really impair the function of healthy sperm. These antibodies attach to sperm, reducing motility and making it more difficult for sperm to pass through cervical mucus. Antisperm antibodies can also force sperm to clump together, making it difficult for the sperm to fertilize an egg.

It is not entirely known why antisperm antibodies develop in some people. Typically, sperm are protected from our immune system by a protective lining, called the blood-testes barrier. This barrier prevents cells from your immune system from getting mixed in with the sperm and killing them. Sometimes, surgery or injury can interfere with this barrier, allowing immune cells to come into contact with sperm cells.

Antisperm antibodies are actually thought to be relatively common in a certain subset of men. While only 1% of fertile men have these antibodies in their blood stream, up to 10% of infertile men have them. Men who have undergone reproductive surgery also seem to have antisperm antibodies; up to 70% of men who have had a vasectomy reversal have antisperm antibodies.

Sometimes, women can develop antisperm antibodies. About 5% of women with unexplained infertility have these antibodies in their blood stream. As a result, sperm are killed before they have chance to fertilize the egg.

Any man can potentially develop antisperm antibodies, as can any woman, so couples facing infertility should be tested for the antibodies. However, certain people are more at risk of developing these antibodies. Men who have experienced the following are at increased risk for developing antisperm antibodies:

  • vasectomy reversal
  • testicular cancer
  • testicular biopsy
  • varicocele
  • testicular torsion
  • infections

These factors increase risk for having blood-testes barrier compromised, which can lead to the growth of antisperm antibodies.

Testing for Antisperm Antibodies
There are a variety of tests that can detect the presence of antisperm antibodies in the body:

Blood Tests: In women, blood tests are commonly used to detect the antibody.

Post-Coital Test: The post-coital test can detect the presence of antisperm antibodies in a woman’s cervical mucus.

SpermTesting: In men, sperm testing is the best way to analyze for antisperm antibodies. The immunobead assay and the mixed agglutination reaction test are both used.

Treating Antisperm Antibodies
There are a variety of treatments available to help couples struggling with antisperm antibodies to conceive. Treatment should only be considered for patients in whom more than 50% of spermatozoa are agglutinated by antibodies, since postcoital tests in patients with lower number of agglutinated spermatozoa are normal.

Intrauterine Insemination(IUI): IUI can help couples to overcome antisperm antibodies as it allows sperm to bypass the cervical mucus. Fertility drugs can also be used.

In-Vitro Fertilization(IVF): IVF is the most successful treatment for couples with antisperm antibodies. This allows the sperm to be directly injected into the egg, without having to travel through the uterus and fallopian tubes.

Condom therapy has not been shown to decrease antisperm antibody titers or increase the pregnancy rates.

Sperm washing: rapid repeated washing of the ejaculate may remove free antibodies in seminal plasma but not those bound to the sperm surface. Variable success rates are reported.

Some attempts have been made to separate the antibody-free spermatozoa employing Sephadex. On the other hand, literature reports the use of protease addition to the culture medium in an attempt to disagglutinate the spermatozoa.


  1. Corticosteroids: Corticosteroids help to decrease the production of antisperm antibodies. Unfortunately, corticosteroids are associated with side effects, including hipbone damage
  2. Cyclosporin: only a limited number of reports are available; none are placebo controlled.


Aspermia is the complete lack of semen (not to be confused with azoospermia, the lack of sperm cells in the semen). Naturally, it is associated with infertility.

One of the causes of aspermia is retrograde ejaculation, which can be brought on by excessive drug use, or as a result of prostate surgery.Absence of seminal fluid after ejaculation.


Assisted reproduction means any medical technique interfering with one or more of the mechanisms or barriers that have to be completed before successful fertilization can occur . It refers to a number of advanced techniques that aid fertilization. These techniques are often used for women who have irreversible damage to their fallopian tubes or cervical mucous problems. It can also benefit couples with unexplained infertility & also incases of male factor infertility.

Identification of a male factor in infertility patients and identifying those for assisted reproduction is handicapped by the lack of uniformity in criteria used. Unlike the clinical male factor which uses pregnancy as a measurable end point ,the end point for male factor in assisted reproduction is usually the fertilization rate. Depending on the basic semen parameters, the results of sperm function tests and semen preparation, it has to be decided if (and if so which form of) assisted reproductive technique should be applied in case of male factor infertility. Although in particular the successful

Bypass cervical mucusYesYesYesYesYes
Selection of sperm on motility and morphologySperm preparationYesYesYesYesYesyesyesyes
Increase number of mature oocytesOvarian hyper- stimulationYes/noYesYesYesYes
Timing of ovulationhCGYes/noYesYesYesYes
Bypass cervical mucusYesYesYesYesYes
Bypass pick up mechanismcollection of oocytesNoNoYesYesYes
Bypass tubal passage spermNoYesYesYesYes
Bypass acrosomal reactionNoNoNoNoNoNoNoYes
Bypass zona bindingNoNoNoNoNoNoYesYes
Bypass zona penetrationNoNoNoNoNoNoYesYes
Bypass fusion with oolemmaNoNoNoNoNoNoNoYes
Selection of oocytes on fertilizationNoNoNoYesNo
Selection of embryos on qualityNoNoNoNoYes
Bypass tubal passage fertilized oocyteNoNoNoNoYes

IUI=intrauterine insemination, DIPI= direct intra aperitoneal insemination,
GIFT= gamete intrafallopian transfer, ZIFT= zygote inrafallopian transfer,
IVF-ET=In vitro fertrilization/embryo transfer, ZD-PZD=zona drilling-partial zona dissection, SUZI= subzonal insemination, ICSI= intracystoplasmic sperm injection

Introduction of intracytoplasmic sperm injection (ICSI) has brought about major changes in the treatment strategies for men with poor semen quality, as a general guideline the following is still valid:


  • Intrauterine insemination needs a minimum of at least 1.5 million motile spermatozoa after preparation.
  • In vitro Fertilization [IVF] requires about 50,000 motile sperm per inseminated oocyte.
  • Indications for ICSI are not clearly defined yet. Usually repeated fertilization failure in previous IVF, sperm parameters that primarily do not meet criteria for IVF or results of sperm function tests indicating that acrosome reaction, zona binding or zona penetration potential are severely impaired are considered to be valid indications for ICSI


What Is IVF (In-Vitro Fertilization)?

IVF is the most well known of assisted reproduction techniques. In this method, the woman takes fertility drugs to stimulate her ovaries to produce more eggs. The physician then retrieves one or more of the eggs by laparoscopy or by passing a needle through the vaginal wall. The partner’s sperm is then mixed with the eggs in a petri dish, and fertilization may take place.

If fertilization occurs, the embryo is allowed to develop outside the womb for a few days. Then it is implanted in the lining of the woman’s uterus with a small plastic tube. Most centers now place two to four embryos in the womb in the hope that one will burrow into the lining and begin to develop normally. Any leftover embryos are frozen to be used later, should the first IVF procedure fail to work. IVF increases the risk of multiple births.

Women with the highest success rate (43%) are ages 20-29 years and have atleast two embryos transferred.
In a variation of IVF called ovum transfer, a donor egg is fertilized with the partner’s sperm and then placed in the woman’s uterus. This technique is often used when the woman has not been able to produce eggs, even with fertility drugs.
The effectiveness of IVF has improved in the past few years but the chance of pregnancy is still only 20 to 40 percent even in the best reproductive centers.

Gamete Intrafallopian Tube Transfer
In this method of assisted reproduction, the woman’s eggs are retrieved but not fertilized. Instead, they are mixed with the man’s sperm and immediately placed into the woman’s fallopian tubes. The woman must have healthy tubes for GIFT to work.

Zygote Intrafallopian Transfer
ZIFT involves placing the fertilized egg itself into the fallopian tubes. This procedure can be more successful than GIFT because the doctor has a greater chance of ensuring that the egg is fertilized. Again, the woman must have healthy tubes for ZIFT.

Intracytoplasmic Sperm Insertion
In this technique, a single sperm is injected into the egg, and the embryo is placed in the fallopian tubes or uterus. This method is often recommended when the male partner has very few sperm or other fertilization methods are not suitable for the couple.

Follicle Aspiration, Sperm Injection, and Assisted Follicular Rupture
In a new method known as FASIAR, the physician punctures the follicle, and then removes the eggs with a syringe that also holds the sperm. This mixture is then immediately injected back into the follicle. FASIAR may reduce the risk of multiple births and is less expensive than other procedures.


Asthenozoospermia` (or `asthenospermia`) is the medical term for reduced sperm motility. It decreases the sperm quality and is therefore one of the major causes of infertility or reduced fertility in men. A condition in males in which large quantities of sperm in an ejaculation are of weakened motility. Because of the low quality sperm, the condition is a common cause of male infertility.

Less than 50% of sperm are progressively motile [World Health Organization). All other semen parameters are normal. As a single abnormality isolated asthenozoospermia has a frequency of 20%. Etiology includes the factors shown in Table

The etiology of Asthenozoospermia




Abnormalities before spermiation including chromosomal aberrations


Structural abnormalities of tail, mix-piece or head [Khartagener’s , short –tail syndrome]


Pathological circumstances; varicocele, infections, toxins, hematospermia, contamination with urine, immobilizing antibodies


Inadequate collection, long interval between ejaculation and examination, or inadequate handling in the laboratory


Azoospermia is the medical condition of a male not having any measurable level of sperm in his semen. It is associated with very low levels of fertility.
Azoospermia has two forms:

  • obstructive azoospermia, where sperm are created, but cannot be mixed with the rest of the ejaculatory fluid due to a physical obstruction, and;
  • non-obstructive azoospermia, where there is a problem with spermatogenesis, as in the condition of hyperprolactinemia.

Azoospermia is a reported side effect of androgen drugs and corticosteroids because they suppress the hypothalamus release of GnRH and therefore FSH. This causes azoospermia in males and amenorrhea in females.
Azoospermia can be congenital, where it can be a manifestation of cystic fibrosis due to agenesis of the vas deferens, among other genetic conditions.
Absence of spermatozoa in the seminal fluid. Etiologically, the following categories can be distinguished.

The Etiology of azoospermia


Disorders of hypothalamic pituitary axis

Gonadotropin deficiency syndromes[e.g.Kallmanns prolactinoma
Androgen insensitivity syndromes
Congenital adrenal hyperplasia


Impaired spermatogenesis

Genetic :XXY, trisomy 21, translocation
Development :cryptorchidism,
Anarchism, germ cell aplasia,
Sertoli cell – only
Environment : heat, drugs, radiation
Post –mumps


Abnormalities epididymis and ejaculatory ducts sexual dysfunction

Congenital :absence vas deferens stenosis
Post-infectious obstruction
Post-surgical obstruction
Retrograde ejaculation

AZOOSPERMIA FACTOR [AZF] This is a gene controlling spermatonesis. It is located within interval 6 of the human Y chromosome’s long arm. Low of the most distal part is associated with severe spermatogenic impairment. The testis shows absent or severely reduced germ cell development.

    Reach us

    Follow us