Atopic Dermatitis Medication: Anti-inflammatory agents, Antihistamines, Immunomodulators, Targeted Biologic Therapies (Interleukin Inhibitors), Dermatologics, JAK Inhibitors, Topical Phosphodiesterase-4 (PDE-4) Inhibitors, Antiviral agents, Antibiotics (original) (raw)

Medication Summary

The basis of treatment for atopic dermatitis (AD) is to provide moisturization for dryness, allay pruritus, and manage inflammation of the eczematous lesions.

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Anti-inflammatory agents

Class Summary

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% (Cortaid)

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 (Beta-Val)

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 (Kenalog Orabase, Kenalog topical, Pediaderm TA)

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.

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Antihistamines

Class Summary

Antihistamines provide symptomatic relief of pruritus associated with acute urticaria in atopic dermatitis patients.

Hydroxyzine (Atarax)

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 (Benadryl)

Diphenhydramine is an antihistamine used for pruritus and allergic reactions.

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Immunomodulators

Class Summary

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 (Neoral, Sandimmune)

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 (Folex PFS, Rheumatrex)

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 (Protopic) ointment 0.03% or 0.1%

Tacrolimus is an immunomodulator that suppresses humoral immunity (T-lymphocyte) activity. It is used for refractory disease.

Azathioprine (Azasan, Imuran)

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 (CellCept, MMF, Myfortic)

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.

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Targeted Biologic Therapies (Interleukin Inhibitors)

Class Summary

Interleukin (IL)–4, IL-5, and IL-13 appear to play critical roles in the etiology of atopic dermatitis in response to activation by epidermal cell–derived cytokines.

Dupilumab (Dupixent)

Dupilumab is a monoclonal antibody that inhibits IL-4 and IL-13 signaling by blocking the shared IL-4Ra. It is indicated for patients aged 6 years or older with moderate-to-severe atopic dermatitis whose disease is not adequately controlled with topical prescription therapies or when those therapies are not advisable. It is administered as a subcutaneous injection every 2 weeks. It may be used with or without topical corticosteroids. It also be coadministered with topical calcineurin inhibitors, but these should be reserved for problem areas only (eg, face, neck, intertriginous and genital areas).

Tralokinumab (Adbry)

Tralokinumab is a human monoclonal antibody that inhibits IL-13. This inhibition prevents IL-13-induced responses (eg, release of proinflammatory cytokines, chemokines, IgE) from occurring. It is indicated for the treatment of moderate-to-severe AD in adults and children aged 12 years and older whose disease is not adequately controlled with topical prescription therapies or when those therapies are not advisable.

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Dermatologics, JAK Inhibitors

Class Summary

The JAK inhibitors block off the overactive pathway of JAK1, JAK2, JAK3 enzymes, which limits cytokine production and reduces eczema symptoms, such as itch and inflammation.

Abrocitinib (Cibinqo)

An oral JAK1 inhibitor indicated for treatment for patients aged 12 years and olderadults with moderate to severe atopic dermatitis whose disease is not adequately controlled with other systemic therapies or for whom those therapies are inadvisable.

Upadacitinib (Rinvoq)

An oral JAK-1 selective inhibitor indicated for refractory, moderate to severe atopic dermatitis in patients aged ≥12 years whose disease is not adequately controlled with other systemic drug products, including biologics, or who are unable to use such therapies.

Ruxolitinib topical (Opzelura)

Indicated for topical short-term and noncontinuous long-term treatment of mild-to-moderate atopic dermatitis (AD) in nonimmunocompromised patients aged 12 years and older whose disease is not adequately controlled with topical prescription therapies or when those therapies are not advised.

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Topical Phosphodiesterase-4 (PDE-4) Inhibitors

Class Summary

A topical PDE-4 inhibitor is a nonsteroidal option for atopic dermatitis treatment.

Crisaborole topical (Eucrisa)

PDE-4 inhibitors allow for cyclic adenosine monophosphate (cAMP) to remain intact in order to decrease the proinflammatory response (eg, cytokine release) associated with atopic dermatitis. Crisaborole is indicated for mild-to-moderate atopic dermatitis in adults and children aged 3 months or older.

Roflumilast topical (Zoryve)

Indicated for mild-to-moderate atopic dermatitis in patients aged 6 years and older.

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Antiviral agents

Class Summary

Antiviral agents are for the management of herpetic infections and to treat atopic dermatitis in patients who develop chickenpox.

Acyclovir (Zovirax)

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.

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Antibiotics

Class Summary

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 (Keflex)

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 (Beepen-VK, Betapen-VK, Veetids)

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 (Cleocin)

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 (Bactroban, Bactroban Nasal, Centany)

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.

Trimethoprim/sulfamethoxazole (Bactrim, Bactrim DS, Cotrim)

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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Author

Brian S Kim, MD, MTR, FAAD Sol and Clara Kest Professor, Vice Chair of Research, Site Chair, Mount Sinai West and Morningside, Director, Mark Lebwohl Center for Neuroinflammation and Sensation, The Kimberly and Eric J Waldman Department of Dermatology, Precision Immunology Institute, Friedman Brain Institute, Icahn School of Medicine at Mount Sinai

Brian S Kim, MD, MTR, FAAD is a member of the following medical societies: American Academy of Dermatology, American Medical Association, Society for Investigative Dermatology

Disclosure: Received research grant from: Doris Duke Charitable Foundation, Celgene Corporation, LEO Pharma, and the National Institute of Arthritis Musculoskeletal and Skin Diseases (NIAMS) of the National Institutes of Health [NIH (K08AR065577 and R01AR070116)]
Consultant for AbbVie, AstraZeneca, Cara Therapeutics, Galderma, GlaxoSmithKline, Pfizer, Regeneron, Sanofi Genzyme, Trevi Therapeutics; Scientific Advisory Board for Abrax Japan, Granular Therapeutics, and Recens Medical. .

Specialty Editor Board

Richard P Vinson, MD Assistant Clinical Professor, Department of Dermatology, Texas Tech University Health Sciences Center, Paul L Foster School of Medicine; Consulting Staff, Mountain View Dermatology, PA

Richard P Vinson, MD is a member of the following medical societies: American Academy of Dermatology, Texas Medical Association, Association of Military Dermatologists, Texas Dermatological Society

Disclosure: Nothing to disclose.

Van Perry, MD Assistant Professor, Department of Medicine, Division of Dermatology, University of Texas School of Medicine at San Antonio

Van Perry, MD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Nothing to disclose.

Chief Editor

William D James, MD Emeritus Professor, Department of Dermatology, University of Pennsylvania School of Medicine

William D James, MD is a member of the following medical societies: American Academy of Dermatology, American Contact Dermatitis Society, Association of Military Dermatologists, Association of Professors of Dermatology, American Dermatological Association, Women's Dermatologic Society, Medical Dermatology Society, Dermatology Foundation, Society for Investigative Dermatology, Washington DC Dermatological Society, Atlantic Dermatologic Society, Philadelphia Dermatological Society, Pennsylvania Academy of Dermatology, College of Physicians of Philadelphia

Disclosure: Received income in an amount equal to or greater than $250 from: Elsevier
Served as a speaker for various universities, dermatology societies, and dermatology departments.

Acknowledgements

Peter Fritsch, MD Chair, Department of Dermatology and Venereology, Medical University of Innsbruck, Austria

Peter Fritsch, MD is a member of the following medical societies: American Dermatological Association, International Society of Pediatric Dermatology, and Society for Investigative Dermatology

Disclosure: Nothing to disclose.

Bernice R Krafchik, MBChB, FRCPC Professor Emeritus, Department of Pediatrics, Section of Dermatology, University of Toronto Faculty of Medicine, Canada

Bernice R Krafchik, MBChB, FRCPC is a member of the following medical societies: American Academy of Dermatology, American Dermatological Association, Canadian Medical Association, College of Physicians and Surgeons of Ontario, Royal College of Physicians and Surgeons of Canada, and Society for Pediatric Dermatology

Disclosure: Nothing to disclose.