Expert Evaluation and Evidence-Based Management
Skin that itches relentlessly at night, inflamed patches that flare without obvious warning, or rashes that keep returning despite everything you’ve tried. If that describes your experience, you’re not imagining it and you’re not alone. Eczema, most commonly in its form called atopic dermatitis, affects more than 31 million Americans and ranks as the most prevalent chronic inflammatory skin disease worldwide.
Atopic dermatitis is not simply dry skin. It’s a complex immune-mediated condition driven by a defective skin barrier, a dysregulated immune response, and a genetic predisposition that makes the skin chronically vulnerable to inflammation and infection. It follows a relapsing-remitting course that can persist for decades. Without proper management, it causes measurable sleep disruption, documented anxiety and depression, and a quality-of-life burden comparable to serious systemic diseases.
At Connolly Dermatology, we provide expert evaluation and eczema treatment guided by evidence-based care. Our board-certified dermatologists accurately diagnose the severity and pattern of your atopic dermatitis, identify your personal triggers, and design a comprehensive treatment plan, from foundational skin barrier repair through advanced biologic therapy when necessary. Every intervention is matched to what your skin actually needs.
If eczema is disrupting your sleep, your skin, or your daily life, a dermatologic evaluation is the most important step you can take. Have your skin assessed by the specialists at Connolly Dermatology and get the answers you need to move forward confidently.
Understanding Eczema (Atopic Dermatitis)
How Atopic Dermatitis Differs From Other Forms of Eczema and Skin Conditions
Eczema is a broad umbrella term covering several distinct inflammatory skin conditions. Atopic dermatitis is the most common form and the one most people mean when they say eczema. It develops at the intersection of three compounding problems: a genetically defective skin barrier that fails to retain moisture and exclude irritants, an immune system skewed toward a Th2-dominant inflammatory response, and environmental triggers that repeatedly activate that response.
The barrier defect is rooted primarily in mutations affecting the filaggrin gene. Filaggrin is a structural protein critical for building the stratum corneum, the outermost protective layer of skin. When filaggrin is reduced or absent, the skin loses ceramide production, transepidermal water loss increases dramatically, and allergens and bacteria penetrate the skin more easily. Staphylococcus aureus, which colonizes more than 90 percent of atopic dermatitis-affected skin, exploits this vulnerability to further amplify inflammation and trigger flares.
Understanding the distinction between atopic dermatitis and other forms of eczema matters because each has different triggers, mechanisms, and treatment requirements. Treating contact dermatitis with an atopic dermatitis protocol, for example, misses the causative allergen entirely.
Types of Eczema
Atopic Dermatitis: The most common form, linked to genetics, immune dysfunction, and skin barrier failure. It typically begins in infancy or early childhood and follows a relapsing-remitting course. The atopic triad, atopic dermatitis alongside allergic rhinoconjunctivitis and asthma, is present in a significant subset of patients. This is the form addressed on this page.
Contact Dermatitis: Triggered by direct skin exposure to an irritant (irritant contact dermatitis) or a specific allergen (allergic contact dermatitis). Common culprits include nickel, fragrances, preservatives, latex, and cleaning chemicals. Patch testing by a dermatologist identifies the causative agent. Avoidance resolves the rash; systemic therapy is rarely needed.
Dyshidrotic Eczema: Produces small, deep-seated, intensely itchy blisters on the palms, fingers, and soles. Triggers include stress, heat, sweating, and certain metals. It follows a seasonal pattern in some patients and is often more resistant to standard topical therapy.
Nummular Eczema (Discoid Eczema): Characterized by coin-shaped, well-demarcated, itchy plaques, typically on the legs and trunk. Often associated with dry skin and cold weather. It can appear as a variant within atopic dermatitis or as a standalone condition.
Seborrheic Dermatitis: Affects oil-rich areas such as the scalp, nasolabial folds, eyebrows, and chest. Driven by an overgrowth of Malassezia yeast. Unlike atopic dermatitis, it produces a greasy, yellowish scale rather than the dry, lichenified patches typical of atopic disease.
Atopic Dermatitis vs. Similar Skin Conditions
Because atopic dermatitis shares surface features with several other conditions, precise diagnosis determines which treatment approach is appropriate. The table below outlines key clinical differences.
| Characteristic | Atopic Dermatitis | Psoriasis | Contact Dermatitis | Seborrheic Dermatitis |
| Primary Mechanism | Skin barrier defect + Th2-skewed immune response | Th17-driven keratinocyte hyperproliferation | Irritant or allergic immune response to contact exposure | Malassezia yeast overgrowth on sebaceous skin |
| Itch Severity | Intense; often disrupts sleep; a defining feature | Moderate; less intense than AD | Variable; often burning or stinging sensation | Mild to moderate; less intense than AD |
| Lesion Type | Dry, scaly patches; lichenification; acute weeping in flares | Thick, well-demarcated, silvery-scaly plaques | Erythema, vesicles, scaling in contact distribution | Greasy yellowish scaling and mild erythema |
| Typical Location | Flexures (elbows, knees); face and neck; hands in adults | Extensor surfaces (elbows, knees, scalp, lower back) | Matches contact area; face, hands, wrists common | Scalp, nasolabial folds, eyebrows, central chest |
| Age of Onset | Infancy or early childhood in most cases | Any age; peaks in 15 to 35 and 50 to 60 years | Any age; driven by exposure history | Infants (cradle cap) and adults over 30 |
| Associated Atopy | Yes; asthma, allergic rhinitis common | No atopic association | Possible in allergic contact type | No atopic association |
| Skin Barrier Defect | Fundamental; filaggrin mutations central | Not a primary feature | Barrier disrupted by repeated exposure | Not a primary feature |
This table reflects typical patterns. Presentations overlap, and more than one condition can coexist. A dermatologist provides the definitive diagnosis when clinical features are ambiguous or when a condition fails to respond as expected.
Is Atopic Dermatitis Dangerous?
Atopic dermatitis is not life-threatening in its typical presentation. However, framing it purely as a skin problem significantly underestimates its consequences.
Undertreated atopic dermatitis carries real risks. Chronic skin barrier failure creates an open door for serious bacterial infections, primarily Staphylococcus aureus and streptococcal species. Eczema herpeticum, a disseminated herpes simplex virus infection spreading across eczematous skin, is a genuine medical emergency requiring prompt antiviral treatment and ophthalmologic evaluation if the eyes are involved. The atopic march, the sequential development of allergic rhinoconjunctivitis and asthma in atopic individuals, represents a systemic immune progression that underscores why atopic dermatitis is not a localized skin problem. Research also consistently documents rates of depression and anxiety in atopic dermatitis patients that parallel those seen in patients with chronic systemic diseases.
Signs and Symptoms of Atopic Dermatitis
Atopic dermatitis presents across an exceptionally wide clinical spectrum, which is part of why it’s so frequently misdiagnosed or undertreated. Its appearance changes with age, fluctuates between flares and remissions, and affects different body regions at different life stages. Knowing what to look for at each stage makes early recognition possible.
The Cardinal Symptom: Itch
Intense, relentless itch is the defining and most debilitating symptom of atopic dermatitis. It precedes visible skin lesions in many patients and drives the itch-scratch cycle that perpetuates and worsens inflammation. Scratching damaged skin releases inflammatory cytokines including TNF-alpha, IL-1, and IL-6 from keratinocytes, further amplifying the inflammatory cascade. The itch is not incidental to the disease. It is central to its pathophysiology. Nighttime itching disrupts sleep architecture, causes chronic sleep deprivation, and contributes significantly to the mood and behavioral impacts documented in children and adults with moderate to severe disease.
Dry Skin (Xerosis)
Even between active flares, the skin of atopic dermatitis patients is persistently dry, rough, and tight. This is a structural consequence of the underlying filaggrin deficiency and ceramide depletion. The skin simply cannot hold water effectively. Xerosis is both a symptom and a driver of flares, as excessively dry skin is more permeable to allergens and irritants that trigger the immune response.
Age-Specific Lesion Patterns
Infants (birth to 2 years): Red, edematous, weeping, and crusting patches typically appear on the face, scalp, and extensor surfaces of the arms and legs. The diaper area is characteristically spared, which helps distinguish atopic dermatitis from seborrheic dermatitis in this age group. Lesions are often intensely inflamed and may ooze.
Children (2 to 12 years): The distribution shifts to the flexural areas, most prominently the antecubital fossae (inner elbows), popliteal fossae (behind the knees), wrists, and ankles. Lesions become less weeping and more scaly. Lichenification, the thickening and exaggerated skin markings that result from chronic scratching and rubbing, becomes more prominent.
Adolescents and Adults: Flexural involvement continues. The hands become a predominant site in adults, often producing a chronic hand eczema that is occupationally disabling. The face and neck are also commonly affected. In severe cases, erythroderma, a widespread inflammatory redness covering more than 90 percent of the body surface, can develop.
Lesion Stages
Acute lesions appear as intensely erythematous, edematous papules and plaques, often with vesicles, weeping, and crusting. These represent active inflammatory flares. Subacute lesions show erythema and scaling with variable crusting as the acute phase resolves. Chronic lesions display the hallmark lichenification, thick, dry, leathery skin with exaggerated surface markings resulting from months or years of scratching.
Associated Atopic Features
Several associated findings support the diagnosis and reflect the systemic atopic constitution. Dennie-Morgan folds are extra skin creases beneath the lower eyelids. The Hertoghe sign is thinning of the outer third of the eyebrows from repeated rubbing. Keratosis pilaris produces rough, follicular papules on the upper arms and thighs. Pityriasis alba appears as pale, slightly scaly patches on the cheeks of children. Hyperlinear palms show exaggerated skin creases on the palms, another reflection of filaggrin insufficiency.
Complications to Recognize
Secondary bacterial infection presents as honey-colored crusting, increased weeping, and worsening inflammation beyond a typical flare. Eczema herpeticum, the most serious complication, presents as a sudden widespread eruption of monomorphic punched-out vesicles and erosions, often with fever and systemic illness. It requires urgent medical evaluation and antiviral treatment. Molluscum contagiosum and viral warts spread more readily across eczematous skin, as does tinea (ringworm).
Symptoms To Watch For
Many people manage mild atopic dermatitis independently. But certain presentations and changes indicate that professional dermatologic evaluation and more targeted treatment are needed.
See a dermatologist if you or your child experience:
- Itching severe enough to disrupt sleep on most nights
- Eczema that has not improved meaningfully after 2 to 4 weeks of consistent over-the-counter moisturizing and mild topical steroid use
- Widespread inflammation covering large body surface areas
- Painful, weeping, or crusted areas suggesting bacterial superinfection
- Sudden onset of widespread blisters or punched-out erosions with fever (possible eczema herpeticum; seek urgent evaluation)
- Eczema significantly affecting school, work, or daily activities
- Anxiety, depression, or behavioral changes in children related to their skin condition
- Chronic hand eczema interfering with occupational function
Earlier intervention produces better long-term skin outcomes, reduces the risk of complications, and prevents the structural skin changes, lichenification and barrier damage, that become harder to reverse with time.
Risk Factors for Developing Atopic Dermatitis
Atopic dermatitis is a multifactorial condition. No single factor causes it. But researchers have mapped a well-defined set of genetic, immunologic, and environmental contributors that substantially elevate the likelihood of developing it and influence how severely it presents.
Family History and Genetics
The genetic contribution to atopic dermatitis is among the strongest of any common inflammatory skin disease. If one parent has atopic disease, more than 50 percent of offspring develop atopic symptoms. If both parents are affected, that figure rises to up to 80 percent. Filaggrin gene loss-of-function mutations are the most well-characterized single genetic risk factor, present in up to 30 percent of atopic dermatitis patients and associated with earlier onset, greater severity, and higher risk of progressing to the full atopic triad.
Atopic Triad: Asthma and Allergic Rhinitis
Atopic dermatitis frequently does not travel alone. The atopic march describes the characteristic progression through which a child with atopic dermatitis develops allergic rhinoconjunctivitis and then asthma as they age. Approximately 30 percent of atopic dermatitis patients develop both asthma and allergic rhinitis. The skin barrier defect present in atopic dermatitis is now understood as the initiating event in this systemic allergic sensitization process, not just a localized skin problem.
Age
Atopic dermatitis is primarily a disease of early childhood. Approximately 60 percent of cases begin within the first year of life, and most have onset before age 5. The childhood prevalence in developed countries ranges from 10 to 30 percent. However, adult-onset atopic dermatitis is increasingly recognized and accounts for a meaningful minority of cases, particularly in women. A senile-onset variant affecting patients over 60 also exists, often presenting with severe pruritus and widespread dry skin.
Skin Barrier Defects
Filaggrin insufficiency is the central structural vulnerability in atopic dermatitis. Without adequate filaggrin, the stratum corneum loses its integrity, ceramide levels fall, and transepidermal water loss increases across both affected and clinically normal-appearing skin. This makes the entire skin surface, not just the visibly inflamed areas, more permeable to environmental triggers. Even among patients without filaggrin mutations, reduced ceramide production and barrier dysfunction remain consistent findings.
Environmental Exposures and Lifestyle Factors
Multiple environmental factors elevate risk and drive flares. Tobacco smoke exposure, both in utero and in the household, is associated with adult-onset atopic dermatitis. Higher latitude and lower humidity environments increase prevalence, likely through reduced sun exposure and greater skin dryness. Early-life exposure to certain allergens, particularly dust mites and animal dander, sensitizes the immune system in genetically susceptible individuals. The hygiene hypothesis suggests that reduced microbial diversity in early childhood, linked to cleaner modern environments, predisposes to the Th2-dominant immune skewing that underlies atopic disease.
Staphylococcus Aureus Colonization
S. aureus colonizes the skin of more than 90 percent of patients with atopic dermatitis, compared with roughly 30 percent of healthy individuals. This bacterium is not merely an opportunistic invader. It actively worsens atopic dermatitis by producing superantigens that stimulate the immune response, disrupting the already-compromised skin barrier, and driving chronic inflammation that perpetuates the itch-scratch cycle. Managing S. aureus colonization is a central therapeutic target in moderate to severe atopic dermatitis.
Psychological Stress
Psychological stress does not cause atopic dermatitis, but it reliably worsens it. Stress activates the hypothalamic-pituitary-adrenal axis and the sympathetic nervous system, releasing neuropeptides and cortisol that modulate skin immunity and lower the itch threshold. Patients routinely report flares during examinations, major life transitions, or periods of sustained workplace stress. Managing stress is a recognized, clinically relevant component of atopic dermatitis management.
Can You Prevent Atopic Dermatitis?
When strong genetic predispositions are present, preventing atopic dermatitis entirely is not currently possible. However, the following strategies meaningfully reduce flare frequency and severity.
Commit to Daily Emollient Use
Applying a fragrance-free, ceramide-containing emollient immediately after bathing, within three minutes of exiting a lukewarm shower, replenishes lost lipids, seals moisture into the skin, and reduces transepidermal water loss. Consistent twice-daily emollient application is the single most evidence-supported prevention strategy for atopic dermatitis and reduces the frequency and intensity of flares significantly.
Identify and Avoid Personal Triggers
Common triggers include harsh soaps and detergents, fragranced skincare products, wool and synthetic fabrics, hot water, excessive sweating, extreme temperatures, dust mites, pet dander, and emotional stress. Keeping a symptom diary helps identify your specific pattern. Trigger avoidance reduces flare frequency without any therapeutic intervention.
Manage the Home Environment
Use fragrance-free, dye-free laundry detergent. Wash new clothing before wearing. Keep indoor humidity at a comfortable level. Use dust-mite-proof mattress and pillow covers. Vacuum regularly. Keep pets out of sleeping areas if animal dander is a known trigger.
Seek Regular Dermatologic Care
Routine appointments allow your dermatologist to adjust treatment as your disease evolves, address emerging superinfections early, and monitor the overall trajectory of your condition. Consistent professional oversight produces significantly better long-term outcomes than crisis-driven care.
Diagnosis and Evaluation of Atopic Dermatitis
Atopic dermatitis is a clinical diagnosis. No single blood test confirms it. No biopsy is required in the vast majority of cases. An experienced dermatologist evaluates your skin directly, characterizes the morphology and distribution of lesions, identifies your triggers, assesses severity, and rules out conditions with overlapping presentations. That clinical evaluation is the foundation every effective treatment plan requires.
During your appointment, your dermatologist uses a systematic, structured approach to confirm the diagnosis and determine the right level of intervention.
Clinical Examination
Your dermatologist performs a comprehensive skin examination, assessing the distribution, morphology, and severity of your eczema. The characteristic flexural pattern in older children and adults, the extensor-predominant pattern in infants, and the presence of associated atopic features such as keratosis pilaris, Dennie-Morgan folds, Hertoghe sign, and hyperlinear palms all contribute to a confident clinical diagnosis. Your history of pruritus, sleep disruption, personal and family atopic history, and response to prior treatments are equally informative.
Severity Assessment
Severity grading drives treatment selection. Your dermatologist uses validated scoring tools to classify your atopic dermatitis objectively. The Eczema Area and Severity Index (EASI) assesses lesion intensity and body surface area involvement. The SCORAD index incorporates both objective skin findings and subjective patient-reported symptoms including itch and sleep disturbance. The Investigator Global Assessment (IGA) scale provides a simplified global severity rating. These tools establish a measurable baseline and allow your dermatologist to track your treatment response at follow-up visits with precision.
American Academy of Dermatology Diagnostic Criteria
The AAD requires the presence of essential features for a definitive diagnosis: chronic or relapsing history, pruritus, and eczematous lesions with typical age-specific morphology and distribution. Important features including early age of onset, personal or family history of atopy, IgE reactivity, and xerosis further support the diagnosis. Associated features such as keratosis pilaris, hyperlinear palms, pityriasis alba, and white dermographism are consistent findings that add diagnostic confidence.
Allergen Testing
Routine allergy testing is not recommended for uncomplicated atopic dermatitis due to high false-positive rates. However, in patients with recalcitrant childhood disease not responding to standard therapy, particularly those with suspected food triggers, targeted allergen-specific IgE testing or skin prick testing helps identify contributing sensitivities. Patch testing is performed when allergic contact dermatitis is suspected as a concurrent diagnosis.
Skin Culture
When secondary bacterial infection is suspected, a skin swab and culture guide antibiotic selection. Nasal swabs may identify S. aureus carriage as a source of recurrent skin colonization. Culture results direct targeted antibiotic therapy and help identify methicillin-resistant S. aureus (MRSA) in patients with repeatedly infected eczema.
Skin Biopsy
Biopsy is rarely needed for typical atopic dermatitis. When the diagnosis is genuinely uncertain, when cutaneous T-cell lymphoma cannot be clinically excluded in an adult with widespread, treatment-resistant disease, or when scabies or another condition needs definitive ruling out, a punch biopsy provides tissue for histopathologic analysis. The histologic findings show a nonspecific eczematous pattern, spongiosis, and epidermal hyperplasia, consistent with but not exclusively diagnostic of atopic dermatitis.
When Should You Get Atopic Dermatitis Evaluated?
You should see a dermatologist if you or your child notice:
- Itching severe enough to disrupt sleep regularly
- Widespread rash not responding to over-the-counter moisturizers and mild steroid creams after 2 to 4 weeks
- Signs of skin infection including honey-colored crusting, swelling, increasing warmth, or fever
- Sudden widespread blisters or erosions with systemic symptoms (seek urgent evaluation)
- Eczema persisting into or first appearing in adulthood
- Eczema significantly affecting school performance, work, or daily activities
- Anxiety or depression related to skin symptoms in children or adults
- Any atopic skin condition that concerns you
A professional evaluation confirms the diagnosis, identifies the severity level driving your treatment decisions, and connects you with interventions that are substantially more effective than anything available over the counter.
Atopic Dermatitis Treatment Options
Effective atopic dermatitis management addresses all four of the condition’s core drivers simultaneously: barrier dysfunction, immune dysregulation, trigger exposure, and microbial colonization. Treatment is stepwise, escalating from foundational skincare through topical therapy to systemic and biologic agents based on disease severity. Here is what the evidence supports at each level.
Foundational Skin Care: Emollients and Barrier Repair
Liberal, consistent application of fragrance-free emollients is the cornerstone of all atopic dermatitis management regardless of severity. Emollients replenish ceramides and lipids in the defective stratum corneum, reduce transepidermal water loss, and decrease the frequency and intensity of flares. Ointments, which have the highest lipid-to-water ratio, provide the most occlusive barrier and are recommended for dry, lichenified skin. Creams and lotions are suitable alternatives for patients who find ointments impractical during the day.
The single most evidence-supported application practice: apply emollient within three minutes of exiting a lukewarm bath or shower, before the skin fully dries. This locks residual moisture into the skin. AAD systematic review evidence from 77 studies gives this practice its highest rating. Twice-daily application is the minimum effective frequency for most patients.
Bathing should be limited to once daily with lukewarm water for 5 to 10 minutes, using a soap-free, fragrance-free, dye-free cleanser. Hot water strips the skin barrier and worsens both dryness and itch.
Topical Corticosteroids
Topical corticosteroids (TCS) remain the first-line anti-inflammatory treatment for atopic dermatitis flares and the most widely used intervention in the world for this condition. They are applied twice daily to inflamed areas until lesions significantly improve, typically within 1 to 2 weeks. The right potency matters. Low-potency steroids are used for sensitive areas including the face, neck, axillae, and groin. Mid- to high-potency formulations address more resistant, lichenified lesions on the body.
Proactive therapy, applying a mid-potency topical corticosteroid twice weekly to areas that typically flare, even when the skin appears clear, significantly reduces flare frequency and total steroid exposure over time. This approach is particularly valuable for patients with frequent, predictable recurrences. Side effects including skin thinning, striae, and telangiectasia are real but largely reversible with appropriate use under dermatologic supervision.
Topical Calcineurin Inhibitors
Tacrolimus 0.03% and 0.1% ointment and pimecrolimus 1% cream are non-steroidal topical immunomodulators that inhibit T-cell activation and inflammatory cytokine production. They’re approved for atopic dermatitis in patients 2 years and older and are particularly valuable for sensitive areas including the face, eyelids, and skin folds where prolonged corticosteroid use carries the highest side effect risk. Applied twice daily, they can also be used as twice-weekly maintenance therapy to extend the intervals between flares. Temporary burning or stinging on application is the most common side effect and typically resolves within days of starting treatment.
Topical PDE-4 Inhibitors and JAK Inhibitors
Crisaborole 2% ointment (Eucrisa) is a phosphodiesterase-4 inhibitor approved for mild to moderate atopic dermatitis in patients 2 years and older. Applied twice daily, it reduces inflammation through a non-steroidal mechanism and is a useful option for patients in whom corticosteroids or calcineurin inhibitors are not suitable.
Ruxolitinib 1.5% cream is a topical JAK inhibitor approved for short-term, non-continuous treatment of mild to moderate atopic dermatitis in immunocompetent patients 12 years and older. Applied twice daily to up to 20 percent of body surface area for up to 8 weeks, it provides rapid itch relief and lesion reduction through targeted intracellular anti-inflammatory signaling.
Tapinarof cream and roflumilast 0.15% cream are newer topical agents added to the 2025 AAD guidelines with strong recommendation and high certainty evidence for adults with moderate to severe and mild to moderate atopic dermatitis respectively.
Wet Wrap Therapy
For moderate to severe flares that are not responding adequately to standard topical therapy, wet wrap treatment provides intensive, accelerated barrier repair and anti-inflammatory benefit. After bathing and applying topical medications, damp cotton wraps are applied over the treated skin and covered with a dry outer layer. This approach drives deeper penetration of topical agents, provides physical protection against scratching, and rapidly reduces inflammation. It is particularly effective for children with widespread, recalcitrant flares.
Bleach Baths
Twice-weekly dilute bleach baths, using half a cup of household bleach in a full 40-gallon bathtub of lukewarm water, reduce S. aureus colonization density on the skin surface and meaningfully decrease both infection frequency and overall disease severity in patients with moderate to severe atopic dermatitis. This simple, low-cost adjunct is supported by clinical evidence and recommended in AAD guidelines for patients with recurrent superinfections or widespread disease.
Phototherapy
Narrow-band ultraviolet B (NB-UVB) phototherapy is the preferred phototherapeutic modality for moderate to severe atopic dermatitis and is conditionally recommended in the 2025 AAD guidelines. It reduces cutaneous inflammation by modulating the immune response within the skin, decreasing T-cell activity and reducing cytokine production. Administered two to three times weekly in a dermatology office, NB-UVB provides meaningful improvement for patients with widespread disease not controlled by topical therapy alone. It is particularly well-suited for adults who prefer to avoid systemic medications or for whom biologics are not accessible.
Biologic Therapy: Dupilumab and Tralokinumab
Biologic agents represent the most significant therapeutic advance in atopic dermatitis management in decades. They target specific inflammatory pathways with precision unavailable to older systemic agents.
Dupilumab (Dupixent) is a fully human monoclonal antibody that blocks the IL-4 receptor alpha subunit, simultaneously inhibiting signaling by both IL-4 and IL-13, the two master cytokines driving Th2-dominant inflammation in atopic dermatitis. It is FDA-approved for moderate to severe atopic dermatitis in patients 6 years and older who are not adequately controlled with topical therapy. Administered as a subcutaneous injection every two weeks following a loading dose, dupilumab produces dramatic improvements in itch, sleep quality, skin clearance, and quality of life. It does not cause the immunosuppression-related side effects of older systemic agents. The most common adverse effects are injection site reactions and conjunctivitis.
Tralokinumab (Adbry) targets IL-13 specifically and is FDA-approved for moderate to severe atopic dermatitis in adults. It offers an effective alternative for patients who do not respond optimally to dupilumab or who prefer a more targeted anti-IL-13 mechanism. Both agents are strongly recommended in the 2025 AAD guidelines with moderate certainty evidence.
Oral JAK Inhibitors
For patients with moderate to severe atopic dermatitis with inadequate response to biologics or other systemic medications, oral JAK inhibitors including upadacitinib (Rinvoq), abrocitinib (Cibinqo), and baricitinib (Olumiant) offer potent anti-inflammatory activity through intracellular signaling blockade. All three carry strong recommendations in the 2025 AAD guidelines. However, they carry a risk profile including serious infections, increased cancer risk, cardiovascular events, and thrombosis that requires careful patient selection, baseline evaluation, and ongoing monitoring. They are FDA-approved for patients 12 years and older (upadacitinib and abrocitinib) and adults (baricitinib).
Traditional Systemic Immunosuppressants
Cyclosporine, methotrexate, azathioprine, and mycophenolate mofetil are traditional immunosuppressants used for severe, refractory atopic dermatitis when biologic agents are not available or appropriate. They broadly suppress T-cell function and provide meaningful disease control. However, their side effect profiles, including nephrotoxicity (cyclosporine), hepatotoxicity (methotrexate), and bone marrow suppression (azathioprine), require regular laboratory monitoring and limit their use for long-term maintenance. In the current treatment landscape, biologics are preferred over traditional immunosuppressants as first-line systemic agents for most patients.
Managing Superinfections
Secondary bacterial infection with S. aureus is the most common complication of atopic dermatitis. Topical antibiotics including mupirocin and fusidic acid treat localized infections. For widespread impetiginization, systemic antibiotics guided by culture and sensitivity results are required. Patients with recurrent infections are evaluated for nasal S. aureus carriage. Eczema herpeticum is a medical emergency treated with systemic acyclovir or valacyclovir and requires ophthalmologic evaluation when eye involvement is possible.
Why Choose Connolly Dermatology for Eczema Treatment
Care Guided by Experience and Clinical Judgment
Atopic dermatitis is one of the most complex conditions in dermatology to manage well. It requires accurate severity assessment, a layered treatment approach calibrated to your disease stage, ongoing monitoring for complications, and the expertise to advance therapy appropriately when earlier interventions fall short. Connolly Dermatology provides that depth of physician-led, evidence-guided care for every atopic dermatitis patient we see.
Board-Certified Dermatologists
Our dermatologists are trained in the full spectrum of atopic dermatitis presentations, from mild childhood eczema to severe adult-onset disease requiring biologic therapy. Every treatment recommendation follows the most current American Academy of Dermatology guidelines, including the 2025 focused update, and reflects the best available clinical evidence. Your care is individualized, not formulaic.
Comprehensive Treatment Options
We offer every evidence-based treatment available for atopic dermatitis: optimized emollient therapy, topical corticosteroids with proactive protocols, topical calcineurin inhibitors, crisaborole, ruxolitinib, wet wrap therapy, bleach bath protocols, narrowband UVB phototherapy, dupilumab, tralokinumab, oral JAK inhibitors, and traditional systemic immunosuppressants when appropriate. Your dermatologist designs a plan matched to your severity, skin type, age, lifestyle, and goals.
Biologic Therapy Expertise
Dupilumab and other biologics represent a genuine paradigm shift in moderate to severe atopic dermatitis care. Our dermatologists have the experience to identify appropriate candidates, manage the initiation and monitoring process, and adjust therapy based on your response. For patients who have spent years suffering inadequately controlled eczema, biologic therapy can be life-changing.
Comprehensive Trigger Identification
Identifying the personal trigger factors driving your individual flare pattern is as therapeutically important as any prescription. We take time to map your triggers, review your skincare routine and home environment, and provide practical, actionable recommendations that reduce flare frequency independently of medication.
Honest Communication About Outcomes
Atopic dermatitis is a chronic condition. Management is a long-term commitment, not a short course of treatment. We set those expectations honestly from the start, discuss what each phase of your treatment plan will achieve, and check in consistently to assess your progress and make adjustments. You’ll never feel like your condition is being minimized or dismissed.
Patient Education and Support
Understanding why each component of your treatment plan is included, how to apply emollients correctly, which triggers to prioritize avoiding, and what warning signs indicate a developing infection empowers you to manage your atopic dermatitis far more effectively between appointments. Clear patient education is built into every visit.
Comfortable, Compassionate Care
The burden of atopic dermatitis on daily life, from disrupted sleep to social withdrawal to the relentless distraction of constant itch, is real and significant. Our team approaches every consultation with the empathy and respect that a condition with this degree of personal impact deserves.
What To Expect During Treatment
Guiding You Through Evaluation and the Next Steps
Starting atopic dermatitis care with a dermatologist, particularly if you or your child have been managing on your own for years with inconsistent results, can feel like both a relief and an unfamiliar step. At Connolly Dermatology, we guide you through every stage of your evaluation and treatment so you know exactly what’s happening with your skin and what to expect as your condition responds.
Before Your Appointment
Preparation helps your dermatologist build a complete clinical picture quickly. Note when the eczema first appeared and how it has evolved. Document the location and pattern of flares, any triggers you’ve already identified, and how the skin responds to those triggers. List every skincare product and medication currently being used on the affected skin. For children, note the impact on sleep and any behavioral or mood changes. Bring information about family history of atopic disease. The more detail you provide, the more precisely your treatment plan can be calibrated from day one.
During the Evaluation
Your dermatologist reviews your history and performs a thorough skin examination. They assess the distribution, morphology, and severity of your lesions, evaluate associated atopic features, check for signs of active superinfection, and classify disease severity using validated scoring tools. If the diagnosis is uncertain or if allergic contact dermatitis is a possible contributor, patch testing may be recommended.
Your dermatologist explains what they’re finding in plain language, identifies your severity level, and discusses your treatment plan clearly before anything is prescribed. Every element of the plan is explained, including what it targets, how to use it correctly, what results to expect, and over what timeframe. You leave the consultation informed and equipped.
For patients being evaluated for biologic therapy, your dermatologist discusses eligibility, the injection schedule, monitoring requirements, and what to realistically expect from treatment. In some cases, a loading dose can be administered in the office on the day of the appointment.
After Your First Visit
Most patients notice meaningful improvement in itch and inflammation within 2 to 4 weeks of starting optimized topical therapy. Biologic therapy typically shows progressive improvement over 4 to 16 weeks. Emollient therapy produces gradual barrier improvement over weeks to months of consistent use.
Follow-up appointments are scheduled at regular intervals to assess your response, identify any side effects, and adjust the treatment plan as needed. If disease severity changes or a new trigger emerges, your plan evolves accordingly. Stable, well-controlled atopic dermatitis transitions to a maintenance plan designed to sustain remission and minimize flare frequency over the long term.
Throughout your care, the team at Connolly Dermatology remains accessible. Questions between appointments are taken seriously. Progress is tracked carefully. And when your skin responds well to treatment, we’ll ensure the strategies that got you there are sustainable for the long run.
Get Clear Answers from Connolly Dermatology
Make Informed Decisions About Your Skin Health
Atopic dermatitis is a chronic, immune-mediated inflammatory skin disease rooted in genetic skin barrier dysfunction and a dysregulated immune response. It is the most common chronic inflammatory skin condition in the world. It follows a relapsing-remitting course that can span decades. And when undertreated, it causes measurable suffering, from chronic sleep deprivation and documented psychological distress to serious skin infections and the progressive atopic march toward asthma and allergic disease.
Effective management requires accurate diagnosis, severity-matched treatment, barrier repair as a continuous priority, trigger identification and avoidance, and access to the full range of therapeutic options, including advanced biologics when the disease demands them. Managing atopic dermatitis well is not a matter of finding the right moisturizer. It’s a matter of having the right clinical partner.
If eczema is affecting your skin, your sleep, or your quality of life, schedule a visit with Connolly Dermatology. Our board-certified dermatologists offer expert evaluation, personalized treatment planning, and the ongoing support needed to bring your atopic dermatitis under real, lasting control.
Schedule a visit with a dermatologist to get clear, informed guidance about your skin.
Care You Can Rely On for Skin Changes and Concerns
Supporting You From Evaluation Through Ongoing Care
At Connolly Dermatology, we review every finding based on your skin’s appearance and medical context. Recommendations are made using established dermatologic standards, with treatment options selected to reflect the specific characteristics of the lesion and the patient’s overall skin health.
If you have noticed a changing mole, a new growth, or a skin lesion that raises concern, our team is here to help and guide you through the next steps. Schedule your evaluation at Connolly Dermatology today.
Our Locations
Linwood Commons
2106 New Road Suite D4
Linwood, NJ 08221
(609) 926-8899
(609) 926-6474 (fax)
The Commons
175 Gunning River Road, Bldg. E
Barnegat, New Jersey 08005
(609) 660-8002
(609) 660-8052 (fax)
409 NJ Route 70
Rear of Building
Cherry Hill, NJ 08034
(856) 772-1333
(856) 772-1997 (fax)
2099 New Albany Road
Cinnaminson, New Jersey 08077
(856) 772-1333
(856) 772-1997 (fax)
Eden Hill Medical Center
200 Banning St., Suite 380
Dover, DE 19904
(888) 377-5177
(302) 672-0879 (fax)
Lacey Medical Arts Building
833 Lacey Road
Forked River, NJ 08731
(609) 660-8002
(609) 660-8052 (fax)
Mainland Professional Centre
310 Chris Gaupp Drive, Suite 102
Galloway NJ 08205
(609) 926-8899
(609) 926-6474 (fax)
392 North White Horse Pike
Hammonton, NJ 08037
(609) 926-8899
(609) 926-6474 (fax)
The Bell Works Building – Purple Lot
101 Crawfords Corner Rd., Suite 1116A
Holmdel, NJ 07733
(732) 722-8437
(732) 722-8438 (fax)
1587 The Fairway, Suite C104, Jenkintown, PA 19046
(215) 774-8290
(267) 807-1479 (fax)
108 Roosevelt Blvd
Marmora, NJ 08223
(609) 926-8899
(609) 926-6474 (fax)
MIAMI, FL
Miami Beach
215 Lincoln Road
Miami Beach, Florida 33139
(786) 485-4182
124 Sleepy Hollow Dr., Ste 100
Middletown, DE 19709
(302) 291-9900
305 Jefferson Ave
Milford, DE 19963
(302) 291-9900
(302) 265-2051 (fax)
740 Bethlehem Pike Montgomeryville, PA 18936
(215) 774-8290
(267) 263-4645 (fax)
3532 West Chester Pike
Suite #20
Newtown Square, PA 19073
(888) 377-5177
(267) 807-1479 (fax)
FISHTOWN
2418 E. York St.
Philadelphia, PA 19125
(215) 774-8290
(267) 807-1479 (fax)
Broad Street
701 S. Broad Street Philadelphia, PA 19147
(215) 774-8290
(267) 807-1479 (fax)
18947 John J Williams Hwy
Suite 306
Rehoboth Beach, DE 19971
(888) 377-5177
(302) 291-2651 (fax)
1178 Route 37 West
Toms River, NJ 08755
(732) 722-8437
(732) 350-1363 (fax)
151 Fries Mill Rd. Suite 405
Washington Twp. NJ 08012
(856) 772-1333
(856) 772-1997 (fax)
1667 E. Landis Avenue
Vineland, NJ 08361
(856) 772-1333
(856) 772-1997 (fax)
108 Lacey Road Suite 38 A
Whiting, NJ 08759
(732) 722-8437
(732) 350-1363 (fax)