Barrier repair in atopic dermatitis

Michelle Withers, MD, FRCPC (biography and disclosures)

What I did before

Atopic dermatitis (AD) is a chronic, itchy relapsing dermatitis that affects up to 20% of North American kids. AD resolves as children age in about 50-70% of cases.  The ultimate cause of AD is unknown, but it is often associated with other atopic features such as hayfever, allergies and asthma, and in many cases there is a genetic predisposition.  Eczema is impacted by a number of intrinsic and extrinsic factors, such as family history, environmental changes, overwashing, contact irritants and possibly dust mites.  It is well recognized that AD patients have very dry skin as part of their clinical picture.  As such, a very important part of discussing the treatment of AD includes the importance of moisturizing the skin on a regular basis to try to ameliorate dryness.

What changed my practice

The epidermis is often conceptualized as a brick wall, with keratinocytes forming the bricks and the intracellular lipids forming the mortar that holds the bricks together. For many years it has been thought that inflammation in the dermis leads to disruption and breakdown of the epidermal barrier. This inflammation was thought to stem from the genetic predisposition of these AD patients. There is new (and older) data that suggests the initial site of abnormality is within the epidermis itself, with primary barrier dysfunction then allowing penetration of allergens, irritants etc which sets up the inflammatory cascade that ultimately makes things worse.  We know that about 50% of patients with AD have a genetic mutation that reduces their levels of filaggrin in the epidermal layer.  Breakdown products of filaggrin create “Natural Moisturizing Factor”, made up of proteins, acids and humectants that help hydrate the skin. In patients without filaggrin, such as ichthyosis and AD patients, the lack of ability to self moisturize worsens the epidermal barrier dysfunction. The old hypothesis is called the inside-out theory, the new is the outside-in theory. It is likely that there is some element of truth to both of these theories and they may work in concert.

There are now on the Canadian market a number of “skin barrier repair” creams which aim to replenish the normal constituents of the intracellular lipid and try to fix the epidermal barrier. These creams are different than that of regular moisturizers or emollients, which serve to seal moisture into the skin and form only a physical barrier. These skin barrier repair creams have various concentrations of ceramides, cholesterol and free fatty acids, which are the components of the intracellular lipid matrix. Some of these lipids are incorporated into keratinocytes and excreted back out into the intracellular space, to fix the brick wall mortar.  It is unclear exactly what concentration of which lipid is most important and there are a number of products all with very different ingredients and percentages.  As such, there is no consensus and we are left with some degree of buyer beware. Skin barrier repair creams are available both in prescription (Epiceram cream) and over the counter preparations (CeraVe cleanser, lotion and cream, Cetaphil Restoraderm cleanser and lotion).

A randomized investigator-blinded study in 2009 compared Epiceram to a low-mid-potency topical steroid cream (fluticasone proprionate 0.05%) BID in 121 moderate to severe AD patients over 28 days. The results showed a similar degree of reduction (~50%) of itch, improvement in specific AD scores and improved sleep habits when looking at both arms of the study. Also, fewer patients in the Epiceram arm required steroid rescue therapy, making it a potential for monotherapy.  Another study in 2011 looked at Epiceram as monotherapy or in combination with various topical steroids.  Of the 207 patients, 54% were clear or almost clear at week 3, in either arm, especially those with mild AD.

CeraVe published in 2008 the use of its cleanser and moisturizing cream in 60 patients with mild to moderate AD. The products were used as adjuvant therapy BID with topical fluocinonide cream 0.05% to see if CeraVe could reduce AD symptom duration. Indeed, the addition of the CeraVe products did increase disease clearance from 15%  (with a mild bar soap, no mositurizer and steroids alone) to 76% (when steroids were used in conjunction with the CeraVe cleanser and cream). There are no similar studies for Cetaphil Restoraderm.  Remember also, these studies are small and not powered for non-inferiority, so results should be interpreted cautiously.

What I do now

Counselling is a significant component of treating AD.  I have always recommended lukewarm, short baths or showers, minimal use of mild cleansers and liberal use of creamy moisturizers.  Now, if I have a patient with AD who is doing all of those things to the best of their ability (and remember, they need regular reminders), I will suggest they try one of the new skin barrier repair creams. These can be used liberally all over or in hot spot areas that always tend to flare.  If a patient has a moisturizer that they like and tolerate, I will not suggest switching, but if they are looking for something new to try, have ongoing xerosis in spite of their moisturizer or aren’t using anything, these are good topical preparations to try. These topicals are only part of the treatment regimen we use when managing AD patients, but a newer tool that may give significant benefit, especially when used in conjunction with active medical therapies.

References

1. Thomas R, Landells I, Lynde C, Withers M et al. Canadian Consensus of Skin Barrier Therapy and Atopic Dermatitis. J Cut Med Surg 2012;16:S1-16.
2. Danby SG, Cork MJ. A new understanding of atopic dermatitis: the role of epidermal barrier dysfunction and subclinical inflammation. J Clin Dermatol 2010;1:33-46
3. Sugarman JL, Parish LC. Efficacy of a lipid-based barrier repair formulation in moderate-to-severe atopic dermatitis. J Drugs Dermatol 2009;8:1106-11

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Barrier repair in atopic dermatitis

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