A Comprehensive Management Guide for Atopic Dermatitis

Jennifer D. Peterson, MD; Lawrence S. Chan, MD

Disclosures

Dermatology Nursing. 2006;18(6):531-542. 

In This Article

Systemic Therapy

Various forms of systemic therapy have been studied for treating atopic dermatitis including oral antihistamines, oral steroids, systemic immunomodulators, phototherapy, and antimicrobials (Darsow et al., 2005; Hanifin et al., 2004). Sedating and nonsedating oral antihistamines are not effective at relieving pruritus in the majority of patients. However, oral antihistamines may provide some benefit to patients who have poor sleep (secondary to pruritus, dermatographism, or allergic rhinitis), dermatographism, urticaria, or allergic rhinitis (Hanifin et al., 2004). Systemic steroids may be employed temporarily to treat severe AD; however, concerns over side effects and a rebound affect that may occur after discontinuation limits their use (Abramovits, 2005).

In severe, recalcitrant AD, immunomodulators may be used, but it is important that the patient be followed closely to detect any side effects and these medications should not be used long-term (Paller et al., 2005). Cyclosporine is an immunosuppressant that works quickly (within 2 weeks) and can treat recalcitrant AD effectively (Abramovits, 2005; Darsow et al., 2005). Adverse effects include renal toxicity, hypertension, nausea, and abdominal pain (Leung et al., 2004; Rudikoff & Lebwohl, 1998). In most cases, this medication should only be used for short periods of time and patients may relapse quickly after the medication is discontinued (Abramovits, 2005). Azathioprine, an anti-inflammatory and antiproliferative medication, has also been used in treating refractory AD. Azathioprine is a slow-acting medication (4 to 6 weeks) (Leung et al., 2004) and has the potential for inducing bone marrow suppression, hepatotoxicity, hypersensitivity reactions, pancreatitis, squamous cell carcinoma of the skin, and non-Hodgkins lymphoma (Abramovits, 2005). Patients who may undergo therapy with azathioprine should have a thiopurine-methyltransferase (TPMT) level monitored, as low levels of TPMT are associated with increase bone marrow suppression and therapy with azathioprine should be avoided in the cases. The adult and pediatric dose of cyclosporine is 3 to 5 mg/kg/day while the adult and pediatric dosage of azathioprine is 2.5 mg/kg/day (Darsow et al., 2005). Myclophenolate mofetil is another immunosuppressant that may be beneficial in treating AD. The adult dosage of myclophenolate mofetil is 2 g/day (Darsow et al., 2005). There is a risk of bone marrow suppression and patients should be treated for only short periods of time (Leung et al., 2004). Data concerning the use of IVIG (intravenous immunoglobin) in treating AD are inconsistent (Hanifin et al., 2004), and clinical trials evaluating the use of methotrexate and biological therapies in AD are lacking (Abramovits, 2005).

Another option for the treatment of recalcitrant atopic dermatitis is ultraviolet (UV) light therapy. Phototherapy has an anti-inflammatory effect on the cells of the immune system (Paller et al., 2005). Types of UV therapy that have been used successfully in treating AD include psoralen plus UVA (PUVA), the combination of broadband UVB/UVA, broadband UVA, broad-band UVB, narrowband UVB (311 nm), and UVA-1 (340-400 nm) (Hanifin et al., 2004; Leung et al., 2004; Paller et al., 2005). PUVA therapy should only be used in patients with severe, widespread, recalcitrant AD (Leung & Bieber, 2003). Topical steroids may be used concomitantly with PUVA therapy and patients may be able to decrease topical steroid use during PUVA therapy (Hanifin et al., 2004, Leung et al., 2004). Combination broadband UVB/UVA therapy, narrowband UVB therapy, and UVA-1 are all superior to broadband UVB therapy alone (Hanifin et al., 2004; Leung et al., 2004). Adverse effects of ultraviolet light therapy include stinging, burning, premature skin aging, pigmentation, and the increased likelihood of squamous cell carcinoma and melanoma (Abramovits, 2005; Paller et al., 2005; Williams, 2005). Relapses, usually within 3 months, are common after therapy is discontinued (Abramovits, 2005).

Finally, as mentioned previously, microbes including bacteria, viruses, fungi, and yeast can all exacerbate atopic dermatitis. Antibiotic treatment is recommended for patients with an active infection or heavy colonization of S. aureus (Darsow et al., 2005; Hanifin et al., 2004). Systemic antibiotics are preferred and first-generation cephalosporins are often prescribed due to the growing number of cases of macrolide-resistant S. aureus. Cultures can be very beneficial for guiding therapy, as the prevalence of methicillin-resistant Staphylococcus aureus is increasing (Paller, 2004). Furthermore, some studies have shown that topical steroids and topical calcineurin inhibitors can decrease S. aureus counts in AD lesions (Leung et al., 2004). Topical antiseptics have limited usefulness in treating AD (Hanifin et al., 2004). Antiviral treatment, often with acyclovir, is critical in patients with eczema herpeticum as this infection can be life threatening in patients with AD. Eczema molluscatum lesions will resolve on their own with time, but treatment decreases further spreading by autoinoculation and accelerates resolution of lesions (Darsow et al., 2005).

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