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Atopic Dermatitis

Atopic dermatitis is the most common chronic inflammatory skin condition in the world and one of the most misunderstood. It is not poor hygiene. It is not a simple allergy. It is a complex skin disease rooted in skin barrier dysfunction and immune dysregulation, where the skin loses its ability to retain moisture and defend against irritants, allergens, and microbes. The result is a relentless itch scratch cycle that disrupts sleep, affects school and work performance, and in severe cases, becomes all-consuming. 

At Shree Hospitals, our atopic dermatitis treatment in Mumbai addresses the skin barrier, the immune driver, and the itch itself, because treating one without the others consistently fails.

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Our Approach in Managing Atopic Dermatitis

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Atopic dermatitis management requires patience — from both the clinician and the patient. It is a condition managed in layers: baseline emollient therapy that never stops, topical anti-inflammatory agents for flares, and escalating systemic or biologic therapy for those whose disease breaks through. Our eczema specialist dermatologist team in Mumbai, India establishes this layered approach at the first visit and adjusts it based on objective severity scoring not subjective impression.

 

  1. Diagnosis & Severity AssessmentAtopic dermatitis is a clinical diagnosis no blood test confirms it.
    • Hanifin and Rajka criteria  major features: pruritus, typical morphology and distribution, chronic relapsing course, personal or family history of atopy (asthma, allergic rhinitis, food allergy)
    • SCORAD (SCORing Atopic Dermatitis)  combines extent, intensity, and subjective symptoms; mild <25, moderate 25–50, severe >50
    • IGA (Investigator's Global Assessment)  simple 5-point scale for clinical practice and treatment response monitoring
    • POEM (Patient-Oriented Eczema Measure) — patient-reported weekly symptom frequency; particularly useful for tracking real-world disease impact
    • Baseline investigations: total IgE, specific IgE or skin prick testing where food or environmental allergy is clinically suspected
    1. Emollient Therapy — The Non-Negotiable FoundationSkin barrier dysfunction is the primary defect in atopic dermatitis. Emollients are not optional add-ons  they are core therapy.
    • Apply within 3 minutes of bathing  the "soak and seal" technique; maximises moisture retention
    • Quantity matters: adults with moderate-severe AD require 500g of emollient per week
    • Emollient selection: ointments (most occlusive, best for dry thick skin), creams (lighter, for daytime), lotions (poor barrier function  generally not recommended in AD)
    • Avoid fragrance, lanolin, and preservatives in emollient products  common contact sensitisers in AD patients
    • Emollient use twice daily at minimum  not just during flares
    1. Topical Anti-Inflammatory Therapy
    • Topical corticosteroids (TCS) — first-line for flares; potency matched to site (mild for face/flexures, moderate-strong for body); fingertip unit guidance for quantity
    • Proactive therapy  twice-weekly TCS application to previously affected sites even when clear  reduces flare frequency significantly; the most underused strategy in AD management
    • Topical calcineurin inhibitors (TCIs)  Tacrolimus 0.1% (adults), 0.03% (children); Pimecrolimus  for face, eyelids, and intertriginous sites; no atrophy risk; steroid-sparing
    • Topical PDE4 inhibitor (Crisaborole)  for mild-moderate AD; non-steroidal; safe for face and sensitive sites
    • Topical JAK inhibitor (Ruxolitinib cream) emerging; rapid itch relief; approved for mild-moderate AD in adults; significant itch reduction within 12 hours

     

    1. Systemic Therapy for Moderate to Severe AD
      When topical therapy fails to control moderate to severe disease:
    • Cyclosporine  rapid onset; first-line systemic for severe AD; BP and renal monitoring; limited to 1–2 years
    • Methotrexate : weekly dosing; slower onset than Cyclosporine; suitable for long-term use; teratogenic counselling
    • Azathioprine  alternative systemic; TPMT enzyme testing before initiation to assess myelosuppression risk
    • Short-course oral Prednisolone  for acute severe flares only; not for long-term control; rebound flare on stopping is common and predictable

    5.Dupilumab & Biologic Therapy

     

      Dupilumab for eczema represents the most significant advance in AD treatment in two decades.

       

      • Dupilumab  anti-IL-4Rα monoclonal antibody; blocks IL-4 and IL-13 signalling — the dominant type 2 inflammatory drivers in AD
      • Every-2-week subcutaneous injection; approved from 6 months of age
      • Response rates: IGA 0/1 (clear or almost clear skin) in 38–44% at week 16; EASI-75 in 51–59%
      • Significantly reduces itch scratch cycle intensity  itch reduction often begins within the first week
      • Common side effect: conjunctivitis  managed with artificial tears and ophthalmology review if persistent
      • Tralokinumab  anti-IL-13; alternative biologic; similar efficacy; monthly dosing after induction
      • JAK inhibitors (Abrocitinib, Upadacitinib, Baricitinib)  oral daily therapy; faster onset than Dupilumab; highly effective for refractory moderate-severe AD; require screening for TB, hepatitis B, and lipids before initiation 

        6.Trigger Identification & Environmental Control

      • House dust mite ;the most important environmental trigger; mattress and pillow encasements, weekly hot washing of bedding, HEPA vacuum
      • Sweat and heat;  exacerbate the itch scratch cycle; cotton loose clothing, cool sleeping environment
      • Food triggers  significant in children under 5 with severe AD; structured elimination and reintroduction under dietetic supervision; not appropriate as first-line management without confirmed sensitisation
      • Contact allergens ; fragrance, nickel, preservatives; patch testing where contact dermatitis is superimposed
      • Skin infections : Staphylococcus aureus colonises AD skin and drives inflammation; antiseptic bath additives, bleach baths (dilute sodium hypochlorite 0.005%) reduce bacterial load

      Happy Patients & Their Case Stories

      Aanya M., 8 years, Dadar (mother attending)  Aanya had moderate to severe eczema from age 2 — constant scratching, disrupted sleep, and repeated school absences. She had been managed with multiple topical steroids without a structured emollient regimen. SCORAD was 47 at first assessment.

       Nikhil R., 29, Powai  An IT professional with severe chronic AD — SCORAD 62, IGA 4, completely disrupted sleep, affecting his work performance. He had failed Cyclosporine and Methotrexate over the preceding two years. Dupilumab for eczema was initiated at Shree Hospitals. By week 4, his itch score had reduced from 8/10 to 2/10. By week 16, IGA was 1.

      How to Identify Atopic Dermatitis ?

       

      Atopic dermatitis has a recognisable pattern  and that pattern changes with age.

      Features across age groups that suggest atopic dermatitis

      Features that point clearly to psoriasis:

       

      • In infants: red, weeping, itchy rash on the face, scalp, and outer limbs appearing from 2–6 months of age
      • In children: rash shifting to the flexures antecubital and popliteal fossae, neck, wrists, and ankles; thickening of the skin from scratching (lichenification)
      • In adults: chronic lichenified plaques on the flexures, hands, and face; hand eczema is a common adult-predominant pattern
      • Intense itch, particularly at night; itch is the defining symptom; itch scratch cycle disrupting sleep is a clinical severity indicator
      • Skin barrier dysfunction signs  skin that feels perpetually dry, rough, and sensitive to soap, sweat, or temperature change
      • Personal or family history of atopy asthma, hay fever, food allergy in the same patient or a first-degree relative
      • A relapsing course ; periods of relative clearance followed by flares; chronicity is part of the diagnostic pictureThe most important question in atopic dermatitis management is not which cream to prescribe , it is whether the emollient regimen is adequate and consistent. An AD patient using 50g of emollient per week instead of 500g will flare regardless of what topical steroid is prescribed. Seek atopic dermatitis treatment in Mumbai from a team that treats emollient therapy as seriously as it treats prescribing dupilumab for eczema.

      Important FAQs: Atopic Dermatitis

      Will my child grow out of eczema?

      Approximately 60% of children with atopic dermatitis improve significantly by adolescence. However, 30% continue into adulthood, and some adults develop eczema for the first time. It is not reliably outgrown.

      Is Dupilumab safe for long-term use?

      Dupilumab has one of the best safety profiles of any biologic in dermatology no requirement for blood test monitoring, no immunosuppression risk, no organ toxicity. It is approved for use from 6 months of age.

      Can atopic dermatitis be triggered by food?

       In children under 5 with severe AD, food allergy  particularly egg, milk, wheat, and peanut  can worsen disease. Food elimination without confirmed allergy testing is not recommended and risks nutritional deficiency.

      Why does eczema get worse at night?

       A serious complication where herpes simplex virus infects eczematous skin  producing widespread painful blisters, fever, and malaise. It requires urgent systemic Acyclovir treatment and is a medical emergency.

      Is bleach bath therapy safe for eczema?

      Dilute sodium hypochlorite baths (0.005% — approximately 1 teaspoon of household bleach in a standard bath) reduce Staphylococcal colonisation and infection rates. Evidence supports twice-weekly use in children with moderate-severe AD prone to skin infections.

      Treatments For Atopic Dermatitis At Shree Hospitals

      Treatments for Atopic Dermatitis at Shree Hospitals. Comprehensive atopic eczema diagnosis and management in Mumbai from structured emollient therapy to biologic and JAK inhibitor treatment.

      Dupilumab Biologic Therapy Dupilumab for eczema

      fortnightly subcutaneous injection targeting IL-4/IL-13 signalling; producing clear or almost-clear skin in moderate-severe AD patients who have failed conventional therapy. Available from 6 months of age.

      JAK Inhibitor Therapy

      Oral Abrocitinib, Upadacitinib, or Baricitinib for moderate-severe AD  faster onset than Dupilumab, highly effective for refractory itch scratch cycle control. Prescribed with pre-treatment screening and regular safety monitoring.

      Proactive Topical Therapy

      Twice-weekly TCS or TCI application to previously affected sites between flares  the most effective strategy for reducing AD flare frequency; dramatically underused in standard practice.

      Phototherapy — Narrowband UVB

       For moderate AD not responding to topicals  3× weekly NB-UVB sessions reducing inflammation and bacterial colonisation; avoids systemic immunosuppression; effective maintenance option between biologic cycles.

      Top Dermatology & Eczema Specialists in Mumbai

      Every doctor and specialist at Shree Hospitals is board-certified and brings an average of 15 or more years of clinical experience in their area of subspecialty.

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