An arm and a leg: A case of rheumatoid vasculitis and antiphospholipid antibody syndrome.

Rheumatoid vasculitis is a rare extra-articular complication of rheumatoid arthritis. The most common manifestation is cutaneous; however, it can manifest in various organ systems and is associated with a high degree of morbidity and mortality. Diagnosis is challenging, and there are no validated diagnostic or classification criteria. Most cases should be confirmed with tissue biopsy when possible given the severity of disease and the extent of immunosuppression required to treat this condition. We report the case of a 54-year-old white woman with long-standing, uncontrolled, and seropositive rheumatoid arthritis with a history of elevated anticardiolipin IgG and IgM antibodies who presented with acute stenosis of her left femoral artery which ultimately required a left above-the-knee amputation. Histopathology revealed findings consistent with vasculitis and thrombosis, and subsequent imaging revealed multifocal arterial and venous thromboses. She was diagnosed with rheumatoid vasculitis and antiphospholipid antibody syndrome, and was treated with high-dose glucocorticoids, cyclophosphamide, and warfarin. Rheumatoid vasculitis is a rare but devastating complication of rheumatoid arthritis, and vigilance for this condition must be maintained, especially in patients with long-standing, seropositive disease.

Persistent Bacteriuria and Antibodies Recognizing Curli/eDNA Complexes From Escherichia coli Are Linked to Flares in Systemic Lupus Erythematosus.

OBJECTIVE: Infections contribute to morbidity and mortality in systemic lupus erythematosus (SLE). Uropathogenic Escherichia coli (UPEC) are known to trigger urinary tract infections (UTIs) and form biofilms, which are multicellular communities of bacteria that are strengthened by amyloids such as curli. We previously reported that curli naturally form complexes with bacterial extracellular DNA (eDNA), and these curli/eDNA complexes induce hallmark features of lupus in mouse models. The present study was undertaken to investigate whether anti-curli/eDNA complex antibodies play a role in the pathogenesis of SLE or development of flares in SLE. METHODS: In total, 96 SLE patients who met at least 4 Systemic Lupus International Collaborating Clinics disease criteria were investigated. Anti-curli/eDNA complex antibodies in the plasma were tested for both IgG and IgA subclasses. Results were compared to that in 54 age-, sex-, and race/ethnicity-matched healthy controls. Correlations of the levels of anti-curli/eDNA antibodies with clinical parameters, lupus disease status, and frequency of bacteriuria were assessed. RESULTS: Anti-curli/eDNA antibodies were detected in the plasma of SLE patients and healthy controls, and their levels correlated with the presence of asymptomatic persistent bacteriuria and occurrence of disease flares in lupus patients. Persistent bacteriuria contained curli-producing UPEC, and this was associated with an inflammatory phenotype. Finally, curli/eDNA complexes cross-reacted with lupus autoantigens, such as double-stranded DNA, in binding autoantibodies. CONCLUSION: These results suggest that UTIs and persistent bacteriuria are environmental triggers of lupus and its flares. Antibodies against curli/eDNA could serve as a sign of systemic exposure to bacterial products in SLE.