Atopic Dermatitis Medication
- Author: Brian S Kim, MD; Chief Editor: William D James, MD more...
The basis of treatment for atopic dermatitis (AD) is to provide moisturization for dryness, allay pruritus, and manage inflammation of the eczematous lesions.
Anti-inflammatory agents provide relief of inflammation of eczematous lesions. The ointment base provides moisturization. White petrolatum is useful to avoid potential sensitization to preservatives in water-based moisturizers.
Hydrocortisone ointment 1% is a mild topical corticosteroid mixed in petrolatum. It has mineralocorticoid and glucocorticoid effects and anti-inflammatory activity. Use 1% ointment 2-3 times daily.
Betamethasone topical is a medium-strength topical corticosteroid for body areas. It decreases inflammation by suppressing the migration of polymorphonuclear leukocytes and reversing capillary permeability. It affects the production of lymphokines and has an inhibitory effect on Langerhans cells. Use 0.05-0.1% ointment in adults and 0.05% ointment in children.
Triamcinolone topical is a medium-strength topical corticosteroid for body areas. It decreases inflammation by suppressing the migration of polymorphonuclear leukocytes and reversing capillary permeability. It affects the production of lymphokines and has an inhibitory effect on Langerhans cells. Use 0.1% ointment in adults and 0.025% ointment in children.
Antihistamines provide symptomatic relief of pruritus associated with acute urticaria in atopic dermatitis patients.
Hydroxyzine is an antihistamine with antipruritic, anxiolytic, and mild sedative effects. It antagonizes H1 receptors in the periphery, and it may suppress histamine activity in the subcortical region of the CNS. Syrup is available as 10 mg/5 mL.
Diphenhydramine is an antihistamine used for pruritus and allergic reactions.
Immunomodulators are for treatment of patients with severe disease in whom conventional therapy is ineffective. In more severe cases and particularly in adults, consider using both MTX and cyclosporine. The latter is more efficacious, but lesions recur when it is stopped.
Cyclosporine has been demonstrated to be helpful in a variety of skin disorders, especially psoriasis. It acts by inhibiting T-cell production of cytokines and ILs. Like tacrolimus and pimecrolimus (ascomycin), cyclosporine binds to macrophilin and then inhibits calcineurin, a calcium-dependent enzyme, which, in turn, inhibits phosphorylation of nuclear factor of activated T cells and inhibits transcription of cytokines, particularly IL-4. Discontinue treatment if no response occurs within 6 weeks.
Methotrexate is an antimetabolite that inhibits dihydrofolate reductase, thereby hindering DNA synthesis and cell reproduction. Satisfactory response is seen 3-6 weeks following administration. Adjust the dose gradually to attain a satisfactory response.
Tacrolimus is an immunomodulator that suppresses humoral immunity (T-lymphocyte) activity. It is used for refractory disease.
Azathioprine is an imidazolyl derivative of mercaptopurine. It works by blocking the pathway for purine synthesis. The 6-thioguanine nucleotide metabolites mediate most of azathioprine’s immunosuppressive and toxic effects.
Mycophenolate mofetil is an inhibitor of inosine monophosphate dehydrogenase (IMPDH), which blocks de novo guanosine nucleotide synthesis. T and B cells are dependent on this pathway for proliferation.
Antiviral agents are for the management of herpetic infections and to treat atopic dermatitis in patients who develop chickenpox.
Acyclovir inhibits the activity of both HSV-1 and HSV-2. It has affinity for viral thymidine kinase and, once phosphorylated, causes DNA-chain termination when acted on by DNA polymerase. Patients experience less pain and faster resolution of cutaneous lesions when used within 48 hours of rash onset. Acyclovir may prevent recurrent outbreaks. Early initiation of therapy is imperative. The zoster dose is 4 times higher than that for herpes simplex. The duration of therapy varies.
Empiric antimicrobial therapy must be comprehensive and should cover all likely pathogens in the context of the clinical setting. For the treatment of clinical infection by S aureus, cloxacillin or cephalexin is used. In streptococcal infections, cephalexin is preferred. If not effective, penicillin and clindamycin in combination are effective. Consider staphylococcal infection in every flare of atopic dermatitis.
Cephalexin is a first-generation cephalosporin that arrests bacterial growth by inhibiting bacterial cell wall synthesis. It has bactericidal activity against rapidly growing organisms. Its primary activity is against skin flora; it is used for skin infections or prophylaxis in minor procedures.
Cephalexin suspension includes mauve granules (125 mg/5 mL) and peach granules (250 mg/5 mL).
Penicillin VK inhibits the biosynthesis of cell wall mucopeptide. It is bactericidal against sensitive organisms when adequate concentrations are reached, and it is most effective during the stage of active multiplication. Inadequate concentrations may produce only bacteriostatic effects.
Clindamycin is a lincosamide for the treatment of serious skin and soft tissue staphylococcal infections. It is also effective against aerobic and anaerobic streptococci (except enterococci). It inhibits bacterial growth, possibly by blocking the dissociation of peptidyl t-RNA from ribosomes, causing RNA-dependent protein synthesis to arrest.
Mupirocin is used as a topical treatment for bacterial skin infections such as furuncle, impetigo, and open wounds. It is also useful in the treatment of methicillin-resistant Staphylococcus aureus (MRSA) infection.
Sulfamethoxazole disrupts bacterial folic acid synthesis and growth via inhibition of dihydrofolic acid formation; trimethoprim inhibits dihydrofolic acid reduction to tetrahydrofolate, resulting in the inhibition of enzymes of the folic acid pathway.
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