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Drug-Induced Autoimmunity
Published in Richard K. Burt, Alberto M. Marmont, Stem Cell Therapy for Autoimmune Disease, 2019
Robert L. Rubin, Anke Kretz-Rommel
Drugs which appear to exacerbate SLE include antibiotics, anticonvulsants, hormones, nonsteroidal anti-inflammatory drugs (NSAIDs), and dermatologic agents. Sulfonamides, tetracyclines, griseofulvin, piroxicam, and benoxaprofen are reported to be photosensitizers of varying frequency; the rash or dermatitis related to these drugs typically has a history of rapid onset and behaves as a drug hypersensitivity-type reaction that may be triggered by exposure to ultraviolet light. The majority of adverse drug reactions in previously diagnosed SLE patients are of this category.10,11 Another, possibly related category of patients are those with acute or subacute cutaneous lupus erythematosus related to photoactive medications; these patients may have systemic disease and can fulfill criteria for a diagnosis of SLE.13 Some of these drugs are also associated with typical drug-induced lupus and are included in Table 2. Drug-induced aseptic meningitis in SLE patients is occasionally associated with ibuprofen and other NSAIDs (e.g., sulindac, tolmetin, diclofenac). Hypersensitivity reactions that have been interpreted as initiating or aggravating factors in SLE are associated with hydralazine, sulfonamides, penicillin, para-aminosalacylic acid, hydrochlorothiazide, cimetidine, phenylbutazone, mesantoin and various NSAIDs. Unknown or suspected environmental chemicals such as hair dyes and permanent wave preparations are also occasionally implicated as aggravating agents in SLE and related diseases.
Genetic variants affecting chemical mediated skin immunotoxicity
Published in Journal of Toxicology and Environmental Health, Part B, 2022
Isisdoris Rodrigues de Souza, Patrícia Savio de Araujo-Souza, Daniela Morais Leme
A potential role of null alleles of GSTM1 and GSTT1 in autoimmunity was suggested by Ollier et al. (1996) as this enables accumulation of ROS, resulting in cell death by apoptosis. Apoptosis is associated with skin autoimmunity because it allows keratinocytes to express surface blebs rich in autoantigens, such as the Ro antigen, that trigger production of anti-Ro antibody. Anti-Ro antibody is a type of anti-nuclear autoantibody associated with many autoimmune diseases (Millard, Fryer, and McGregor 2008). Apoptosis, under this context, may lead to a breakdown of the immune tolerance to Ro proteins or an exposure of Ro proteins to circulating anti-Ro antibodies results in autoimmunity (Millard, Fryer, and McGregor 2008; Ollier et al. 1996). Subacute cutaneous lupus erythematosus (SCLE) is an autoimmune skin disease associated with this biological process (Casciola-Rosen and Rosen 1997; Sontheimer 1989). SCLE presents outbreaks of erythematous, annular and/or papulosquamous lesions in a characteristic distribution and presenting Ro/SS-A autoantibodies and granular deposition of IgM, IgG and C3 in a band-like array at the dermal-epidermal junction (Lowe et al. 2011). SCLE was already induced by chemicals that induce ROS, including psoralen with UVA and environmental exposure to hydrazine-containing insecticides (Lowe et al. 2011; Shapiro et al. 2004).