Anti-Helicobacter pylori antibodies, autoimmunity, aldosterone and infertility: Causal or casual association with polycystic ovary syndrome?

Dear Editors, We thank Yavasoglu and Kucuk for their interesting comment [1]. The most important aspects of the whole problem are: (i) IgG anti-Helicobacter pylori antibodies (antiHPAb) block sperm motility in vitro and at the level of cervical mucus [2], (ii) 85% of patients with Hashimoto thyroiditis are positive for antiHPAb [3], (iii) 40% of patients with polycystic ovary syndrome (PCOS) and 20% of controls are positive for antiHPAb [4], (iv) 30% of patients with PCOS have Hashimoto's thyroiditis [5], (v) PCOS and Hashimoto are associated with reduced fertility or with increased abortivity, (vi) HP infection has been associated with autoimmune gastritis [6], (vii) PCOS, Hashimoto and HP infection are associated with increased inflammatory reaction, and (viii) PCOS is associated with increase of aldosterone which is the principal inflammatory steroid [7]. AntiHPAb could be involved in couple sterility by blocking the sperm at the level of cervical mucus and although it is difficult to clearly demonstrate their presence in vaginal smears, some authors have identified them in follicular fluid after ovarian stimulation for in vitro fertilization [8]. The authors have addressed an important question: are antiHPAb a new etiological factor for development of PCOS or is this an incidental association? AntiHPAb have been found in 40–50% of healthy subjects but these studies do not take into account the possible presence of PCOS or other autoimmune diseases in otherwise healthy subjects. Considering the association of PCOS and Hashimoto, and Hashimoto and gastritis we would consider antiHPAb and PCOS as possible components of some autoimmune polyendocrine syndromes. The action of these antibodies at the level of sperm tail or of ovarian follicle could be an additive factor for reduced fertility. AntiHPAb might be implicated in several autoimmune disorders since the infected patients may have an enhanced autoimmune response against epithelial cells of various organs particularly of the thyroid and ovary, stimulating the production of free radicals, damaging the spermatozoa and affecting oocyte function. We do not believe that the antiHPAb are the cause of PCOS since PCOS is frequently familial, is already present in adolescence and is more related to insulin resistance. It is indeed probable that PCOS patients are more prone to the chronic immune reaction to the HP infection. Another factor which could play a similar role is increased aldosterone, which is involved in the inflammatory state of PCOS and may be associated with the autoimmune response. Recently we have found an increase of aldosterone or aldosterone to renin ratio in PCOS [7]. In the light of research carried out in recent years, it seems that aldosterone may produce a complex proinflammatory effect. Excessive aldosterone secretion may stimulate the development and/or progression of autoimmune disorders. In a case of association of primary aldosteronism and Hashimoto's thyroiditis, surgical removal of an aldosterone-producing tumor improved thyroid function and decreased thyroid autoimmunity [9]. Hyperaldosteronism may exacerbate the clinical course of autoimmune thyroiditis and probably also of other autoimmune disorders and favor the inflammatory reaction in PCOS.