Background

The relationship between systemic lupus erythematosus (SLE) patients treated with rituximab and nocardiosis remains unclear.

Cases Report

A 55-year-old female with lupus nephritis II and smoking history, was treated with high-dose steroids, immunoglobulins, rituximab, and azathioprine. She developed infectious loci in the lungs, hip, and brain. N. farcinica was detected in bronchoalveolar lavage and abscess culture. She was treated with linezolid, trimethoprim/sulfamethoxazole (TMP/SMX), minocycline, and amoxicillin/clavulanic acid, achieving complete cure at 12 months. The second patient, a 73-year-old male with lupus nephritis V, autoimmune thrombocytopenia, antiphospholipid syndrome (APS), and alveolar hemorrhage, was treated with high-dose steroids, azathioprine, mycophenolate, and rituximab. He developed infections in the lungs, prostate, and possibly colon. N. farcinica was detected in blood cultures. Despite treatment with imipenem, linezolid, TMP/SMX, and moxifloxacin, he died from bronchoaspiration.

Methods

A systematic review was conducted using PubMed, Embase, Web of Science, and Scopus. The search terms were (systemic lupus erythematosus OR SLE) AND (rituximab) AND (nocardia), with a timeframe up to 15 March 2024. Inclusion criteria were confirmed cases of Nocardia infection in SLE patients treated with rituximab in the previous year. Non-original studies and secondary research were excluded.

Results

Only one article was included, describing a 34-year-old male with APS and lupus nephritis IV, treated with high-dose steroids, cyclophosphamide, and rituximab. He had infections in the lungs and brain, with N. farcinica detected in blood cultures. Despite treatment with TMP/SMX and fluoroquinolones, he died from thrombotic complications.

Conclusion

Nocardiosis is more likely in SLE patients due to T lymphocyte immune dysfunction caused by the disease itself, rituximab, and other immunosuppressants. Diagnosis requires a high level of clinical suspicion, supported by long-time blood cultures and 16S rRNA. Beta-lactams and quinolones are reasonable alternatives to TMP/SMX and linezolid, which can worsen the hematological situation, and amikacin, which may worsen lupus nephritis.