Vasectomy: an experimental autoimmune disease state.

This paper summarizes recent laboratory findings which deal with: 1) the postvasectomy humoral antibody and cell-mediated autoimmune responses 2) postvasectomy orchitis and 3) the role of antisperm autoantibodies as the mechanism responsible for postvasovasostomy infertility. Only 50-60% of vasectomized subjects develop antisperm autoantibodies. This correlates with the finding that within a species antisperm antibody responsiveness is strain-dependent. It is shown by the use of quantitative antibody assay that the postvasectomy IgG autoantibody response to sperm surface autoantigens (TSDA) in vasectomized guinea pigs is controlled by a single dominant autosomal. The development of postvasectomy autoiummune orchitis has been conclusively demonstrated in the guinea pig and rabbit. Data from in vitro fertilization experiments demonstrate that antisperm autoantibodies isolated from the sera of vasectomized guinea pigs can essentially interfere with all prefertilization and fertilization events. These findings support the concept that serum antisperm autoantibodies present in vasovasostomized individuals may in part be responsible for the high rate of infertility following vasovasostomy. Vasectomy appears to have a striking atherogenic effect in subhuman primates. The pathogenetic mechanism of postvasectomy atherosclerosis is likely to be the result of intimal injury. An alternative hypothetical model based on the physical-chemical nature of some unusual sperm autoantigens is presented. Glycolipid autoantigens released from the testis after vasectomy may insert into the plasma membrane of endothelial cells rendering these previously insusceptible cells susceptible to immunologic injury by antisperm glycolipid autoimmune reactions. The attendent intimal injury may then lead to atherosclerosis potentially the most serious complication of vasectomy.