In addition to utilizing the most common treatments for AD, including topical steroids and calcineurin inhibitors, keeping the skin efficiently moisturized is a very effective strategy for improving quality of life for patients with AD.
Atopic dermatitis breaks down the stratum corneum, the outermost epidermal layer of the skin. This dense layer of skin is responsible for preventing epidermal water loss and serves as a barrier to bacteria, irritants and allergens. People with atopic dermatitis (AD) have a weaker skin barrier than people with uncompromised barrier hydration; the skin of AD patients also has a depressed immune function and lacks normal lipophilic bacteria. The disease is responsible for creating breaks and cracks in the skin that allow bacteria and viruses to enter more easily and result in infection. The infection causes the skin to flare again, thus perpetuating the cycle of atopic disease.
People with AD often have recurrent infections caused by bacteria. These individuals are particularly susceptible to Staphylococcus aureus, as well as fungi and viruses. The lesions caused by AD are believed to provide an environment that is conducive to the harboring, growing and replicating of these infection-causing organisms. As this cycle continues, the AD worsens and can become resistant to traditional emollients and topical treatments, allowing for more bacteria to enter the body.
Bacterial infections are very common in patients who suffer from atopic dermatitis. Antibiotics are often required to combat bacterial infections. In rare instances, the bacterial infection can be especially severe, involving much of the skin surface and causing sepsis. Patients with AD are also at greater risk for developing an infection from the herpes simplex virus.
The Pathophysiology Of Atopic Dermatitis
Developing understanding of the pathophysiology of AD indicates that genetic abnormalities that result in deficiencies of the skin barrier are the first risk factor; this converges with acquired diseases to alter the skin’s structure and function. Immune system activation follows, which has a further negative impact on the skin barrier.
While current therapy has been largely directed toward lessening inflammation and pruritus, Mark Boguniewicz, MD, and Donald Y. M. Leung, MD, PhD, write: “Naturally occurring CD4+CD25+ FoxP3 expressing T regulatory (Treg) cells with normal immunosuppressive activity appear to be expanded in the peripheral blood of patients with AD. However, after stimulation by the superantigen (SAg), staphylococcal enterotoxin B (SEB), Treg cells lose their immunosuppressive activity, suggesting a novel mechanism by which SAgs could augment T-cell activation in patients with AD.”1
In addition to treating the hallmarks of AD — dry, cracked skin and itching — it is important to address the bacterial and fungal infections that patients with AD have an increased susceptibility to. Importantly, these bacteria can be present even in skin that visually appears to be uncompromised.
Traditional treatment of atopic dermatitis is multifactorial and based on the severity of a patient’s conditions. Topical corticosteroids are used as first-line treatment for plaques of AD; potency should be based on severity and thickness of plaques. Creams or ointments that contain coal tar or anthralin may also be used. Treatment with topical immunomodulators (TIMs), including tacrolimus (Protopic) or pimecrolimus (Elidel), can aid in long-term management of AD. Suppression of inflammation can be achieved with corticosteroid creams, while successful immunosuppression can be obtained with immunomodulator creams.
Topical calcineurin inhibitors (TCIs) are indicated in the management of mild to moderate AD (pimecrolimus) and moderate to severe AD (tacrolimus). TCIs inhibit T-cell activation and the release of cytokines that cause inflammation. Side effects can include skin irritation and burning at the beginning of therapy, but most patients report these reactions subside with time. However, the long-term safety is unknown, and rare reports of malignancies have surfaced. TCIs are generally used in patients who are unresponsive to traditional therapy or who show unacceptable side effects to the traditional options.
Severe recalcitrant AD may require treatment with oral systemic medications such as cyclosporine, azathioprine, mycophenolate mofetil and methotrexate.
Researchers at the University of Rochester Medical Center (URMC) have undertaken a clinical trial of pioglitazone (Actos) that is funded by the National Institutes of Health to see if off-label uses provide long-term benefit for patients with AD. The drug, which is intended for the treatment of diabetes complications, may be effective at strengthening the skin barrier and reducing symptoms in patients with AD. Actos works to shift the Th2 response to a Th1 response; such a shift would be beneficial for patients by suppressing the over-activated Th2 response and helping to relieve the inflammatory component of the disease.
Also, recent studies have proven the importance of ceramides and natural moisturizing factor in repairing the skin barrier. Researchers from the University Of California, San Francisco departments of dermatology and pediatrics and the Veterans Affairs Medical Center in San Francisco have shown that a ceramide-dominant, barrier repair emollient is a safe, useful addition to the treatment of childhood AD.2 The researchers introduced these emollients into the treatment regimen of 24 children who were also receiving standard therapy for stubborn-to-recalcitrant AD; after 3 weeks, most of the children showed improvement.2
Benefits of Repairing the Skin Barrier
Keeping the skin efficiently moisturized is a very effective strategy for improving quality of life for patients with AD. The protective coating reduces moisture loss and prevents overdrying, lessening the cycle of itching, drying and cracking skin. For some patients, application of a moisturizer is needed four times or more daily.
Barrier-repair emollient may repair the damaged stratum corneum over time. Emollient therapy maintains hydration levels and epidermal barrier defenses, reducing the frequency and severity of AD flares while soothing the skin. While emollients are not proven to directly improve AD, they continue to be widely recommended for improving the appearance and symptoms of the disease.
It is important to prevent scratching of irritated areas; scratching leads to a more widespread area of rash, which in turn leads to greater irritation. Some patients report that wearing light gloves while sleeping can help prevent scratching during the night.
Prevention of infection and inflammation is also important. When washing or bathing, patients should keep water contact as brief as possible and use gentle body washes and cleansers instead of regular soaps. Short, cooler baths are better than long, hot baths. Gentle drying and scrubbing is also preferred over vigorous methods. Topical creams and ointments should be applied while the skin is still damp to increase moisture retention.
Care to avoid allergens that will irritate the skin should also be exercised. This includes avoiding irritating fabrics like wool, strong clothing soaps and detergents, sudden changes in body temperature, smoking or exposure to smoke and other allergic triggers.
Dr. Crandell is co-owner of Southern Tier Dermatology & Aesthetics. She founded the practice, which specializes in medical, surgical and cosmetic dermatology, in 2006. Dr. Crandell is a Fellow of the American Academy of Dermatology, an active member of the American Society of Dermatologic Surgery and a recognized expert in medical, surgical and cosmetic dermatology.
Dr. Fenkl is co-owner of the practice. He has undergone extensive training and professional development in all areas of medical, surgical and cosmetic dermatology.
Disclosure: The authors have no conflicts of interest to report.