Polycystic Ovarian Disease (PCOS)

The Basics Polycystic ovarian syndrome (PCOS) is an extremely common endocrine disorder. Despite the lack of specific population-based studies, the prevalence of PCOS is conservatively estimated to occur in 5-10% of reproductive-aged women and has been recognized since at least the 1930's. While a clinical diagnosis of PCOS may encompass several distinct subsets of patients, most experts in the field agree that there are some common clinical and laboratory aspects of this prevalent disorder. Most women with PCOS have ovulatory dysfunction or absent ovulation. If the egg is not released from the ovary each month in a normal fashion, this can obviously lead to infertility. Anovulation may also manifest itself by infrequent or irregular menstrual cycles. In the absence of ovulation, the ovary does not make the hormone progesterone in the second half of the menstrual cycle. Without progesterone, the lining of the uterus is not shed in an efficient and timely manner. After a number of years, this can place women with PCOS at risk for an abnormal buildup of the lining of the uterus (endometrial hyperplasia) or even cancer. For this reason, women with PCOS who are not trying to get pregnant should be treated with progesterone-like medications to induce a normal menstrual period at least every 2-3 months. Another common feature to PCOS is clinical or laboratory hyperandrogenism. This means that women with PCOS have either increased circulating amounts of or increased responsiveness to "male" hormones like testosterone or DHEAS. This may result in oily skin or acne and excess hair on the face, between the breasts, or on the lower abdomen. In order for the diagnosis of PCOS to be made, these abnormalities must exist in the absence of other related hormonal disorders. A qualified doctor can distinguish these disorders. Most women with PCOS also display changes in the ovaries as viewed by ultrasound. In fact, the name itself describes the typical ultrasound findings seen in this disorder: poly (many), cystic (small collections of fluid). When the eggs in the ovaries do not develop to maturity, many small "follicles" (small fluid-filled sacs containing immature eggs) develop and can be seen on ultrasound. The ovaries of women PCOS are often enlarged as well. However, most women with PCOS do not have the kind of "cysts on the ovary" that we normally think of as problematic or requiring surgery. Another common feature of PCOS is increased body weight. Women with PCOS tend to be heavy and have trouble losing weight. One underlying mechanism behind the ovulatory irregularity and the increase in body weight is probably insulin resistance. This means that the cells of women with PCOS do not respond as well to their bodies' own insulin as those of someone without PCOS. This puts women with PCOS at higher risk for developing diabetes during pregnancy or later in life. Treatment Strategies Treatment for PCOS depends largely on an individual woman's fertility desires. For those women not desiring immediate pregnancy, there are basically two options to help regulate menstrual cyclicity and prevent endometrial hyperplasia. The most common option is the use of oral contraceptives (birth control pills; BCPs). BCPs will give most women normal bleeding patterns and prevent hyperplasia. Since ovulation can occur unpredictably in women with PCOS, BCPs also provide adequate contraception. The hormones in BCPs will also help reduce acne and facial hair in most patients with PCOS. In women who do not require oral contraception, progesterone given for 10-12 days every 30-60 days will induce a reliable menses. In women for whom unwanted hair growth is particularly bothersome, significant improvement can be obtained with a combination of medications. As already mentioned, BCPs are extremely useful in this regard. Other medications may include drugs that reduce the secretion of androgen hormones or interfere with their action in the skin and hair cells. Alternatively, for women with PCOS who desire pregnancy, ovulation induction is often necessary. This involves medical treatment in order to help the ovaries release an egg each month in a reliable fashion. For many women this involves simple and relatively inexpensive oral medication. Others may require more intensive and expensive therapies utilizing injectable medications. Finally, there are some new therapeutic options available for women with PCOS. As already mentioned, insulin resistance may represent the underlying problem for a lot of PCOS patients. A relatively new class of drugs that help sensitize the cells to the action of insulin, thereby reducing insulin resistance, has recently been shown to help induce ovulation in women with PCOS who failed previous simple therapies. Certain of these agents may also help women with PCOS to lose weight. Some of the more common drugs that increase insulin sensitivity are Metformin (GlucophageÒ) and Troglitazone (RezulinÒ). Because these agents can have serious side effects, they should be taken only under the careful supervision of an experienced physician. Troglitazone can cause hepatic damage. Patients taking this medication must have blood work every month. Patients taking Metformin typically do not require regular blood work. In women who cannot tolerate oral medications or have failed several different regimens of medication, surgical induction of ovulation can also be attempted. So-called "ovarian drilling" utilizes laser or electrosurgical techniques to place small holes in the ovaries in an effort to normalize the hormonal environment and allow ovulation to occur. PCOS is a common, readily treatable disorder.

Immunological Factors & Infertility

Introduction The immune system provides us with a multilayer defense against invading microbes and foreign intruders. It can recognize the difference between normal (self) and alien (non-self) cells, trigger a local or widespread inflammatory response, and retain the memory of the offending organism to repel it again if it should ever return. Like any finely-tuned machine, however, the system can break down and leave us open to the threat of infection, or, conversely, turn against our own healthy tissues, as occurs in such diseases as rheumatoid arthritis or lupus. The immune system also plays an important role in human reproduction. Inflammatory cells and their secretory products are involved in the processes of ovulation and preparation of the endometrium for implantation of a fertilized egg. Dysfunction of the immune system can interfere with the normal reproductive processes and result in infertility. It has been estimated that an immune factor may be involved in up to 20% of couples with otherwise unexplained infertility. Although many of these associations with infertility remain unproven, there is solid scientific evidence to implicate the formation of antibodies against sperm as an important infertility factor. Antisperm Antibodies: How common are they? Sperm are relatively protected from the immune system by a natural protective mechanism called the blood-testes barrier. Tight connections between the cells lining the male reproductive tract keep immune cells from gaining entry to the sperm within. If an injury breaches this barrier, then the immune system has access to sperm and antibodies are formed. Antisperm antibodies have been reported in approximately 10% of infertile men, compared to less than 1% of fertile men. The prevalence of antibodies jumps dramatically in men who have had surgery on their reproductive tract: nearly 70% of men who have undergone a vasectomy reversal will have antibodies present on their sperm. Women have a much lower chance for developing antibodies to sperm: less than 5% of infertile women can be shown to have antisperm antibodies, and it is unclear who is at risk for their formation. Who is at risk for antisperm antibodies? Anything that disrupts the normal blood-testes barrier can result in the formation of antisperm antibodies. This may include any of the following conditions: Vasectomy reversal Varicocele (dilation of the veins surrounding the spermatic cord) Testicular torsion (twisting of the testicle) Congenital absence of the vas deferens Testicular biopsy Cryptorchidism (failure of testicular descent) Testicular cancer Infection (orchitis, prostatitis) Inguinal hernia repair prior to puberty Fortunately, intrauterine insemination (the placement of washed sperm into the uterine cavity - a common fertility treatment) has not been shown to cause antisperm antibody formation. Despite the long list of risk factors, most men with antisperm antibodies have not had any of the conditions listed above. Therefore all infertile men are potentially at risk, and consideration should be given to testing infertile men for antisperm antibodies, especially if no other reasons for the infertility have been detected by the diagnostic workup. How do antisperm antibodies cause infertility? Antibodies that attach to the sperm may impair motility and make it harder for them to penetrate the cervical mucus and gain entrance to the egg; they may also cause the sperm to clump together, which is occasionally noted on a routine semen analysis. Antibodies may also interfere with the ability of the sperm to fertilize the egg. What is the best way to detect antisperm antibodies? Over the years, many tests have been developed to detect antisperm antibodies. In women, blood tests for antisperm antibodies in women may be more practical than trying to measure antibodies in the cervical mucus, which is the primary site where her immune system interacts with sperm. The postcoital test, which has been a standard part of the infertility evaluation, may suggest the presence of antisperm antibodies. By examining the cervical mucus following intercourse near the time of ovulation, antisperm antibodies may result in either a lack of sperm or in the presence of sperm, which are shaking in place rather than actively swimming through the mucus. In men, a direct examination of their sperm for attached antibodies is more reliable than testing blood for the presence of antibodies. Two commonly used tests are the immunobead assay and the mixed agglutination reaction (MAR). Both tests use antibodies bound to a small marker, such as plastic beads or red blood cells, which will attach to sperm that have antibodies on their surface. The results are read as a percentage of sperm bound by antibodies. What treatments are available for antisperm antibodies? Suppressing the immune system with corticosteroids may decrease the production of antibodies but can result in serious side effects, including severe damage to the hipbone. Intrauterine insemination, with or without the use of fertility medications, has been used for the treatment of antisperm antibodies. It is believed to work by delivering the sperm directly into the uterus and fallopian tubes, thus bypassing the cervical mucus. In vitro fertilization appears to be the most effective treatment for antisperm antibodies, especially when there are very high levels of antibodies (near 100% of sperm are bound by antibodies). There is no clear guidance on whether intracytoplasmic sperm injection (ICSI), the direct fertilization of an egg with a single sperm, is required for the treatment of antisperm antibodies, unless there had been a complete absence of fertilization on a prior attempt at in vitro fertilization For women with recurrent miscarriage, there are a group of antibodies that appear to attack an early developing pregnancy, resulting in either a miscarriage or severe preeclampsia with risk of intrauterine growth retardation or even fetal death. Collectively these belong to a class of antibodies known as antiphospholipid antibodies, which include the lupus anticoagulant and the anticardiolipin antibody. Testing for these antibodies are an integral part of the workup for recurrent pregnancy loss. However, it is unclear whether these antibodies play any role in the ability to conceive. Some physicians believe that the presence of antiphospholipid antibodies may decrease the chance for pregnancy through in vitro fertilization. Although this is a controversial subject, one of the largest studies that looked for these antibodies in women undergoing in vitro fertilization found that these antibodies were no more likely to be detected in those who did not become pregnant as in women who did conceive.

INFERTILITY EDUCATION CENTER

we are to adhere to strict medical definition, recurrent pregnancy loss is three or more miscarriages. Purists frequently will not start to evaluate a couple who have had only two losses, but my feeling is that we should not be too rigid. Certainly if the lady is over 35, she is at greater risk for miscarriage than is her 25 year old "sister", but she is also at greater risk of not being able to conceive again. Couples whose only two pregnancies have been lost are also deserving of some greater consideration as well. In this discussion, I would like to outline some of the causes of recurrent pregnancy loss and offer some suggestions as to evaluation and treatment. Causes of Miscarriage Probably the most common cause of any pregnancy loss is a chromosome abnormality in the conception. The contribution of the inappropriate number of chromosomes usually comes from the egg. Best estimates are today that only about one half the eggs a woman makes in her reproductive lifetime are capable of a successful pregnancy. Most of these chromosomally abnormal eggs are never identified as pregnancies. Either they do not divide to produce an embryo or fetus, or the conception is lost very soon after implantation of the early embryo. A woman is a few days late for her menstrual period and thinks nothing of it. Eggs and sperm, collectively known as gametes, form differently than other cells in the body. With the exception of gametes, all normal cells in the human contain 46 chromosomes. There are 22 paired chromosomes called autosomes. These direct the overall formation of the body. There is also a twenty-third pair of chromosomes, often referred to as sex chromosomes. In women and girls, there is a matched pair of "X" chromosomes, which are responsible for, among other things, the formation of the ovaries. In men and boys, one of the "X" chromosomes is replaced with a much shorter "Y" chromosome. The "Y" chromosome carries the determinants for maleness. Formation of gametes (sperm and eggs) requires the separation of pairs of chromosomes into singletons, which on fertilization of the egg recombine to form the 23 pairs of a new individual. Some times in the formation of a gamete, some genetic material gets lost. It may be the result of the loss of a part of a chromosome or even an entire chromosome. The missing genetic material may be attached to another chromosome and be surplus genetic material in another gamete. Large deletions or excesses of genetic material are lethal conditions for the conception and it will be lost. Examinations of products of conception, which have been passed, are rarely helpful. For couples with repeated losses, it is better to evaluate their chromosomes to determine if one of them is at increased risk of making gametes with the improper number of chromosomes. If one has such a problem, it is appropriate to consider donor sperm or donor egg. Risk of Miscarriage There is a certain overall or background risk to pregnancy loss. The risk increases with age. Below is a table published in Fertility and Sterility. Maternal age (years) Risk of Miscarriage (%) 15-19 9.9 20-24 9.5 25-29 10.0 30-34 11.7 35-39 17.7 40-44 33.8 44 & older 53.2 Fertility and Sterility: vol.46, p 989; 1986 Since there is a parallel increased risk of chromosome abnormalities in live births in women over 35, we assume the same mechanisms are responsible for increased risk of miscarriage. Abnormalities of the uterus may increase the potential for pregnancy loss. Fibroid tumors of the uterus may increase the risk to some degree, but are not as great a risk as incomplete formation of the uterus. The uterus is formed by the fusion of two tubular structures in the early fetus. It is not uncommon to find incomplete fusion. At its most severe, there may be complete duplication of structures as the cervix, uterine body and cavity, as well as the upper one third of the vagina. More commonly we find a duplication of only the uterine body and cavity. Such a uterus is described as "bicornuate" or two horned. It actually looks like the horns of a steer. The risk of pregnancy loss in this condition is approximately one third (30%-35%, depending on whose series you read). Still more common is a less severe incomplete fusion referred to as a septate uterus. The septum or wall, which either partially or completely divides the uterine cavity, has very poor blood supply. We believe the poor blood supply to the septum is responsible for the two-thirds probability of losing a pregnancy in a septate uterus. Where as a partial septum increases the risk to 60%-75%; a total septum carries a risk for loss of up to 90%. Today a relatively simple surgical procedure can remove a uterine septum. DES and Miscarriage Diethylstilbestrol (DES) was used many years ago with the mistaken belief that it could prevent miscarriages. We know today, that in addition to increasing the risk of a very rare vaginal cancer in exposed women, there is decreased fertility and increased risk of pregnancy loss. Diagnosis of the uterine abnormality associated with DES can be easily accomplished with a properly done hysterosalpingogram (HSG, X-ray of the uterus and fallopian tubes). Other Miscarriage Information So far our discussion has been about first trimester loss. A common cause of second trimester loss is an "incompetent cervix". The incompetent cervix painlessly dilates in early to mid second trimester and the pregnancy literally falls out. The woman has a gush of water and then begins to cramp as the uterus begins to contract, expelling what remains of the pregnancy. Placing special sutures in a purse string fashion around the cervix helps prevent a future loss. Some infectious agents have been incriminated in pregnancy loss, but the evidence that they are guilty is open to many questions. The focus has primarily been on Mycoplasma hominis, and Ureaplasma urealyticum. The studies in which these bacteria are incriminated are interesting, but have some significant weakness from the standpoint of study design. Another germ, which has been blamed, is Chlamydia. The data supporting Chlamydia's role as a cause for pregnancy loss is even less strong than for the other two. Approximately 10% of couples with recurrent pregnancy loss have recognized immune problems. The immunology problem is tagged with the misnomer "lupus anticoagulant". It is not related to the disease lupus and it is not an anticoagulant. Instead, the immunology problem actually enhances clotting. As such it may cause clotting in small blood vessels of the placenta. Testing for lupus is not helpful in making a diagnosis. We must test for clotting activity. The best treatment to date seems to be low dose aspirin and low dose heparin. Cortisol and related drugs have been tried, but are of no greater benefit and significantly increase the risks to the woman's health. Several years ago, much discussion was publicized about "blocking factor" and how inadequate "blocking factor" increased the risk of miscarriage. Forget it! We have never been able to find blocking factor. The original studies cited the Hutterite communities of the mid-west and their high rate of pregnancy loss. They have a very high compatibility of tissue-typing antigens (HLA) and, therefore, make fairly good organ donors for each other. The hypothesis arose that husband and wife were immunologicly too similar and for that reason, she did not produce adequate "blocking factor" to protect the early placenta and fetus from maternal antibodies. None of this could be proven. A carefully done genetic study hints that there may be a lethal mutant gene in the same area on the chromosome that carries the genes for the HLA antigens. Many OB-GYN's have guessed that some women do not make enough progesterone to support an early pregnancy. Although this seems to be unusual, I believe it may, on some occasions, be responsible for pregnancy loss. In a few of my patients I have been able to find no other cause for repetitive loss except low progesterone levels in early pregnancy. I supplemented them with progesterone and the pregnancy was successful. Did I really help with the progesterone? I don't know! I will, however, take the credit. There are times we can identify poor preparation of the endometrium (uterine lining) to support a new pregnancy. Hormonal evaluation, such as thyroid function, progesterone secretion by the ovary after ovulation, and prolactin levels, need to be evaluated. Specific treatment can then be designed. Very poorly understood and worse documented is the observation that delayed ovulation, beyond cycle day 16, seems to be associated with poor retention of the early pregnancy. Is the egg too old by the time it is released from the ovary and then fertilized? Again, using the anecdotal discussion, ovulation induction to move egg release forward to cycle day 13 or 14 seems to be helpful. The information provided is neither exhaustive nor detailed. It is meant as an overview of a serious problem for those who experience it. Please contact a well trained Reproductive Endocrinologist for assistance if you are having a problem.

In vitro fertilization (IVF) and other "high tech" procedures are now referred to as the assisted reproductive technologies (ART). These procedures all involve collecting the oocytes (eggs) and placing them in direct contact with sperm. Together they form an alphabet soup of techniques including: IVF, GIFT, ZIFT, ICSI, and FET. In its simplest term, IVF is simply the uniting of egg and sperm in vitro (in the lab). Subsequently the embryos are transferred into the uterus through the cervix and pregnancy is allowed to begin. IVF was the first of the ART techniques to be developed. The first birth was in 1978 in England. The procedure was pioneered by a Gynecologist and a Ph.D. (Drs. Steptoe and Edwards). Next came GIFT, which stands for gamete (egg and sperm) intrafallopian transfer. This procedure requires laparoscopy, which is a small incision surgery and requires a general anesthetic. With existing technology, pregnancy rates are similar with IVF and GIFT. Since IVF does not require surgery, it has supplanted GIFT. ZIFT involves IVF and then a laparoscopic surgical procedure to transfer the embryos into the fallopian tube. Since transferring embryos through the cervix with IVF gives the same pregnancy rate as ZIFT, and is nonsurgical, IVF has also supplanted GIFT. As the years have passed, IVF has become the dominant ART technology due to its simplicity, efficacy and lack of invasiveness. A typical IVF cycle begins with shutting down the ovaries. This is done with a medication known as a GnRH agonist. The most common drug such used is Lupron. Lupron is given for approximately two weeks after which the ovaries are shut down temporarily. The next phase involves stimulation of the ovaries with potent ovulation medications such as Pergonal. For a full description of these agents go to the page on ovulation medication. These injections are given for approximately 10 days. When the eggs are ready for harvesting, a final step is to give hCG to induce final maturation. The eggs are then harvested by a process called ultrasound guided vaginal retrieval. Under heavy sedation, and with ultrasound guidance, a thin needle is passed a short distance into the ovaries and the eggs are suctioned from the follicles. Typically 5-15 eggs are collected. Typically the eggs are fertilized by adding approximately 100,000 motile sperm to each egg. If the sperm will not fertilize the eggs naturally we can perform intracytoplasmic sperm injection (ICSI). This procedure involves puncturing the egg directly under a microscope and injecting one sperm in the egg. The day following retrieval, we can document fertilization under the microscope. We then observe the embryos for 3-6 days. The current trend is to observe longer. Typically 3-4 embryos are then placed in a catheter and transferred through the cervix into the uterus. This is a simple procedure much like a Pap smear. At the present time, embryos can be transferred either 3 or six days following retrieval. A 3-day embryo is usually at the 6-8-cell stage: It is also possible now to perform advanced stage or blastocyst embryo transfers. These embryos are further along and usually fewer of them need to be transferred: Two weeks later a pregnancy test can be obtained. Two weeks after the pregnancy test, an ultrasound can be performed and the fetal hear beat can be seen. If more embryos were generated than can be replaced, freezing (cryopreservation) can save these additional embryos. Frozen embryos can be stored for future replacement at much lower cost than the original IVF cycle. As the years have passed, IVF has improved greatly. Today it is arguably the most effective technique to treat infertility when compared with others on a month by month basis. IVF has created a lot of controversy also. First, it is expensive. An IVF cycle can cost $6,000 to $7,000. It may not work on the first cycle. Multiple pregnancies can result. The truth is that it is a powerful technology and must be used carefully. Some patients may have very high odds of success: 45 - 60% chance per attempt. Others may due to their situation have only a 20% chance of success. The multiple pregnancy risk varies with age. Younger patients need fewer embryos to be replaced, and older patients need more. The worst thing that has happened with IVF is the various centers entering into a race to see who can get "the best statistics". This has encouraged centers to transfer high numbers of embryos to get the statistics while accepting too high a risk of multiple pregnancy. Also in order to get the best statistics, some patients will be refused care in order to "protect the statistics". f) cells, trigger a local or widespread inflammatory response, and retain the memory of the offending organism to repel it again if it should ever return. Like any finely-tuned machine, however, the system can break down and leave us open to the threat of infection, or, conversely, turn against our own healthy tissues, as occurs in such diseases as rheumatoid arthritis or lupus. The immune system also plays an important role in human reproduction. Inflammatory cells and their secretory products are involved in the processes of ovulation and preparation of the endometrium for implantation of a fertilized egg. Dysfunction of the immune system can interfere with the normal reproductive processes and result in infertility. It has been estimated that an immune factor may be involved in up to 20% of couples with otherwise unexplained infertility. Although many of these associations with infertility remain unproven, there is solid scientific evidence to implicate the formation of antibodies against sperm as an important infertility factor. Antisperm Antibodies: How common are they? Sperm are relatively protected from the immune system by a natural protective mechanism called the blood-testes barrier. Tight connections between the cells lining the male reproductive tract keep immune cells from gaining entry to the sperm within. If an injury breaches this barrier, then the immune system has access to sperm and antibodies are formed. Antisperm antibodies have been reported in approximately 10% of infertile men, compared to less than 1% of fertile men. The prevalence of antibodies jumps dramatically in men who have had surgery on their reproductive tract: nearly 70% of men who have undergone a vasectomy reversal will have antibodies present on their sperm. Women have a much lower chance for developing antibodies to sperm: less than 5% of infertile women can be shown to have antisperm antibodies, and it is unclear who is at risk for their formation. Who is at risk for antisperm antibodies? Anything that disrupts the normal blood-testes barrier can result in the formation of antisperm antibodies. This may include any of the following conditions: Vasectomy reversal Varicocele (dilation of the veins surrounding the spermatic cord) Testicular torsion (twisting of the testicle) Congenital absence of the vas deferens Testicular biopsy Cryptorchidism (failure of testicular descent) Testicular cancer Infection (orchitis, prostatitis) Inguinal hernia repair prior to puberty Fortunately, intrauterine insemination (the placement of washed sperm into the uterine cavity - a common fertility treatment) has not been shown to cause antisperm antibody formation. Despite the long list of risk factors, most men with antisperm antibodies have not had any of the conditions listed above. Therefore all infertile men are potentially at risk, and consideration should be given to testing infertile men for antisperm antibodies, especially if no other reasons for the infertility have been detected by the diagnostic workup. How do antisperm antibodies cause infertility? Antibodies that attach to the sperm may impair motility and make it harder for them to penetrate the cervical mucus and gain entrance to the egg; they may also cause the sperm to clump together, which is occasionally noted on a routine semen analysis. Antibodies may also interfere with the ability of the sperm to fertilize the egg. What is the best way to detect antisperm antibodies? Over the years, many tests have been developed to detect antisperm antibodies. In women, blood tests for antisperm antibodies in women may be more practical than trying to measure antibodies in the cervical mucus, which is the primary site where her immune system interacts with sperm. The postcoital test, which has been a standard part of the infertility evaluation, may suggest the presence of antisperm antibodies. By examining the cervical mucus following intercourse near the time of ovulation, antisperm antibodies may result in either a lack of sperm or in the presence of sperm, which are shaking in place rather than actively swimming through the mucus. In men, a direct examination of their sperm for attached antibodies is more reliable than testing blood for the presence of antibodies. Two commonly used tests are the immunobead assay and the mixed agglutination reaction (MAR). Both tests use antibodies bound to a small marker, such as plastic beads or red blood cells, which will attach to sperm that have antibodies on their surface. The results are read as a percentage of sperm bound by antibodies. What treatments are available for antisperm antibodies? Suppressing the immune system with corticosteroids may decrease the production of antibodies but can result in serious side effects, including severe damage to the hipbone. Intrauterine insemination, with or without the use of fertility medications, has been used for the treatment of antisperm antibodies. It is believed to work by delivering the sperm directly into the uterus and fallopian tubes, thus bypassing the cervical mucus. In vitro fertilization appears to be the most effective treatment for antisperm antibodies, especially when there are very high levels of antibodies (near 100% of sperm are bound by antibodies). There is no clear guidance on whether intracytoplasmic sperm injection (ICSI), the direct fertilization of an egg with a single sperm, is required for the treatment of antisperm antibodies, unless there had been a complete absence of fertilization on a prior attempt at in vitro fertilization Are there other antibodies that affect fertility? For women with recurrent miscarriage, there are a group of antibodies that appear to attack an early developing pregnancy, resulting in either a miscarriage or severe preeclampsia with risk of intrauterine growth retardation or even fetal death. Collectively these belong to a class of antibodies known as antiphospholipid antibodies, which include the lupus anticoagulant and the anticardiolipin antibody. Testing for these antibodies are an integral part of the workup for recurrent pregnancy loss. However, it is unclear whether these antibodies play any role in the ability to conceive. Some physicians believe that the presence of antiphospholipid antibodies may decrease the chance for pregnancy through in vitro fertilization. Although this is a controversial subject, one of the largest studies that looked for these antibodies in women undergoing in vitro fertilization found that these antibodies were no more likely to be detected in those who did not become pregnant as in women who did conceive.

The Fertility Netwo