Abstract:We propose to determine routinely the existence of an H. pylori infection in men and women with reduced fertility. Our proposal is based on the following observations: a) the infection is more prevalent in patients than controls, b) the infection could negatively affect semen quality, c) the presence of H. pylori influences the levels of inflammatory cytokines in the blood stream and stimulates the production of antibodies that, being also present in follicular fluids, vaginal mucous and semen of infected people, could possibly hamper the meeting of sperm with the oocyte.
LETTERReproductive disorders are steadily increasing. Figura et al.,[1] proposed H. pylori infection as a possible concomitant cause of reduced fertility and sperm damage: the infection is significantly more common in both men and women with trouble procreating; infected individuals have specific antibodies in semen, follicular fluid and vaginal secretions, which may cross react in vitro with spermatozoa, suggesting the existence of autoimmune phenomena; the amino acid alignment of the human tubulin, a major sperm flagellar constituent, with H. pylori peptides may indicate the existence of an antigenic mimicry with the cytotoxinassociated gene A protein (CagA) and other H. pylori antigens.Other groups have shed new light on this topic. Kurotsuchi et al., [2] found that H. pylori infection was twice as prevalent in women with procreation problems, in whom the search for the most common causes of reduced fertility had yielded negative results. Ambrosini et al.,[3] have recently found that in vitro sperm motility through cervical mucous was significantly reduced in infected women and they concluded that anti-H. pylori antibodies could possibly hamper the meeting of sperm with the oocyte. These findings suggest that H. pylori infection, in both men and women, could contribute to decrease the probability of pregnancy.These observations are derived from solid bases of biological plausibility: H. pylori infected men, especially those with serum antibodies to the CagA protein (i.e. that they are infected by bacterial genotypes endowed with an increased inflammatory potential), have a) increased systemic levels of tumor necrosis factor-alfa, a proinflammatory cytokine that may cause sperm damage; b) reduced sperm motility in vitro and c) a greater number of necrotic and apoptotic spermatozoa in their ejaculates [4]. The partial results of still another unpublished study from