Atopic dermatitis (AD), also known as atopic eczema, is the most common chronic inflammatory condition of the skin, and it is characterized by relapsing pruritic lesions.1 The 2003 National Survey of Children's Health reported a prevalence ranging from 8.7% to 18.1% for patients younger than age 17 years in the United States, with disease onset occurring before age 5 years in 85% of patients.2 These data represent an ongoing increase in AD prevalence over the past 30 years. Comorbid asthma and allergic rhinitis occur in 22.8% and 30.7% of patients, respectively.2 National cost estimates range widely, from $364 million to $3.8 billion US dollars per year.3 Costs will continue to rise with increasing prevalence.4
AD is part of the atopic triad, along with asthma and allergic rhinitis. In addition to food allergies, these are the most well-established AD comorbidities. The term “atopic march” expresses the idea that some patients will develop each of these in sequence: eczema and food allergies as infants, asthma as children, and allergic rhinitis as adults.5 Efforts at interrupting this “march” through early intervention have thus far failed;6 however, early use of emollients in children at high risk has shown promise, possibly due to effects on skin barrier properties and the cutaneous microbiome.7
AD negatively impacts quality of life. A recent meta-analysis and systematic review identified a higher prevalence of depression in patients with AD compared to patients without AD (19.2% vs 14.1%). Parents of patients with AD are also more likely to report depression (29.3% vs 20.3%). One in eight patients with AD has suicidal ideation.8 The cause of psychosocial comorbidity is incompletely understood. Intractable pruritus and associated sleep loss in the context of a chronic, incurable condition are likely contributors. The role of systemic inflammation has also been questioned. Children with AD are at increased risk of attention-deficit/hyperactivity disorder (ADHD).9 Although inattention and fatigue at school may result from pruritus-induced sleep loss, pediatricians should remain mindful of this independent association. Anemia, headaches, obesity, and many other associations have been linked with AD; however, further study will be required to establish causality. The strength of these associations, including impact of AD on quality of life, correlate positively with AD severity.10
The pathogenesis of AD is multifactorial (Figure 1). A null mutation in the epidermal structural protein filaggrin (FLG) is a strong risk factor. FLG is a critical component of a healthy skin barrier, and absent or diminished FLG promotes increased transepidermal water loss (TEWL) as well as increased penetration of allergens and microbes. This corelates with some of the hallmark clinical features of AD, including xerosis, and an increased risk of both allergies and skin infection. Recent work has focused specifically on interactions between the skin barrier, microbiome, and host immune response.10 The majority of patients with AD are colonized with Staphylococcus aureus. This organism adversely affects skin barrier function through enhanced protease activity and TEWL exacerbation. During flares, microbial diversity is reduced, and S. aureus overgrowth occurs, increasing the risk of frank superinfection.11 Emerging data suggest that diminished antimicrobial peptide-producing Staphylococcus epidermidis or gram-negative species (eg, Roseomonas) may also contribute to AD flares and superinfection.12–14
Atopic dermatitis pathogenesis. CARD 11, caspase recruitment domain-containing protein 11; Stat 3, signal transducer and activator of transcription 3. Reprinted from Williams and Gallo10 with permission.
AD is fundamentally a disease of immune dysregulation. It remains a matter of debate as to how dysregulation begins. The “inside-out” hypothesis posits that an inflammatory process induces alterations in filaggrin production with subsequent downstream effects on the skin. However, accumulating data (including the recent microbiome work) support the “outside-in” construct, in which an abnormal skin barrier triggers the inflammatory cascade that characterizes AD.15
In acute lesions of AD, Th2 cells secrete several cytokines including interleukin (IL)-4, IL-13, and IL-5. IL-4 and IL-13 work through a common receptor (IL-4 alpha), to downregulate filaggrin and antimicrobial peptides, inhibit keratinocyte terminal differentiation, recruit eosinophils, and disrupt the skin barrier.16,17 In chronic lesions of AD, Th1 cells predominate, producing IL-2, interferon-gamma, tumor necrosis factor-alpha, lymphotoxin, and other cytokines that promote immune responses against intracellular pathogens. IL-31, produced by both Th1 and Th2 cells, mediates itch transmission to the central nervous system. The development of new therapies has capitalized on this granular detail of the AD inflammatory cascade.18
The most important therapeutic intervention in AD is counseling and education. Parents are often confused about very basic elements of AD care, and time spent discussing issues such as proper bathing and moisturization, identifying and avoiding triggers, signs and symptoms of infection, and the safe use of prescription medications (in particular topical corticosteroids), will improve adherence and outcomes.19
Bathing and Moisturization
Moisturizers are the foundation of AD care. Moisturizers have a combination of ingredients that maintain skin hydration: emollients that lubricate the skin, occlusive agents that prevent water evaporation, and humectants that attract and hold water into the stratum corneum. Moisturizers should be applied liberally and frequently as needed, especially after any activity that wets the skin (eg, bathing, hand washing, swimming). The choice of a specific moisturizer will depend upon several factors including climate, vehicle, and patient preference. In more humid climates, thicker occlusive emollients may not be well tolerated. Independent of ambient conditions, ointments are more effective than creams or lotions, but a patient must be willing to use the product for it to be effective. Asking older patients, especially teens, for an honest assessment of their willingness to use certain products will optimize the chances of useful recommendations.
Although a matter of strong opinion, there is no evidence to support a specific bathing frequency. Many parents are told in no uncertain terms that bathing is either inherently good or bad for atopic skin. This is not supported by evidence. Bathing can indeed dry out the skin if not rapidly followed by application of either topical medications or moisturizers. Similarly, if products are applied quickly after a bath or shower the cutaneous hydration will likely improve (ie, “soak and smear”). An effective routine for most patients is to take a bath or shower with warm water every 2 to 3 days, lasting from 5 to 15 minutes, followed by application of prescription medications to inflamed skin first, then emollients to unaffected skin. In general, emollients need not be put “on top” of areas just treated with prescription topical medications (although many often recommend this to simplify the regimen). Cleansers should be hypoallergenic, fragrance-free, and with a neutral to low pH.20
Antihistamines and Triggers
The use of oral antihistamines for AD is controversial. Sedating agents such as diphenhydramine or hydroxyzine can be helpful for patients with disturbed sleep secondary to itch, but use of antihistamines specifically for itch reduction in AD is not indicated. A recent systematic review did not find evidence that second-generation, less-sedating antihistamines (eg, cetirizine, loratadine) are effective in improving the signs and symptoms of atopic dermatitis.21 An exception may occur in patients who describe allergic co-morbidities such as rhinitis “driving” their dermatitis. In such patients, effectively treating the rhinitis with an antihistamine can confer benefit to the skin as well.
Patients should try to learn what exacerbates their AD and minimize exposure to these triggers. Avoidance may lead to longer intervals between flares and even complete disease clearance in some cases. Common triggers for AD may include environmental allergens, infections, harsh soaps and detergents, fragrances, sweat, excess saliva, and psychosocial stress. Allergens differ by age group: young children are more likely to have food allergy, whereas older children are more likely to have sensitivity to aeroallergens. A good rule of thumb to follow is skin care first, allergy care second (if at all).
Recognition and Treatment of Superinfection
In 2002, Ong et al.22 demonstrated deficient antimicrobial peptides in the skin of AD patients, which places them at greater risk for skin infections. S. aureus carriage occurs in up to 90% of patients with AD. Cultures are indicated only in atypical presentations or if concern for resistant organisms (eg, methicillin-resistant S. aureus) might influence therapy. Localized crusting or impetiginization should be treated topically (eg, with mupirocin); however, more extensive involvement may require systemic antibiotics (eg, cephalexin).23
Patients with AD are also at increased risk for disseminated herpes simplex infection, also known as eczema herpeticum; new vesicles and “punched out” erosions should trigger testing for this potentially severe presentation.23 Coxsackievirus A6 (CAV6) can cause an exuberant presentation of hand, foot, and mouth disease that may mimic eczema herpeticum. The primary morphology, discrete vesicles, and punched out erosions may be identical, as can accentuation in areas of atopic dermatitis (eczema coxsackium). Patients with CAV6 typically present with a prodrome, followed by simultaneous development of skin lesions diffusely and symmetrically in and around the mouth, the palms, soles, and buttocks.24 Affected children may have lesions extending onto their extremities (Figure 2).
Discrete vesicles and punched out erosions in a child with eczema coxsackium.
Dilute Bleach Baths
Dilute bleach baths or sodium hypochlorite (NaOCl) body washes have been used as a maintenance therapy for AD in children, particularly in those prone to recurrent infection and AD flares. Huang et al.25 demonstrated that twice weekly bleach baths and intranasal mupirocin decreased bacterial superinfections and improved AD severity. Although a meta-analysis suggested bleach baths are no more effective than water baths at reducing AD severity, more recent work has shown them to be well tolerated and effective in reducing the use of topical corticosteroids (TCS).26Table 1 details appropriate use of bleach baths in patients with AD.
Bleach Baths for Atopic Dermatitis
TCS are first-line pharmacologic therapy for AD. TCS reduce acute and chronic inflammation by anti-inflammatory, anti-proliferative, and vasoconstrictive actions. Age, distribution, and vehicle preferences must be taken into account when choosing dosage and potency of TCS. There are seven potency classes ranging from lowest (VII) (eg, hydrocortisone 1%) to highest (I) (eg, clobetasol 0.05%). Low-potency agents in class VI or VII are generally applied twice daily to affected areas involving the face, neck, skin folds, and genitalia, whereas mid-potency topical steroids (eg, triamcinolone 0.1% ointment) are more appropriate for the trunk and extremities. Caution should be exercised if steroids are occluded or used in areas of natural occlusion (eg, axillae), as this can increase absorption and effectively increase potency. Education is critical to effective use of topical steroids When attempting to induce remission, TCS may be used twice daily for up to several weeks consecutively; however, safe maintenance will ultimately require breaks from daily use. A simple goal of a day off for every day used (eg, half the month or less) will help prevent adverse effects. Patients and parents should be instructed to use TCS only on inflamed skin; intuitive guidance such as the “touch test” can help parents better understand the difference between actively inflamed skin and healing skin with residual dyspigmentation: if the skin is red, itches, and is palpable, it should be treated with TCS; otherwise emollients alone should suffice. Patients should be educated regarding possible adverse effects including cutaneous atrophy, hypertrichosis, and adrenal axis suppression; however, adverse effects are infrequent when TCS are used intermittently and in appropriate potencies.19
Topical Calcineurin Inhibitors
Topical calcineurin inhibitors (TCIs) are nonsteroidal anti-inflammatory agents approved for use in patients with atopic dermatitis. Tacrolimus 0.03% ointment is indicated in children age 2 years and older; the 0.1% formulation is recommended for older children and adults (age 15 years and older). Pimecrolimus 1% cream is indicated for mild to moderate AD (age 2 years and older). TCIs are bacteria-derived macrolides that inhibit calcineurin-dependent T-cell activation and block the production of proinflammatory cytokines. TCIs may be used on any site, including the face. Local reactions such as application site stinging and burning occur in up to 10% of patients, but usually improve with continued use. TCIs can be used daily during acute flares or 2 to 3 times a week after disease stabilization to prevent recurrences.19 In 2005, the US Food and Drug Administration (FDA) issued a warning advising against TCI use in infants younger than age 2 years due to concerns for excessive systemic absorption and theoretical risks of malignancy. To date, these concerns have proven unfounded.27
Phosphodiesterase 4 Inhibition
Crisaborole, a topical phosphodiesterase inhibitor, was approved by the FDA in 2017 for mild to moderate AD in patients age 2 years and older. This represented the first new molecule indicated for AD in more than 15 years. Phosphodiesterase 4 (PDE4) regulates inflammatory cytokine production. In pivotal phase trials, crisaborole was superior to vehicle at 1 month (33% vs 25%, P < .04%).28 Application site burning and stinging was infrequent (4.4% vs 1.4% vehicle), although it is seemingly much more common in general use. There are several other topical phosphodiesterase inhibitors in development.
When patients fail standard treatment, phototherapy should be considered. Phototherapy reduces inflammation by inducing apoptosis and decreasing S. aureus colonization. Narrow-band ultraviolet light B is usually used due to its favorable efficacy and safety profile. There are considerable barriers, including cost and convenience, as most protocols require treatment 3 times weekly for weeks to months.23 Access can be challenging as well because many pediatric dermatology practices do not have phototherapy units and not all adult dermatologists are comfortable treating children. Phototherapy can be an effective modality for bridging patients from systemic therapy back to topical treatment once better.
Until the approval of dupilumab in 2017, the only FDA-approved systemic medication for AD was prednisone. Because systemic steroids are an inappropriate choice for long-term control due to adverse effects, off-label nonsteroidal systemic immunomodulators such as cyclosporine, methotrexate, mycophenolate, and azathioprine have been the only alternatives. Cyclosporine is a calcineurin inhibitor that inhibits T-cell–dependent immune responses. Dosed at 3 to 5 mg/kg per day divided twice daily, cyclosporine can decrease itch and improve rash within several weeks. Renal function and blood pressure must be monitored, and continuous use for more than 1 year is discouraged due to malignancy concerns. Methotrexate at a dose of 0.3 to 0.8 mcg/kg per week can be used for a longer duration but its onset of action is slower; full effect may take up to 3 months. Routine laboratory monitoring with particular attention to hepatic function and white blood cell count is required. Mycophenolate mofetil and azathioprine are used less commonly in AD. Systemic agents are indicated when (1) diagnosis is confirmed; (2) adherence to treatment recommendations is good; (3) AD remains uncontrolled despite good skin care and appropriate use of conventional therapy; and (4) patients have negative physical, emotional, or social impact from their disease. Systemic corticosteroids should be avoided if possible; adverse effects include hypertension, glucose intolerance, weight gain, adrenal suppression, increased infections, and decreased bone density. Systemic steroids should be reserved for severe exacerbations or as short-term bridge therapy to other treatments. Treatment decisions must always be individualized.23
Dupilumab, a human monoclonal antibody against IL-4 receptor alpha, is approved in patients age 12 years and older with moderate to severe AD. Studies are ongoing in patients as young as age 6 months. Prescribing details are outlined in Table 2. Ocular adverse effects, seen in up to 10% of patients, can include noninfectious conjunctivitis, blepharitis, ocular pruritus, and dry eye. Up to 8% of AD patients have pre-existing ocular disease, and it is this population that is at greatest risk for dupilumab-induced ocular adverse effects. Nasopharyngitis, injection-site reactions, gastrointestinal disturbances, and back pain may occur. Improved response may be seen when used in combination with TCS. For patients who do not respond completely to dupilumab, other systemic therapy may be added.
Dupilumab Fact Sheet
What Is New in Ad Therapy?
JAK inhibitors. The Janus kinase (JAK) signal transducer and activator of transcription-signaling pathway is an essential part of the inflammatory cascade in many dermatoses. JAK inhibitors have shown promise in psoriasis, alopecia areata, and AD. Tofacitinib is a JAK 1 and JAK 3 inhibitor; topical use inhibits cytokines such as IL-4 directly and has shown favorable results in phase II clinical trials.29
Tapinarof. Tapinarof is a nonsteroidal topical agent representing a unique class of anti-inflammatory compounds called therapeutic aryl hydrocarbon receptor modulating agents. Tapinarof has demonstrated both anti-inflammatory and barrier-enhancing properties, inducing production of ceramides known to be deficient in skin of patients with AD. Folliculitis and contact dermatitis have been noted but safety profiles are otherwise excellent.29
Nemolizumab. Nemolizumab is an antibody that blocks IL-31, the “itch” cytokine. It is a subcutaneous injection given monthly that has shown rapid reduction in itch. Adverse effects include asthma exacerbation, nasopharyngitis, peripheral edema, and creatine phosphokinase elevation.30
Baricitinib. Baricitinib is a systemic inhibitor of JAK1 and JAK2 that has been recently approved for the treatment of rheumatoid arthritis in several countries. Phase 3 data suggest baricitinib reduces eczema severity scores, pruritus, and sleep loss. Almost 60% of patients receiving two doses of baricitinib in a 16-week course had one or more adverse events such as headache, serum creatine kinase increase, AD exacerbation, nasopharyngitis, or cellulitis.30
AD is a complex multifactorial disorder caused by the interaction of genetic, environmental, and immune factors. Foundational elements of care have not changed: good skin care, trigger avoidance, and topical steroids are considered first-line interventions. However, awareness of new comorbidities and associations such as ADHD and depression, and the availability of new targeted therapies such as crisaborole and dupilumab, will continue to improve outcomes.
- Weidinger S, Beck LA, Bieber T, Kabashima K, Irvine AD. Atopic dermatitis. Nat Rev Dis Primers. 2018;4(1):1. doi:10.1038/s41572-018-0001-z [CrossRef] PMID:29930242
- Shaw TE, Currie GP, Koudelka CW, Simpson EL. Eczema prevalence in the United States: data from the 2003 National Survey of Children's Health. J Invest Dermatol. 2011;131(1):67–73. doi:10.1038/jid.2010.251 [CrossRef] PMID:20739951
- Ellis CN, Drake LA, Prendergast MM, et al. Cost of atopic dermatitis and eczema in the United States. J Am Acad Dermatol.2002;46(3):361–370. doi:10.1067/mjd.2002.120528 [CrossRef] PMID:11862170
- Mancini AJ, Kaulback K, Chamlin SL. The socioeconomic impact of atopic dermatitis in the United States: a systematic review. Pediatr Dermatol. 2008;25(1):1–6. doi:10.1111/j.1525-1470.2007.00572.x [CrossRef] PMID:18304144
- Davidson WF, Leung DYM, Beck LA, et al. Report from the NIAID workshop in atopic dermatitis and the atopic march: mechanisms and interventions. J Allergy Clin Immunol. 2019;143(3):894–913. doi:10.1016/j.jaci.2019.01.003 [CrossRef] PMID:30639346
- Schneider L, Hanifin J, Boguniewicz M, et al. Study of the atopic march: development of atopic comorbidities. Pediatr Dermatol. 2016;33(4):388–398. doi:10.1111/pde.12867 [CrossRef] PMID:27273433
- Glatz M, Jo JH, Kennedy EA, et al. Emollient use alters skin barrier and microbes in infants at risk for developing atopic dermatitis. PLoS One. 2018;13(2):e0192443. doi:10.1371/journal.pone.0192443 [CrossRef] PMID:29489859
- Patel KR, Immaneni S, Singam V, Rastogi S, Silverberg JI. Association between atopic dermatitis, depression, and suicidal ideation: A systematic review and meta-analysis. J Am Acad Dermatol. 2019;80(2):402–410. doi:10.1016/j.jaad.2018.08.063 [CrossRef] PMID:30365995
- Strom MA, Fishbein AB, Paller AS, Silverberg JI. Association between atopic dermatitis and attention deficit hyperactivity disorder in U.S. children and adults. Br J Dermatol. 2016;175(5):920–929. doi:10.1111/bjd.14697 [CrossRef] PMID:27105659
- Williams MR, Gallo RL. Evidence that human skin microbiome dysbiosis promotes atopic dermatitis. J Invest Dermatol. 2017;137(12):2460–2461. doi:10.1016/j.jid.2017.09.010 [CrossRef] PMID:29169458
- Paller AS, Kong HH, Seed P, et al. The microbiome in patients with atopic dermatitis. J Allergy Clin Immunol.2019;143(1):26–35. doi:10.1016/j.jaci.2018.11.015 [CrossRef] PMID:30476499
- Chernikova D, Yuan I, Shaker M. Prevention of allergy with diverse and healthy microbiota: an update. Curr Opin Pediatr. 2019;31(3):418–425. doi:10.1097/MOP.0000000000000766 [CrossRef]
- Nakasuji T, Chen TH, Narala S, et al. Antimicrobials from human skin commensal bacteria protect against Staph aureus and are deficient in atopic dermatitis. Sci Transl Med. 2017;9(378):eaah4680. doi:10.1126/scitranslmed.aah4680 [CrossRef] PMID:28228596
- Myles IA, Earland NJ, Anderson ED, et al. First-in-human topical microbiome transplantation with Roseomonas mucosa for atopic dermatitis. JCI Insight. 2018;3(9):120608. doi:10.1172/jci.insight.120608 [CrossRef] PMID:29720571
- Silverberg NB, Silverberg JI. Inside out or outside in: does atopic dermatitis disrupt barrier function or does disruption of barrier function trigger atopic dermatitis?Cutis. 2015;96(6):359–361. PMID:26761930
- Brunner PM. Early immunologic changes during the onset of atopic dermatitis. Ann Allergy Asthma Immunol. 2019;123(2):152–157. doi:10.1016/j.anai.2019.03.033 [CrossRef] PMID:30953783
- Bieber T. Atopic dermatitis. N Engl J Med. 2008;358(14):1483–1494. doi:10.1056/NEJMra074081 [CrossRef] PMID:18385500
- Kalamaha K, Reis E, Newton S, et al. Atopic dermatitis: a review of evolving targeted therapies. Expert Rev Clin Immunol. 2019;15(3):275–288. doi:10.1080/1744666X.2019.1560267 [CrossRef] PMID:30577713
- Eichenfield LF, Tom WL, Berger TG, et al. Guidelines of care for the management of atopic dermatitis: section 2. Management and treatment of atopic dermatitis with topical therapies. J Am Acad Dermatol. 2014;71(1):116–132. doi:10.1016/j.jaad.2014.03.023 [CrossRef] PMID:24813302
- Tollefson MM, Bruckner ALSection on Dermatology. Atopic dermatitis: skin-directed management. Pediatrics. 2014;134(6):e1735–e1744. doi:10.1542/peds.2014-2812 [CrossRef] PMID:25422009
- Matterne U, Böhmer MM, Weisshaar E, Jupiter A, Carter B, Apfelbacher CJ. Oral H1 antihistamines as ‘add-on’ therapy to topical treatment for eczema. Cochrane Database Syst Rev. 2019;1:CD012167. doi:10.1002/14651858.CD012167.pub2 [CrossRef] PMID:30666626
- Ong PY, Ohtake T, Brandt C, et al. Endogenous antimicrobial peptides and skin infections in atopic dermatitis. N Engl J Med. 2002;347(15):1151–1160. doi:10.1056/NEJMoa021481 [CrossRef] PMID:12374875
- Sidbury R, Davis DM, Cohen DE, et al. American Academy of Dermatology. Guidelines of care for the management of atopic dermatitis: section 3. Management and treatment with phototherapy and systemic agents. J Am Acad Dermatol. 2014;71(2):327–349. doi:10.1016/j.jaad.2014.03.030 [CrossRef] PMID:24813298
- Mathes EF, Oza V, Frieden IJ, et al. “Eczema coxsackium” and unsual cutaneous findings in an enterovirus outbreak. Pediatrics. 2013;132(1):e149. doi:10.1542/peds.2012–3175 [CrossRef] PMID:23776120
- Huang JT, Abrams M, Tlougan B, Rademaker A, Paller AS. Treatment of Staphylococcus aureus colonization in atopic dermatitis decreases disease severity. Pediatrics. 2009;123(5):e808–e814. doi:10.1542/peds.2008-2217 [CrossRef] PMID:19403473
- Majewski S, Bhattacharya T, Asztalos M, et al. Sodium hypochlorite body wash in the management of Staphylococcus aureus-colonized moderate-to-severe atopic dermatitis in infants, children, and adolescents. Pediatr Dermatol. 2019;36(4):442–447. doi:10.1111/pde.13842 [CrossRef] PMID:30983053
- Margolis DJ, Abuabara K, Hoffstad OJ, Wan J, Raimondo D, Bilker WB. Association between malignancy and topical use of pimecrolimus. JAMA Dermatol. 2015;151(6):594–599. doi:10.1001/jamadermatol.2014.4305 [CrossRef] PMID:25692459
- Paller AS, Tom WL, Lebwohl MG, et al. Efficacy and safety of crisaborole ointment, a novel non-steroidal phosphodiesterase inhibitor (PDE4) for the topical treatment of atopic dermatitis in children and adults. J Am Acad Dermatol. 2017;76(4):777. PMID:28169014
- Suga H, Sato S. Novel topical and systemic therapies in atopic dermatitis. Immunol Med; 2019;42(2):1–10. doi:10.1080/25785826.2019.1642727 [CrossRef] PMID:31318324
- Alexander H, Patton T, Jabbar-Lopez ZK, Manca A, Flohr C. Novel systemic therapies in atopic dermatitis: what do we need to fulfil the promise of a treatment revolution?F1000 Res. 2019;8:8. doi:10.12688/f1000research.17039.1 [CrossRef] PMID:30774935
Bleach Baths for Atopic Dermatitis
||1 teaspoon per gallon of water or a maximum of one-quarter cup per full tub
||Per individual preference but generally 5 to 15 minutes
Rinse at conclusion of bath
||Per routine, apply prescription topicals to inflamed skin and emollients to unaffected skin immediately after bath
||Nonsteroidal adjunctive therapy to decrease risk of skin infection and improve eczema severity
Use as maintenance not for acute flares
Dupilumab Fact Sheet
||Weight >60 kg
Loading dose = 600 mg SQ on day 1
Maintenance dose = 300 mg SQ on day 14 and every 2 weeks thereafter
|Weight <60 kg
Loading dose = 400 mg SQ on day 1
Maintenance dose = 200 mg SQ on day 14 and every 2 weeks thereafter
||10% will develop ocular inflammation (ie, conjunctivitis); greatest risk is in patients with pre-existing ocular disease
Injection site reactions
|Onset of action
||Continue emollients and good skin care practices
May use topical corticosteroids or other prescription agents that are needed concurrently
||Document moderate or severe disease
Document failed prior therapies
Document impact on quality of life