Trigger factors of cutaneous lupus erythematosus: a review of current literature

Abstract

It is currently believed that autoimmune conditions are triggered and aggravated by a variety of environmental factors such as cigarette smoking, infections, ultraviolet light or chemicals, as well as certain medications and vaccines in genetically susceptible individuals. Recent scientific data have suggested a relevant role of these factors not only in systemic lupus erythematosus, but also in cutaneous lupus erythematosus (CLE). A variety of environmental factors have been proposed as initiators and exacerbators of this disease. In this review we focused on those with the most convincing evidence, emphasizing the role of drugs in CLE. Using a combined search strategy of the MEDLINE and CINAHL databases the following trigger factors and/or exacerbators of CLE have been identified and described: drugs, smoking, neoplasms, ultraviolet radiation and radiotherapy. In order to give a practical insight we emphasized the role of drugs from various groups and classes in CLE. We also aimed to present a short clinical profile of patients with lesions induced by various drug classes.

Drug-induced subacute cutaneous lupus erythematosus caused by amlodipine

“…Serological markers of DI-SCLE include anti-Ro/SS-A antibodies, occasionally coexisting with anti-La/SS-B antibodies. Conversely, anti-histone antibodies (AHA), typically associated with DI-SLE, rarely accompany DI-SCLE (20-40%) and cannot be regarded as a serological marker of the condition [6,15]. There are no differences between SCLE and DI-SCLE in terms of histopathological findings and DIF results [13].…”

“…DI-SCLE develops as a result of exposure to certain drugs, usually hypotensive agents: calcium channel blockers (CCBs), diuretics, angiotensin-converting-enzyme inhibitors, β-blockers and antifungal medications (chiefly terbinafine) [12]. Common causative factors also include proton pump inhibitors, ticlopidine and chemotherapeutics (typically taxanes) [16,17], and less commonly antihistamines and statins [15]. The period between the initiation of drug therapy and the onset of pathological lesions (i.e.…”

“…Among medications used in the treatment of arterial hypertension, CCBs and thiazide diuretics are most commonly reported as the causative factors of DI-SCLE [15]. Both dihydropyridine and nondihydropyridine CCBs are responsible for inducing DI-SCLE, however the vast majority of reported cases are attributed to verapamil and diltiazem, and rarely to nifedipine and nitrendipine.…”

“…Markerem serologicznym DI-SCLE są również przeciwciała anty-Ro/SS-A, które niekiedy współistnieją z przeciwciałami anty-La/SS-B. Natomiast przeciwciała przeciwhistonowe (anti-histone antibodies -AHA), typowe dla DI-SLE rzadko występują w przebiegu DI-SCLE (20-40%) i nie mogą być uznane za jego marker serologiczny [6,15]. Obraz histologiczny oraz DIF nie wykazują różnic między SCLE i DI-SCLE [13].…”

“…Do rozwoju DI-SCLE dochodzi wskutek ekspozycji na niektóre leki, najczęściej przeciwnadciśnieniowe: inhibitory kanału wapniowego (calcium channel blockers -CCB), diuretyki, inhibitory konwertazy angiotensyny, β-adrenolityki, oraz leki przeciwgrzybicze (przede wszystkim terbinafinę) [12]. Częstym czynnikiem sprawczym są również inhibitory pompy protonowej, tiklopidyna i chemioterapeutyki (najczęściej taksany) [16,17], a rzadziej leki przeciwhistaminowe i statyny [15]. Czas między rozpoczęciem stosowania leku a pojawieniem się zmian chorobowych (tzw.…”