Effect of <i>Helicobacter pylori</i> infection on bone mineral density in patients with rheumatoid arthritis

The ability of Helicobacter pylori (H. pylori) to develop and maintain chronic inflammation, induce general immune response, to affect blood lipid metabolism and insulin resistance, and negative impact on bone mineral density (BMD) requires a closer look at the association between H. pylori infection and secondary osteoporosis (OP) in patients with rheumatoid arthritis (RA). The effects of H. pylori infection on BMD at the axial skeletal sites were assessed in 85 women with RA (35 patients were diagnosed with OP). Blood serum samples from RA patients were tested for the presence of IgG class antibodies to H. pylori (anti-Hp-IgG) and total antibodies to H. pylori CagA antigen (anti-CagA). When anti-Hp-IgG was determined, a positive result was recorded in 70.6% of cases. Anti-CagA was also detected in 34 patients with chronic H. pylori infection. In the total group of patients infected with H. pylori, there was a decrease in spinal BMD at the level of L1-4 (BMDL1-L4, p = 0.008), but not in total hip BMD (BMDTotal) (p = 0.06). The analysis of variance demonstrated a significant decrease in both BMDL1-L4 (p = 0.01) and individual BMD parameters of the proximal femur (BMD of the femoral neck, BMDNeck, p = 0.048 and BMD in the Ward’s zone, BMDWards, p = 0.02) detectable only among patients positive for anti-CagA. Among RA patients with a confirmed diagnosis of OP, the incidence of H. pylori infection was significantly higher than in the group of RA patients without osteoporosis (÷2, p = 0.021), and the major proportion of patients with OP were also positive for anti-CagA (73.3%). In patients with significantly high titers of anti-CagA (n = 16), the decrease in BMD was most pronounced and differed from the BMD values for axial skeletal support sites in the group of patients with low titers of these antibodies (BMDL1-L4, p = 0.003; BMDNeck, p = 0.011; BMDTotal, p = 0.049). Infection with H. pylori strains expressing CagA may be considered not only as a risk factor of osteopenia and osteoporosis, but also as a possible risk factor for low-energy fractures in RA patients. Moreover, it seems that the high anti-CagA titers may predict a risk of developing OP in H. pylori-infected patients with RA, rather than simple detection of helicobacteriosis or infection with a CagA-expressing strain. In summary, the presence of chronic H. pylori infection is accompanied by a decrease in BMD across axial skeletal support sites, and H. pylori infection should not be ignored in the treatment of osteoporotic complications in patients with RA.