Atopic dermatitis -Management
How do we treat AD?
Multipronged
approach that involves
Elimination
of exacerbating factors
Restoration
of the skin barrier function and hydration of the skin,
Patient education,
and
Pharmacologic
treatment of skin inflammation.
CLICK HERE FOR CLINICAL FEATURES AND DIAGNOSIS OF AD
How can we assess severity of AD?
As per NICE guidelines (National Institute for Health and Care Excellence)Mild – Areas
of dry skin, infrequent itching (with or without small areas of redness);
little impact on everyday activities, sleep, and psychosocial well-being
Moderate –
Areas of dry skin, frequent itching, redness (with or without excoriation and
localized skin thickening); moderate impact on everyday activities and
psychosocial well-being, frequently disturbed sleep
Severe –
Widespread areas of dry skin, incessant itching, redness (with or without
excoriation, extensive skin thickening, bleeding, oozing, cracking, and
alteration of pigmentation); severe limitation of everyday activities and
psychosocial functioning, nightly loss of sleep.
There are various disease severity scores like:
Scoring of
Atopic Dermatitis [SCORAD] index,
Eczema Area
and Severity Index [EASI], and the Patient-Oriented Eczema Measure [POEM]) and
patient quality-of-life measurement scales have been tested and validated for
use in clinical trials, but they are not commonly used in clinical practice.
What is the general approach for AD patients?
Patient
education and counselling have been shown to improve the clinical symptoms.
It is
essential to identify and eliminate triggering factors for AD, both during the period
of acute symptoms and on a long-term basis to prevent recurrences.
Patients with
AD should use soaps with minimal defatting properties and a neutral pH.
New clothing
should be laundered before wearing to decrease levels of formaldehyde and other
chemicals.
Residual
laundry detergent in clothing may trigger the itch-scratch cycle; using a
liquid rather than powder detergent and adding a 2nd rinse cycle facilitates
removal of the detergent.
Use of SPF
sunscreens should be used.
Avoidance of
aeroallergen and food allergen.
What is the use of moisturizers?
Skin
hydration is a key component of the overall management of patients with atopic
dermatitis.
To maintain
skin hydration, emollients should be applied at least two times per day and
immediately after bathing or hand washing.
Thick creams,
which have a low water content, or ointments (eg, petroleum jelly), which have
zero water content, better protect against xerosis, but some patients may
complain that they are greasy.
Since atopic
skin is deficient in stratum corneum lipids (especially ceramide) and
"natural moisturizing factor" (a mixture of hygroscopic amino acids
resulting from filaggrin breakdown), moisturizers that contain those
ingredients may be beneficial. There are a number of topical moisturizers
available in the market by prescription. There are few data demonstrating their
efficacy, but one randomized trial suggests that they are no more effective
than over-the-counter emollients.
What is the data regarding bathing?
Warm soaking
baths or showers using mild or soap-free cleansers should be part of the
routine skin care for patients with atopic dermatitis. Some controversy exists
concerning the frequency of bathing and whether showering or bathing is
preferable in patients with atopic dermatitis.
Most experts
recommend a hydrating bath followed by immediate emollient application, but
others recommend a shower of short duration.
Till now there
are no studies that has clearly supported the above claims by the experts.
Can we use bath additives for AD?
In absence of high-quality studies providing evidence of benefit, bath emollient additives (e.g., liquid paraffin, oils with or without emulsifiers, colloidal oatmeal) are widely used to improve skin hydration in children and adults with atopic dermatitis, especially in Europe, where their use is supported by national and international guidelines.How do we treat pruritis?
Non-pharmacological therapy
Pharmacological therapy
What is the non-pharmacological therapy?
Proper skin hydration and moisturization
Tepid baths to hydrate and cool the skin
followed by application of emollients
Wet wraps can be used.
Occlusive ointments
are sometimes not well tolerated because of interference with the function of
the eccrine sweat ducts and may induce the development of folliculitis. In
these patients, less occlusive agents should be used.
Hydration by
baths or wet dressings promotes transepidermal penetration of topical glucocorticoids.
Dressings may
also serve as effective barriers against persistent scratching, in turn
promoting healing of excoriated lesions.
Wet dressings
are recommended for use on severely affected or chronically involved areas of
dermatitis refractory to skin care. It is critical that wet dressing therapy be
followed by topical emollient application to avoid potential drying and fissuring
from the therapy.
Wet dressing
therapy can be complicated by maceration and secondary infection and should be
closely monitored by a physician.
What are the pharmacological therapies for itching?
Topical
steroids and calcineurin inhibitors
Systemic immunosuppressants
Dupilumab
Oral
antihistamines
What is the role of oral antihistamines?
Systemic
antihistamines act primarily by blocking the histamine H1 receptors in the
dermis, thereby reducing histamine-induced pruritus.
Histamine is
only one of many mediators that induce pruritus of the skin, so patients may
derive minimal benefit from antihistaminic therapy.
Because
pruritus is usually worse at night, sedating antihistamines (hydroxyzine, diphenhydramine)
may offer an advantage with their soporific side effects when used at bedtime.
Doxepin hydrochloride
has both tricyclic antidepressant and H1 - and H2 -receptor blocking effects.
Short-term
use of a sedative to allow adequate rest may be appropriate in cases of severe
nocturnal pruritus.
Studies of
newer, non-sedating antihistamines have shown variable effectiveness in
controlling pruritus in AD,
although they
may be useful in the small subset of patients with AD and
concomitant
urticaria
What are the pharmacological therapies for AD?
Topical
steroids
Topical
calcineurin inhibitors
Phosphodiesterase
inhibitors
Tar
preparations
Antihistamines
Systemic
steroids
Cyclosporine
Monoclonal
antibody therapy
MMF,
Methotrexate
Azathioprine
Topical steroids are the cornerstone of therapy of AD.
What are the types of topical steroids?
There are 7 groups
based on potency.
How do we
prescribe topical steroids?
Mild cases less potent steroids like desonide, hydrocortisone are usedApplied 1-2
per day for 2-4 weeks
For moderate
AD
Medium to
high potency steroid (group 3 and 4) are used. e.g. triamcinolone,
betamethasone dipropionate.
n patients with acute flares, super high-
or high-potency topical corticosteroids (groups 1 to 3 can be used for up to
two weeks and then replaced with lower-potency preparations until the lesions
resolve.
The face and
skin folds are areas that are at high risk for atrophy with corticosteroids.
Initial therapy in these areas should start with a low-potency steroid, such as
desonide 0.05% ointment.
High-potency
topical corticosteroids are generally avoided in skin folds and on the face.
However, limited, brief use (five to seven days) of potent corticosteroids may
produce a rapid response, after which patients can be switched to lower-potency
preparations.
Use of Topical calcineurin inhibitors:
Non-steroidal
immunomodulating agent which do not cause skin atrophy and other steroid
related side effects.
They can be
used as an alternative to topical corticosteroids for the treatment of mild to
moderate atopic dermatitis involving the face, including the eyelids, neck, and
skin folds.
Tacrolimus
ointment and pimecrolimus cream are applied twice a day.
Tacrolimus
comes in two strengths. The 0.1% formulation is appropriate initial therapy for
adults (and those >15 years old), and the 0.03% formulation is appropriate
for children and for adults who do not tolerate the higher dose.
In patients
who do not tolerate tacrolimus because of burning or stinging, pimecrolimus may
be better tolerated.
US FDA has
approved use of tacrolimus and pimecrolimus for use in children above 2 years of
age.
What is the mechanism of action of tacrolimus?
Inhibits cytokine
production and alters APCs function in skin.
What are the
side effects of tacrolimus?
Pruritis,
erythema and transient burning sensation. They are as efficacious as a medium potency
steroid.
When are tacrolimus prescribed?
Topical
calcineurin inhibitors may be better than topical corticosteroids in the
treatment of patients whose AD is poorly responsive to topical steroids,
patients with steroid phobia, and those with face and neck dermatitis, in whom
ineffective, low-potency topical corticosteroids are typically used because of
fears of steroid-induced skin atrophy.
What is the use of Phosphodiesterase inhibitors?
Crisaborole
is a topical phosphodiesterase 4 (PDE4) inhibitor approved by the FDA for the
treatment of mild to moderate atopic dermatitis in adults and children three
months of age and older.
After initial therapy how to prescribe maintenance therapy?
After
induction of remission, intermittent therapy with moderate- to high-potency
topical corticosteroids (groups 3 to 5) should be started.
The steroid
should be applied once daily to previously affected skin areas for two
consecutive days per week (eg, weekends) and may be continued for up to 16
weeks.
Emollients
can be liberally used multiple times per day.
How do we treat flare?
Flares of
atopic dermatitis that occur during intermittent treatment may be treated by
resuming continuous use of topical corticosteroids or calcineurin inhibitors
that have been effective for the patient in the past.
Those
children who have frequent flares can be treated with low potency steroids
intermittently for 2 consecutive days in a week.
How do we treat acute exacerbations of chronic AD?
In
adolescents and adults, an acute exacerbation of chronic atopic dermatitis can
sometimes be aborted by a short course of systemic glucocorticoids (eg,
prednisone 40 to 60 mg/day for three to four days, then 20 to 30 mg/day for
three to four days). This strategy is not recommended for infants and young
children.
How do we treat cases refractory to topical steroid and calcineurin inhibitors?
Phototherapy
or
Systemic Immunomodulatory
therapy
Role of
phototherapy
Narrow Band UV-B
phototherapy as first-line therapy for adult patients with moderate to severe
atopic dermatitis that is not controlled with topical therapy.
Phototherapy
is usually administered two to three times per week. Topical corticosteroids
can be continued as needed during phototherapy. Additional emollients may be
necessary since phototherapy may increase skin dryness.
Phototherapy is not suitable for
infants and young children.
Systemic therapies:
Dupilumab is
a fully human monoclonal antibody that binds to the alpha subunit of the
interleukin (IL) 4 receptor and inhibits downstream signaling of IL-4 and IL-13.
It is useful
for patients with moderate to severe AD not responding to topical therapy and
in whom phototherapy is not feasible or acceptable.
Dupilumab is
also an option for patients who are not candidates for or failed previous
treatment with conventional immunosuppressive agents, such as cyclosporine,
methotrexate, mycophenolate mofetil, or azathioprine.
Compared with
conventional immunosuppressive agents, dupilumab has a favorable safety profile
and may be used for long-term treatment of atopic dermatitis.
However, cost
may be a major consideration with dupilumab.
Exacerbation
or new onset of head and neck dermatitis ("dupilumab facial redness")
has been reported in approximately 4 to 10 percent of adult patients treated
with dupilumab after a median time of 65 days after initiating dupilumab.
Cyclosporine:
Cyclosporine
(5mg/kg/day) for short-term and long-term (1 yr) use has been beneficial for children
with severe, refractory AD.
Oral
cyclosporine is not recommended in infants and young children with atopic
dermatitis. In older children and adolescents, the use of cyclosporine should be
reserved for the most severe cases that failed to respond to optimal topical
treatment and where there is a significant, negative impact on quality of life.
Cyclosporin
forms a complex with an intracellular protein, cyclophilin, and this complex in
turn inhibits calcineurin, a phosphatase required for activation of NFAT (nuclear
factor of activated T cells), a transcription factor necessary for cytokine
gene transcription.
Methotrexate,
MMF and Azathioprine can be used in severe cases.
What are the other unproven therapies?
Probiotics
containing Lactobacillus rhamnosus strain GG
Human
recombinant IFN-γ
Allergen
immunotherapy
Chinese
herbal medicine
Vitamin D
Melatonin
How do we treat infections in AD?
Bacterial infection
by Staph aureus is common in AD
Treat with
oral macrolides in case of MSSA and oral cephalosporin in cases of MRSA.
Dilute bleach
baths (cup of bleach in 40 gallons of water) twice weekly may be also
considered to reduce S. aureus colonization.
In one
randomized trial, the group who received the bleach baths plus intranasal
mupirocin (5 days/mo) had significantly decreased severity of AD at 1 and 3 mo
compared with placebo.
Patients
rinse off after the soaking. Bleach baths may not only reduce S. aureus abundance
on the skin but also have anti-inflammatory effects.
For HSV
infection in AD
Topical
corticosteroids should be temporarily discontinued if HSV infection is
suspected. Reports of life-threatening dissemination of HSV infections in
patients with AD who have widespread disease mandate antiviral treatment.
Treat with
oral acyclovir.
Persons with
AD are also susceptible to eczema vaccinatum , which is similar in appearance
to eczema herpeticum and historically follows smallpox(vaccinia virus)
vaccination.
Antifungal agents
for dermatophytal infection.
What are the complications?
Skin
infections
Exfoliative dermatitis
Atopic
keratoconjuctivitis
Keratoconus
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