Are You Confident of the Diagnosis?
Discoid lupus erythematosus (DLE) is a form of chronic cutaneous lupus erythematosus (CCLE). A diagnosis of discoid lupus erythematosus can be made with the characteristic clinical appearance and location of cutaneous lesions together with histopathologic confirmation. It is a photosensitive dermatosis, but there may not be a clear temporal association between sun exposure and its development.
Discoid lupus erythematosus can be limited, involving only the head and neck, or diffuse. Those patients with diffuse lesions below the head and neck are more likely to develop systemic lupus erythematosus (SLE). Arthralgias may be present in patients with DLE.
• Characteristic findings on physical examination
Characteristic discoid lesions are erythematous and sometimes indurated lesions with keratotic scale that vary in size. Dilated follicles plugged with keratin, or follicular plugging, are common and can best be seen on the scalp. If the scale from these follicular areas is lifted, conical projections may extend downward giving the “carpet tack” sign. Atrophic scars and dyspigmentation remain after the active lesions resolve. Typically there is a hypopigmented atrophic center surrounded by hyperpigmentation at the periphery. This is most dramatic in darker skin-type patients (Figure 1, Figure 2).
Scarring alopecia on the scalp may also be a prominent feature. Discoid lesions follow a photodistributed pattern that involves the scalp, face and ears (particularly the conchal bulb), but can also involve areas below the neck, mucosal surfaces, and sun-protected sites. Variants of DLE include hypertrophic DLE (thick hyperkeratotic plaques, which may be confused with squamous cell carcinoma clinically and histologically), mucosal DLE (oral, conjunctival, nasal, and genital lesions), and lichenoid DLE (DLE and lichen planus overlap).
• Expected results of diagnostic studies
There is no confirmatory laboratory test to diagnose discoid lupus and only 10% to 30% of patients present with positive antinuclear antibodies (ANA). A skin biopsy is warranted to confirm the clinical diagnosis of DLE. A biopsy of an active lesion will show hyperkeratosis, thickened dermal-epidermal and follicular basement membrane, and interface dermatitis with perivascular and periadnexal lymphohistiocytic infiltrate (Figure 3, Figure 4, Figure 5).
If routine histology and clinical presentation are definitive, direct immunofluorescence (DIF) is not necessary. In ambiguous cases, a DIF can be helpful. Skin direct immunofluorescence demonstrates granular IgG and/or IgM deposition at the dermo-epidermal junction and around hair follicles.
Who is at Risk for Developing this Disease?
DLE is the most common subset of CCLE. African-Americans are at increased risk of developing DLE. In DLE the number of female to males affected is similar, unlike the female predominance seen in other CLE subsets and SLE.
What is the Cause of the Disease?
CLE, including DLE, is an autoimmune disease felt to be due to an interplay of genetics, hormones and environment. Given that lupus is more common in women of childbearing age, estrogen is felt to be a cause. However, given the equal number of males and females with DLE, hormones are less likely to play a role in this subset. In terms of genetics, genes encoding cytokines, cytokine receptors, adhesion molecules and apoptosis genes are felt to contribute to the development of lupus erythematosus.
The most well-known environmental trigger of SLE and most CLE lesions, particularly DLE, is ultraviolet light. UV light induces pro-inflammatory cytokines, chemokines, and adhesion molecules leading to tissue injury. UVB, UVA and visible light can all contribute to induction of CLE skin lesions. Trauma or koebnerization may also play a role in CLE development through pro-inflammatory factors.
Specific autoantibodies are often not seen in discoid lupus. ANA titers tend to be low or nonexistent in patients with DLE. Skin direct immunofluorescence testing can detect deposition of immunoglobulins and complement at the dermal-epidermal junction in patients with DLE. The role of these antibodies in the local induction of clinical lesions is unknown.
Overall, this complex inflammatory cascade between necrosis, apoptosis, autoantibodies, T and B cells, and vascular changes leads to the development of CLE. However, a complete understanding of the pathophysiology of CLE is unknown.
Systemic Implications and Complications
The risk of progression to SLE in patients with DLE lesions is 5% to 10%, with greatest risk for those with disseminated skin lesions. Patients with DLE should be screened for underlying SLE with clinical history, physical examination and laboratory evaluation to assess for central nervous system, renal, hematologic, pulmonary and cardiovascular system involvement.
There is a limited number of pediatric patients with DLE reported in the literature. In most of the studies, the rate of SLE development in pediatric patients (<16 years old) with DLE, was greater than rates seen in adults. However, it may correlate with a milder phenotype of systemic disease.
An initial ANA, complete blood count (CBC) and urinalysis is sufficient for those without other symptoms. Given that an ANA assay has a 99% negative predictive value, it is rare for a patient with SLE to have a negative ANA. This is also a more cost-effective way to use specific autoantibody tests. If the ANA is elevated (≥ 1:160) or a patient has symptoms suggestive of SLE, further testing is warranted. These may include anti-dsDNA, anti-Smith, CBC with differential, creatinine, albumin, total protein, erythrocyte sedimentation rate, urinalysis, and complement (C3,C4).
Treatment options are summarized in the Table I.
|Sun protection and avoidanceBroad spectrum UVA and UVBsunscreen protectionSmoking cessationTopical
Topical steroids, class I or II (may use lower strength on face)Topical calcineurin inhibitors with or without topical steroidTacrolimus 0.1% ointmentPimecrolimus1% creamIntralesional triamcinolone 3 to 5mg/mLTopical retinoid (especially hypertrophic DLE)Tazarotene gel 0.05%, tretinoin 0.025%/0.05% creamImiquimod 5% cream daily × 3 weeks
|585 nm Pulse Dye Laser: fluence 5.5J/cm2, 0.45 millisecond pulse duration, 7mm diameter spot size|
|SystemicAntimalarials:Hydroxychloroquine 6.0 to 6.5mg/kg/day ideal body weight (IBW)Hydroxychloroquine + quinacrine 100mg daily|
|Chloroquine ≤3.5mg/kg/day IBW +/− quinacrine 100mg daily|
|Thalidomide 50–200mg/dayMethotrexate 5 to 25mg/weekMycophenolate Mofetil 2–3gm/dayAzathioprine 1 to 2.5mg/kg/dayIVIG 0.4mg/kg/day for 5 daysAcitretin 0.2 to 1.0mg/kg/day IBW|
IBW, ideal body weight
Optimal Therapeutic Approach for this Disease
The treatment goal for DLE is to decrease the inflammation and induration in active lesions and hopefully avoid severe dyspigmentation and scarring. Assessment of treatment response should be focused on improvement in erythema and scale. Established dyspigmentation and scarring will not resolve with the above treatments, but may slowly improve over time. Cosmetics such as Covermark and Dermablend may be used for dyspigmentation in cosmetically sensitive areas, such as the face.
DLE is highly photosensitive, thus sun avoidance and sun protection is the first step to therapy and must be discussed with all patients. The use of broad spectrum sunscreens to cover the UVB and UVA spectrum is necessary. Products with helioplex, mexoryl, and physical blockers (titanium dioxide, zinc oxide) offer the broadest protection. An SPF of at least 50 should be applied daily to all sun exposed areas.
Cigarette smokers are more likely to develop CLE and SLE and suffer from more severe disease. Antimalarials may be less effective in smokers, and smokers are more likely to have skin disease that is refractory to all therapies. This is particularly true for discoid lupus. As a result, all patients with CLE and SLE should be counseled on smoking cessation.
Topical therapy with steroids can be initiated as first-line therapy, with or without calcineurin inhibitors. Class I or II topical steroids should be tried in patients with mild skin disease prior to starting systemic therapies. Lower steroid strengths (class V, VI) can be used on the face. Topical calcineurin inhibitors have been shown to be effective in DLE, and offer a decreased risk of telangiectasia development compared with topical steroids. Combining topical steroids and calcineurin inhibitors may provide an added benefit.
Other lesion-directed therapies include intralesional triamcinolone for chronic, recalcitrant, hyperkeratotic lesions. Low doses of 3 to 5mg/mL may be used on local areas monthly as needed. However, risks of skin atrophy and dyspigmentation should be discussed with the patient. This therapeutic modality is particularly effective for scalp lesions. For hypertrophic DLE, tazortene gel 0.05% or tretinoin cream 0.025%/0.05% can also be effective, especially when combined with topical steroids. A small amount of topical retinoid should be used to avoid irritation.
After sunscreen and topical therapies, antimalarials are the next step in the therapeutic ladder and are highly effective in DLE.
Antimalarials are recommended as first-line systemic therapy for CLE and SLE given their effectiveness in prevention and treatment of symptoms, such as photosensitivity, acute malar rash, DLE, oral ulcers, alopecia, arthritis, pleuritis, and pericarditis. The majority of patients with DLE respond to single-agent or combination antimalarial therapy.
Hydroxychloroquine is the treatment of choice over chloroquine given its lower ocular toxicity risk. Typically, hydroxychloroquine is started at 200mg to 400mg a day. To avoid ocular toxicity, the daily dose should not exceed 6.5mg/kg ideal body weight per day.
Ideal body weight is calculated as follows: 45.5kg (use 50kg for males) + 2.3 kg for each inch over 5 feet; or 45.5kg + 2.3kg * (height [inches]-60).
Antimalarials take 2 to 3 months for improvement to be noticed and up to 6 months for a complete response. After 8 to 12 weeks, if improvement is not satisfactory, quinacrine 100mg daily may be added. Quinacrine can only be obtained at compounding pharmacies. It may cause yellow discoloration of the skin.
If the combination of hydroxychloroquine and quinacrine has not provided complete response after 6 months, changing to chloroquine plus quinacrine is an option. Chloroquine is typically started at a dose of 250mg 5 to 7 days a week and should not exceed 3.5mg/kg ideal body weight per day. The lowest possible effective dose should be used for maintenance therapy. Antimalarials may be used safely for long periods of time.
The recommended doses listed in Table I are based on the maximal safe dose from an ocular safety perspective. The retinopathy associated with antimalarials (chloroquine) is often irreversible. The blurred vision and corneal deposition that may occur is reversible. The use of hydroxychloroquine necessitates eye examinations every 6 months and with chloroquine every 4 months. The eye examination should include visual acuity, visual fields, and fundoscopic examination. Patients with a history of retinopathy should not get hydroxychloroquine or chloroquine.
Patients who get a drug exanthem with hydroxychloroquine may be able to tolerate chloroquine, while an urticarial reaction from hydroxychloroquine would preclude use of chloroquine. Other side effects include nausea, headaches, myopathy, and bluish-gray hyperpigmentation of the skin.
In addition to a baseline eye examination, a CBC and liver function tests are recommended at baseline and after 1 month of use.
If antimalarials are not effective, second-line systemic therapies including thalidomide and immunosuppressives may be required. Specifically, if refractory and widespread DLE lesions persist, or patients have concomitant SLE symptoms, they may benefit from these steroid-sparing immunosuppressants. In some instances, these immunosuppressants are initially used in combination with prednisone. Once the medication takes effect, the goal is to taper off the prednisone. However, prednisone is not often used in DLE as high doses are usually necessary to achieve a response.
If antimalarials are ineffective, thalidomide can be used as a second-line agent together with antimalarials. Thalidomide is also an option for patients who are unable to tolerate antimalarials. Thalidomide produces relatively rapid improvement, as early as 2 to 3 weeks, and clinical remission is typically achieved within 8 weeks. Up to 90% of patients respond to thalidomide therapy. A starting dose of 50mg nightly of thalidomide is recommended and may be increased to normally 100mg at night over 6 to 8 weeks for peak effect, assuming tolerable side effects.
Thalidomide dose can often be decreased once CLE lesions are improved. The dose of thalidomide can be decreased to 50mg per day and then 50mg every 2 or 3 days as maintenance if continued therapy is needed. Thalidomide can also be used in short courses for disease flare in patients on maintenance antimalarials. Of note, thalidomide is effective for CLE and associated arthralgias, but has little effect on the visceral symptoms associated with SLE.
Thalidomide is known to be efficacious in CLE, but its utility in clinical practice is limited by its toxicities. The most common side effects of thalidomide are dose-related sedation, headaches, and amenorrhea. Severe side effects include teratogenicity, reversible sensory neuropathy and venous thromboembolic events. Sensory neuropathy can present with tingling or numbness in the distal extremities but can also be clinically asymptomatic yet have abnormal sensory nerve action potentials.
The dose can be decreased or discontinued if symptoms are severe. To prevent birth defects, physicians are required to enroll in the Thalomid Risk Evaluation and Mitigation Strategy (REMS)™ program (formerly known as the S.T.E.P.S.® program). To decrease the risk of deep vein thrombosis, the use of an antimalarial or aspirin is recommended.
Methotrexate (MTX) in lupus erythematosus can be used in doses of 5 to 25mg weekly. MTX typically takes 3 to 4 weeks for clinical improvement. A typical test dose is 5mg, and then increase 5mg weekly to the dose needed to control symptoms. The lowest possible maintenance dose needed to control disease should be used. Doses as low as 5mg a week have been successfully used to maintain clinical remission.
A potential for hepatotoxicity with long-term use and pulmonary toxicity are important considerations. Patients who drink alcohol should not receive methotrexate, and underlying viral hepatitis, obesity and diabetes are associated with an increased risk of hepatotoxicity, including liver fibrosis.
Bone marrow suppression is a severe adverse reaction. Risk factors for this side effect include drug interactions (trimethoprim/sulfamethoxazole [TMP/SMX] and non-steroidal anti-inflammatory drugs [NSAIDS]), renal insufficiency, older age (>65) and no folate supplementation. Frequent CBCs are important to monitor for this adverse reaction and all patients should be on folate supplementation.
Baseline laboratory tests should include CBC, complete metabolic panel (liver and renal function), hepatitis B and C serologies, and HIV testing. After the first dose of MTX, a CBC and liver function studies should be done in 1 week. If results are normal, repeat testing of CBC and liver function, every week as the dose is increased and then monthly thereafter for 3 months, is warranted. After a year of a stable dose with no serious toxicity, blood monitoring can decrease to every 3 months.
Renal function can be evaluated once a year, or sooner if renal dysfunction is suspected.
Weekly intramuscular injections may improve gastrointestinal (GI) intolerance due to oral MTX.
Mycophenolate mofetil (MMF) is well tolerated and has been shown to be effective in CLE, including widespread DLE and SLE. The most common adverse reaction from this therapeutic is gastrointestinal (GI) side effects, including nausea, vomiting, diarrhea, and abdominal cramps. These symptoms are typically dose dependent and may be avoided by starting at a lower dose.
In patients with GI side effects, one can start with 500mg once or twice a day and then titrate dose up, per tolerability every 2 to 4 weeks to goal dose of 2 to 3g/day. As with any immunosuppressant, MMF can increase the risk of infections. Less common side effects include myelosuppression and transaminitis. MMF typically takes approximately 4 weeks to take effect.
Baseline laboratory tests include CBC with differential and liver function tests. Laboratory tests should be checked 2 weeks after starting therapy and 2 weeks after increases in dose. Monthly CBC and liver function tests for the first year, then every 3 months, is recommended. Maintenance doses of 1.5 to 3g a day can be used safely.
Azathioprine is an immunosuppressant that has been extensively studied in lupus erythematosus as a steroid-sparing agent. An initial dose of 50mg a day is suggested to determine acute toxicity/sensitivity. The dose can be increased by 25mg every 2 weeks with a goal of achieving a range between 2 to 3mg/kg/day. In CLE, azathioprine doses of 100 to 150mg are commonly needed to achieve desired effects. Clinical effects are typically seen in 4 to 8 weeks. The maintenance dose can range from 50 to 150mg daily and may be continued for years.
Side effects include GI symptoms of nausea, vomiting and abdominal cramping. Pancreatitis and hepatotoxicity have also been reported. Hypersensitivity reaction, aseptic meningitis and increased cancer risk are also known adverse reactions. Flu-like symptoms may occur within the first 2 weeks of use.
Prior to the use of azathioprine, a thiopurine methyltransferase (TPMT) enzyme level can be performed, particularly if doses above 50mg a day are used initially. Low levels increase the risk of myelosuppression and potentially fatal neutropenia. A CBC and liver function tests should be performed every 2 weeks while the dose is being adjusted, then every month for the first year, and then every 3 months.
For resistant cases, acitretin has been used at doses ranging from 10mg to 75mg a day, but not to exceed 1mg/kg ideal body weight per day. Starting with a 25mg dose and increasing to 50mg in 4 weeks, assuming limited side effects, is reasonable. Most patients show response within 3 to 4 weeks and system remission was seen in 12 weeks. If no improvement is noted by 8 to 10 weeks, the medication can be stopped. Decreasing acitretin to the lowest effective dose as soon as possible to avoid side effects is recommended. A maintenance dose as low as 10mg can be effective.
The most common side effects are dry lips and skin, pruritus and alopecia. Severe adverse events include teratogenicity, hyperlipidemia (particularly triglyceridemia), pancreatitis and hepatotoxicity. Acitretin is pregnancy category X, thus use is not recommended in women of child-bearing age. However, if it is used in severe and refractory cases in this population, all female patients must use 2 forms of effective contraception 1 month prior to treatment start, during treatment and up to 3 years after.
Baseline CBC, complete metabolic panel (liver and renal function) and fasting lipid profile should be obtained. As the dose is being increased, repeat testing of liver function and fasting lipids should be done every 2 weeks. Once a stable dose is achieved, monthly testing of liver function and fasting lipids is warranted. For the limited number of patients that require long-term therapy (> 6 months), liver function test and fasting lipid profiles should be obtained every month for the first year and then every 3 months.
Pulse-dye laser (585nm), as a physical treatment, was found to be effective and safe for active discoid lupus lesions. No improvement was seen in damaged areas. The best results were achieved with a fluence of 5.5J/cm2, 7mm diameter spot size, and pulse duration of 0.45ms. One pass over each lesion is sufficient, and 2 to 3 treatments may be needed for improvement. Treatment intervals can be spaced every 4 to 6 weeks.
All patients newly diagnosed with CLE should be counseled on the specific disease course, including any potential risk for scarring and disfigurement. The vast majority of patients with CLE, particularly CCLE, have disease that primarily affects the skin. These patients should be reassured that their disease progression is relatively benign. Patients with generalized DLE should be aware that their risk of progression to SLE is slightly higher than those with limited disease.
The next step is to provide patients with therapeutic modalities that minimize disease progression and improve treatment response. All patients must be counseled on sun avoidance and protection, including avoidance of artificial tanning beds and photosensitizing medications. On a similar note, the role of smoking in disease severity must be stressed at the initial visit. All patients should be encouraged to stop smoking and should begin a smoking cessation program.
The goal of any therapy for DLE is to improve the patient’s appearance and minimize the development of new lesions to prevent more areas of potential scarring and dyspigmentation. Mainstay therapies for DLE include topical therapies and antimalarials. Both of these modalities have limited severe adverse reactions. However, patients with refractory or widespread disease may need treatment with therapies that carry higher side effect risks. It is important to discuss all side effects and monitoring guidelines prior to initiating therapy.
After antimalarials, there is no one agent that is superior in the treatment of DLE lesions. Thus, when ascending the therapeutic ladder, individualizing therapy for each patient based on their co-morbidities is necessary. Furthermore, after clearance of DLE lesions, therapies should be reduced to the lowest effective dose, or discontinued.
If the initial evaluation is normal, yearly screening (or sooner if symptoms develop) for underlying SLE with a complete review of systems and physical examination to assess for central nervous system, renal, hematologic, pulmonary and cardiovascular system involvement is warranted.
A CBC, ANA, and urinalysis is sufficient for those patients without other symptoms. If the patient develops symptoms suggestive of systemic lupus, further testing may include anti-dsDNA, anti-Smith, CBC with differential, creatinine, albumin, total protein, erythrocyte sedimentation rate, urinalysis, and complement (C3,C4). A repeat ANA is not necessary if it was positive on an initial evaluation.
Unusual Clinical Scenarios to Consider in Patient Management
Squamous cell carcinomas may rarely occur within long-standing DLE lesions, in Caucasians and in persons of color. Consider a biopsy of DLE lesions that may be growing in such a manner that suggest the possibility of squamous cell carcinoma, especially if those lesions are recalcitrant to treatment.
Family planning is important for patients with DLE. Ideally, planning for pregnancy once DLE is inactive for at least 6 months is recommended. However, even if the disease is controlled, DLE patients may flare during pregnancy. Prior to conception, if not already done, checking for antiphospholipid antibodies is necessary, as anticoagulation therapy during pregnancy may be indicated. Checking for anti-SSA and anti-SSB antibodies is necessary because there is a small risk of congenital heart block in women with these antibodies.
During pregnancy, monitoring for development of SLE with review of systems and physical examination is warranted. Depending on the severity of disease, a high-risk obstetrician may be necessary. Particularly, if the patient has disseminated DLE, or active SLE with lupus nephritis, history of congenital heart block, and antiphospholipid syndrome, a high-risk obstetrician and close follow-up with a rheumatologist is essential.
There is little evidence regarding treatment of DLE during pregnancy. Typically, patients with active DLE and mild disease are managed during pregnancy with topical steroids. Hydroxychloroquine has evidence for its safety and efficacy during pregnancy; however, it is still considered a class C drug by the Food and Drug Administration. If the disease is more severe, treatment with corticosteroids and azathioprine may be used. At this time, there is not enough safety information on the use of mycophenolate mofetil in pregnancy.
What is the Evidence?
Knott, HM, Martinex, JD. “Innovating management of lupus erythematosus”. Dermatol Clin. vol. 28. 2010. pp. 489-99. (Through table summaries, this article discusses novel CLE treatments and new approaches to monitoring treatment response.)
Bockle, BC, Sepp, NT. “Smoking is highly associated with discoid lupus erythematosus and lupus erythematosus tumidus: analysis of 405 patients”. Lupus. vol. 24. 2015. pp. 669-74. (A retrospective descriptive study of 405 patients at a tertiary care referral hospital reported that smokers were more common among patients with cutaneous LE, especially those with LE tumidus or discoid LE.)
Miot, HA, Bartoli-Miot, LD, Haddad, GR. “Association between discoid lupus erythematosus and cigarette smoking”. Dermatology. vol. 211. 2005. pp. 118-122. (Through a case-control study the authors investigate the association of cigarette smoking and DLE. The study reveals a statistically significant odds ratio of 14 between cigarette smoking and development of DLE.)
Arkin, LM, Ansell, L, Rademaker, A. “The natural history of pediatric-onset discoid lupus erythematosus”. J Am Acad Dermatol. vol. 72. 2015. pp. 628-33.
Madan, V, August, PJ, Chalmers, RJ. “Efficacy of topical tacrolimus 0.3% in clobetasol proprionate 0.05% ointment in therapy-resistant cutaneous lupus erythematosus: a cohort study”. Clin Exp Dermatol. vol. 35. 2010. pp. 27-30. (This study reveals that the combination of clobetasol and tacrolimus were more effective than each of these agents used alone.)
Wu, JJ, Huang, DB, Pang, KR, Hsu, S, Tyring, SK. “Thalidomide: dermatological indications, mechanisms of action and side effects”. Br J Dermatol. vol. 153. 2005. pp. 254-73. (A comprehensive discussion of the use of thalidomide for dermatologic conditions, adverse reactions and monitoring recommendations.)
Cuadrado, MJ, Karim, Y, Sanna, G, Smith, E, Khamashta, MA, Hughes, GR. “Thalidomide for the treatment of resistant cutaneous lupus: efficacy and safety of different therapeutic regimens”. Am J Med. vol. 118. 2005. pp. 246-50. (The use of thalidomide in 48 patients with CLE is discussed, including their response to therapy and side effects. In this study, 27% of patients developed peripheral neuropathy. Given these findings, the authors propose that thalidomide would be most useful in refractory CLE cases when seeking disease remission.)
Diez, MT, Boixeda, P, Moreno, C, Gonzalez, JA, Zamorano, ML, Olasolo, PJ. “Histopathology and immunohistochemistry of cutaneous lupus erythematosus after pulsed dye laser”. Dermatol Surg. vol. 37. 2011. pp. 971-981. (A prospective study of nine patients with CLE (6 DLE) treated with PDL reported immunohistologic improvement. After treatment there was reduction of the dermal lymphocytic infiltrate, basal damage; as well as improved epidermal changes. Eighty-nine percent had clinical improvement, without side effects.
Erceg, A, Bovenschen, HJ, van de Kerkhof, PC, de Jong, EM, Seyger, MM. “Efficacy and safety of pulse dye laser treatment for cutaneous discoid lupus erythematosus”. J Am Acad Dermatol. vol. 60. 2009. pp. 626-32. (This study focused on treatment of active DLE lesions with three PDL treatments using a set spot size and fluence. The authors used the Cutaneous Lupus Erythematosus Disease Area and Severity Index (CLASI) to standardize assessment of treatment response.
Wenzel, J, Brahler, S, Bauer, R, Bieber, T, Tuting, T. “Efficacy and safety of methotrexate in recalcitrant cutaneous lupus erythematosus: results of a retrospective study in 43 patients”. Br J Dernatol. vol. 153. 2005. pp. 157-62. (A retrospective investigation of 139 patients with CLE. The authors reported disease activity, additional treatment, laboratory parameters and side effects for all patients. Nearly all patients had improvement in cutaneous lesions, but 16% of patients had to discontinue therapy due to reversible side effect.)
Gerdsen, R, Wenzel, J, Uerlich, M, Bieber, T, Petrow, W. “Successful treatment of chronic discoid lupus erythematosus of the scalp with imiquimod”. Dermatology. vol. 205. 2002. pp. 416-8. (A case of DLE successfully treated with imiquimod 5% daily in 2 cycles over 3 weeks is described. Disease remission persisted for 12 months.)
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