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Paul Chabert, Hatem Kallel
2020-10-19
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We present the case of a 25-year-old woman without medical history, presenting with acute respiratory failure needing mechanical ventilation. Aetiologic screening showed PVB19 primary infection and concomitant SLE flare-up. We discuss the causative interactions between PVB19 and SLE in the pathogenesis of the disease. Difficulty diagnosing inaugural SLE flare-up concomitant with PVB19 infection can lead to delayed diagnosis and treatment. Inversely, overtreating a SLE-mimicking PVB19 infection with immunosuppressive agents can be highly detrimental.
Roxana González-Mazarío, Luisa Suárez Álvarez, Luisa Micó, Inés Moret Tatay, Miguel Salavert Lletí
2015-02-06
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Immunologic storm simulating systemic lupus erythematosus following parvovirus B19 infection.: 0
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Background: The appearance of symptoms compatible with systemic autoimmune diseases has been described in relation to several viral infections like HIV, cytomegalovirus and especially PVB19, depending on the evolution of the immunological condition of the host and their age. We present a young immunocompetent male patient, with clinical manifestations simulating systemic lupus erythematosus (SLE) with important activation of cytokines.
Methods: For quantification of the different cytokines in plasma, a commercially available multiplex bead immunoassay, based on the Luminex platform (Cat # HSCYTO-60SK-08, Milliplex® MAP High Sensitivity, Millipore), was used according to the manufacturer’s instructions. All samples were run in duplicate and the data (mean fluorescence intensity) were analyzed using a Luminex reader. The mean concentration was calculated using a standard curve.
Results: The clinical evolution was favourable without the need for any specific treatment, showing complete recovery after two months. Whilst the symptoms and viral charge were disappearing, the anti-DNA continued to increase and we demonstrate important activation of IL-10, IL-6 and TNF? cytokines as a result of a hyperstimulating response by an immunocompetent hyperfunctional system, which persists after clinical improvement. We should emphasize the behaviour of two cytokines: IL-12p70 and IL-2, which showed opposite tendencies.
Conclusions: Viral infections, especially PVB19, can produce or simulate several autoimmune diseases as a hyperstimulation response from an immunocompetent hyperfunctional system. Consequently, a persistent increase of autoantobodies and important activation of cytokines, even after clinical improvement and seroconversion, can be demonstrated.
2.1 = | 1.730 Cit. to date |
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