Discoid lupus is an unpredictable and highly variable disorder. While the condition is benign, it can cause devastating complications, often leading to high morbidity and a poor quality of life. The disorder frequently waxes and wanes. The outcome is much improved for patients with only skin and musculoskeletal involvement.
DLE is more common in skin of colour. For example, in New Zealand, Māori, and Pacific people have a significantly higher relative risk of discoid lupus erythematosus compared to the European population. This ethnic disparity has also been observed in the USA with those with skin of colour having an increased incidence of DLE.
2. ◦ Subjective findings :
A 46 years old male patient with
weight of 44kg’s came to the hospital with chief
complaints of small coin sized lesions on scalp
& body since 5 years.
Increase in much.
H/O: Fever, joint pains, oral ulcers.
Past Medical history: k/c/o
HANSEN’S Disease used 3 years treatment for
it.
3. Physical examination:
DISCOID PLAUQUES, ATROPHY, CRUSTING Present on scalp, face,
upper and lower limbs.
On derma scopy: telangiectasia+ crusting+ atrophy seen
4. ◦ Objective findings :
◦ Random blood sugar: 74 mg/dl,
◦ AFB test : positive
◦ ANA: positive
◦ CUE & LFT are normal.
◦ Assessment :
Based on subjective and objective findings the patient was diagnosed with
“DISCOID LUPUS ERYTHEMATOUS’’.
5. About Disease:
◦ Definition:
◦ Discoid lupus erythematosus (DLE) is a chronic scarring skin condition. It is the
most common form of cutaneous lupus.
◦ DLE is a sub-type of chronic cutaneous lupus erythematosus. It is characterised
by persistent scaly plaques on the scalp, face, and ears which subsequently
can progress to scarring, atrophy, dyspigmentation, and permanent hair loss in
affected hair-bearing areas.
6. Causes:
◦ The causes of DLE are endogenous and exogenous.
◦ Endogenous factors include:
• Genetic predisposition with major histocompatibility complex alleles HLA-DQA1 and DRB1.
• Single nucleotide polymorphism TYK2, IRF5, CTLA4 are also associated.
• Interferon, particularly type 1, is a key cytokine in pathogenesis.
• IRF5 and TYK2 are involved in interferon regulation.
• ITGAM polymorphisms confer a greater risk for DLE than systemic lupus erythematosus (SLE).
◦ Exogenous factors include:
• Smoking which is more common in those with DLE and which also impairs the efficacy of
antimalarials
• Ultraviolet radiation can provoke DLE as it is a photosensitive disorder. However, it can be found
in non-sun exposed areas.
◦
7. ◦ Symptoms: Typical signs of localized DLE include:
• Initial dry red patches evolve to form red plaques with
adherent scale. Follicular hyperkeratosis (plugs of keratin within hair follicles) is common.
When this scale is removed using sticky tape the horny plugs can be seen giving rise to the
“carpet-tack” sign.
• As DLE progresses atrophic scarring and scarring alopecia is common. This is associated
with hyper- and or hypo- pigmentary change and is especially noticeable in those with skin of
colour.
• DLE is typically located on the nose, cheeks, ear lobes, and conchal bowl (Shuster sign). It
may involve lips, oral mucosa, nose, or eyelids.
◦ Signs of generalised DLE include:
• The morphology of the lesions is similar to that on the face and scalp but they are distributed
widely including the anterior chest, upper back, dorsum of hands and less commonly on the
lower limbs, palms, and soles. Rarely, there is involvement of the anogenital mucosa.
8. ◦ Complications:
• DLE commonly scars causing facial disfigurement and permanent alopecia. Pigmentary change
may improve over long periods.
Diagnosis:
◦ A patient with DLE should undergo a complete examination for other manifestations of lupus.
• A skin biopsy usually confirms diagnosis.
• Features vary depending on the stage of the DLE but include an interface dermatitis also involving hair follicles and
a perivascular and peri-appendageal lymphocytic infiltrate in the upper and lower dermis.
• There is epidermal vacuolation and apoptotic basal cells and hyperkeratosis.
• The basement membrane may become thickened and dermal mucin may be present.
• As lesions evolve further, the inflammatory infiltrate subsides and there is dermal fibrosis.
• Blood tests include a full blood count, renal function, and antinuclear antibodies (ANA). ANA is frequently
not detected.
• Urine analysis.
9. ◦ Treatment:
◦ General measures
• Careful year-round protection from sun exposure using clothing and generously applied high SPF broad-
spectrum sunscreens. Sunscreens alone are not adequate.
• While indoors, some patients may also need to stay away from glass windows, or these can be treated with UV-blocking
films.
• Vitamin D supplements should be recommended for those who strictly avoid the sun.
• Smoking cessation.
◦ Specific measures
◦ Local therapy
• Intermittent courses of potent or ultrapotent topical corticosteroids applied for several weeks are the first treatment for
localised DLE. Intralesional injections of corticosteroids are sometimes used.
• Calcineurin inhibitors — tacrolimus ointment and pimecrolimus cream can also be used.
• Cosmetic camouflage and wigs are useful and improves self-confidence when there is extensive scarring.
◦ Systemic therapy
• Short term
• Systemic corticosteroids such as prednisone or prednisolone can be used for short term control.
• Longer-term
• The following have been used and sometimes in combinations; hydroxychloroquine, chloroquine,
mepacrine, clofazimine, methotrexate, oral retinoids (isotretinoin and acitretin), mycophenolate
mofetil, ciclosporin, cyclophosphamide, azathioprine, dapsone, thalidomide, intravenous immunoglobulins,
and biologic agents (belimumab and rituximab).
10. ◦ Plan:
S.NO
GENERIC
NAME
BRAND
NAME
DOSE ROA FREQUENCY Days
of
treatme
nt
01
Tab.
PREDNISOLONE
WYSOLONE 5mg P/O OD
for 1
month
02 Tab. HYDROXY
CHLOROQUINE
HCQ 200mg P/O OD for 1
month
03
Tab.
LEVOCITRIZINE
LEVOCIZ 5 mg L/A BD
for 1
month
04 Lotion.
MOMETASONE
FUROATE
MONOSONE 0.1% L/A OD at night
for 1
month
11. Patient Counselling :
Shower daily & avoid scrubbing your skin.
Use sunscreen
You can eat soft and healthy food and drink plenty of water to enhance your own resistance.
Use a mild soap and body wash.
Use lukewarm water.
Manage your stress.
Sun protection.
Don’t scratch or pick at the lesions.
Wear soft cotton & linen materials.
Avoid direct sun exposure wear tightly woven clothing and broad brimmed hats.
Decrease Alcohol intake.
