Eczema (Atopic Dermatitis) in India — Triggers, Treatment, Climate Effects & Why Most Patients Get Steroid Withdrawal Before Diagnosis

India has between 50 and 70 million eczema patients. By the time an adult Indian patient sees a qualified dermatologist for the first time, the average history is 7 to 12 years of over-the-counter steroid creams from neighbourhood chemists, “ayurvedic” balms that turn out to be clobetasol in disguise, and three generations of family advice that mostly makes things worse.

This is not because eczema is harder to treat in India. It is because the system around the patient is uniquely broken. Triple-combination steroid creams are dispensed without prescription. Hard water in Delhi and Gurgaon is well above the eczema-trigger threshold but never mentioned in an OPD. Monsoon humidity drives Malassezia overgrowth that gets misdiagnosed as “worsening eczema,” and the antifungal-steroid combo prescribed in response masks the cycle for years.

This guide covers what actually matters for Indian eczema patients in 2026 — the real climate and water triggers by city, the topical steroid withdrawal (TSW) epidemic almost nobody is naming, the working treatment ladder with real Indian prices, when biologics like Dupixent are worth the ₹13 lakh a year they cost, and the at-home protocols (wet wraps, bleach baths, pH-acidic moisturisers) that change outcomes without changing budget.

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What Atopic Dermatitis Actually Is — And Why Indian Eczema Is Not European Eczema

Atopic dermatitis (eczema) is a chronic, itchy, relapsing skin condition driven by a defective skin barrier and Th2-skewed immune inflammation. It typically begins in infancy, often on cheeks and scalp, then moves to the elbow folds, behind the knees, on the wrists and neck. It cycles between flares and quiet periods, and is closely linked to the “atopic march” — eczema first, then food allergy, then asthma, then allergic rhinitis.

In white European populations, the dominant driver is a loss-of-function mutation in the filaggrin gene (FLG) that wrecks the skin barrier. Around 25–50% of moderate-to-severe European eczema patients carry FLG mutations.

In Indian patients, FLG mutations are far less common. Indian eczema is dominated by:

• Environmental insult — pollution, hard water, fabric allergens, climate extremes
• Th2 immune skewing with elevated IL-4, IL-13, and IgE
• Secondary infection — Staphylococcus aureus (60–90% colonised), Malassezia, dermatophytes
• Microbiome disruption more than barrier-gene loss

Why this matters clinically: dupilumab (Dupixent), an anti-IL-4 and anti-IL-13 monoclonal, works particularly well in Indian patients because Indian eczema is more cytokine-driven than barrier-driven. Filaggrin-replacement strategies that get attention in European research are largely irrelevant here.

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The Topical Steroid Withdrawal (TSW) Epidemic Indian Dermatology Won’t Name

If you stop steroids and your skin turns angry red, burns, swells, oozes, and flakes in a pattern noticeably different from your original eczema — you are not “having a bad flare.” You are likely in topical steroid withdrawal (TSW), also called Red Skin Syndrome.

TSW happens after prolonged, usually unsupervised, use of moderate-to-potent topical steroids. In India, the prolonged exposure is built into the retail pharmacy system:

• Panderm Plus, Quadriderm RF, Cosvate-GM, Skin Lite — triple-combination steroid creams (steroid + antifungal + antibiotic) sold without prescription at any chemist
• Used by patients for years for any rash, eczema, ringworm, melasma, or pigmentation
• Marketed historically as “fairness creams,” then continued as eczema relief
• CDSCO has been trying to schedule these since 2016 — enforcement is patchy

The Indian Association of Dermatologists, Venereologists and Leprologists (IADVL) has flagged the OTC sale of these triple-combinations multiple times. Yet most general physicians and many dermatologists still hand them out for non-specific itchy rashes.

How to recognise TSW vs an eczema flare:

Feature	Atopic Eczema Flare	Topical Steroid Withdrawal
Onset	Gradual, follows trigger	Within days to weeks of stopping steroid
Skin colour	Patchy red, scaly	Bright burning red “sleeve” — wrist to elbow, ankle to knee
Distribution	Classic eczema sites	Often goes beyond original eczema area
Sensation	Itch dominant	Burning, stinging dominant
Improvement	Improves with steroid	Initial improvement with steroid, escalating frequency needed
Sweating	Normal	Often impaired in affected skin

If your skin pattern fits the TSW column, escalating the steroid will not fix it. A dermatologist familiar with TSW (still rare in India) will manage with calcineurin inhibitors (tacrolimus, pimecrolimus), wet wraps, antihistamines, sometimes oral immunomodulators, and a long, painful taper. Recovery takes anywhere from 6 months to 3 years.

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Indian Climate Triggers — City by City

Indian eczema is not one disease. The trigger profile of a Delhi software engineer is almost opposite to that of a Kochi schoolchild. Treating both with the same advice is why so many patients never get better.

Delhi / NCR — Pollution, Hard Water, Winter Xerosis

• PM2.5 spikes Oct–Feb correlate with adult-onset eczema flares. AIIMS Delhi dermatology now flags “pollution dermatitis” as an emerging diagnosis since 2022.
• Groundwater TDS 500–900 ppm in most NCR localities. Calcium carbonate is well above the 200 mg/L threshold associated with childhood eczema in UK and EU studies.
• Room heaters and dry winter air strip the skin in December and January.
• Action: indoor air purifier with HEPA, RO softener or shower-head filter, humidifier in bedrooms, increase emollient frequency from twice daily to four times daily in winter.

Mumbai / Chennai / Kochi — Monsoon Fungal Flares

• Humidity above 80% for 3–4 months drives Malassezia and Staphylococcus aureus overgrowth on broken eczematous skin.
• What dermatologists miss: patients are told their “eczema is worsening” when the actual problem is secondary fungal folliculitis. Antifungal-steroid combos seem to work, reinforcing wrong treatment. The pattern overlaps with fungal acne versus regular acne diagnosis — the same Malassezia yeast is involved.
• Action: ketoconazole 2% shampoo as a body wash 2–3 times a week during monsoon, dilute bleach baths weekly, never use thick occlusive ointments in humid months — switch to lighter ceramide creams.

Bangalore — Air Conditioner Mould and Dry-Cool Paradox

• Year-round AC use combined with dry winters causes confusing flares.
• Cladosporium and Aspergillus spores from uncleaned split AC units are an under-recognised chronic trigger. Patients blame “cold air” — the problem is the spore exposure.
• Action: AC service every 3 months including coil cleaning, run a HEPA purifier in AC rooms, switch to humidifier in winter.

Kolkata / North-East — Damp Walls and Dust Mites

• Monsoon-induced wall dampness in older homes harbours moulds.
• House dust mite (HDM) is a year-round sensitiser.
• Action: anti-allergen mattress and pillow encasements, hot-wash bedding weekly at >60°C, regular sun-airing of mattresses.

Rajasthan / Gujarat / Punjab — Extreme Dryness and Xerotic Eczema

• 45°C summers and very low humidity in winter create severe xerosis (extremely dry skin).
• Action: heavy occlusive moisturisers (petrolatum-based), aggressive emollient frequency, urea-based creams (10–20%) for thickened areas.

Kerala / Coastal Karnataka — Less Dry, More Lichenified

• High humidity prevents xerosis but encourages lichenification (thickened, leathery skin from chronic rubbing).
• Action: focus on itch control, tacrolimus on lichenified plaques, short courses of potent steroid for breakthrough flares.

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The Hard Water Problem That Indian Dermatologists Almost Never Ask About

UK NHS-funded research and the EU GEO-EPI consortium have repeatedly linked domestic water hardness above 200 mg/L calcium carbonate to higher prevalence of childhood atopic eczema.

Delhi NCR groundwater commonly runs 500–900 ppm total dissolved solids, with calcium carbonate well above the 200 mg/L eczema threshold. Bangalore, parts of Mumbai, and many tier-2 cities are similarly hard.

What happens on the skin:

• Hard water + soap → soap scum (calcium stearate) deposits on skin
• This scum disrupts the lipid barrier and raises skin surface pH from healthy 4.5–5.5 to >7.0
• Eczematous skin already has elevated pH (6.5–7.2 in untreated patients) — hard water makes it worse
• Staphylococcus aureus thrives at neutral-to-alkaline pH; lactobacilli (skin commensals) thrive at acidic pH

Realistic interventions, in increasing cost order:

1. Switch to syndet (synthetic detergent) bars — Cetaphil bar, Sebamed Olive Face & Body Bar, Aveeno cleansing bar (₹250–₹450). Plain soap leaves much more calcium scum than syndets.
2. Acidic moisturisers — anything containing lactic acid 5%, urea 10%, or glycolic acid restores barrier pH. Brands like Atogla, Venusia Max, Restoraderm.
3. Shower-head filter — KDF + Vitamin C cartridges, ₹2,500–₹6,000. Replace cartridge every 3 months.
4. Whole-house RO softener — ₹35,000–₹70,000 installed. Realistic for severe cases in NCR.

Within 4–6 weeks of any meaningful water-quality intervention, most NCR patients see a measurable drop in flare frequency. Almost no Indian dermatologist leads with this advice.

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Real Treatment Cost Ladder — India 2026

Treatment	Indian Brand / Generic	Indian Cost	US Equivalent	Where It Fits
Plain white petrolatum	Vaseline, generic	₹150–₹300 / 450g	$5–$8	Daily emollient base
Cetaphil moisturising cream	Cetaphil	₹500–₹900 / 250g	$20	Sensitive skin maintenance
Indian ceramide cream	Atogla, Venusia Max	₹400–₹800 / 200g	$25–$40	First-line moisturiser
Mometasone furoate 0.1%	Elocon, Momate	₹120–₹250 / 15g	$30	Mild-moderate flare
Fluticasone propionate 0.05%	Flutivate	₹180–₹350 / 15g	$40	Moderate flare
Clobetasol propionate 0.05%	Tenovate	₹80–₹150 / 15g	$40	Short courses, thick skin only
Tacrolimus ointment 0.1%	Tacroz Forte, Protopic	₹250–₹680 / 10g	$200–$400	Face, folds, maintenance
Pimecrolimus cream 1%	Elidel	₹500–₹850 / 15g	$300–$500	Mild facial eczema
Crisaborole 2%	parallel import	₹4,000–₹7,000 / tube	$600–$900	PDE4 inhibitor, less needed in India
Difamilast 1%	not yet in India	not launched	$500–$800	See Difamilast India guide
Cyclosporine	Sandimmun, Imusporin	₹2,500–₹4,500 / month	$300–$500	Short-term severe eczema
Methotrexate	Folitrax	₹150–₹400 / month	$40–$80	Chronic moderate-severe
NB-UVB phototherapy	hospital chambers	₹400–₹1,500 / session	$200–$500	35–50 sessions needed
Dupilumab (Dupixent)	Sanofi	₹40,000–₹55,000 / syringe	$1,500–$1,800	Severe refractory eczema
Upadacitinib (JAK)	Sun, Cipla	₹6,000–₹12,000 / month	$5,000+	Severe refractory eczema
Baricitinib (JAK)	Lupin, Sun	₹3,000–₹8,000 / month	$2,500+	Severe refractory eczema

Hidden costs people do not budget for:

• GOTS-certified cotton clothing — ₹400–₹800 per kid shirt vs ₹150 regular
• Replacement bedding every 6 months — ₹3,000–₹6,000
• Patch testing (Indian Standard Series) — ₹3,000–₹8,000 one-time
• Total IgE and specific IgE food allergen panel — ₹4,000–₹8,500
• Vitamin D supplementation — ₹100–₹300 per month
• Lost school and work days — Indian severe eczema kids miss 20–40 school days a year on average

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The Working Treatment Ladder for Indian Eczema

Step 1 — Foundation (Everyone)

1. Soak-and-seal bathing — short (5–10 minute) lukewarm bath, pat dry, apply emollient within 3 minutes while skin is still slightly damp.
2. Fragrance-free syndet cleanser instead of soap. Avoid antiseptic soaps in non-infected eczema.
3. Emollient at least twice daily. Plain white petrolatum is non-inferior to ₹2,000 moisturisers for the body. Ceramide creams (Atogla, Venusia Max) for face and visible areas.
4. Cotton clothing, mild detergent (no enzymes, no fragrance), double-rinse cycle.
5. Identify and remove individual triggers — hard water, AC mould, dust mites, fabric softeners, perfumes.

Step 2 — Active Flare Management

1. Topical corticosteroid appropriate to severity and site:
   • Face, eyelids, folds — hydrocortisone 1% or weak steroid, max 5–7 days
   • Body — mometasone 0.1% or fluticasone 0.05%, twice daily for 7–14 days
   • Thickened skin (palms, soles, lichenified plaques) — clobetasol short courses under supervision
2. Use the fingertip unit (FTU) rule — one FTU = amount squeezed from fingertip to first crease, covers two adult palms. Most Indian patients under-apply.
3. Antihistamine if itch is wrecking sleep — cetirizine, levocetirizine, or hydroxyzine.

Step 3 — Maintenance and Proactive Therapy

1. Calcineurin inhibitors (tacrolimus 0.03% or 0.1%, pimecrolimus 1%) on previously affected sites twice weekly to prevent flares. Excellent for face and folds where steroids cause atrophy.
2. Twice-weekly dilute bleach bath for moderate-to-severe disease with frequent infection.
3. Treat secondary infection — short course of cloxacillin or cefadroxil if frank impetigo, ketoconazole shampoo body-wash for monsoon Malassezia.
4. Vitamin D supplementation — Indian eczema patients are nearly universally deficient; 1000–2000 IU/day for adults, 400–1000 IU for children.

Step 4 — Phototherapy and Systemic

1. NB-UVB phototherapy — 35–50 sessions, twice weekly, ₹400–₹1,500 per session. Available at most government medical colleges and large private hospitals.
2. Cyclosporine — for short-term (3–6 month) severe disease control. Watch BP and creatinine.
3. Methotrexate — slower onset, safer long-term. Common Indian dose 7.5–15 mg/week, with folic acid 5 mg/week.

Step 5 — Biologics and JAK Inhibitors

1. Dupilumab (Dupixent) — first-line biologic, 600 mg loading then 300 mg every two weeks. Strong evidence, safe profile, but ₹10–13 lakh per year out of pocket in most Indian cases.
2. Upadacitinib, baricitinib — oral JAK inhibitors, cheaper in India (₹3,000–₹12,000/month) but need bloodwork monitoring.

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The Pediatric Indian Eczema Picture — What Mothers Are Not Told

About 60% of Indian eczema patients first present before age 5. Distinct issues in this group:

• Vitamin D deficiency is near-universal in Indian children with eczema. Supplementing measurably lowers SCORAD scores in tropical-climate trials.
• Cow milk protein allergy is over-suspected and under-confirmed. Blanket dairy elimination without confirmed sensitisation (sIgE + supervised oral challenge) worsens childhood nutrition without fixing eczema.
• Coconut oil application is widespread in Indian homes and is contraindicated in active flares — lauric acid disrupts the skin microbiome. Sunflower seed oil has slightly better evidence; mustard oil is too pungent for infants and is an irritant under age 2.
• Probiotics during late pregnancy and infancy — Cochrane meta-analyses suggest a modest reduction in eczema risk with specific Lactobacillus rhamnosus GG strains. Few Indian obstetricians prescribe them.
• Atopic march — Indian children with severe early eczema have higher rates of progression to food allergy, allergic rhinitis, and asthma. Aggressive early eczema control may reduce sensitisation. The autoimmune-atopic family link also overlaps with thyroid problems in India, and many Indian eczema families have a thyroid history worth investigating with a thyroid panel.
• AIIMS Delhi runs a pediatric eczema clinic on Thursdays — OPD fee ₹10, waitlist 3–4 months. Most parents instead pay ₹1,500–₹2,500 at cosmetic-skewed chains where evidence-based care is rare.

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Eczema on Brown Skin — What Indian Patients See That Western Guides Don’t Show

Indian skin (Fitzpatrick III–VI) reacts to inflammation differently:

• Redness looks like dusky purple or grey-brown, not bright pink — eczema is often under-recognised on darker skin.
• Post-inflammatory hyperpigmentation (PIH) appears in 50–70% of Indian eczema patients after each flare. The marks can persist 6–18 months even after the eczema itself heals. The mechanism is identical to post-acne dark spots and PIH on Indian skin, and the treatment overlaps — sun protection, niacinamide, azelaic acid, tranexamic acid, and azelaic-kojic combinations.
• Lichenification (thickened, leathery, deeply pigmented plaques) is much more common than in white-skinned eczema. Chronic rubbing and scratching is the driver.
• Post-inflammatory hypopigmentation (lighter patches after a flare) is also common, especially on cheeks of children — known as pityriasis alba and often confused with vitiligo by anxious parents.

Cosmetic concerns are not vanity in this context. Visible eczema and PIH on faces affects marriage prospects, employment, and mental health in conservative Indian family contexts. Recognising this as part of disease burden — not a separate concern — changes treatment urgency.

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Wet Wrap Therapy and Bleach Baths — At-Home Protocols Indian OPDs Won’t Demo

Wet Wrap Therapy

Used for moderate-to-severe eczema not controlled by topical steroids alone. Despite being globally recommended, it is almost never demonstrated in Indian OPDs because consultations average 4–7 minutes.

Method:

1. Soak in lukewarm water 10 minutes.
2. Pat dry, apply prescribed topical steroid to affected areas.
3. Apply emollient generously over and around steroid areas.
4. Cover with a damp layer of cotton tubigauze, soft cotton clothing or specialised garments.
5. Cover with a dry second layer.
6. Leave on 2–8 hours, or overnight for severe cases.

Repeat once daily for 3–7 days during severe flare, never more than 14 days continuously. Steroid absorption is amplified — use a milder strength than usual.

Dilute Bleach Bath

For Staphylococcus-colonised moderate-to-severe eczema.

Method:

1. Fill a standard 40-litre bathtub with lukewarm water.
2. Add about 30 ml (one bottle-cap) of regular 4–5% sodium hypochlorite (Domex, Sanifresh — read the label, not scented variants).
3. Soak from neck down for 5–10 minutes.
4. Rinse with plain water at the end (some skip this — both work).
5. Pat dry, apply emollient within 3 minutes.

Twice a week is the standard schedule. The concentration is too low to bleach skin or hair, similar to chlorinated swimming-pool water. Clinical trials show roughly 50% reduction in flare frequency in S. aureus-colonised patients.

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Diet and Food Allergy — What Indian Dermatologists Get Wrong

The single most common Indian eczema myth: “Cut out dairy and gluten and the eczema will clear.”

The actual evidence:

• Only 30–35% of moderate-to-severe pediatric eczema has a true food trigger, and only 5–10% of adult eczema does.
• Blanket elimination without confirmation worsens nutrition (especially calcium, protein, vitamin D in dairy-elimination) without fixing eczema.
• The correct workflow is symptom-suspicion → specific IgE blood test or skin prick → supervised oral food challenge to confirm before elimination.

Top food triggers in Indian children with confirmed sensitisation: cow’s milk, egg, peanut, wheat, soy, fish, tree nuts. The same as global lists.

Adult eczema is rarely food-driven. Adult patients chasing food triggers usually have aero-allergens (house dust mite, mould, pollens), contact allergens (nickel, fragrance, PPD in hair dye, mehendi), or stress as the real driver.

Specific Indian-context flags:

• Mango — oral allergy syndrome and contact dermatitis around mouth in sensitised individuals.
• Cashew, jackfruit, brinjal, mushroom — common minor sensitisation panel positives in Indian patients.
• Buffalo milk vs cow milk — different protein profile; some milk-allergic children tolerate buffalo milk, though this needs supervised challenge.

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When To See a Real Dermatologist — Red Flags

See a dermatologist (not a GP, not a chemist, not an ayurvedic kiosk) if you have any of these:

• Eczema not controlled despite 4–6 weeks of correctly-used topical steroid and emollient
• Frequent infections (yellow crusts, oozing, fever)
• Sleep disruption from itch more than twice a week
• Sudden worsening with red sleeve, burning, or skin pattern beyond original eczema (think TSW)
• Eczema in a child under 6 months with poor growth or persistent vomiting (rule out atopic march + food allergy)
• Visible eczema on face affecting work, school, or mental health
• Eczema-like rash that does not respond to standard care (rule out cutaneous lymphoma, scabies, contact dermatitis, tinea incognito)

Top centres known for evidence-based atopic dermatitis care in India:

• AIIMS Delhi — pediatric eczema clinic Thursdays; long waitlist but research-grade care
• PGI Chandigarh — strong dermatology research, TSW recognition
• CMC Vellore — patch testing, biologics access
• KMC Manipal, St. John’s Bangalore — tropical dermatology research
• NIMHANS Bangalore — behavioural dermatology clinic for stress-eczema overlap (almost no one knows this exists)
• Apollo Indraprastha, Max Saket, Fortis Memorial Gurgaon — for Dupixent access, infusion day care

This is structurally similar to how Indian patients have to navigate the acne treatment ladder — start with a dermatologist who follows guidelines, not a chemist or a fairness-cream clinic. The same chemist-shop steroid pipeline that drives eczema TSW also drives PIH on Indian skin. And for hormonally driven adult eczema patterns in women, ruling out the same axis covered in PCOS hormonal acne and thyroid disease is reasonable.

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Stress, Sleep and the Indian Eczema Cycle

The itch-scratch-sleep-loss-stress-flare cycle is bidirectional. Cortisol from chronic stress increases Th2 inflammation and worsens eczema. Disrupted sleep increases pain perception and reduces skin barrier repair overnight.

In India, the mental-health side of eczema is almost completely unaddressed. No Indian dermatologist refers to a psychologist, despite NIMHANS Bangalore actually running a behavioural dermatology clinic. The pattern overlaps with what is documented in depression and burnout in India’s IT sector — high stress, poor sleep, no support, somatic skin presentations.

Practical interventions Indian patients can build into routine:

• Habit-reversal training for scratching (replace scratch with light pinch or cold compress)
• 7–8 hours sleep with skin moisturised and antihistamine if needed at night
• Yoga and pranayama (Surya Namaskar, Bhramari, Anulom Vilom) for cortisol regulation
• CBT for sleep disturbance if available

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Sources and References

• Indian Association of Dermatologists, Venereologists and Leprologists (IADVL) — Atopic Dermatitis Treatment Guidelines, 2024
• Indian Journal of Dermatology, Venereology and Leprology — Topical Steroid Misuse in India, 2017–2024
• World Allergy Organization (WAO) — Atopic Dermatitis Guidelines, 2023
• National Eczema Association — Wet Wrap Therapy and Bleach Bath Protocols
• Central Drugs Standard Control Organization (CDSCO) — Advisories on triple-combination topical preparations
• AIIMS Delhi Department of Dermatology — Pollution Dermatitis publications, 2022–2025
• Cochrane Database of Systematic Reviews — Probiotics for prevention of allergic disease
• Indian Council of Medical Research (ICMR) — Vitamin D deficiency in Indian children
• British Journal of Dermatology — Water Hardness and Childhood Eczema (UK BAMSE/GEO-EPI), 2016–2021
• Sanofi India — Dupixent (dupilumab) prescribing information and patient assistance programme, 2026
• National Institute of Mental Health and Neurosciences (NIMHANS), Bangalore — Behavioural Dermatology Clinic protocols

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Medical Disclaimer: This article is for informational purposes only and is not medical advice. Eczema treatment must be individualised by a qualified dermatologist. Do not start, stop, or change any prescription medication including topical steroids, calcineurin inhibitors, immunosuppressants, or biologics based solely on this content. If you suspect topical steroid withdrawal, secondary infection, or severe flare, see a dermatologist in person. Reviewed by Fittour India Editorial Team in line with current Indian and international atopic dermatitis guidelines.