The purpose of the present study was to determine whether the presence of one or more multinucleated blastomeres during early embryonic development is associated with chromosomal abnormalities in sibling blastomeres of that embryo. Embryos with multinucleated cells (n = 47) detected on day 2 or 3 or development were compared to dividing embryos without multinucleation. Arrested embryos were excluded from this study. Chromosome abnormalities were detected using fluorescent in-situ hybridization (FISH) with X, Y, 18 and 13/21 chromosome-specific probes. Of 47 embryos included in this study, 76.6% were chromosomally abnormal, compared to 50.9% in the control group (P < 0.001). Excluding aneuploidy, which is originated in the gametes and not the embryo, the differences were even higher, with 74.5% of multinucleated embryos being chromosomally abnormal compared to 32.3% of non-multinucleated embryos (P < 0.001). Day of multinucleation appearance, number of nuclei per cell, number of multinucleated cells per embryo and developmental quality of the embryos as well as the type of fertilization (intracytoplasmic sperm injection versus standard insemination) were not found to affect the rate of chromosomal abnormalities in embryos with multinucleated cells. These results suggest that embryos with multinucleated cells may not be suitable for replacement and should be excluded unless no other embryos are available.
The relationship between a localized genital tract humoral immune response to Chlamydia trachomatis and the presence of antisperm antibodies on the surface of motile spermatozoa in the ejaculate was examined in 227 asymptomatic male partners of infertile couples with no history of exposure to C.trachomatis. Semen and serum samples were assayed for immunoglobulin (Ig) A and IgG antibodies to C.trachomatis by enzyme-linked immunosorbent assay employing a recombinant Chlamydia-specific lipopolysaccharide fragment (Medac, Hamburg, Germany), while motile spermatozoa were tested for bound autoantibodies by immunobead binding. Semen samples from 24.7 and 10.9% of the men were positive for IgA and IgG antibodies to C.trachomatis respectively. In comparison, antichlamydial IgA was less prevalent in sera (14.5%) than in semen (P = 0.01), while antichlamydial IgG was most prevalent (21.5%) in sera (P = 0.003). In 75.0% of the men with antichlamydial IgA in their semen, this antibody was undetectable in sera obtained at the time of semen collection. Conversely, 84.0% of the men with seminal antichlamydial IgG were also IgG seropositive. Antisperm IgG and/or IgA were detected on motile spermatozoa from 16.3% of the men; their occurrence was strongly correlated with the presence of antichlamydial IgA in semen (P < 0.0001). Weaker associations between antisperm antibodies and either seminal IgG antibodies to C.trachomatis (P = 0.01) or circulating IgA and IgG antichlamydial antibodies (P = 0.03) were also observed. Men with antichlamydial IgA in their semen had a lower median sperm count (82 versus 144 x 10(6)/ml) than those men without (P = 0.003); sperm morphology and motility were comparable in both groups. These data suggest that asymptomatic male genital tract exposure to C.trachomatis is a frequent event among this population and that the presence of a humoral immune response to this organism is correlated with the development of an autoimmune response to spermatozoa.
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