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Discoid Lupus Erythematosus

Cutaneous Lupus Erythematosus

Discoid lupus erythematosus (DLE) is a chronic autoimmune skin condition characterized by erythematous lesions with scaly and crusty appearances. Discoid lupus erythematosus can be categorized into localized, generalized, and childhood DLE [1].


Most patients with discoid lupus erythematosus are asymptomatic, however, some patients may experience pain and pruritus in the lesions. A recent study revealed that 16% of patients with DLE may develop systemic manifestations of the disease within 3 years of onset of diagnosis. [3].

Systemic involvement of DLE presents with clinical features of SLE, therefore , there should be a detailed evaluation to detect serologic abnormalities, hematologic disorders, serosal inflammation such as pleuritis and pericarditis, neurological sequalae, and renal abnormalities

Malignant transformation of DLE is rare, however, skin cancer may be more common among blacks because of the absence of pigmentation in the chronic lesions, coupled with the chronic inflammation and continuous sun exposure. Risk factors for squamous cell carcinoma include lip involvement of lesions, early age of onset, smoking,  male gender, and recalcitrance of the disease [10].

Porphyria cutanea tarda is predominant in patients with cutaneous lupus erythematosus. Porphyria cutanea tarda may be triggered by antimalarial therapy as may lichen planus in these patients.

Lesions in DLE are usually characteristic comprising of erythematous papules or plaques with scaly appearances. As the lesions progress, the scales become thickened and coalescent. There may be central hypopigmentation of the lesions with hyperpigmentation at the active peripheral borders of the lesions. Lesions appear in a centrifugal pattern and may coalesce. These lesions heal with scars. The lesions may present with dilation of the follicular openings which are closed by keratinous plugs. Lesions are mainly found in the sun-exposed areas of the body.

The early lesions may be indistinguishable from those which occur in subacute cutaneous lupus erythematosus. The scalp is a very common site of occurrence of the skin lesions an it may result in irreversible alopecia.

In DLE, the lesions may be localized or generalized. Lesions are said to be localized if they involve only the head and neck regions, and when they affect additional areas of the body, they are described as generalized DLE. Generalized DLE is mostly associated with hematologic abnormalities and abnormal serologic findings. Furthermore, generalized DLE is more refractory to treatment and is more likely to be associated with SLE. The palms and soles are affected in less than 2% of patients with DLE. [11].

Some cases of DLE present with hypertrophic lesions which have a wart-like appearance, these lesions commonly affect the extensor arms and are generally unresponsive to treatment [12].

Lupus panniculitis is a form of chronic cutaneous lupus erythematosus which is characterized by inflammatory and destructive changes in the subcutaneous adipose tissue. This condition may coexist with DLE [13].

Raynaud Phenomenon
  • The presence of Raynaud's phenomenon, swollen fingers, a high anti-nuclear antibody titer, and the results of a biopsy revealed limited-type systemic sclerosis (lSSc).[ncbi.nlm.nih.gov]
  • Raynaud's phenomenon. Sun sensitivity. Joint pain. Itching and swelling on the skin. Pale or blue lips. Fast heart rate. Rapid breathing. Chest pain. Irregular heartbeat. Inability to urinate.[epainassist.com]
  • ’s phenomenon When a person experiences one or some of the mentioned symptoms, it is highly recommended to consult a physician receive proper treatment.[healthzene.com]
  • If a patient does not have any signs of systemic lupus erythematosus, such as generalized hair loss, ulcers in the mouth or nose, Raynaud's phenomenon, arthritis, or fever at the time that he develops discoid lupus, he will most likely only have discoid[en.wikipedia.org]
  • Raynaud’s phenomenon Raynaud’s phenomenon is a condition in which the blood vessels in the hands and/or feet go into spasm, causing restricted blood flow.[lupus.org]
  • She complained of joint pain and fatigue. Clinical presentation, laboratory data, and histopathologic features were consistent with systemic lupus erythematosus in a patient with generalized chronic discoid lupus erythematosus.[ncbi.nlm.nih.gov]
  • We ask about general symptoms (anxious mood, depressed mood, fatigue, pain, and stress) regardless of condition. Last updated: January 30, 2019[patientslikeme.com]
  • Continued Sometimes, changes in blood counts (low red cell count, or anemia ), may cause fatigue, serious infections (low white cell count), or easy bruising or bleeding (low platelet count).[webmd.com]
  • Other symptoms include: Severe fatigue Swollen or painful joints Clotting disorders Anemia Raynaud’s phenomenon (reduced blood flow to fingers or toes in response to cold or stress causing them to turn white then blue and red).[news-medical.net]
  • Rarely, fingers or toes with aggressive ulceration and gangrene may require amputation. Therefore, it is very important that you notify your doctor of any skin abnormalities.[hopkinslupus.org]
  • Areas of dead skin can appear as sores or small black spots at the ends of the fingers or around the fingernails and toes, causing gangrene (death of soft tissues due to loss of blood supply).[lupus.org]
Easy Bruising
  • Continued Sometimes, changes in blood counts (low red cell count, or anemia ), may cause fatigue, serious infections (low white cell count), or easy bruising or bleeding (low platelet count).[webmd.com]
Abdominal Pain
  • Other symptoms depend on which part of the body is affected: Brain and nervous system: Headaches, numbness, tingling, seizures, vision problems, and personality changes Digestive tract: Abdominal pain, nausea, and vomiting Heart: Valve problems, inflammation[medlineplus.gov]
  • Manifestations may include abdominal pain resulting from serositis, nausea, vomiting, manifestations of bowel perforation, and pseudo-obstruction. SLE rarely causes parenchymal liver disease.[merckmanuals.com]
Oral Ulcers
  • Other lesions associated with ACLE include oral ulcers, hives, and temporary hair loss, which are replaced by new hair once the disease flare is treated.[americanskin.org]
  • Mouth ulcers Formation of thick scales may spread to the interior region of the mouth, causing open sores or oral ulcers. These open lesions in the mouth can often be painful. These may also multiply if allowed to spread further.[phaa.com]
  • As this dog also exhibited an intermittent fever, oral ulcers, a persistent proteinuria, a Coombs’ positive hemolytic anemia, a thrombocytopenia, a suspected pleuritis and hepatitis and elevated serum anti-nuclear autoantibodies, he was diagnosed has[doi.org]
  • Oral ulcers (open mouth sores). Arthritis, pain, inflammation, or swelling of the joints. Kidney disorder, either excess protein in the urine ( proteinuria ) or red blood cells in the urine. Neurological disorder, seizures, or psychosis.[webmd.com]
  • A 28-year-old woman presented with a 2-year history of idiopathic, chronic blepharitis unresponsive to several courses treatment of corticosteroid eye drops.[ncbi.nlm.nih.gov]
  • Patients with this presentation will likely be treated as chronic blepharitis or eczema (7).[scielo.br]
  • In addition to their skin lesions, they may also have swelling and redness around their eyes, as well as blepharitis. Darker-skinned patients are often left with severe scarring and skin color changes even after the lesions get better.[en.wikipedia.org]
  • Patient 2 Presenting with a 6-month history of sore and itchy eyes, a 48-year-old Afro-Caribbean female had been managed locally for blepharitis without improvement.[nature.com]
Retinal Pigmentation
  • pigment epithelial atrophy resembling retinitis pigmentosa. 16 This is dose related and can largely be avoided.[doi.org]
  • Up to 50% of patients with subacute cutaneous LE may also have a mild form of SLE, resulting in arthralgia (painful joints) or arthritis (joint disease) and low blood counts. Severe SLE is rare in patients with subacute cutaneous LE.[dermnetnz.org]
  • Common manifestations may include arthralgias and arthritis, Raynaud phenomenon, malar and other rashes, pleuritis or pericarditis, renal or CNS involvement, and hematologic cytopenias. Diagnosis requires clinical and serologic criteria.[merckmanuals.com]
  • Spinal radiographs, myelogram and cerebrospinal fluid analysis and stifle and hock joint aspirates were performed in dogs suffering from intermittent arthralgia, but they failed to identify any underlying abnormality [ 34 ].[doi.org]
  • Some of the more common symptoms include: Achy joints (arthralgia) Unexplained fever (more than 100 F) Swollen joints ( arthritis ) Prolonged or extreme fatigue Skin rash Ankle swelling and fluid accumulation Pain in the chest when breathing deeply ([webmd.com]
Joint Swelling
  • They may sometime have symptoms of joint pain and joint swelling. In about 5% of the individuals with discoid lupus erythematosus symptoms of systemic lupus erythematosus may be seen.[steadyhealth.com]
  • Common symptoms include: severe fatigue joint pain joint swelling headaches a rash on the cheeks and nose, which is called a “butterfly rash” hair loss anemia blood-clotting problems fingers turning white or blue and tingling when cold, which is known[healthline.com]
  • We report two cases of sarcoidal alopecia originally thought to represent DLE scarring plaques of the scalp. A subsequent histopathologic diagnosis of sarcoidal alopecia was made.[ncbi.nlm.nih.gov]
  • We report a case of DLE, presenting with a six-month history of ulcerated fungating plaques and small crusted nodules superimposed on DLE plaques over both the forearms.[ncbi.nlm.nih.gov]
  • Erosions and ulcers were common but granulation tissue was limited and fibrosis (scarring) was not seen.[doi.org]
  • Previously, a discoid lupus erythematosus-like eruption linked to its use was rarely reported in patients with rheumatoid arthritis. We present a case of rheumatoid arthritis which developed such an eruption after treatment with infliximab.[ncbi.nlm.nih.gov]
  • The dyspigmentation of older lesions often presents as central hypopigmentation and peripheral hyperpigmentation. Patients may have scalp lesions only or may have concomitant lesions on the face, neck, and especially the external ears.[dermnet.com]
  • Over time, lesions slowly expand, producing areas of peripheral inflammation or hyperpigmentation, leaving a central region of scarring with telangiectasia and hypopigmentation.[bestpractice.bmj.com]
  • Fig. 7 Clinical characteristics of canine mucocutaneous lupus erythematosus. a : anal erosions with peripheral hyperpigmentation in a German shepherd dog; ( b ): multifocal perigenital erosions with peripheral hyperpigmentation are often seen in female[doi.org]
  • In this study 20 patients developed side effects; 17(85%) patients had transient hyperpigmentation which fade after 3-6 months and 3 (15%) patients had hypopigmentation.[edoj.org.eg]
Skin Plaque
  • It is characterized by the presence of discoid skin plaques showing varying degrees of edema, erythema, scaliness, follicular plugging, and skin atrophy. Lesions are surrounded by an elevated erythematous border.[sideeffects.embl.de]
  • A chronic form of cutaneous lupus erythematosus that is characterized by the presence of discoid skin plaques showing varying degrees of swelling, redness, scaliness, and skin atrophy.[patientslikeme.com]
  • It is characterized by discoid skin plaques with edema, erythema, scaliness, follicular plugging, and skin atrophy surrounded by an elevated erythematous border.[medicine.academic.ru]
Malar Rash
  • In patients with malar rash, AMS scores at one (8.30   6.80, p CONCLUSIONS: Malar rash may be a marker of more severe systemic disease over time, while DLE has no significant impact on general SLE disease activity. The Author(s) 2015.[ncbi.nlm.nih.gov]
  • In SLE, a malar rash in a butterfly pattern may appear across the nose and cheeks of the patients, or red rashes may develop in reaction to sunlight.It's possible for discoid lupus to spread to your internal organs, although this is rare.[lupus.about.com]
Facial Lipoatrophy
  • We want to report a young male patient with progressive symmetrical facial lipoatrophy. In addition, he has discoid lupus erythematosus and celiac disease.[ncbi.nlm.nih.gov]
Kidney Failure
  • Calcinosis can develop from a reaction to steroid injections or as a result of kidney failure. Cutaneous vasculitis lesions Cutaneous vasculitis lesions occur when inflammation damages the blood vessels in the skin.[lupus.org]
  • failure SLE can have serious negative effects on your body during pregnancy.[healthline.com]
  • People with this problem may develop kidney failure. They may need dialysis or a kidney transplant. A kidney biopsy is done to detect the extent of damage to the kidney and to help guide treatment.[medlineplus.gov]
  • This is because symptoms can range from a mild rash and arthritis to kidney failure and seizures — “with a whole spectrum in between.” Symptoms may mimic other diseases and conditions, such as infections or cancer.[everydayhealth.com]
  • Pain in the chest after taking a deep breath Unexplained fever Edema (swelling), often in the legs or around the eyes Mouth sores Unexplained hair loss Raynaud’s phenomenon (characterized by cold fingers and/or toes that are pale or purple in color) Headaches[lifeextension.com]
  • Common symptoms include: severe fatigue joint pain joint swelling headaches a rash on the cheeks and nose, which is called a “butterfly rash” hair loss anemia blood-clotting problems fingers turning white or blue and tingling when cold, which is known[healthline.com]
  • Vascular headaches, epilepsy, or psychoses may be initial findings. Manifestations referable to any organ system may appear. Periodic exacerbations (flares) may occur.[merckmanuals.com]
  • […] teratogenicity and polyneuropathy. 20 However, in a retrospective study of 18 patients with chronic DLE, Brocard et al 21 found low-dose thalidomide treatment was efficacious with good tolerance, with the most frequent side effect being usually mild asthenia[doi.org]


Baseline laboratory blood test is necessary in the diagnosis of DLE. These include complete blood count with the white blood cell count often reduced and erythrocyte sedimantation rate (ESR) which is typically raised. Rheumatoid factor may be positive in DLE. A negative result doesn't exclude DLE.

Serology is also important in the diagnosis of discoid lupus erythematosis. Serology reveals positive antinuclear antibody(ANA) findings in 20% of cases of DLE. Complements are often reduced. 

Urinalysis may be necessary to exclude renal involvement. Albuminuria suggests kidney involvement.

These laboratory investigations should be ordered periodically to determine the absence or presence of systemic progression.

Biopsy is the most sensitive and specific investigation for DLE. The features on histology are usually characteristic but may depend on the type and duration of the disease. A direct positive immunoflourescence is observed in the biopsy samples in most cases of DLE.

Antinuclear Autoantibodies
  • Wallace ; Antinuclear autoantibodies in cutaneous lupus erythematosus: biochemical and cell biological characterization of Ro/SSA / Anna von Mikecz -- Part IV: Treatment and management of cutaneous lupus erythematosus.[worldcat.org]
  • Mycophenolate is an ester prodrug of mycophenolic acid, initially isolated from Penicillium species. 26 Goyal and Nousari 27 described 2 cases of refractory discoid lupus involving the palms and soles that responded satisfactorily to mycophenolate mofetil[doi.org]


Treatment is aimed at controlling the existing skin lesions, preventing development of new lesions, preventing complications, and improving cosmesis.

Topical corticosteroids and antimalarials are the main drugs of choice for treating DLE.

Intralesional corticosteroids are the preferred form of administration of corticosteroids and are administered into the individual lesions. Oral corticosteroids are avoided because of adverse effects of prolonged use of the drug. A medium-strength corticosteroid such as triamcinolone is usually administered topically first. Low-strength corticosteroids such as hydrocortisone are preferable for facial lesions. However, if both forms of corticosteroids fail to resolve the symptoms, a high-strength corticosteroid such as bethametasone becomes necessary. These high potency corticosteroid are also recommended as first-line for hypertrophic lesions.

If the lesions remain unresolved upon treatment with topical and intraleional corticosteroid, antimalarials are considered with hydroxychloroquine being the drug of choice. If hydroxychloroquine produces no resolution of the lesions after a period of two months of therapy, chloroquine should be used. However, antimalarial therapy should be provided continuously for 1 to 2 years for complete resolution of the lesions. Corticosteroid treatment should be given concurrently with antimalarial treatment and should be discontinued after completion of antimalarial treatment.

In cases where antimalarial treatment is unsuccessful, immunosuppressant treatment is considered next. Effective immunosuppressants include azathioprine, mycophenolate mofetil, and methotrexate. These are also particularly effective in the treatment of refractory cases of DLE.

Oral thalidomide is considered if all other treatments have failed. However, thalidomide is recommended only for remission induction because of its tendency for neural damge. Although thalidomide neurotoxicity is not dose-dependent, low doses could be safe.

Studies have identified topical tacrolimus and pimecrolimus as useful alternative drugs in the treatment of DLE and other CLE lesions. These studies have not provided concrete evidence to establish their safety and effectiveness.

Supportive treatment for DLE include limited sun exposure especially during the hours when sunlight is most intense, usually between 10 am to 3 pm. Occlusive clothing and sunscreens are recommended. Smoking cessation is also critical in preventing progression and worsening of the disease. Cosmetic products to mask the lesions are also recommended.

In cases of DLE with telegiectasia and chronic erythema, surgery including photothermolytic ablation of the dilated vessels may be recommended. This procedure is called pulsed eye laser treatment and it has been shown to be very effective for recalcitrant cases of DLE. Surgical excision of scarred lesions is also effective, although it may reactivate latent lesions.


Discoid lupus erythematosus may not cause mortality, however, it may be associated with significant morbidity. The condition may cause significant burning and pain caused by the lesions, and considerable cosmetic problems. In a few cases, discoid lupus erythematosus may cause fatal sequelae if there is systemic involvement. Although malignant transformation of the lesions are rare, prompt skin biopsy is recommended in case of suggestive malignant lesions [10]. Sunlight is a known exacerbating factor of DLE lesions.


Several studies have identified smoking as a risk factor for DLE. These studies have also indicated ultraviolet radiation as a precipitating and aggravating factor of DLE [5] [6]. DLE may also develop within areas of skin which have been injured or affected by physical trauma, this is known as koebner phenomenon.

DLE is thought to be a result of autoimmune mechanisms as it has been linked to some major histocompatibility complex antigens. Other studies indicate that genetic factors may contribute to the etiology of DLE [7].


SLE has a worldwide prevalence of 17 to 48 cases per 100,000 people. SLE most commonly occurs in individuals aged 40-60 years with onset at the age of 20-30 years. SLE is commoner in women than men with a female to male ratio of 10:1.

DLE accounts for 50-85% of all cases of cutaneous lupus erythematosus and it is more common among women than men with a female to male ratio of 3:1.

DLE is also more common among African Americans than whites or Asians. DLE occurs most commonly among persons aged between 20 and 40 years, however, it may occur at any age.

Sex distribution
Age distribution


The exact mechanism of development of cutaneous lupus erythematosus in general is not clearly understood. However, leading theories have indicated that an autoimmune process may be responsible for the disease. This is because of the identification of IgG and C3 in the epidermal basement membrane which is the site of the autoimmune damage [8].

In chronic DLE, as compared to acute and subacute cutaneous lupus erythematosus, there is a much higher concentration of inflammatory infiltrates which mostly comprise of T cells. Additionally, in chronic DLE , the inflammatory cell infiltrates extend to the deeper reticular dermis and subcutaneous tissue in contrast to findings in subacute and acute chronic lupus erythematosus in which the inflammatory cell infiltrates are confined to the outer dermis.

Researchers have suggested that apoptosis of keratinocytes may be the critical occurrence in the etiology of cutaneous lupus erythematosus [9].


To reduce triggers or flares of the lesions in discoid lupus erythematosus, restriction of exposure to sunlight is advised. This can be achieved by using occlusive clothing and sunscreens. UV-blocking films may be applied to window glasses to prevent reflection of sunlight into the rooms. However, vitamin D supplements are necessary because of the sunlight restriction. Smoking cessation also prevents precipitation of flares of DLE.


There are 3 subtypes of cutaneous lupus erythematosus (CLE) based on the onset and duration of lesions: acute, subacute and chronic. Each subtype presents with characteristic lesions.

Acute CLE is characterized by malar rash which may spread across the nasal bridge. The lesions do not involve the nasolabial folds. Furthermore, acute CLE may present with generalized morbilliform eruptions on the hands sparing the joint areas. Subacute CLE is characterized by annular plaques affecting sun-exposed areas only. Chronic CLE consists of three subdivisons including discoid lupus erythematosus, lupus panniculitis, and timid lupus.

The lesions in discoid lupus erythematosus are erythematous or violaceous plaques with a scaly appearance and a characteristic keratinous plugging on the openings of each lesion.The lesions typically heal with scarring.

DLE may be localized to the skin without systemic features. However, in other cases, it may progress to systemic lupus erythematosus (SLE). Approximately 16.7% of cases of DLE progress to SLE within 3 years from onset of DLE [2] [3]. Often, the secondary SLE manifestations do not fulfill more than 4 of the 11 criteria for the diagnosis of SLE as set by the American College of Rheumatology [4] 

Diagnosis of DLE is mainly clinical, however, series of laboratory investigations may be necessary to exclude systemic involvement. Serology may be needed to confirm antinuclear antibody (ANA) titers. Skin biopsy is the most sensitive test for DLE.

Treatment of choice for DLE is topical corticosteroid and antimalarials. Corticosteroids are the first line of treatment, while antimalarials and immunosupressants are used respectively if the preceeding medical therapy fails. Surgery may be considered for certain lesions.

Patient Information


Discoid lupus erythematosus (DLE) is a rare skin disease characterized by scaly and crusty rashes affecting mainly the sun-exposed areas of the body. Discoid lupus erythematosus is within a spectrum of skin diseases called cutaneous lupus erythematosus and it is characterized by only skin lesions. Another disease condition in this broad group is called systemic lupus erythematosus which causes both skin rashes and disorders of the internal organs. All of these diseases are worsened by sunlight.


Although the cause of this skin condition is not fully understood, some researchers have suggested that it may result from autoimmune mechanism, which refers to a phenomenon whereby the body's antibodies attack different tissues in the body. This results because the antibodies confuse these tissues for foreign harmful materials from which they must protect the body. In the case of DLE, the antibodies confuse the normal skin cells for foreign objects and attack them causing the skin lesions . it is typically worsened by exposure to sunlight. Tobacco smoking and physical trauma to the skin have also been suggested to contribute to the development of this condition.


DLE affects both sexes and all age groups, however, it is most common among women aged between 20 and 40 years.


The skin presents with red, itchy, and scaly or crusty rashes which heal with bad scars. In some patients , there may be no symptoms at all. The only problem in patients with DLE is the bad appearance of their skin.

DLE typically causes skin rashes in the face and scalp, although could affect every other skin area. In the scalp, DLE could result in irreversible hair loss.


Typically, a skin biopsy may be necessary to make a diagnosis of DLE, the biopsied sample is viewed under the microscope to detect unique features of this disease. Laboratory blood and urine tests are needed to exclude SLE which is the type that affects internal organs.


DLE doesn't have a cure, the available drugs just help to reduce the symptoms of the disease. First of these drugs to be recommended and prescribed by a doctor is corticosteroid ointments or injections which are administered directly into the skin rashes. Corticosteroid tablets have more detriments than benefits, so would be avoided by doctors for the treatment of DLE.

If these drugs have been administered for a period, but the skin rashes do not improve, antimalarials would be prescribed. Now these drugs are not used because of their antimalarial effect, but because of their additional ability to suppress inflammation significantly. The commonest antimalarial used is hydroxychloroqine which could also be prescribed with mepacrine, another antimalarial , to increase its safety and effectiveness. The only concern with hydroxychloroquine is its ability to cause eye problems if taken at high doses. Doctors would conduct eye tests to determine if this drug is suitable for you.

After about 2 months of receiving antimalarial treatment, if no improvement is recorded, certain drugs which serve as suppressants of the immune system would be prescribed. Examples of these include methotrexate and azathioprine.

Self care is also important in the management and control of DLE. Important self-care tips include limiting your exposure to sunlight by using a good sunscreen and wearing clothes that cover your arms, shoulders and legs well. Dark clothing is preferable to reflect sun rays from the cloth. A hat is advised to reduce sun exposure to the face and scalp.



  1. James, William; Berger, Timothy; Elston, Dirk. Andrews' Diseases of the Skin: Clinical Dermatology. (10th ed.) Saunders. Chapter 8. 2005.
  2. Prystowsky SD, Gilliam JN. Discoid lupus erythematosus as part of a larger disease spectrum. Correlation of clinical features with laboratory findings in lupus erythematosus. Arch Dermatol. 1975 Nov; 111(11):1448-52.
  3. Grönhagen CM, Fored CM, Granath F, Nyberg F. Cutaneous lupus erythematosus and the association with systemic lupus erythematosus: a population-based cohort of 1088 patients in Sweden. Br J Dermatol. 2011 Jun; 164(6):1335-41. 
  4. Tan EM, Cohen AS, Fries JF, et al. The 1982 revised criteria for the classification of systemic lupus erythematosus. Arthritis Rheum. 1982 Nov; 25(11):1271-7.
  5. Gallego H, Crutchfield CE 3rd, Lewis EJ, et al. Report of an association between discoid lupus erythematosus and smoking. Cutis. 1999;63:231-234.
  6. Miot HA, Bartoli Miot LD, Haddad GR. Association between discoid lupus erythematosus and cigarette smoking. Dermatology. 2005;211:118-122.
  7. Knop J, Bonsmann G, Kind P, et al. Antigens of the major histocompatibility complex in patients with chronic discoid lupus erythematosus. Br J Dermatol. 1990;122:723-728.
  8. Seitz CS, Brocker EB, Trautmann A. Linear variant of chronic cutaneous lupus erythematosus: a clue for the pathogenesis of chronic cutaneous lupus erythematosus? Lupus. 2008;17:1136-1139.
  9. Lin JH, Dutz JP, Sontheimer RD, et al. Pathophysiology of cutaneous lupus erythematosus. Clin Rev Allergy Immunol. 2007;33:85-106.
  10. Tao J, Zhang X, Guo N, et al. Squamous cell carcinoma complicating discoid lupus erythematosus in Chinese patients: review of the literature, 1964-2010. J Am Acad Dermatol. 2012 Apr; 66(4):695-6.
  11. Parish LC, Kennedy RJ, Hurley J. Palmar lesions in lupus erythematosus. Arch Dermatol. 1967 Sep. 96(3):273-6. 
  12. Spann CR, Callen JP, Klein JB, Kulick KB. Clinical, serologic and immunogenetic studies in patients with chronic cutaneous (discoid) lupus erythematosus who have verrucous and/or hypertrophic skin lesions. J Rheumatol. 1988 Feb; 15(2):256-61.
  13. Martens PB, Moder KG, Ahmed I. Lupus panniculitis: clinical perspectives from a case series. J Rheumatol. 1999 Jan; 26(1):68-72.

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Last updated: 2019-07-11 20:22