Drug-induced Cutaneous Lupus Erythematosus Research Articles

Drug-induced photosensitivity associated with anticancer therapies.

Despite the promising results in terms of effectiveness of anticancer treatments, a wide range of dermatologic adverse reactions have been reported. Among them, skin photosensitivity, defined as a range of dermatologic conditions caused or exacerbated by sunlight exposure, is an emerging adverse event. A review of the current literature was performed to report the most characteristic phototoxic and photoallergic reactions associated with anticancer therapies, as well as other characteristic manifestations potentially related to photo-exposure, including UV recall, vitiligo-like reactions, drug-induced cutaneous lupus erythematosus, and UV-induced hyperpigmentation. A total of 30 manuscripts were collected in the present review, reporting several phototoxic and photoallergic reactions associated with anticancer therapies. Photosensitivity reactions are an increasing challenge in cancer management. The raising awareness about this adverse event has increased the identification of potential photosensitizing drugs as well as its prevention and the management. However, more studies are required to improve the knowledge of this cutaneous toxicity and to define a personalized treatment strategy.

Analysis of clinical characteristics of drug-induced cutaneous lupus erythematosus in men

Analysis of clinical characteristics of drug-induced cutaneous lupus erythematosus in men

Drug-Induced Cutaneous Lupus Erythematosus: A Case Series of Five Patients with Bupropion-Associated Disease.

Drug-Induced Cutaneous Lupus Erythematosus: A Case Series of Five Patients with Bupropion-Associated Disease.

Drug-Induced Cutaneous Lupus Erythematosus

Drug-Induced Cutaneous Lupus Erythematosus

Drug-induced cutaneous lupus erythematosus: 88 new cases.

An increasing number of drugs have been linked to drug-induced subacute cutaneous lupus erythematosus (DI-SCLE). The recognition and management of DI-SCLE can be challenging, as the condition may be triggered by different classes of drugs after variable lengths of time. To determine the proportion of patients with cutaneous lupus erythematosus (CLE) whose drugs are an inducing or aggravating factor. We conducted a retrospective chart review of patients diagnosed with CLE at a dermatological department over a 21-year period. We registered clinical, serological, and histological data with a focus on drug intake. Of 775 consecutive patients with a diagnosis of lupus erythematosus (LE) or suspected LE, a diagnosis of CLE could be confirmed in 448 patients. A total of 130 patients had a drug intake that could suggest DI-SCLE. In 88 cases, a drug was evaluated to be definitely, probably, or possibly triggering CLE using the Naranjo probability scale. The most common drugs involved were proton pump inhibitors (PPIs), thiazide diuretics, antifungals, chemotherapeutics, statins, and antiepileptics. The incubation period varied widely with a median of eight weeks. The characteristics of DI-SCLE patients were more widespread rash relative to the other patients, with inflamed skin lesions or atypical variants which could resemble erythema multiforme. We present 88 patients with DI-SCLE, which is the largest case series reported, to date. DI-SCLE represented 20% of patients with CLE seen at our department. We conclude that DI-SCLE should be considered in every case of SCLE.

LÚPUS ERITEMATOSO CUTÂNEO INDUZIDO POR FÁRMACOS

As Estatinas são um grupo farmacológico muito utilizado atualmente. São habitualmente bem toleradas, no entanto, podem estar implicadas na génese/agravamento de doenças auto-imunes como Lupus Eritematoso Cutâneo. Descreve-se o caso de uma doente caucasóide, de 74 anos que, 18 meses após início de terapêutica com sinvastatina, desenvolveu uma dermatose localizada à raiz dos membros superiores e dorso, constituída por pápulas e placas eritematosas, anulares e com superfície descamativa. Analiticamente era de salientar presença de ANA e anticorpos anti-SSA. O exame histopatológico foi consistente com a hipótese clínica de Lupus Eritematoso Cutâneo Subagudo. Após a suspensão da Sinvastatina assistiu-se à resolução completa do quadro clínico e laboratorial. O Lupus Eritematoso Cutâneo induzido por fármacos é uma entidade muitas vezes indistinguível das formas idiopáticas. Apesar de frequentemente ter uma evolução e prognóstico favoráveis, salienta-se a sua importância pelo possível envolvimento sistémico associado e pelas sequelas cutâneas, por vezes desfigurantes.

Susceptibility of T cell receptor-alpha chain knock-out mice to ultraviolet B light and fluorouracil: a novel model for drug-induced cutaneous lupus erythematosus.

The anticancer agent 5-fluorouracil (FU) frequently induces cutaneous lupus erythematosus (LE) lesions on sun exposed sites. Based on this observation, we have tried to establish a cutaneous LE model of C57BL/6 J (B6) mice, B6 T cell receptor (TCR)-alpha(-/-) mice and B6 TCR-delta(-/-) mice treated with FU and/or ultraviolet B light (UVBL) in order to clarify the role of T cells and the cytokine profile of cutaneous lupus lesions. Cutaneous LE-like skin lesions could be induced in TCR-alpha(-/-) mice with low FU (0.2 mg) plus UVBL, and in B6 mice treated with a high dose of FU (2.0 mg) plus UVBL. In contrast, low FU plus UVBL induced such skin lesions in TCR-delta(-/-) mice at a very low incidence. Specifically, the skin lesions of TCR-alpha(-/-) mice with low FU plus UVBL appeared more rapidly and were more severe than lesions in B6 mice. The former had the common characteristic features of human chronic cutaneous LE such as typical histology, positive IgG at the dermoepidermal junction, low antinuclear antibody and low mortality. Furthermore, a Th1 response was induced in the development of drug-induced cutaneous LE. FU and UVBL-induced cutaneous LE-like eruption is an excellent model for better understanding the pathomechanisms of skin lesion development in LE.

Drug-induced cutaneous lupus erythematosus, a distinct syndrome that is frequently unrecognized

J Am Acad Dermatol 2001;45:315-6.