נוגדנים עצמוניים

ראי: http://www-medlib.med.utah.edu/asrm/autoimmune.html Autoantibodies AND Infertilty The antiphospholipid syndrome is a cause of recurrent pregnancy loss (RPL) in a small proportion of women. The antiphospholipid syndrome requires one clinical (venous clot, arterial clot, OR two OR more losses of clinically recognized pregnancies), AND one laboratory criterion (lupus anticoagulant OR IgG anticardiolipin antibody greater than 20 GPL units) to confirm the diagnosis. Some investigators have hypothesized that immune dysfunctions similar to the antiphospholipid syndrome may also affect very early pregnancies AND could potentially explain some cases of infertility. Hypothetical explanations include the possibility that autoantibodies OR associated unrecognized antibodies may be directed at eggs, sperm OR other components critical to fertilization. Furthermore, antibodies could potentially impair embryo development, implantation, OR continued growth. Circumstantial clinical evidence suggests that further well-designed research is warranted. Available studies supporting immune dysfunction with infertility consist of observations linking the prevalence of various autoantibodies to clinical situations like endometriosis, unexplained infertility , pelvic disease, and/or IVF failures. Equally convincing data is also available suggesting that antiphospholipid antibodies play no role in infertility. Those evaluating the literature on autoantibodies AND infertility must consider the following limitations. First, the study populations in the literature are inconsistent. Second, there is no consistency in the laboratory criteria required to establish a diagnosis AND there are no historical OR physical findings that identify an individual with autoimmune infertility. Third, appropriate control groups have not been consistently utilized. Fourth, the majority of studies utilize autoantibody assays which are not standardized AND no long term follow up studies show consistently positive autoantibody titers in the patient groups studied. Furthermore, even upper respiratory infections can induce false positive autoantibody findings. Fifth, normal standards are not consistently used. Sixth, multiple testing for different autoantibodies can result in an incidence of autoantibody positivity in over 50% of individuals tested AND yet there is no consensus that any specific autoantibody is a marker for autoantibody-mediated infertility. In summary, until multi-centered, prospective, randomized clinical trials clarify the value, if any, of screening AND treatment for the presumed diagnosis of autoantibody-mediated infertility, the use of intravenous gamma globulin, prednisone, and/or aspirin should be considered research protocol. Informed consent documents are required in authorized research protocols which fully inform patients of the potential risks AND benefits of proposed interventions.