Non-Pharmacologic Management of Atopic Dermatitis

October 1, 2009

Reprinted from Skin Therapy Letter FP 5(1):4-7 (April 2009) due to content update

M. Weinstein, MD, FRCPC (Pediatrics), FRCPC (Dermatology)

Assistant Professor of Pediatrics and Medicine, University of Toronto, Toronto, ON, Canada
Staff Dermatologist, Division of Pediatric Medicine, Department of Pediatrics, Hospital for Sick Children, Toronto, ON, Canada

Background

Atopic dermatitis (AD) or eczema is a chronic, relapsing skin condition that can lead to xerosis, pruritus, and patches of dermatitis. Coping with the physical and emotional aspects of AD can significantly impact the quality of life. It is most common in childhood, as many patients seem to outgrow the condition by adulthood. The etiology of AD is complex and not fully understood, but contributing factors include a dysfunctional skin barrier that allows moisture to escape and irritants to enter, as well as inflammatory mediators. There is increasing interest in exploring the feasability and efficacy of using non-drug alternatives as adjuncts to conventional pharmacologic approaches. Lifestyle modifications that can aid AD management will also be reviewed.

Diagnostic Features

Chronic or chronically relapsing dermatitis
Typical morphology and distribution (e.g., flexural erythema, excoriations, lichenification, xerosis)
- Facial and extensor involvement in infants and children; flexural dermatitis and lichenification in adults
Early age of onset – AD affects up to 20% of children¹
Intensive itching that can cause disruptive sleep or difficulties in concentration
- Breaks in the skin from scratching can lead to secondary infection
Personal or family history of atopy (i.e., asthma, allergic rhinitis, AD)
Hyperreactivity to environmental triggers

Defects in the Skin Barrier

There is growing data to support the longstanding theory that AD may be caused by a genetic defect in the epidermis, permitting environmental irritants, microbes, and allergens to penetrate, which in turn elicit inflammatory responses.²

The filaggrin gene contributes to the formation and function of the skin.
Deviations in the gene coding for filaggrin can cause skin barrier defects that contribute to AD.
Defects in skin barrier development prevent adequate levels of antimicrobial peptides to form in the epidermis. Consequently, bacterial and viral infections may occur in affected lesions.

Treatment Options

Avoidance of triggers
Emollients/moisturizers
- Standard adjunct for prevention and maintenance
Topical corticosteroids
- The cornerstone of AD therapy
- Potential for tachyphylaxis, skin atrophy, and systemic side-effects, especially in long-term use
Topical calcineurin inhibitors (TCIs)
- Useful when conventional therapies fail or are unsuitable
- In 2006, an FDA boxed warning was issued for TCIs over concerns of immunosuppression and the potential risk of malignancy following long-term or continuous use
Antimicrobials for infection
- Topical or oral antibiotics may be prescribed to treat infected lesions
- Overuse or prolonged treatment increase the risk for developing antibiotic resistance
- Oral antivirals can be used for cases of eczema herpeticum (eczema infected with herpes virus)
Oral antihistamines for pruritus
- Often tried for intractable itch, but little evidence exists to support their antipruritic effect
Systemic corticosteroids, systemic immunosuppressants and phototherapy
- Reserved for severe disease

Moisturizing and Bathing

Moisturizers

Daily moisturization is essential for managing AD, both during and between flare-ups.
A randomized controlled study demonstrated that moisturizers can improve the barrier function of skin; however, the effects are determined by individual product composition.³
Basic essential components of moisturizers include emollients and humectants.
- Emollients provide a protective film by filling-in spaces between cells and restoring lost lipids to prevent transepidermal water loss (TEWL).
  - Commonly used emollients include animal oils, butyl stearate, cocoa butter, lanolin, lipids, mineral oil, petrolatum, and shea butter.
  - Petrolatum is the gold standard emollient; its non-sensitizing and highly occlusive properties are effective against TEWL.
  - Ceramides are lipid molecules that are important components of skin structure; they improve the skin barrier by limiting TEWL and preventing the entry of irritants.
  - AD patients have significantly fewer ceramides in their stratum corneum.
  - Lipids can be replaced topically with a ceramide-dominant emollient.
- A new class of emollients, now available in the US, aims to replenish certain molecules that are deficient in the skin of AD patients. These nonsteroidal moisturizers are very expensive, but study findings indicate their efficacy and safety for mild to moderate AD.⁴
- Humectants aid in the absorption and retention of moisture, and soften thickened skin.
  - Commonly used humectants include glycerin, hyaluronic acid, lactic acid, propylene glycol, panthenol, silicones, and urea.
  - Glycerin’s high affinity to attract moisture to the skin makes it the most widely used.
  - Panthenol (vitamin B5) functions as a humectant, emollient, and moisturizer. Studies examining adjuvant care with panthenol showed improved hydration and reduced dryness, itching, and inflammation.⁵

Choosing a Moisturizer

Generally, the greasier the better. Bland ointments, such as petrolatum, are non-irritating and provide an excellent barrier, but they can be perceived by patients as being too thick.
Less greasy creams and lotions may be more irritating.
Some acids (e.g., salicylic acid and lactic acid) and humectants (e.g., urea) can be poorly tolerated by eczematous skin. Avoid their use in infants and small children due to the risk of systemic absorption.

Bathing

Bathing first, and then applying a moisturizer while the skin is still damp, will help trap moisture in the skin. Medicated treatments should be applied to any dermatitis and moisturizers to unaffected skin.
Bathing more than once daily is not always practical. Although, during flare-ups, several short baths followed by daytime applications of a moisturizer can be helpful.
Baths (or showers) should be taken with warm (not hot) water and limited in duration.

Advancements in the Use of Natural Anti-inflammatories

Increasingly, patients prefer to supplement medical treatments with over-the-counter skin care products that incorporate natural ingredients. Plant-derived extracts are one of the largest categories of additives found in moisturizers. A few notable compounds have emerged following scientific evaluation, which supports their therapeutic benefits for alleviating symptoms associated with AD and other inflammatory skin conditions.⁶

Aloe Vera

Applications include its use as an anti-inflammatory, analgesic, antipruritic, antioxidant, and wound healing agent.
Chamomile (Matricaria recutita)
Topical use can relieve skin irritation. The active components (á-bisabolol, á-bisabolol oxide A and B, matricin) inhibit enzymes that mediate inflammation and suppress histamine release.
Its anti-inflammatory effect is approximately 60% of that elicited by hydrocortisone 0.25%.⁷

Colloidal Oatmeal

It has multiple active components that include enzymes, flavonoids, lipids, proteins, polyphenols (avenanthramides), polysaccharides, and vitamins.
Avenanthramides are potent phytochemicals that inhibit the release of proinflammatory cytokines, resulting in reduced contact hypersensitivity and inflammation.⁸
It also has antioxidant, anti-irritant, antihistaminic, and immunomodulatory effects.
Colloidal oatmeal is one of few natural ingredients approved as a skin protectant by the US FDA.

Feverfew (Tanacetum parthenium)

Its broad spectrum of clinical applications is attributable to its potent anti-inflammatory, antioxidant and anti-irritant properties.
Parthenolides are compounds in feverfew that can produce skin sensitivities. Development of a purified extract that is free of parthenolides has been shown to have strong anti-inflammatory activity through inhibition of proinflammatory cytokine release.⁹

Licorice Extracts (Glycyrrhiza glabra, Glycyrrhiza inflata)

Glycyrrhiza glabra (contains glabridin) reduces irritation, inflammation, and melanin production.
Glycyrrhiza inflata (contains licochalcone A) decreases irritation and inflammation.
Twice daily application of a licochalcone A-containing lotion for 8 weeks by patients with mild to moderate red facial skin produced statistically significant improvements in erythema scores.¹⁰

Avoidance of Triggers

Avoidance of triggers is a key AD management strategy. Each patient and his or her physician need to identify and eliminate relevant triggers.

Food

While AD patients are more prone to food allergies (type 1 hypersensitivity), it is unclear if certain foods can cause a flare-up, which is more of a type 4 hypersensitivity reaction.
If there appears to be a food trigger, parents or patients should keep a diary to track foods eaten and flare-ups. Food elimination diets should be physician supervised.
If type 1 allergic symptoms develop in response to a particular food, avoid ingestion until testing can be undertaken. If a food source is unclear, it may be useful to involve an allergist.

Aeroallergens

Certain aeroallergens (e.g., dust mites or seasonal allergens) can trigger AD flares.^11,12
Confirmatory testing may be useful in refractory
patients. If results are positive, deploy dust mite prevention strategies (e.g., frequently laundering mattress covers and avoid stuffed toys, feather pillows, duvets, and carpets).

Humidity/Sweating

Sweating can aggravate itching and humid conditions that increase perspiration can induce flares. Frequently cooling off, changing clothes, and adjusting activities in humid weather can help.
Heat and sweating can promote nighttime scratching. Recommend one layer each of sleepwear and covering. The bedroom should also be kept cool (but not cold).

Low Humidity/Dry Weather

Due to the dry weather, most patients have worse flares in the winter. Moisturizing several times per day is crucial. Use of a cool mist humidifier in the bedroom can be helpful.

Infection

AD patients are commonly colonized with Staphylococcus aureus (S. aureus) and have problems with S. aureus killing mechanisms.¹³ This frequently presents as a worsening of AD that is not responsive to therapy. Infected areas can appear as wet, oozing, or crusted lesions that require topical or oral antibiotics.
S. aureus may drive AD flares through superantigen mechanisms, even in the absence of an actual clinical infection.¹⁴ Therefore, patients who have frequent flare-ups may need strategies to reduce S. aureus colonization and inflammation.

Environmental Irritants

AD patients can be especially sensitive to dry grass, perfumes or fragrances in skin care products, and certain fabrics (wool and synthetics).
Wearing cotton clothing can be helpful. Some evidence suggests that specially treated silk or silver-coated fabrics may also be beneficial.^15,16

Chlorine

Swimming can be a good sport for AD patients, because sweating is not a concern. However, to avoid irritation, they should rinse off thoroughly afterwards and apply a moisturizer.
There is a lack of data to confirm if salt water or chlorinated pools are better for AD patients.

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Normal Routines

School

Children with severe eczema may engage in school-avoidance behaviours that are caused by fatigue due to nocturnal pruritus, or anxiety from being teased. These issues must be addressed promptly to re-establish a normal school routine.

Sunscreen

Many sunscreen products contain irritating ingredients. If regular sunscreens are unsuitable, suggest using sensitive skin formulations or physical sunblocks (e.g., titanium dioxide or zinc oxide).
A comprehensive sun protection strategy combines regular sunscreen use, avoidance of peak sun exposure times, and wearing hats and protective clothing.

Sleep

Sleep disturbance from pruritus can be a major problem for many patients and their families, particularly if parents sleep with their AD-afflicted child and help to scratch or restrain their child’s hand to prevent scratching.¹⁷ Both practices should be discouraged and may indicate a need to increase antipruritic therapy and the use of emollients.
Poor sleep can lead to patient and/or parental difficulties in concentration, irritability, and fatigue.

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Additional Tips

Keep nails short to minimize tissue damage from scratching.
Keep moisturizing creams in the refrigerator, as the cold sensation is soothing to itchy skin.
For topical medical therapy, ointments are usually better tolerated than creams or lotions.
Ask families if sleep routines are satisfactory and if sleep is disturbed. Many families do not volunteer this information to physicians.
Patients should be steered toward good sources of information (e.g., http://www.eczemahelp.ca).

Conclusion

Successful AD management is best undertaken with a step-wise approach that considers multiple factors including disease severity, therapeutic side-effects, patient preferences, itch intensity, and sleep quality. As well, psychosocial impacts from AD cannot be overlooked. The regimented use of moisturizers can improve the skin barrier and significantly reduce xerosis and itch. As such, it can serve as useful adjunctive care for maintenance and flares. The new research realm directed at the epidermal barrier and the important immune factors carries the hope that innovative therapeutic approaches will lead to reduced infections and improved management of AD patients.

References

Williams H, et al. J Allergy Clin Immunol 103:125-38 (1999 Jan).
Hanifin JM. J Invest Dermatol 129(2):320-2 (2009 Feb).
Buraczewska I, et al. Br J Dermatol 156(3):492-8 (2007 Mar).
Boguniewicz, M, et al. J Pediatr 152:854-9 (2008 Jun).
Eichenfield LF, et al. Cutis 80(6Suppl):2-16 (2007 Dec).
Wu J. J Drugs Dermatol 7(7 Suppl):s13-6 (2008 Jul).
Albring M, et al. Methods Find Exp Clin Pharmacol 5(8):575-7 (1983 Oct).
Sur R, et al. Arch Dermatol Res 300(10):569-74 (2008 Nov).
Martin K, et al. Parthenolide-free feverfew: an extract with effective anti-irritant activity in vitro. Presented at: 63rd Annual Meeting of the American Academy of Dermatology; New Orleans, LA; February 18-22, 2005. Poster #P1039.
Weber TM, et al. J Cosmet Dermatol 5(3):227-32 (2006 Sep).
Boralevi F, et al. Allergy 63(2):205-10 (2008 Feb).
Ponyai G, et al. J Eur Acad Dermatol Venereol 22(11):1346-55 (2008 Nov).
Kisich KO, et al. J Allergy Clin Immunol 122(1):62-8 (2008 Jul).
Schlievert PM, et al. Clin Infect Dis 46(10):1562-7 (2008 May 15).
Koller DY, et al. Pediatr Allergy Immunol 18(4):335-8 (Jun 2007).
Gauger A, et al. J Eur Acad Dermatol Vernereol 20(5):534-41 (2006 May).
Chamlin SL, et al. Arch Pediatr Adolesc Med 159(8):745-50 (2005 Aug).