Prevalence of Helicobacter pylori Infection in Male Patients with Osteoporosis and Controls
- 153 Downloads
Cytokines that regulate bone turnover (tumor necrosis factor-α, interleukin-6, etc.) may influence the pathogenesis of skeleton disorders, such as osteoporosis. Since Helicobacter pylori infection increases the systemic levels of inflammatory cytokines, we investigated the possibility that this infection increases the risk of developing osteoporosis and affects the bone metabolism in a group of male patients with osteoporosis. We examined 80 osteoporotic male patients and 160 controls for serum antibodies to H. pylori and the CagA protein and determined, in patients alone, the most important biochemical and instrumental parameters of the disease. Fifty-one patients (63.7%) and 107 controls (66.8%) were seropositive for H. pylori infection (nonsignificant); 30 infected patients (58.8%) and 43 infected controls (40.1%) were positive for anti-CagA antibodies (P = 0.028; OR = 2.13). Levels of estradiol in infected CagA-positive patients were significantly lower than in infected CagA-negative patients (28.5 [SD = 10.18] vs. 39.5 [SD = 14.50] pg/ml; P = 0.002) and uninfected patients (35.2 [SD = 12.7] pg/ml; P = 0.028). Levels of urinary cross-laps(a marker of bone resorption) were increased in patients infected by CagA-positive strains compared to patients infected by CagA-negative strains (282.9 [SD = 103.8] vs. 210.5 [SD = 150.1] μ g/mmol; P = 0.048) and uninfected patients (204.3 [SD = 130.1] μ g/mmol; P = 0.016). Differences among uninfected and infected patients, independent of CagA status, were observed for other markers of bone turnover, but they did not reach statistical significance. Infection by CagA-positive H. pylori strains is more prevalent in men with osteoporosis, who show reduced systemic levels of estrogens and increased bone turnover. H. pylori infection by strains expressing CagA may therefore be considered a risk factor for osteoporisis in men.
Key WordsHelicobacter pylori CagA protein osteoporosis estrogens bone turnover cytokines
Unable to display preview. Download preview PDF.
- 5.Kowalski M, Konturek PC, Pieniazek P, Karczewska E, Kluczka A, Grove R, Kranig W, Nasseri R, Thale J, Hahn EG, Konturek SJ: Prevalence of Helicobacter pylori infection in coronary artery disease and effect of its eradication on coronary lumen reduction after percutaneous coronary angioplasty. Digest Liver Dis 33:222–229, 2001CrossRefGoogle Scholar
- 8.Xiang Z, Censini S, Bayeli PF, Telford JL, Figura N, Rappuoli R, Covacci A: Analysis of expression of CagA and VacA virulence factors in 43 strains of Helicobacter pylori reveals that the clinical isolates can be divided into two major types and that CagA is not necessary for expression of the vacuolating toxin. Infect Immun 63:94–98, 1995PubMedGoogle Scholar
- 13.Bulun SE, Noble LS, Takayama K, Michael MD, Agarwal V, Fisher C, Zhao Y, Hinshelwood MM, Ito Y, Simpson ER: Endocrine disorders associated with inappropriately high aromatase expression J Steroid Biochem Mol Biol 61:133–139, 1997Google Scholar
- 14.Giannini E, Fasoli A, Borro P, Chiarbonello B, Malfatti F, Romagnoli P, Botta F, Testa E, Fumagalli A, Polegato S, Savarino V, Testa R: Impairment of cytochrome P-450-dependent liver activity in cirrhotic patients with Helicobacter pylori infection. Alim Pharmacol Ther 15:1967–1973, 2001CrossRefGoogle Scholar