The Open Rheumatology Journal

ISSN: 1874-3129 ― Volume 10, 2016

Anti-Tumor Necrosis Factor-α Induced Systemic Lupus Erythematosus§

Hani Almoallim*, 1, 2, Yahya Al-Ghamdi 1, Haneen Almaghrabi 1, Omnia Alyasi 1
1 Department of Medicine, Umm Alqura University, Makkah, Saudi Arabia
2 Alzaidi Chair of Research in Rheumatic diseases, Umm Alqura University, Makkah, Saudi Arabia


Anti-tumor necrosis factor-alpha induced lupus (ATIL) represents a major diagnostic and therapeutic challenge. Most cases of ATIL are caused by infliximab, followed by etanercept and adalimumab. Symptoms can range from common, mild cutaneous lesions to rare, serious pleural or pericardial effusions, deep venous thrombosis, life-threatening pneumonitis, and neuritis. Constitutional symptoms often present in association with positive autoantibody serology. Diagnosis can be considered if there is a temporal relationship between symptoms and anti-tumor necrosis factor-α (TNF- α) therapy and at least one serologic and one non-serologic American College of Rheumatology criteria. Since it is contraindicated to use anti-TNF-α drugs in patients with systemic lupus erythematosus, it is recommended to perform a thorough immunological screening in any patient with polyarthritis to assure accurate diagnosis. In addition, prior to anti- TNF therapy, baseline immunological investigations (including antinuclear antibodies) should be performed, and there should be close follow up to assess the development of lupus manifestations. The main approach in the treatment of ATIL is withdrawal of the offending drug. Traditional therapy with corticosteroids and immunosuppressive agents may be required to achieve full resolution of lupus symptoms. In this review, we discuss the pathogenesis, clinical manifestations, and management of ATIL.

Keywords: Anti-tumour necrosis factor alpha, disease modifying anti-rheumatic drugs, drug-induced lupus, rheumatoid arthritis, systemic lupus erythematosus..

Article Information

Identifiers and Pagination:

Year: 2012
Volume: 6
First Page: 315
Last Page: 319
Publisher Id: TORJ-6-315
DOI: 10.2174/1874312901206010315

Article History:

Received Date: 30/9/2012
Revision Received Date: 22/10/2012
Acceptance Date: 26/10/2012
Electronic publication date: 16/11/2012
Collection year: 2012

© Almoallim et al.; Licensee Bentham Open.

open-access license: This is an open access article licensed under the terms of the Creative Commons Attribution Non-Commercial License ( which permits unrestricted, non-commercial use, distribution and reproduction in any medium, provided the work is properly cited.

* Address correspondence to this author at the Department of Medicine, Umm Alqura University, Makkah, Saudi Arabia; Tel: 00966505703935; E-mails:,


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