Rheumatoid arthritis is the major risk factor for septic arthritis in rheumatological settings

Abstract

Septic arthritis (SA) is a clinical emergency with considerable morbidity and mortality that can lead to rapid joint destruction and irreversible functional loss. The reported incidence varies from 2–5 cases/100,000 person-years in the general population to 70 cases/100,000 person-years among patients with rheumatoid arthritis. In fact, individuals with rheumatoid arthritis are at particular risk for developing SA. This may be due to several reasons: joint disease predisposes to bacterial joint colonization and RA itself and its treatment with corticosteroids, disease-modifying antirheumatic drugs (DMARDs) and biological therapies may decrease the immune function required for protection from pathogens. Steroids and DMARDs seem to affect the leukocyte synovial count; indeed, RA patients with SA have a leukocyte count in synovial fluid (SF) lower than patients with SA without underlying rheumatic diseases. The diagnosis of SA in RA patients can be difficult because the development of a hot painful joint is often confused with a relapse of the underlying joint disease leading to delay in diagnosis. For this reason the microscopic analysis and culture of synovial fluid are crucial to exclude septic arthritis.

Introduction

Rheumatoid arthritis (RA) is the most common inflammatory arthritis and is associated with increased morbidity and a shortened lifespan. A high frequency of infections complicating RA has been reported during the last 40years. In particular high rates of septic arthritis (SA), a disabling condition that requires prompt diagnosis and treatment and that may cause synovial joint destruction and death, have been described [1], [2]. The finding that up to 40% of patients with SA have RA further support the evidence of the increased risk in patients with RA [3]. This may be due to several reasons: joint disease predisposes to bacterial joint colonization and RA itself and its treatment with corticosteroids, disease-modifying antirheumatic drugs (DMARDs) and biological therapies may decrease the immune function required for protection from bacterial pathogens. Staphylococcus aureus is the bacterium responsible for up to 80% of joint infections in patients with RA [4] and it has been shown that S. aureus and other gram-positive bacteria are potent inducers of TNF-α secretion from macrophages [5] and that a local increase of TNF-α levels might improve host defences against staphylococcal foreign body infections [6]. The aim of our study therefore was to retrospectively evaluate all septic arthritis cases admitted to our Rheumatology Unit in the last 12 years to assess the causative microorganisms and the risk factors, and to look at the underlying rheumatic diseases and the effect of DMARDs on the likelihood of developing SA.