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Part Two: Atopic Dermatitis Management

*Disclaimer: For optimal management and successful outcomes managing Atopic Dermatitis, Dermal Clinicians are educated on the broader management options and treatment strategies available to clients. This includes staying up to date with current best practice and emerging therapies through evaluation of scientific literature. This blog is for educational purposes only. It is intended to provide a general understanding of therapies available by Medical professionals within an interdisciplinary framework for the management of Atopic Dermatitis. Dermal Clinicians do not prescribe or claim to prescribe any medication or treatments mentioned that are Medical practitioner only.*

Management and treatment of Atopic Dermatitis/ Eczema

Once a confirmed diagnosis of atopic dermatitis (AD) has been made, eliminating possible

differential diagnoses such as allergic contact dermatitis, a multidisciplinary approach to

treatment may be suggested. Treatment involves relieving symptoms during active occurrences, preventing periods of acute worsening (flares) and pro-active maintenance therapy once acceptable remission is achieved. Patient education is paramount and aims to improve treatment adherence, once appropriate treatment approaches have been identified based on the condition of the particular individual. Before treating, physicians will take a detailed medical history and establish immunoglobulin E (IgE) levels, establish disease severity, and assess and monitor their patients using valid, reproducible clinical tools such as SCORing Atopic Dermatitis (SCORAD), Eczema Area and Severity Index (EASI), and Six Area Six Sign Atopic Dermatitis Severity index (SASSAD.)

The aim of treatment is to stablise the condition and strengthen the impaired epidermal barrier, relieving symptoms such as pruritus and cosmetic concerns, and improving patient quality of life by reducing restrictions in their daily life caused by AD.

There are many treatment options available which should be individually tailored based on severity, patient preference and contraindications, with combination therapies often yielding the best results. A treatment algorithm is proposed based on evidence within literature, and considers patient age, severity of condition, type, site and extent of lesions, presence or absence of infection and responses to any previous treatments.

Mild AD responds to optimal skin care including regular use of moisturisers containing agents such as emollients (for example, glycol), occlusives (e.g.: petrolatum), and humectants which attract and hold water (e.g.: urea, glycerol) to relieve xerosis and reduce trans-epidermal water loss. Moisturisers can be enough to treat the condition if it is mild, as well as useful as a maintenance therapy and in the prevention of flares. Amount and frequency of application will depend on severity of xerosis and delivery system of the product (e.g.: cream, lotion, gel) as well as patient preference.

It makes sense to avoid known trigger factors that will exacerbate the condition such as

detergents, solvents and other irritants. Stress and anxiety can worsen the symptoms,

especially pruritus, therefore psychological support and interventions such as the control of

serotonin levels, can be used in management. There is insufficient evidence to recommend

dietary supplements or prebiotics/probiotics, however food allergies may co-exist and could

possibly trigger flares.

Vitamin D supplementation however, is an area of recent interest as an add-on therapy as it is theorised that vitamin D could have a role in AD pathogenesis. Oral vitamin D supplementation has been shown to improve the incidence of AD, which for many

individuals, worsens in winter when vitamin D deficiency is possible.

Pharmacologic topical agents are the backbone of treatment, comprising topical corticosteroids, calcineurin inhibitors, antimicrobials and antihistamines, which can be used alone or in combination because they aim to treat different facets of the AD pathogenesis.

Topical corticosteroids (TCS) such as aceponate and methylprednisolone act on T lymphocytes, monocytes, macrophages and dendritic cells, suppressing the release of proinflammatory cytokines. They are effective, safe, highly recommended as level 1 evidence and should be used once or twice daily under physician direction for active inflammation, or one to two times weekly for maintenance and prevention.

TCS potency should be adjusted to suit the anatomical location of use, and a rebound effect may occur if usage is not reduced gradually.

Calcineurin inhibitors such as tacrolimus for moderate to severe AD, and pimecrolimus for mild to moderate AD, are immune modulators and block the production of proinflammatory cytokines and mediators of AD inflammation. During significant flares, wet wraps may be indicated for relief for 5 – 7 days, when steroids diluted with emollients are applied and wrapped in bandages for improved penetration and patient comfort.

Phototherapy can be considered second line treatment after emollients/skin care and topical

corticosteroids and calcineurin inhibitors for children and adults, under careful monitoring and dosed according to minimal erythema dose and Fitzpatrick skin type. Narrowband UVB (311 –313 nanometers), UVA (340 – 400 nm) and UVA plus 8-methoxypsoralen (PUVA) is used for 15 to 36 sessions. Phototherapy can be used alone or in combination with emollient and TCS use, however it is not recommended to be used in conjunction with TCI.

Systemic treatments may be used if topicals and non pharmacologicals have not been

successful, and after considering an individual’s disease severity, risks, benefits and disease

impact on the patient’s quality of life. Systemic immunomodulatory agents work by decreasing proliferation of B or T cells during inflammation, and include azathioprine, dupilmab, methotrexate, cyclosporine, and mycophenolate mofetil. Cyclosporine (prescribed most commonly) suppresses T cell activation by inhibiting transcription of interleukin 2 and other cytokines, and low doses serve as an immune modulator by increasing the population of regulatory T cells.

Contraindications for use of systemic immunomodulatory agents include:

  • pregnancy

  • active infection

  • abnormal renal function

  • uncontrolled hypertension.

Interferon gamma is a cytokine acting in the innate and adaptive immune cascades, an alternative therapy useful for individuals contraindicated to other systemics.

Systemic steroids may be considered however more study is needed to address gaps in

research in this area. Atopic dermatitis patients may be prone to secondary bacterial or viral

infections due to their impaired barrier; hence systemic antimicrobials may be prescribed.

Also, oral antihistamines may be beneficial to relieve pruritus caused by histamine production during AD flares. Other options for control of pruritus include antileukotrienes (e.g.: montelukast), Naltrexone, serotonin modifiers, ondansetron and doxepin. To control infection, the use of prescribed topical or systemic antibiotics or antivirals is recommended.

Moderate AD responds to a maintenance regime of TCS or TCI’s, oral corticosteroids such as prednisone to reduce flares and then gradually reduce, emollient and corticosteroid wet wrap dressings, cyclosporine to reduce flares then gradually reduce, and finally medium doses of narrowband UVB phototherapy treatment.

For severe AD, studies have found the following are recommended:

  1. Cyclosporine (oral)

  2. Azathioprine (oral)

  3. Methotrexate

  4. Mycophenolate motefil

  5. Psoralen UVA

  6. IV immunoglobulins

  7. Interferon (family of immunoregulators)

  8. Hydroxychloroquine

  9. Omalizumab (monoclonal antibody which inhibits binding of IgE to receptors on mast cells and basophils)

  10. Rituximab (monocloncal antibody)

  11. Alefacept (immunosuppressive drug, T cell blocker)

  12. TNF inhibitors

Recent studies around the human microbiome suggest a disrupted balance between

commensal and pathogenic organisms fosters a proinflammatory environment, and as such

may play a role in the development of inflammatory skin conditions. Interventions which target the skins microbiome aiming to restore it to a stable and diverse anti-inflammatory state are an emerging area of AD therapy.

There is also an association between obesity and atopic dermatitis, as adipocytes act as a neuroendocrine organ, reducing immune tolerance. Studies hypothesise that the gut microbiome is implicated in the connection between AD and obesity.

Impact of COVID-19

The use of alcohol based hand sanitisers is a convenient, effective, low cost and simple method of protecting against cross-contamination of infections in general, not only at this time. The current necessity of frequent sanitisation however, increases the prevalence of skin irritation and therefore maintenance of healthy skin for AD patients is particularly crucial at this time.

While it is essential to follow strict hand washing and sanitising guidelines during this pandemic, it is recommended to apply a hypo-allergenic emollient hand cream frequently in addition. Such products usually contain humectants, fats, and oils intended to increase skin hydration and replace depleted skin lipids, maintaining an effective skin barrier.

The impact of the COVID-19 pandemic has been profound across the world, and health

professionals such as those in dermatology practice face unprecedented challenges in dealing with transmission of the virus and also caring for patients in vastly different environments. Tele-health consultations are taking over from face-to-face patient interactions, and non-urgent dermatology procedures may need to be postponed.

COVID-19 poses considerable concern for AD patients taking systemic immune-modulating

treatments, however recommendations by European Task Force on Atopic Dermatitis (ETFAD) warn against ceasing such treatment over COVID concerns, fearing an exacerbation of AD symptoms. The task force advises careful monitoring of pre-existing dermatological conditions such as AD, and to continue all treatment, even immune suppressive therapy or if necessary, utilise topical treatment on dermatologist advice instead.



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