The presence of ASA in the IVF culture medium results in an impairment of fertilization. Immunoglobulins of the IgA class appeared to be more effective in impairing fertilization than IgG. More critical examination of the results of IVF in women with isoimmunity to sperm revealed both diminished fertilization rate and diminished embryonic cleavage rate, and reduced chance of pregnancy as shown by the study of Vasquez-Levin [25]. On the other hand, significant pregnancy rates can be achieved despite the presence of ASA. These antibodies cannot be eliminated from the egg by washing. Pagidas et al. [31] claimed that IVF is not significantly affected by the presence of ASA in female sera used to supplement the culture media or by antibodies bound to inseminated sperm. Inhibition of IVF fertilization may be caused by a synergistic effect of IgG and/or IgA classes of ASA. In IVF trials, other authors did not find any differences between antibody positivity and antibody negativity in the outcome of the IVF embryo transfer attempt [28].

Menge and Naz [9] suggested three mechanisms by which ASA can affect embryo survival. The first mechanism consists of the possibility that sperm surface antigens are incorporated into the zygotic membrane at fertilization. Fertilization involves the possibility of sperm made oolemma plasma membranes moving to a mixture of antigens. The second mechanism proposed is that similar epitopes are present on spermatozoa and embryos. Several common antigens have been found. The last proposed mechanism to account for postfertilization reproductive loss mediated by ASA is via an indirect effect of antibodies on embryo development.

A woman whose partner has ASA following a vasectomy, inflammation process, or testicular tumors often produces also ASA [10, 16, 29]. In humans, clinical evidence of an association between early pregnancy loss and immunity to sperm is not definitively clear. Approximately 15 % of women produce antibodies to sperm in the cervical mucus and in the blood. Over 50 % of men with low sperm motility have been found to carry these antibodies in semen plasma and in serum. Sperm cells have unique surface antigens that elicit an immune response.

Beer also speculated [10] about the rising incidence of ASA in women. It may be due to delaying pregnancy until late in life, by which time they will probably have had several sexual relationships. This increases the risk of immune sensitization. If ASA in woman are present that agglutinate and/or immobilize partner’s sperm and those from any sperm donor, we consider non partner-specific ASA. Beer studied [10] ASA levels in over 100 prostitutes and compared them with those of 40 age-matched women. More than 40 % of prostitutes had ASA compared with just 5 % among the control group. Over 60 % of these women who had never used any form of contraception became infertile within 9 years.

The same author also observed [10] that ASA can be associated with antibodies to phospholipids. They are strong indication that the woman will have anti-DNA antibodies in addition to elevated levels of circulating natural killer cells and CD19+/5+ B-cells that produce the ASA. Such a problem can manifest itself as repeated IVF failure where embryo is implanted, but later it leads to very early miscarriage. Immunotherapy is an effective way of treating women with antibodies to sperm who experience this problem. A number of autoimmune and/or isoimmune conditions of the reproductive system are associated with poor fertility. Several topics [13, 23] have described the relationship between ASA and pregnancy prognosis. Also allergies to heavy metals can negatively influence reproduction, because in sensitive persons they are able to alter the immune reactions including production of autoantibodies. The altered immune reaction can then cause infertility. In patients with metal intolerance diagnosed by the MELISA test, the release of metal ions from dental materials can be one of the stimulating factors which may adversely affect fertility [11]. An Italian group [50] studied the presence of ASA in 190 patients with testicular cancer 1 month after orchiectomy and before radiotherapy or chemotherapy. The results support the hypothesis that testicular cancer is not a cause of ASA and infertility. Marconi et al. [29] did not find any relationship between ASA detected by mixed agglutination reaction or immunobead test and chronic inflammation and infection of the seminal tract.

Presence of sperm antibodies connected or not connected with pathology in semen such as azoospermia and severe oligospermia (oligoasthenospermia) is a reason to make examination of genetic causes of male infertility. Our genetic laboratory investigates karyotype, on an exclusion of Y chromosome microdeletions in AZF area, and on exclusion of mutations in the CFTR gene. If chromosomal aberrations and DNA mutations in our patients are found, their offsprings will be at an increased risk of transmitting genetic alterations. We recommend to perform preimplantation genetic diagnosis (PGD) to select embryos without genetic changes. Nowadays, the most commonly used method PGD/PGS (preimplantation genetic screening) includes the examination of cells of trophectoderm of early embryo, which is taken on the fourth to fifth days of the development stage of blastocyst in vitro. DNA isolation from trophectoderm follows. The VeriSeq PGS Kit offers a highly sensitive screening of all 24 chromosomes for selection of euploid embryos. We exclude by the VeriSEq PGS method both numerous and extensive structural aberrations, but also to detect microdeletions and microduplications. If genetic cause in male patient exists we use sperm cells from healthy and anonymous donor without ASA. The examination of ASA in donors is required.

In men with severe obstructive oligospermia and/or azoospermia, we use the surgical sperm retrieval option such as microsurgical epididymal sperm aspiration (MESA), testicular sperm aspiration (TESA), or percutaneous sperm aspiration (PESA).