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Inflammatory Physician Reviewed

Eczema — managed by dermatologists, not steroid guesswork

India's most undertreated chronic skin condition, addressed with structured flare control and barrier repair at DermaVue's 7 clinics across Kerala & Tamil Nadu.

Atopic Dermatitis Atopic Eczema Endogenous Eczema Flexural Eczema Neurodermatitis
Affects Face, Neck, Flexures, Hands
Age Group 0 – 60+ years
Contagious No
Treatment 4 – 8 sessions
Consultation ₹300
At a Glance
0–20%
of children in India affected by atopic dermatitis
0–5%
of Indian adults live with chronic eczema flares
0%+
DermaVue patient satisfaction across 7,400+ reviews
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7 clinics · Kerala & Tamil Nadu · ₹300 consultation

What Is It

Understanding Eczema

Reviewed by Dr. Minu Liz Mathew, MBBS MD DVL — February 2026

Eczema is a chronic skin condition where the skin barrier doesn't hold moisture properly, making it dry, itchy, and prone to inflammation. In India, triggers range from humidity and sweat to dust mites, hard water, and synthetic fabrics — all common in daily life across Kerala. Left unmanaged, the itch-scratch cycle damages skin further and opens the door to infections and permanent thickening. DermaVue dermatologists use a structured protocol — barrier repair, targeted anti-inflammatory therapy, and trigger avoidance — personalised to your skin type and flare pattern.

Atopic dermatitis (AD) is a chronic, relapsing inflammatory dermatosis characterised by defective filaggrin-mediated epidermal barrier function, Th2-skewed immune dysregulation, and cutaneous dysbiosis. Pathogenesis involves loss-of-function mutations in the FLG gene reducing natural moisturising factor (NMF) synthesis, increased transepidermal water loss (TEWL), and enhanced penetration of allergens and irritants through a compromised stratum corneum.[1] The resulting Th2 cytokine milieu — IL-4, IL-13, IL-31, and TSLP — drives pruritus, IgE hyperproduction, and the characteristic eczematous morphology.[2] Indian Fitzpatrick IV–VI skin phenotypes frequently present with follicular accentuation, lichenification, and prominent post-inflammatory hyperpigmentation that complicates clinical assessment and treatment monitoring.

M
Dr. Minu Liz Mathew, MBBS MD DVL
Consultant Dermatologist · RealSelf Recognised · DermaVue Kochi
Last reviewed: February 2026
Signs & Symptoms

What does Eczema look like?

Symptoms range widely in severity. Identifying which type you have determines the right treatment.

Intense Itching (Pruritus)
The hallmark of eczema — relentless itching that worsens at night, disrupting sleep. Severity often disproportionate to visible skin changes.
Moderate
Dry, Rough Skin (Xerosis)
Generalised skin dryness due to impaired barrier function. Feels rough, scaly, and tight — especially after bathing or in air-conditioned environments.
Mild
Red or Darkened Patches
Inflamed areas appearing red on lighter skin or dark brown/greyish on Indian Fitzpatrick IV–VI skin — often missed or misdiagnosed in darker tones.
Moderate
Oozing and Crusting
Acute flares produce vesicles that weep clear fluid and form yellowish crusts. Indicates active inflammation requiring prompt treatment.
Mod. Severe
Lichenification
Thickened, leathery skin with exaggerated skin lines from chronic scratching. Common on neck, wrists, and antecubital fossae in long-standing cases.
Mod. Severe
Post-Inflammatory Pigmentation
Dark marks left after flares resolve — highly visible and persistent in Indian skin (Fitzpatrick IV–VI). Often the primary cosmetic concern for patients.
Moderate
Cracked, Fissured Skin
Deep painful cracks, especially on hands and feet. Entry point for secondary bacterial infection (<em>S. aureus</em>) — common in tropical climates.
Mod. Severe
Secondary Infection Signs
Honey-coloured crusting, increased pain, and spreading redness indicate bacterial superinfection — requires urgent antibiotic intervention.
Severe
Root Causes

What actually causes Eczema?

Multiple factors act together — understanding them helps prevent recurrence after treatment.

🧬
Genetic Barrier Defect (Filaggrin)
Loss-of-function mutations in the filaggrin gene weaken the skin's outer barrier, allowing moisture to escape and irritants to penetrate. Family history of eczema, asthma, or hay fever (the "atopic triad") strongly increases risk.
Immune Dysregulation (Th2 Shift)
An overactive Th2 immune response produces excess IL-4, IL-13, and IgE — driving chronic inflammation, itching, and allergic sensitisation even to mild environmental triggers.
🦠
Skin Microbiome Imbalance
<em>Staphylococcus aureus</em> colonises eczematous skin in up to 90% of patients, forming biofilms that worsen inflammation and increase infection risk. Reduced microbial diversity perpetuates flares.
☀️
Kerala Climate & Humidity
Kerala's tropical heat and humidity trigger sweating that irritates barrier-compromised skin. Paradoxically, air-conditioned environments then over-dry the skin — both extremes provoke flares.
🏠
Environmental Allergens
Dust mites (abundant in Kerala's humid homes), pet dander, mould, pollen, and cockroach allergens penetrate the defective skin barrier and trigger IgE-mediated flares.
🧴
Irritant Contact Triggers
Soaps, detergents, synthetic fabrics, hard water, and fragranced products strip residual barrier lipids. Self-prescribed steroid creams — rampant in India — cause rebound flares and skin atrophy.
🍚
Dietary & Stress Triggers
Food allergens (dairy, eggs, wheat, seafood) trigger flares in a subset of patients — especially children. Chronic psychological stress elevates cortisol and neuropeptides that amplify Th2 inflammation.
Who gets eczema in India?
  • 15–20% of Indian children develop atopic dermatitis before age 5 — one of the highest childhood prevalence rates globally
  • 3–5% of Indian adults live with chronic eczema, with urban populations affected more than rural due to pollution and lifestyle factors
  • Kerala and South India report higher prevalence linked to humidity, dust mite density, and water hardness in certain districts
  • Atopic triad (eczema + asthma + allergic rhinitis) clusters in families — if one parent has atopy, the child has a 50% risk; if both, 80%
  • Indian patients with Fitzpatrick IV–VI skin present with follicular prominence and post-inflammatory hyperpigmentation that requires modified treatment protocols
Diagnosis Process

What happens at your DermaVue consultation?

A structured clinical assessment — not a quick glance and a prescription pad. Here's exactly what to expect.

01
Clinical History & Hanifin-Rajka Criteria
Dermatologist evaluates onset age, flare pattern, family atopic history, and applies Hanifin-Rajka diagnostic criteria (3 of 4 major + 3 minor features). SCORAD or EASI scoring quantifies severity.
02
Skin Examination & Dermoscopy
Full-body skin assessment for distribution pattern — flexural in children, hand/eyelid/neck in adults. Dermoscopy identifies subtle features and rules out fungal infection, psoriasis, and contact dermatitis. Baseline photography recorded.
03
Allergy & IgE Testing
Total serum IgE and specific IgE panels for common Indian allergens — dust mites, cockroach, pet dander, dairy, egg, wheat, seafood. Patch testing if contact allergen component suspected.
04
Infection & Barrier Assessment
Bacterial swab if secondary infection suspected. Skin pH and TEWL measurement assess barrier integrity. In India, steroid misuse history is specifically evaluated — topical steroid-damaged skin requires a distinct treatment approach.
05
Personalised Management Plan
Written protocol combining emollient prescription, step-up anti-inflammatory regimen, trigger avoidance list (specific to Kerala environment), and follow-up schedule — tailored to disease severity, age, and skin phototype.
Available at DermaVue

Eczema treatments we offer

All procedures by board-certified MD DVL dermatologists. US-FDA approved equipment. No technician-only protocols — ever.

Emollient & Barrier Repair Therapy
Prescription-grade ceramide-based emollients applied within 3 minutes of bathing to trap moisture and restore the lipid barrier. The foundation of all eczema management — reduces flare frequency by 50% when used consistently.
All eczema grades — daily maintenance
Topical Anti-Inflammatory Therapy
Tailored corticosteroid potency matched to body site and severity, with calcineurin inhibitors (tacrolimus, pimecrolimus) for steroid-sparing maintenance on face and flexures. Structured step-down protocol prevents rebound.
Mild–moderate flare control
Phototherapy (NB-UVB)
Narrowband UVB therapy 2–3 times weekly reduces Th2 inflammation and pruritus without systemic immunosuppression. Particularly effective for widespread eczema unresponsive to topicals alone.
Moderate–severe widespread eczema
Systemic Immunomodulators
Cyclosporine, methotrexate, or azathioprine for severe refractory eczema — prescribed with regular monitoring. Dupilumab (anti-IL-4Rα biologic) available for eligible patients with inadequate response to conventional therapy.
Severe refractory atopic dermatitis
HydraFacial & Gentle Peels
Modified gentle HydraFacial with barrier-safe serums hydrates and calms eczema-prone skin during remission phases. Mild lactic acid peels address post-inflammatory pigmentation once flares are controlled.
Post-flare pigmentation & skin texture
Allergy Desensitisation & Counselling
Structured allergen avoidance based on IgE testing results. Environmental modification guidance specific to Kerala (dust mite control in humid homes, water softening, fabric selection). Itch management and sleep hygiene counselling.
Trigger-driven recurrent flares
Glutathione & Antioxidant Therapy
IV glutathione and oral antioxidant supplementation reduce oxidative stress markers elevated in chronic eczema, while supporting barrier recovery and fading post-inflammatory hyperpigmentation.
Post-eczema pigmentation & barrier support
Find Eczema Treatment Near You
Treatment Journey

Your Eczema treatment timeline

Results are gradual, progressive, and lasting with the right protocol.

Week 1
Consultation, severity scoring (SCORAD/EASI) & baseline photos. Allergy panels ordered. Emollient regimen and rescue anti-inflammatory prescribed.
Immediate itch relief protocol started. Steroid misuse detox initiated if applicable. Trigger diary introduced.
Month 1
Acute flare controlled. Itching reduced significantly. Skin hydration improving with consistent emollient use. Sleep quality beginning to normalise.
Allergy test results reviewed. Trigger avoidance plan refined. Phototherapy course started if indicated.
Month 2–3
Flare frequency decreasing. Barrier function measurably improved. Topical steroid stepped down to maintenance potency or replaced with calcineurin inhibitors.
Post-inflammatory pigmentation treatment initiated. 40–60% overall improvement expected in moderate cases.
Month 4–6
Sustained remission in most patients. 70–85% symptom reduction. Emollient-only maintenance sufficient for mild cases. Biologics assessed for severe refractory patients.
Environmental modifications established. Seasonal flare prevention plan in place for Kerala monsoon and summer.
Month 6+
Long-term management phase. Quarterly dermatologist review. Proactive weekend therapy protocol to prevent subclinical flares.
Most patients maintain controlled disease with emollients and intermittent low-potency anti-inflammatories.
FAQ

Frequently asked questions about Eczema

No, eczema is not contagious. You cannot catch eczema by touching, hugging, or sharing items with someone who has it. Eczema is caused by a combination of genetic barrier defects and immune system dysregulation — it is not caused by bacteria, viruses, or fungi that can transfer between people. The rash may look alarming during flares, but there is zero risk of transmission.

Kerala's tropical climate presents specific triggers: high humidity causes sweating that irritates barrier-compromised skin, while air-conditioned offices over-dry it. Dust mites thrive in humid homes year-round. Hard water in certain Kerala districts strips skin lipids. Monsoon season increases mould exposure. Synthetic fabrics in humid conditions trap sweat against skin. DermaVue dermatologists create trigger avoidance plans specific to your local environment.

Eczema is a chronic condition — there is currently no permanent cure. However, it can be very well controlled. Many children outgrow atopic dermatitis by adolescence. In adults, the goal is sustained remission: long flare-free periods with minimal medication. With consistent barrier repair, trigger avoidance, and proactive anti-inflammatory maintenance, most patients achieve excellent disease control and normal quality of life.

DermaVue consultation fee is ₹300 at most branches. Emollient and topical prescriptions typically cost ₹500–2,000 per month depending on severity. Phototherapy sessions range ₹800–1,500 per session (typically 2–3 per week for 8–12 weeks). Allergy testing panels cost ₹2,000–5,000. All costs are discussed transparently at your first consultation — no hidden charges or pressure to buy packages.

Topical corticosteroids are safe and effective when prescribed by a dermatologist with appropriate potency, duration, and body-site matching. Problems arise from self-prescribed use — applying high-potency steroids to the face, using them continuously without breaks, or using combination creams containing steroids with antifungals. DermaVue dermatologists use structured step-down protocols and steroid-sparing agents (calcineurin inhibitors) to minimise long-term steroid dependence.

Eczema and psoriasis can look similar but differ in key ways. Eczema typically starts in childhood, affects flexural areas (elbow creases, behind knees), causes intense itching, and is associated with allergies. Psoriasis usually appears after age 15, affects extensor surfaces (elbows, knees), produces thick silvery scales, and is associated with joint involvement. A dermatologist can distinguish them clinically — treatment approaches differ significantly.

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