Periprosthetic joint infection during biologic therapy in rheumatoid arthritis: two cases successfully managed without implant removal—a case report

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Background Periprosthetic joint infection (PJI) is a devastating complication of arthroplasty, and in patients with rheumatoid arthritis (RA) receiving biological disease-modifying antirheumatic drugs (b-DMARDs), its diagnosis and management are particularly challenging. Because b-DMARDs blunt the acute-phase response, PJI in these patients may present with attenuated fever and C-reactive protein (CRP), delaying diagnosis. Whether late acute hematogenous PJI arising during biologic therapy can be managed with retention of the prosthesis remains uncertain. Case presentation We report two Japanese women with long-standing RA who developed late acute hematogenous PJI during b-DMARD therapy. Case 1, a 77-year-old Japanese woman on etanercept plus methotrexate (MTX) 9 years after left bipolar hemiarthroplasty, presented in septic shock with methicillin-susceptible Staphylococcus aureus (MSSA) bacteremia and multifocal abscesses (left hip, right acromioclavicular joint, bilateral iliopsoas). Case 2, a 63-year-old Japanese woman on tocilizumab plus MTX 2 years after total elbow arthroplasty, had progressive elbow pain and a draining sinus despite a CRP of 0.01 mg/dL; cultures yielded Listeria monocytogenes . In both cases, b-DMARDs were discontinued and pathogen-directed antibiotics were administered. The prostheses were retained: in Case 1 after bedside incision and drainage of the affected joints without formal debridement (because of hemodynamic instability), and in Case 2 after open debridement with polyethylene liner exchange. Neither prosthesis has shown recurrence at 5-year follow-up, and RA has subsequently been controlled with conventional synthetic DMARDs (cs-DMARDs) alone. Conclusions Two learning points emerge. First, b-DMARDs—particularly interleukin-6-receptor blockade—can markedly attenuate the clinical and laboratory signature of PJI, so a high index of suspicion is essential even when fever and CRP are absent. Second, these two cases illustrate that, in carefully selected patients, late acute hematogenous PJI arising during biologic therapy can be managed with retention of the prosthesis when b-DMARDs are promptly discontinued, the causative pathogen is identified, and adequate source control is achieved. These observations are hypothesis-generating and do not establish the general effectiveness of debridement, antibiotics, and implant retention (DAIR) in this population. Both patients were maintained on cs-DMARDs without biologic reintroduction; whether biologics should be permanently discontinued after PJI should be decided individually.