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Chronic erythematous rash on the face
Published in Richard Ashton, Barbara Leppard, Differential Diagnosis in Dermatology, 2021
Richard Ashton, Barbara Leppard
An erythema on the face associated with fever and arthralgia in a female patient is suggestive of SLE. The rash characteristically occurs in a ‘butterfly’ distribution (cheeks and bridge of nose), but does not always do so. There is also nail fold telangiectasia with ragged cuticles. Although the site may be similar to rosacea, there are no papules or pustules. The patient may have renal involvement, psychiatric or neurological symptoms, pericarditis, pleurisy or abdominal pain. Chilblains and Raynaud's phenomenon are likely. A positive anti-nuclear factor will confirm the diagnosis. An illness identical to SLE can be caused by drugs such as procainamide, hydralazine, minocycline and the anti-TNF monoclonal biologic therapies. Subacute cutaneous lupus erythematosus looks like SLE and there may be positive auto-antibodies, but systemic symptoms are absent.
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.
Photosensitivity and Photoreactions
Published in Gabriella Fabbrocini, Mario E. Lacouture, Antonella Tosti, Dermatologic Reactions to Cancer Therapies, 2019
Cecilia A. Larocca, Mackenzie Asel, Mario E. Lacouture
Cancer therapies may cause dermatologic conditions that are exacerbated by exposure to ultraviolet radiation (Table 4.5). Chemotherapy, targeted therapies, and immunotherapy have all been reported to induce connective tissue diseases, such as subacute cutaneous lupus erythematosus, a photosensitive autoimmune condition (59–63). In particular, hydroxyurea has been associated with several photosensitive connective tissue diseases and is the most common trigger of drug-induced dermatomyositis (64–66). Tegafur has also caused dermatomyositis and lupus-like syndromes (11).
Cutaneous adverse events of immune checkpoint inhibitor therapy: incidence and types of reactive dermatoses
Published in Journal of Dermatological Treatment, 2022
Thomas K. Le, Subuhi Kaul, Laura C. Cappelli, Jarushka Naidoo, Yevgeniy R. Semenov, Shawn G. Kwatra
Of the 1857 patients treated with anti-PD-1 ICIs, there were 1079 patients treated with nivolumab, 821 patients treated with pembrolizumab, and 43 patients treated with both pembrolizumab and nivolumab. There were 254/1857 (13.7%) patients who developed one of the 28 different dermatoses identified from the literature review following anti-PD-1 ICIs. Eleven reactions, although reported in the literature, had an incidence n < 5: xerosis (n = 4), Stevens-Johnson syndrome (n = 2), paronychia (n = 2), panniculitis (n = 2), onycholysis (n = 2), maculopapular eruption (n = 2), bullous pemphigoid (n = 2), alopecia areata (n = 2), acral erythema (n = 2), Grover’s disease (n = 2), and erythema multiforme (n = 2), as reported in Table S1. 6 reactions had an incidence of n = 0. This included dermatomyositis, erythroderma/pityriasis rubra pilaris, granuloma annulare, hyperkeratosis, photosensitivity, and subacute cutaneous lupus erythematosus (Table S1).
Safety of topical interventions for the treatment of actinic keratosis
Published in Expert Opinion on Drug Safety, 2021
Elias A. T. Koch, Anja Wessely, Theresa Steeb, Carola Berking, Markus V. Heppt
Other uncommon side effects of topical IMQ have been reported in the literature. Many reports describe an exacerbation or manifestation of skin conditions such as generalized psoriasis, pityriasis rubra pilaris, subacute cutaneous lupus erythematosus, severe eczema, contact pemphigus, pemphigus foliaceus, pemphigus-like symptoms, erosive cheilitis, erosive pustular dermatosis, morbilliform exanthema, and eruptive epidermoid cysts [65–75]. Furthermore, vasodilatory AE such as angioedema and urticaria have been described [76]. Also several cases with cSCC development after IMQ treatment have been reported. Singh et al. described the case of an 80-year-old male receiving IMQ 5% for AK. Six weeks after the treatment, he developed a well‐differentiated cSCC in an area of radiodermatitis [77]. Two further cases of histologically verified cSCC in the application site after treatment of cSCC in situ with 5% IMQ once a day for 6 weeks were published by Goh et al. One Patient developed a cSCC along with cervical lymph node metastasis 2 months after treatment. Another cSCC was reported in a patient with chronic lymphocytic leukemia 4 months after treatment with IMQ [78].
Animal models of systemic lupus erythematosus and their applications in drug discovery
Published in Expert Opinion on Drug Discovery, 2022
Yue Xin, Bo Zhang, Junpeng Zhao, Qianmei Liu, Haoyuan Yin, Qianjin Lu
Imiquimod (IMQ) is an immunomodulator topically applied to treat superficial cutaneous tumors that activates TLRs and induces proinflammatory cytokine production. IMQ-induced subacute cutaneous lupus erythematosus (SCLE) at the drug application site or distant sites has been observed occasionally [56]. Based on effect of TLR on initiating SLE in the BXSB and MRL/lpr strains, Yokogawa et al. constructed a new lupus model from wild-type mice, including FVB/N, BALB/c, C57BL/6 strains, by topically applying the TLR7 agonist IMQ in the ears 3 times a week, and the animals developed systemic autoimmune manifestations, including nephritis, hepatitis, hypertension, carditis, and photosensitivity [57]. Significantly elevated IgG2a titers were observed at the age of 4 w, similar to the appearance of immune complex-mediated glomerulonephritis. Activated TLR increased the IFN-α level, which was responsible for lupus induced by IMQ. Recent studies revealed that type II IFN (IFN-γ) and type III IFN (IFN-λ) are also related to the dysregulation of immunity and organ injury in individuals with lupus, with the alleviation of nephritis and skin lesions occurring after the deletion of the IFN-λ receptor [58,59]. Another TLR7 agonist, resiquimod (R848), has also been shown to exert a similar effect as IMQ, as treated C57BL/6 mice exhibit significant splenomegaly and early death without nephritis, which is not an ideal model of SLE. However, resiquimod is capable of serving as an autoimmune accelerator in mice with genetic backgrounds such as the NZM 2410 strain in which aggravated nephritis and some fatal secondary are complications present, including histiocytic sarcoma and macrophage activation syndrome-like disease [60].