PMC:7102591 / 10269-11472 JSONTXT

{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/7102591","sourcedb":"PMC","sourceid":"7102591","source_url":"https://www.ncbi.nlm.nih.gov/pmc/7102591","text":"It has now been more than 70 years that corticosteroids (CS) are pivotal for RA management and their role as remission inducer and bridging therapy for the management of disease flare has recently been renewed by the latest update of EULAR recommendations for RA treatment [36]. Even though CS efficacy in rapidly suppressing inflammation during RA initial course or flares is well recognized [37], their downside is the broad spectrum of adverse events, including severe infections and the high risk of developing comorbidities further increasing the risk of infection [27,38]. Although RCTs conducted in the past with CS showed no higher risk of infections in RA patients [[39], [40], [41]], cohort and case-control studies reported increased rates of overall infections in RA patients treated with CS, according to a dose-dependent fashion [42]. The majority of these infectious events are of bacterial etiology, but RA patients receiving CS exhibit a greater risk of developing even viral infections. As an example, a 2012 retrospective cohort-study demonstrated an increased risk of Herpes Zoster infections with an incidence rate of 8.54 cases per 1000 patient-years in CS treated population 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