Published on 16/03/2015 by admin
Filed under Dermatology
Last modified 16/03/2015
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Jeffrey P. Callen and Courtney R. Schadt
Evidence Levels: A Double-blind study B Clinical trial ≥ 20 subjects C Clinical trial < 20 subjects D Series ≥ 5 subjects E Anecdotal case reports
Subacute cutaneous lupus erythematosus (SCLE) is a non-scarring, non-atrophic variant of lupus erythematosus (LE) that was first distinguished from other cutaneous variants in 1979. At least half of the patients with SCLE have or develop four or more of the features that allow classification as systemic LE using the criteria of the American College of Rheumatology. In general, however, their prognosis is better than that of unselected patients with systemic LE and these patients have less likelihood of having renal or neurologic disease (Black, D.R., et al, 2002. Arch Dermatol 138 (9),1175–1178).
Therapy of cutaneous lesions in patients with LE involves both an empiric and a scientific approach. Unfortunately, there are few double-blind, placebo-controlled trials of drugs used in the treatment of cutaneous LE.
The goals of management of SCLE are to improve the patient’s appearance, relieve the symptomatology, and prevent the development of dyspigmentation. Cosmetic problems are often of major importance to the patient with cutaneous LE. Dyspigmentation may follow SCLE, and may be effectively hidden by agents such as Covermark™ or Dermablend™.
Once a diagnosis of subcutaneous LE has been made, management must involve sun avoidance and sun protection, and elimination of medications that might be responsible for the skin lesions. Treatment with the most benign drugs possible should be stressed. Topical corticosteroids and oral antimalarials are the most commonly prescribed medications. Although systemic corticosteroids may be highly effective, attempts should be made to reduce their dosage and use other medications in their place to avoid corticosteroid-associated side effects.
Thorough evaluation to exclude systemic disease
History of drug ingestion that might be responsible for the disease
History of smoking
The cornerstone of the management of SCLE is correct diagnosis and thorough evaluation. The patient should have a careful history, physical examination, and laboratory studies directed at uncovering systemic manifestations that might occur in LE. The risk of serious systemic involvement (renal, central nervous system, or cardiopulmonary involvement) in patients with SCLE is probably around 10%, though many patients with SCLE – more than 50% – have sufficient criteria to classify them as having systemic lupus erythematosus (SLE).
Srivastava M, Rencic A, Diglio G, Santana H, Bonitz P, Watson R, et al. Arch Dermatol 2003; 139: 45–9.
This study detailed only patients with cutaneous disease who were anti-Ro/SS-A positive. However, it was found that, among 70 such patients, 15 had a link to a new drug within 6 months of the diagnosis of SCLE. Most of these instances were linked to antihypertensive agents, but two patients with statin-induced disease were reported.
Grönhagen CM, Fored CM, Linder M, Granath F, Nyberg F. Br J Dermatol 2012; 167: 296–305.
This study is a first in which population-based data for diagnosis of cutaneous LE were compared with a national database on prescription drug use. In this study, the authors linked SCLE to terbinafine (OR [odds ratio]=38.5, 95% CI 6.6–∞), tumor necrosis factor-α (TNF-α) inhibitors (OR=8.0, 95% CI 1.6–37.2), antiepileptics (OR=3.4, 95% CI 1.9–5.8) and proton pump inhibitors (OR=2.9, 95% CI 2.0–4.0). They did not find a significant OR for thiazides, or other antihypertensive agents, which they speculated might be due to a longer latency between the time of prescription and the onset of disease.
A complete list of the patient’s medications will assist in the exclusion of drug-induced cutaneous LE. Drugs that have been linked as causes of SCLE primarily include antihypertensive agents such as hydrochlorothiazide, calcium channel blockers, statins, proton pump inhibitors, terbinafine, tumor necrosis factor-α antagonists, and angiotensin-converting enzyme inhibitors. Because of the growing list of agents linked to SCLE development or exacerbation, any newly introduced drug should be considered as a possible trigger.
Lowe G, Henderson CL, Grau RH, Hansen CB, Sontheimer RD. Br J Dermatol 2011; 164: 465–72.
This report details a literature review of 117 cases of drug-induced SCLE. Antihypertensive medications and antifungals are the most commonly reported medicines. The reaction often occurs after months of therapy and most of the implicated agents are photosensitizers.
Although reports of antifungal medications as causes of SCLE are numerically greater, the most frequently implicated drug remains hydrochlorothiazide.
Gallego H, Crutchfield III CE, Lewis EJ, Gallego HJ. Cutis 1999; 63: 231–4.
These authors suggest that cutaneous LE is more severe in patients who smoke.
Jewell ML, McCauliffe DP. J Am Acad Dermatol 2000; 42: 983–7.
These authors compared antimalarial-responsive patients to those who did not respond. Their results indicate that patients with cutaneous LE who smoke are significantly less likely to respond to antimalarial therapy.
Wahie S, Daly AK, Cordell HJ, Goodfield MJ, Jones SK, Lovell CR, et al. J Invest Dermatol 2011; 131: 1981–6.
In a multicenter observational and pharmacogenetic study of 200 patients with discoid LE treated with hydroxychloroquine these authors failed to demonstrate an effect of cigarette smoking on responsiveness to antimalarial therapy. However, severity of cutaneous disease as measured by body surface extent and the presence of SLE were predictive of poor responsiveness.
Piette EW, Foering KP, Chang AY, Okawa J, Ten Have TR, Feng R, Werth VP. Arch Dermatol 2012; 148: 317–22.
In this study smokers with LE had worse disease and quality of life, and were more often treated with a combination of hydroxychloroquine and quinacrine than were non-smokers, suggesting that their response to antimalarials is impaired. Never and past smokers showed greater improvement when treated with antimalarial agents plus at least one additional immunomodulator.
Regardless of whether smoking impacts the effectiveness of antimalarial agents, patients who smoke should be encouraged to stop for the benefit of their skin disease.
Lehmann P, Holze E, Kind P, Goerz G, Plewig G. J Am Acad Dermatol 1990; 22: 181–7.
The action spectrum was defined by photoprovocation testing and includes UVA, UVB, and occasionally visible light.
Broad-spectrum sunscreens, protective clothing, and sun avoidance are important parts of any therapeutic regimen.
Stege H, Budde MA, Grether S, Krutmann J. Photodermatol Photoimmunol Photomed 2000; 16: 256–9.
These authors examined the capacity of three sunscreens to prevent the development of skin lesions by provocative phototesting. Although each of the three sunscreens tested prevented lesions, the extent to which they did so varied greatly. The sunscreen that was most effective contained Octocrylene as the UVB protectant, Mexoryl SX, Mexoryl XL, and Parsol 1789 as UVA protectants, and titanium oxide. This sunscreen’s SPF was 60. Their study was of only 11 patients (nine men and two women), of whom eight had SCLE and three had discoid LE.
Callen JP. J Rheumatol 1985; 12: 630–3.
Intralesional injections of corticosteroids are often effective in patients with lesions that are refractory to topical corticosteroids. Small amounts of triamcinolone acetonide 3 mg/mL may be injected with a 30-gauge needle into multiple areas. These injections are often very effective in control of the lesions, but do not prevent the development of new lesions.
The potential for cutaneous atrophy and/or dyspigmentation similar to that seen with the disease should be discussed with the patient; however, in most cases an experienced dermatologist is able to inject without a great risk. Alternative agents for intralesional injection have not been well tested.
Feldmann R, Salomon D, Saurat JH. Dermatology 1994; 189: 425–7.
Treatment of Skin Disease Comprehensive Therapeutic Strategies 4e
Cosmetics
Sunscreens and protective clothing
Corticosteroids
Antimalarials
Topical retinoids
Topical tacrolimus or pimecrolimus
