• rheumatoid arthritis

Proton pump inhibitors are commonly prescribed for the treatment of acid-related gastrointestinal diseases. The association between proton pump inhibitors therapy and other subsequent comorbidities has been extensively explored.1 Recently, a cohort study in USA conducted by Ozen et al published in the Annals of the Rheumatic Diseases reported that proton pump inhibitors therapy was not associated with increased fracture risk in patients with rheumatoid arthritis (HR=0.92; 95% CI 0.80 to 1.06).2 Ozen et al’s study is an important one and deserves a practical value. Some points not shown in the original article are shared with the readers. First, in order to test this issue in a different country, a preliminary population-based cohort study was conducted using the 2005–2012 database of the Taiwan National Health Insurance Program with 23 million residents living in Taiwan.3 Patients ≥20 years old with a diagnosis of rheumatoid arthritis were included in the study. In order to reduce the biased results, those patients who had a cumulative periodof proton pump inhibitors therapy ＜3 months were excluded from the study. The main outcome was a new diagnosis of any major osteoporotic fractures including fractures of the spine, humerus, forearm, wrist and hip. Table 1 shows that the incidence of major osteoporotic fractures is 1.33-fold higher in patients with proton pump inhibitors therapy than those without use, but it does not reach statistic significance (1.24 vs 0.94 per 100 person-years; 95% CI 0.86 to 2.06, p=0.2049) which was compatible with Ozen et al’s study reporting that no association could be observed between proton pump inhibitors therapy and fracture risk in patients with rheumatoid arthritis.2 Second, previous research has suggested that no significant association can be detected between proton pump inhibitors therapy and fracture risk in older adults.4 Ozen et al’s and our studies further confirm that even in patients with rheumatoid arthritis, such an association still does not exist. Third, I agree with Sugiyama’s comments published in the Annals of the Rheumatic Diseases reporting that no conclusive evidence supports a cause–effect relationship between proton pump inhibitors therapy and fracture risk, regardless of the population studied.5 Fourth, currently no research definitely proves that proton pump inhibitors therapy can change bone mineral density. So, the American Gastroenterological Association does not recommend that patients on long-time therapy of proton pump inhibitors need to routinely assess bone mineral density.6 Fifth, based on the above discussion, patients with rheumatoid arthritis who are on long-time therapy of proton pump inhibitors do not need to routinely examine bone mineral density and do not need to worry about fracture risk.