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Erschienen in: Zeitschrift für Rheumatologie 5/2021

11.03.2021 | Übersichten

Anti-TNF-α-induced lupus syndrome

Two case reports and review of current literature

verfasst von: Cristiana Sieiro Santos, MD, Carolina Álvarez Castro, MD, PhD, Clara Moriano Morales, MD, Elvira Díez Álvarez, MD

Erschienen in: Zeitschrift für Rheumatologie | Ausgabe 5/2021

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Abstract

Anti-tumor necrosis factor‑α (TNF-α)-induced lupus (ATIL) represents a diagnostic and treatment challenge. Most cases are caused by infliximab and in some cases by etanercept and adalimumab. Symptoms can range from cutaneous manifestations to more rare and serious conditions. Diagnosis requires a temporal relationship between symptoms and positive autoantibody determination. Arthritis and cutaneous symptoms are the most common manifestations accompanied by positive antinuclear antibody (ANA) and anti-double strand DNA (dsDNA) determinations. The etiology of ATILS remains to be definitively established. Several mechanisms have been proposed for anti-TNF-α-induced lupus, including apoptosis, immunosuppression and humoral autoimmunity. Treatment includes discontinuation of anti-TNF‑α agents and in some cases corticosteroids and immunosuppressors. Questions to be answered: (1) Are soluble TNF receptor fusion proteins such as etanercept and anti-TNF chimeric antibodies equally likely to cause ATIL? (2) Can patients with ATIL switch from one anti-TNF‑α antagonist to another? (3) Can the concurrent use of a conventional synthetic disease-modifying antirheumatic drug (csDMARD) like methotrexate or hydroxychloroquine reduce the probability of ATIL?
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Metadaten
Titel
Anti-TNF-α-induced lupus syndrome
Two case reports and review of current literature
verfasst von
Cristiana Sieiro Santos, MD
Carolina Álvarez Castro, MD, PhD
Clara Moriano Morales, MD
Elvira Díez Álvarez, MD
Publikationsdatum
11.03.2021
Verlag
Springer Medizin
Erschienen in
Zeitschrift für Rheumatologie / Ausgabe 5/2021
Print ISSN: 0340-1855
Elektronische ISSN: 1435-1250
DOI
https://doi.org/10.1007/s00393-021-00983-8

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