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Principles of therapy
Goals of Therapy
The
goals of therapy in atopic dermatitis are to reduce symptoms, achieve clear or
almost clear skin, prevent exacerbations, and maintain long-term remission.
Other goals would be a 75% improvement in severity scores, improved quality of
life, minimized therapeutic risks, and avoidance of drug-related toxicities.
Topical Therapy
Fingertip
unit rule (FTU), which is the amount of ointment expressed from a tube with a
5-mm nozzle and measured from the distal skin crease to the tip of the index
finger and measuring about 0.5 gram, should be followed in applying topicals
including anti-inflammatory agents. It covers approximately 2% of an adult body
surface area.
Atopic Dermatitis_Management 1There are two approaches to topical anti-inflammatory therapy namely reactive management and proactive management.
Reactive management is when topical anti-inflammatory is applied to skin lesions and stopped or rapidly tapered once visible lesions are cleared or almost cleared.
Proactive management is a combination of predefined, long-term anti-inflammatory treatment applied two times a week to previously affected skin areas in combination with liberal daily use of emollients on the entire body. It begins after treatment of an acute flare when lesions have been successfully treated with regular anti-inflammatory therapy. The duration depends on the severity and persistence of atopic dermatitis.
Systemic Therapy
Systemic therapy is recommended for patients with a high composite score (eg SCORAD >50), patients unresponsive to optimized topical therapy, or patients unable to perform normal activities of daily living while following an adequate treatment regimen. This is recommended if signs and symptoms of atopic dermatitis are not controlled sufficiently with appropriate topical therapy and ultraviolet (UV)-light therapy.
It is recommended to reduce the total amount of topical corticosteroids in patients needing large amounts of potent topical corticosteroids for large body areas over prolonged periods to control atopic dermatitis.
Pharmacological therapy
Topical Corticosteroids
Topical
corticosteroids are used as first-line treatment for mild to severe atopic
dermatitis and when non-pharmacological interventions have been unsuccessful. They
provide rapid symptomatic relief for acute flare-ups and are also used for the prevention
of relapses.
The
choice of product will depend on the severity of the flare-up, distribution and
site of the lesions, patient’s age and preference, and other factors like
humidity.
They
provide anti-inflammatory and antipruritic activity through several mechanisms.
They induce alterations in leukocyte number and activity, suppress mediator
release (histamine, prostaglandins), and promote enhanced response to agents
that increase cyclic adenosine monophosphate (prostaglandin E2 and histamine via the histamine-2 receptor).
Recommended
restrictions should be followed regarding the intensity and duration of use
especially in children on delicate skin areas (eg face, neck, and skin folds).
Intermittent use (1 to 2 times per week) in combination with moisturizers is
historically the standard therapy for atopic dermatitis. Continuous use can
lead to adverse effects.
Topical
corticosteroids are available in different potencies from mildly potent to very
potent. Potency is also affected by the vehicle the product is formulated in
(eg ointment, cream, and lotion in decreasing order of efficacy). The potency
of topical corticosteroids does not relate to the percentage stated (eg
Hydrocortisone 2.5% versus Betamethasone dipropionate 0.05%). The least potent
but effective product should be used, especially if for long-term use. Mid- and
high-potency preparations may be used (except when lesions are on the face,
groin, or axillae) to control acute flares and then follow with lower potency
preparations after clinical improvement is seen. Rebound flaring can occur if
higher potency preparations are discontinued abruptly. A gradual decrease in
potency should follow the use of higher potency preparations. Therapy-resistant
lesions may require potent topical corticosteroids used under occlusion.
Solutions
Solutions
are useful for the scalp or other hirsute areas. The alcohol content may be
irritating when used on inflamed lesions.
Lotions
Lotions
are useful for minimal application to a large area or on hirsute areas. They may
also be used on exudative lesions and in hairy areas.
Creams
Creams
are usually preferred for moist or weeping lesions. They may be preferred
during periods of excessive heat or humidity. They are easier to apply but may
be less effective.
Ointments
Ointments
are generally used for dry, scaly, or lichenified lesions or if a more
occlusive effect is needed (most occlusive vehicle). There are usually lesser
additives used in ointments. Evaporative losses are also decreased.
Systemic Corticosteroids1
Short-term
treatment (up to 1 week) with systemic corticosteroids should only be
considered in treatment-resistant atopic dermatitis, acute severe exacerbations,
and as a bridge therapy to other steroid-sparing systemic treatments. The recommended
dose is 0.5 mg/kg body weight.
They
improve lesions but rebound flare-up usually occurs upon discontinuation. They
should be used only for the short term. To decrease the chance of rebound
effect, taper the oral form slowly while increasing topical corticosteroid treatment
and continuously hydrating the skin.
1Various
oral corticosteroids are available. Please see the latest MIMS for specific
formulations and prescribing information.
Calcineurin Inhibitors - Topical
Immunomodulators
Steroid-sparing
agents for acute and maintenance therapy, topical calcineurin inhibitors
inhibit inflammatory cytokine transcription in activated T cells and other
inflammatory cells through the inhibition of calcineurin.
They
are considered second-line therapy for moderate to severe atopic dermatitis.
They are considered first-line treatment over topical corticosteroids when
atopic dermatitis is unresponsive to steroid therapy, when atrophy or telangiectasia
is present secondary to steroid use, when affected areas are either the face,
anogenital area, and/or skin folds, and for long-term treatments. They are also
used in patients with inadequate response or contraindication to other topical
therapeutic agents.
They
may be used on all body locations for extended periods of time, especially the
face, hands, and feet. There is no evidence of a causal link between the use of
calcineurin inhibitors and cancers.
Pimecrolimus
The
safety and efficacy of Pimecrolimus have been shown in children >2 years of
age and adults with mild-moderate atopic dermatitis. Pruritus relief has been
seen as early as day 3 of use and it does not cause atrophy. It prevents
flare-ups and results in significant steroid-sparing effect when used for up to
12 months. When used in the early stages of the disease, it has been shown to
be therapeutically advantageous over typical moisturizers plus topical
corticosteroids with long-term use.
Tacrolimus
Tacrolimus
is recommended for moderate to severe atopic dermatitis. It rapidly decreases
the signs and symptoms of atopic dermatitis in adults and children >2 years
of age. Improvement is seen within 3 to 7 days of therapy and sustained for at
least 12 months. It is well-tolerated with transient skin burning or irritation
and has less incidence of atrophy compared to steroids.
Studies have confirmed the efficacy of Tacrolimus 0.03% compared to
low-potency topical corticosteroids in children and the efficacy of Tacrolimus
0.1% compared to mid-potency topical corticosteroids in adults.
Phosphodiesterase Type-4 (PDE-4)
Inhibitors
Apremilast
Apremilast
may be considered in patients with moderate to severe atopic dermatitis
unresponsive to standard treatments, but further studies are needed to
establish its efficacy and safety.
Crisaborole
Crisabarole
may be considered for mild to moderate atopic dermatitis in patients ≥3 months
old. Studies showed improvement in symptoms (ie erythema, induration, oozing) with
Crisaborole use.
Immunosuppressants2
Abrocitinib
Abrocitinib
is an oral Janus kinase (JAK) 1 inhibitor used for the treatment of refractory
moderate to severe atopic dermatitis which is inadequately controlled with
other systemic drugs (including biologics) or when the use of those therapies
is not advisable. It may be used with or without topical corticosteroids. It is
not recommended to be used in combination with other JAK inhibitors, biologic
immunomodulators, or with other immunosuppressants.
A
large, randomized, safety clinical trial showed an increased risk of malignancy
(lymphoma and lung cancer), all-cause mortality (including sudden
cardiovascular death), major adverse cardiovascular events (MACE; defined as
cardiovascular death, myocardial infarction, and stroke), and thrombosis
(including pulmonary embolism and venous and arterial thrombosis) with another
JAK inhibitor compared to tumor necrosis factor (TNF) inhibitors in patients with
rheumatoid arthritis.
Azathioprine
Azathioprine
is used for severe or refractory disease unresponsive or with contraindications
to Ciclosporin therapy and most children respond to low doses. There is
increasing evidence supporting its efficacy in severe refractory atopic
dermatitis.
It
may cause nausea, fatigue, myalgia, liver dysfunction, and bone marrow
depression in patients deficient in thiopurine methyltransferase (TPMT). TPMT
levels should be monitored while the patient is on Azathioprine to test for
myelosuppression.
Baricitinib
Baricitinib
is an oral selective JAK1 and JAK2 inhibitor which blocks signals of immune
response and inflammation. It may be given as an option for treatment of
moderate to severe atopic dermatitis in adults who are unresponsive or
contraindicated to at least one systemic immunosuppressant (eg Ciclosporin,
Methotrexate, Azathioprine, Mycophenolate mofetil). It may be an alternative to
Dupilumab with the best supportive care and may be offered with topical
corticosteroids.
Studies
showed Baricitinib, with or without corticosteroids, can reduce the severity and
symptoms of atopic dermatitis compared with a placebo.
It is important to assess patients after 8 weeks of treatment if there
is an adequate response. An adequate response is defined as a reduction of at
least 50% in EASI-50 score and at least 4 points in DLQI from the start of the
treatment.
Ciclosporin (Cyclosporin A)
Ciclosporin
is a first-line option for short-term use in chronic, severe refractory disease
in adults who require systemic immunosuppressive treatment. The condition tends
to return after discontinuation of therapy but not always at the original
severity level.
It
may be used in children and adolescents with refractory or severe disease. Long-term
use is not justified because of the risks of hypertension and renal and liver
dysfunction. Combination therapy with UV light (eg UVA, UVB, PUVA) is not
recommended due to the increased risk of skin cancer.
Methotrexate
Methotrexate
may be considered for severe or refractory disease unresponsive or with
contraindications to Ciclosporin therapy. Studies showed that the efficacy of
Methotrexate for atopic dermatitis is comparable to that of Azathioprine and
Ciclosporin.
Mycophenolate mofetil
Mycophenolate
mofetil may be considered for severe or refractory disease unresponsive or with
contraindications to Ciclosporin therapy.
Ruxolitinib
Topical
Ruxolitinib is a selective JAK1 and JAK2 inhibitor that is approved by the
United States Food and Drug Administration (US FDA) for short-term therapy of
mild to moderate atopic dermatitis in immunocompetent patients ≥12 years old
whose disease is not controlled with other topical therapies.
Upadacitinib
Upadacitinib
is an oral selective and reversible inhibitor of JAK enzymes (preferentially
JAK1 or JAK1/3), which are intracellular enzymes involved in the stimulation of
hematopoiesis and immune cell function through a signaling pathway.
It
is used in patients ≥12 years old with refractory moderate to severe atopic
dermatitis which is inadequately controlled with other systemic drugs
(including biologics) or when the use of those therapies is not advisable.
It
is not recommended to be used in combination with other JAK inhibitors,
biologic immunomodulators, or with other immunosuppressants.
A
large, randomized, safety clinical trial showed an increased risk of malignancy
(lymphoma and lung cancer), all-cause mortality (including sudden
cardiovascular death), MACE (defined as cardiovascular death, myocardial
infarction, and stroke), and thrombosis (including pulmonary embolism and venous
and arterial thrombosis) with another JAK inhibitor compared to TNF inhibitors
in patients with rheumatoid arthritis.
2Various immunosuppressants
are available. Please see the latest MIMS for specific formulations and
prescribing information.
Biologic Therapy
Dupilumab
Dupilumab
is a human immunoglobulin (Ig) G4 monoclonal antibody approved for use in
patients ≥12 years of age with moderate to severe atopic dermatitis
uncontrolled by first-line treatments and who are candidates for systemic
therapy. It binds to the interleukin-4Ra (IL-4Ra) subunit thereby inhibiting
IL-4 and IL-13 cytokine-induced responses which include proinflammatory
cytokine, chemokines, and IgE release. Combination with emollients and
as-needed topical anti-inflammatory agents are recommended.
Tralokinumab
Tralokinumab
is recommended for adult patients with moderate to severe atopic dermatitis
uncontrolled by topical therapies and are candidates for systemic therapy. It
is a human, high-affinity IgG4 monoclonal antibody which acts by neutralizing
IL-13. Combination treatment with topical corticosteroids, topical calcineurin
inhibitors, and UV light is possible.
Other Biologicals
Further studies are needed to prove the efficacy of Nemolizumab,
Rituximab, Mepolizumab, Omalizumab, and Ustekinumab for atopic dermatitis. Trial
treatment with Mepolizumab may be considered in select patients unresponsive to
standard therapies. Lebrikizumab, Nemolizumab, Tralokinumab, and Tezepelumab are
being studied for atopic dermatitis.
Retinoid
Alitretinoin
is a derivative of Isotretinoin with anti-inflammatory effects used for severe
chronic hand atopic dermatitis unresponsive to first-line treatments. Concomitant
treatment with topical corticosteroids, topical calcineurin inhibitors, and
emollients is possible.
Allergen-specific Immunotherapy
Allergen-specific
immunotherapy may be considered for select patients with severe disease with
house dust mite, birch, or grass pollen sensitization, and concomitant history
of clinical exacerbation after exposure or positive atopy patch test.
Antihistamines3
Oral
sedating antihistamines are typically used for soporific effects to facilitate
sleep, to prevent an increase of itch intensity at night, and as an adjunctive
therapy to topical anti-inflammatory therapy. Studies of oral non-sedating
antihistamines have shown variable results in controlling pruritus; however,
they may be useful in a small group of patients with associated urticaria. Topical
antihistamines are usually not helpful in relieving pruritus and may cause
allergic contact dermatitis.
3Various
antihistamines are available. Please see the latest MIMS for specific
formulations and prescribing information.
Skin Infections4
Clinical
infections at treatment sites should be cleared before starting
anti-inflammatory agents. Reservoirs of the disease may need to be treated to
prevent recurrence (eg nose, groin).
Bacterial Infections
Staphylococcus
aureus is commonly cultured from eczematous skin and is
often the cause of localized infections.
Short-term
topical therapy may be used to treat localized areas. Fusidic acid, Mupirocin,
Neomycin, and Retapamulin are treatment options. Retapamulin is recommended for
children >9 months. Neomycin may cause allergic contact dermatitis.
Oral
therapy is usually necessary to treat widespread infected lesions. Anti-staphylococcal
penicillins (eg Flucloxacillin), macrolides (eg Clarithromycin, Erythromycin), first-
and second-generation cephalosporins, and Clindamycin are treatment options. Flucloxacillin
is recommended as the first-line therapy for patients with secondary bacterial infections.
Alternative treatments to Flucloxacillin include Clarithromycin and
Erythromycin.
Fungal Infections
Fungal infections may be considered as a possible complication of atopic
dermatitis. Antifungal therapy (eg topical Ketoconazole or Ciclopirox olamine,
systemic Itraconazole or Fluconazole) may be considered in patients with head and/or
neck involvement or with IgE-sensitization to Malassezia spp. Superficial
dermatophytosis and Pityrosporum ovale may be treated with systemic or
topical antifungals.
Viral Infections
Patients
may develop secondary herpes infections inclusive of eczema herpeticum and
Kaposi’s varicelliform eruption and may require systemic Acyclovir or
Valaciclovir treatment in a hospital setting. Topical agents such as potassium
hydroxide (KOH), Cantharidin, Tretinoin, or Cidofovir, and physical treatments
such as cryotherapy and curettage, may be used for eczema molluscatum.
4Various antibiotics,
antifungals, and antivirals are available. Please see the latest MIMS for
specific formulations and prescribing information.
Other Pharmacotherapeutic
Options
Further
studies are needed to prove the efficacy of probiotics, topical sodium
cromoglycate, vitamin D, Tofacitinib, mast cell stabilizers, and leukotriene
antagonists (eg Montelukast) in atopic dermatitis. Vitamin D supplementation and
the use of prebiotics or probiotics may reduce symptoms but are not routinely
recommended.
Patient Education
Patient or Caregiver
Education
Discuss
the chronic nature of atopic dermatitis, exacerbating factors, and appropriate
treatment options with the patient or caregiver. Emphasize that atopic
dermatitis tends to decrease with increase in age. Convey that the goal of
treatment is control rather than “cure”. Discuss that many factors probably
contribute to flare-ups and usually a specific cause cannot be found.
Educate
the patient about proper skin care (eg bathing, hydration, and use of
moisturizers). The patient or caregiver should be instructed to apply
emollients liberally 3 minutes after taking a bath two to three times daily or
frequently as the skin gets dry even in the absence of symptoms. Studies showed
that correct and adequate instructions for the use and application of
moisturizers when done properly reduce disease severity and the overall topical
corticosteroid use. This may improve disease awareness, manage expectations, and
enhance treatment adherence.
Supportive
stress-reduction training, including relaxation training and cognitive
behavioral therapy, and behavioral therapy to stop habitual scratching, should
be discussed with the patient.
Explain
the importance of therapy adherence, appropriate drug therapy, and potential
side effects of medications when used over extended periods of time. Apply
topical steroids 10 to 15 minutes after the application of emollients.
Advise
patients to keep their fingernails trimmed short and to use cotton gloves at
night to limit scratching.
Lifestyle Modification
Avoidance of Trigger
Factors
Identify and Eliminate
Trigger Factors
Identify
potential allergens by careful history and selective allergy tests. Skin prick
tests and serum tests for allergen-specific IgE are only useful if there is a
suspected allergen. Negative results are useful for ruling out suspected
allergens. In vitro allergy tests or positive skin prick tests do not
always correlate with the clinical symptoms (especially foods) and controlled
food challenges, atopy patch tests, or elimination diets may be needed. Limited
food allergy testing may be considered in children <5 years with
moderate-severe or refractory disease and/or a history of an allergic reaction
after a particular food exposure. Most children will outgrow food
hypersensitivity within the first few years of life. Patch tests may be done if
contact dermatitis is suspected such as palmar or facial dermatitis.
Advise patients to avoid
foods identified as allergens in controlled food challenges. Avoidance of aeroallergens
(eg house dust mites) may improve symptoms. Advise patients to use dust
mite-proof encasings on pillows, mattresses, and box springs, wash bedding
weekly in hot water (>58°C), remove bedroom carpeting and curtains, and decrease
indoor humidity to levels below 60%. Evidence suggests that allergen-specific
immunotherapy may be an option in treating select patients with sensitivity to
aeroallergens.
In
most cases, trigger factors cannot be specifically identified, thus advise the
patient to apply a holistic approach to avoidance since trigger factors are
usually multiple.
Common trigger factors
for atopic dermatitis include wool clothing, pollen, extreme temperature,
sweat, products with perfumes or preservatives, foods, cigarette smoke, and animal
dander. Psychological factors may also trigger atopic dermatitis. Emotional
factors (eg anxiety, stress, and anger) cause disease exacerbation, induce
immune activation, and increase pruritus and scratching. Psychological
evaluation and counseling should be considered in patients with difficulty with
emotional triggers or psychological problems.
Skin Care
Emphasize
the importance of a holistic skincare routine which includes cleansing,
moisturizing, treatment, and sun protection. Improvement in symptoms and reduction
in side effects of topical therapy such as corticosteroids in atopic dermatitis
improve adherence to treatment.
Appropriate skin care reduces the incidence of flares and increases the
time between flares. Hydration of skin with emollients and restoration of skin
barrier function are essential to the treatment of atopic dermatitis. Regular
skin cleansing with the use of soaps, synthetic detergent (syndet) bars, and
topical antiseptics and antibiotics helps reduce abnormal microbial
colonization to restore the skin microbiome.
Bathing1
Bathing
helps cleanse the skin by removing scales, crusts, bacteria, allergens, and
irritants. Soap substitutes with minimal defatting activity,
moisturizer-containing, fragrance-free, hypoallergenic, and a neutral to low pH
are preferred.
The
ideal hot water temperature for bathing or showering is approximately 38-40°C since
a skin temperature of ≥42°C induces an itching response. Once- or twice-daily,
short, lukewarm water baths followed by immediate application of moisturizers
are recommended for atopic dermatitis patients.
Advise
patients that, if possible, limit soap use to hands, feet, genitalia, and axillae
and limit bathing to once daily for 5 to 10 minutes using warm water. Advise
them to pat dry after a bath and apply moisturizer or bath oils within 2 to 3
minutes of a bath.
Studies
have shown a decrease in bacterial infection (eg staphylococcal, methicillin-resistant
Staphylococcus aureus [MRSA]), disease severity, and flare-ups in
patients taking regular bleach baths (1:1200 dilution of 6% hypochlorite
bleach; 10-minute soak, three times per week). Bleach baths with intranasal
Mupirocin are highly recommended for patients with moderate to severe disease with
recurrent secondary bacterial infection. Topical antiseptic agents (eg Sodium
hypochlorite 0.005% bath) may be considered in patients with chronic,
treatment-resistant disease.
Salt
baths may also be used to help shed dead keratin materials from the skin. Oatmeal
products added to baths may be soothing but do not increase water absorption by
the skin. Thermal spring water balneotherapy may be considered in patients with
mild to moderate disease. Topical medications are best applied after bathing
because of greater penetration of hydrated skin.
1Various
products are available. Please see the latest MIMS for specific formulations
and prescribing information.
Moisturizers1
Moisturizers
are considered the mainstay of atopic dermatitis treatment as they improve skin
barrier function, reduce the incidence of flares, increase the time between
flares, and have steroid-sparing effects.
Atopic Dermatitis_Management 2They are recommended for all levels of atopic dermatitis severity ‒ for primary prevention, maintenance, during acute flares, and for prevention of relapse. Moisturizers should contain anti-inflammatory and antioxidant properties.
Water-in-oil emollients are preferred, although occlusive agents and humectants are also used. They are useful for the treatment of active disease and in both prevention and maintenance therapy as they help reestablish and preserve the stratum corneum.
For the effects, emollients (eg Glycerol stearate, lanolin, soy sterols) provide lubrication, improve the epidermal barrier, and help soften the skin surface. Newly developed emollients contain ingredients that positively influence the skin microbiome of atopic dermatitis patients. Occlusive agents (eg Dimeticone, Mineral oil, petrolatum) provide a physical barrier against water evaporation. Humectants (eg Urea, Glycerol, Lactic acid, pyrrolidone carboxylic acid [PCA]) help retain moisture in the stratum corneum. Urea, lactate, PCA, and amino acids (eg Arginine) are components of the natural moisturizing factor which maintains adequate hydration of the skin thus optimizing the barrier function of the stratum corneum.
A comparative review of different clinical studies on moisturizers revealed that proper use reduces pruritus, reduces topical corticosteroid use, and prevents flares and recurrences. A clinically significant reduction in disease severity with moisturizer use compared to no moisturizers was seen. Moisturizer combined with Fluticasone propionate applied twice weekly was more effective in preventing flares than moisturizers alone. Better efficacy was noted in patients who used topical active treatment combined with moisturizers compared to using topical active treatment alone.
Patient preference and treatment area will determine the formula used in moisturizers (eg Ceramides, Hydroxypalmitoyl sphinganine, Palmitoylethanolamide [PEA], Liquid paraffin, Mineral oils, Glycerin, Hyaluronic acid, Shea [Butyrospermum parkii] butter, Telmesteine, Glycyrrhetinic acid, Lactic acid). Urea-containing moisturizers reduce the rate of flares but may cause transient burning and stinging after application. Oat- and Glycerol-containing moisturizers also reduce the rate of flares but with lesser side effects and lessen the use of topical corticosteroids. Glycyrrhetinic acid and Allantoin have anti-inflammatory properties that help reduce pruritus. The anti-inflammatory and antibacterial properties of Licochalcone contained in some moisturizers are comparable to the efficacy of combination therapy of moisturizers and 1% Hydrocortisone acetate cream. Niacinamide and sunflower seed oil improve skin barrier function by reducing transepidermal water loss.
Emollients should be applied at least three times daily (in the morning and afternoon immediately after bath and at night before bedtime) or in flare-up condition every 3 to 4 hours.
Products with preservatives or fragrances should be avoided and if the product stings and/or burns, expert advice should be sought. Reports of studies suggest that the use of emollients in infants might prevent atopic dermatitis development in high-risk patients.
1Various products are available. Please see the latest MIMS for specific formulations and prescribing information.
Photoprotection
Regular use of broad-spectrum sunscreens with SPF30+ and with inorganic ultraviolet filters (eg titanium dioxide, zinc oxide) is recommended; however, it should not be applied over inflamed skin.
Other Therapy
Wet Wrap Therapy
Wet
wrap therapy may be used for chronic and refractory lesions or for moderate to severe
weeping lesions. It cools inflamed skin, maintains hydration, and decreases
scratching. It can help reduce water loss and disease severity in patients with
moderate to severe atopic dermatitis. When combined with topical
corticosteroids, it can be effective in treating refractory cases.
Phototherapy
Phototherapy
is considered in patients with recalcitrant disease or when first-line therapy
with topical agents has been unsuccessful.
Atopic Dermatitis_Management 3Broadband UVB and UVA, narrowband UVB and UVA-1, or combined UVA and UVB can be useful. They treat chronic lichenified forms of moderate-severe disease, effectively reduce colonization of Staphylococcus aureus and Malassezia sp, and mediate cytokine production. Narrowband UVB and medium-dose UVA-1 are recommended for patients with moderate to severe atopic dermatitis. They may be used in children and adolescents after skin type assessment but only for a short period. Other phototherapy modalities (eg broadband UVB and UVA, balneophototherapy) may be considered as second-line modalities.
Photochemotherapy with Psoralens and UVA (PUVA) should be restricted to patients with widespread severe atopic dermatitis. PUVA therapy may be considered only when previous treatment cycles with other phototherapies are ineffective or when approved drug therapies are contraindicated, ineffective, or with adverse effects.
Phototherapy may be combined with corticosteroids and emollients in phases of acute flares and to prevent future flare-ups. Relapse after therapy cessation frequently occurs.
The short-term adverse reactions of phototherapy include erythema, skin pain, pigmentation, and itching. The long-term adverse reactions include premature skin aging and the potential for cutaneous malignant diseases. It is therefore not recommended in patients with a history of skin cancer or with an increased risk of skin cancer. It is also not recommended in patients who are treated with systemic immunosuppressants (eg Azathioprine, Ciclosporin) due to the increased risk of cancer.
Immunoadsorption
Immunoadsorption is a treatment option for patients with severe, treatment-refractory disease with high serum IgE levels. It is an extracorporeal technique that utilizes immunoadsorption columns to deplete the IgE serum level which may lead to the reduction of disease activity. Studies showed a significant decrease in SCORAD and disease activity improvement.
Prevention
The identification and elimination of triggering factors are the mainstay for the prevention of flares as well as for the long-term treatment of atopic dermatitis.
Breastfeeding or feeding with hypoallergenic hydrolyzed formula milk was shown to be beneficial. If the patient with atopic dermatitis is also diagnosed with food allergy, the mother should be advised to eliminate all identified food allergens from her diet.
Immunization against varicella-zoster virus infection should be encouraged to prevent secondary local or systemic bacterial infection in children with atopic dermatitis. Probiotics may also reduce the incidence or severity of atopic dermatitis, however, more studies are needed to prove this benefit.