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English Abstract
Journal Article
[Role of sperm antibodies and cellular autoimmunity to sperm in the pathogenesis of male infertility].
Ceská Gynekologie 2002 January
OBJECTIVE: To test the hypothesis of relationship between sperm pathology and elevated humoral and/or cell-mediated antisperm autoimmunity in male partners from infertile couples.
DESIGN: Analytic study.
SETTING: Department of Immunobiology, Institute for the Care of Mother and Child, Prague.
METHODS: Sperm samples were evaluated according to WHO rules. Sperm-bound antisperm autoantibodies (ASA) were determined by SpermMar Test (FertiPro N. V., Sint-Martens-Latem, Belgium). For evaluation of cell-mediated antisperm autoimmunity (CMAA) the authors used their own modification of migration-inhibition test (Dimitrov et al., J. Immunol. Methods 154: 147, 1992).
RESULTS: The pool of men was divided into groups according to the result of sperm examination: normozoospermia (740 men), asthenozoospermia (244), teratozoospermia (191), oligoasthenozoospermia levis (61), oligoasthenozoospermia gravis (29), oligoteratozoospermia (82), and azoospermia (54). Subgroup of fertile men (32) consisted of normozoospermic men--fathers of child younger than 3 years. Percentage of sperm-bound ASA-positive samples was significantly higher in asthenozoospermia in comparison with normozoospermia in both IgA (20.8% versus 10.6%) and IgG classes (13.8% vs 6.8%). Positivity of CMAA was significantly more frequent in group of asthenozoospermic (52%) than in normozoospermic (28.5%) and fertile (12.5%) men.
CONCLUSION: Antisperm autoimmunity, namely its cell-mediated form, appears to play a significant role in impairment of spermiogenesis. Sperm-bound autoantibodies were found more frequently in asthenozoospermia, but also in some men with normozoospermia they may impair fertility.
DESIGN: Analytic study.
SETTING: Department of Immunobiology, Institute for the Care of Mother and Child, Prague.
METHODS: Sperm samples were evaluated according to WHO rules. Sperm-bound antisperm autoantibodies (ASA) were determined by SpermMar Test (FertiPro N. V., Sint-Martens-Latem, Belgium). For evaluation of cell-mediated antisperm autoimmunity (CMAA) the authors used their own modification of migration-inhibition test (Dimitrov et al., J. Immunol. Methods 154: 147, 1992).
RESULTS: The pool of men was divided into groups according to the result of sperm examination: normozoospermia (740 men), asthenozoospermia (244), teratozoospermia (191), oligoasthenozoospermia levis (61), oligoasthenozoospermia gravis (29), oligoteratozoospermia (82), and azoospermia (54). Subgroup of fertile men (32) consisted of normozoospermic men--fathers of child younger than 3 years. Percentage of sperm-bound ASA-positive samples was significantly higher in asthenozoospermia in comparison with normozoospermia in both IgA (20.8% versus 10.6%) and IgG classes (13.8% vs 6.8%). Positivity of CMAA was significantly more frequent in group of asthenozoospermic (52%) than in normozoospermic (28.5%) and fertile (12.5%) men.
CONCLUSION: Antisperm autoimmunity, namely its cell-mediated form, appears to play a significant role in impairment of spermiogenesis. Sperm-bound autoantibodies were found more frequently in asthenozoospermia, but also in some men with normozoospermia they may impair fertility.
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