Abstract

Abstract Antinuclear antibody detection by indirect immunofluorescence (IIF) is considered a hallmark for the diagnosis of systemic autoimmune rheumatic diseases. Proliferating cell nuclear antigen (PCNA) pattern is being increasingly detected in infectious diseases. Infections can mimic features of autoimmune disease and may trigger autoimmunity in genetically predisposed individuals. These may lead to a diagnostic dilemma in certain situations. A middle-aged woman, with comorbidities of diabetes mellitus and systemic hypertension, presented with a history of polyarthralgia, fever, altered sensorium, and status epilepticus. Examination showed hepatosplenomegaly and axillary lymphadenopathy. Investigations revealed elevated acute phase reactants, bicytopenia, transaminitis, and wedge infarct in spleen with coexistence of urosepsis with Escherichia coli and tropical infection. Immunological tests detected PCNA by IIF and immunoblot. The patient was treated with sensitive parenteral antibiotics and on improvement discharged. Possible explanation could be due to synthesis of biofilm by invading bacteria would have resulted in formation of an amyloid scaffold such as curli. This could have transported and presented antigens for autoantibody production. Diabetes mellitus, a state of chronic inflammation, would have accentuated NETosis. Differentiating systemic lupus erythematosus from infectious diseases is challenging. They share similar pathogenesis and clinical features. The need for the initiation of immunosuppressive therapy in lupus necessitates for absolute need for new biomarkers and tests for its differentiation from infectious diseases.

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