Women with H. pylori infection were more likely to be older and have a higher body mass index (BMI) than those without H. pylori infection.

Women with Helicobacter pylori (H. pylori) infection are about 25% more likely to have osteoporosis than those without the infection, independent of risk factors and confounding factors, according to a South Korean study in the Journal of Gastroenterology and Hepatology.

The large-scale, longitudinal, retrospective cohort study comprised 10,482 healthy women aged 20 years or older (mean age 50.2 years) without osteoporosis at baseline. Subjects participated in a comprehensive health-screening examination at the Center for Health Promotion of the Samsung Medical Center, in Seoul, South Korea, from January 2000 to December 2019.1

Each participant underwent at least two screening examinations that included an H. pylori-specific immunoglobulin G antibody test and dual-energy x-ray absorptiometry (DXA) to assess bone mineral density (BMD). The baseline prevalence of H. pylori infection was 57.3% (n = 6,009).

During the 77,515.3 person-years of follow-up, women with H. pylori infection had a higher risk of osteoporosis than those without H. pylori infection: hazard ratio (HR) 1.23; 95% confidence interval (CI): 1.03 to 1.45.

Women with H. pylori infection were more likely to be older and have a higher body mass index (BMI) than those without H. pylori infection. Women with infection were also more likely to use proton pump inhibitors.

The risk of osteoporosis was more pronounced in women with osteopenia at baseline compared to women with normal BMD at baseline: HR 2.76; 95% CI: 2.26 to 3.37

Non-obese (BMI < 25) and postmenopausal women also had an increased risk for osteoporosis: HR 2.08; 95% CI: 1.61 to 2.70; and HR 1.68; 95% CI: 1.31 to 2.16, respectively.

However, no significant differences were observed between the two groups in smoking, comorbidities (including hypertension, diabetes, dyslipidemia, stroke, and ischemic heart disease) or history of corticosteroid use.

Although the precise mechanism linking H. pylori infection to osteoporosis has yet to be elucidated, “several possible mechanisms might explain the potential role of H. pylori in the predisposition to and causation of the decrease in BMD,” wrote the authors.

For example, H. pylori infection is associated with chronic inflammation from the release of inflammatory cytokines. The pro-inflammatory response and inflammatory cytokines are known to result in bone resorption.

In addition, H. pylori bacteria containing the cytotoxin-associated gene A (CagA) is a strong pathogenic factor related to peptic ulcer disease and gastric cancer, and deemed more virulent and capable of inducing an increased systemic inflammatory response.

However, regional differences exist as to the frequency of CagA strains in H. pylori infections, which are observed in roughly 90% of cases in East Asian countries such as Korea and Japan, compared to only 30% to 40% of cases in Western countries.

Moreover, there are two types of genetic polymorphism in CagA: East Asian type and non-East Asian type. The former induces more severe gastritis and mucosal atrophy; hence East Asian type CagA strains might be more potent than the non-East Asian type.

The East Asian type CagA is not only the most prevalent type in East Asia, but is not even detected in Western countries; thus the likely explanation for contradictory results of previous studies about the association between H. pylori infection and osteoporosis.

The current study’s findings “support the hypothesis that H. pylori may contribute to the pathogenesis of decreased BMD,” concluded the authors. “Physicians should, in turn, pay more attention to women with H. pylori infection by using DXA scan, especially in postmenopausal women or women with lower BMIs.”

 

Source: Kim, T. J.Lee, H.Min, Y. W.Min, B.‐H.Lee, J. H.Rhee, P.‐L., and Kim, J. J. (2020Cohort study of Helicobacter pylori infection and the risk of incident osteoporosis in womenJournal of Gastroenterology and Hepatologyhttps://doi.org/10.1111/jgh.15181.