Simultaneous Presentation of Parvovirus B19 Infection and Sy
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The differential diagnosis between parvovirus B19 primary infection and systemic lupus erythematosus flare-up can be difficult. Parvovirus B19 primary infection can elicit authentic severe systemic lupus erythematosus flare-up that requires urgent immunosuppressive therapy. Parvovirus B19 primary infection can also mimic systemic lupus erythematosus.

A 25-year-old woman was admitted to intensive care unit, for febrile acute respiratory failure, polyarthralgia and rash. She had no medical history and no anterior apparent SLE-compatible symptoms. The first symptoms appeared 2 weeks earlier with febrile diffuse arthromyalgia and cough. Clinical findings at admission showed: sinus tachycardia without murmur, bilateral crackles, oxygen desaturation, no joint swelling, malar macular rash, digital purpura and buccal ulcerations.

Chest CT showed bilateral interstitial infiltration, with alveolar opacities and bilateral pleural effusion. Initial echocardiography found normal left ventricular systolic function, with little pericardial effusion. The patient received empiric antibiotherapy with cefotaxime and levofloxacin and diuretic therapy. Despite this, the respiratory state worsened and the patient required invasive protective mechanical ventilation. Transitory deterioration of left ventricular global systolic function was noted

She received corticosteroid boluses, intravenous immunoglobulins and cyclophosphamide. In a second phase, while thrombocytopenia persisted, haptoglobin plummeted, reticulocytes increased and schistocytes reached 4.7%. She developed a transient moderate acute kidney injury. Renal biopsy objectified class II mesangial proliferative lupus glomerulonephritis, and capillary thrombi consistent with thrombotic microangiopathy. ADAMTS13 activity was normal. All abnormalities scaled back without plasma exchange.

The patient was weaned from mechanical ventilation and discharged from hospital. Long-term follow-up confirmed the persistence of biological auto-immunity and the diagnosis of SLE, its clinical course being now stabilized with oral corticosteroid and immunosuppressive drugs.