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Autoimmune / Inflammatory Physician Reviewed

Psoriasis — managed by dermatologists, not concealed

A chronic immune-mediated condition affecting 2–3% of Indians, treated with evidence-based protocols at DermaVue's 7 clinics across Kerala & Tamil Nadu.

Plaque Psoriasis Psoriasis Vulgaris Scalp Psoriasis Guttate Psoriasis Chronic Plaque Disease
Affects Scalp, Elbows, Knees, Lower Back, Nails
Age Group 15 – 60 years
Contagious No
Treatment 6 – 12+ sessions
Consultation ₹300
At a Glance
0–3%
of India's population affected — over 30 million people living with psoriasis
0%
of cases are plaque psoriasis — the most common and treatable subtype
0%+
DermaVue patient satisfaction across 7,400+ reviews
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7 clinics · Kerala & Tamil Nadu · ₹300 consultation

What Is It

Understanding Psoriasis

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

Psoriasis is a chronic autoimmune condition where the immune system mistakenly speeds up skin cell production, causing thick, scaly patches that itch, crack, and sometimes bleed. It is not an infection, not caused by poor hygiene, and cannot be passed to another person. In India, over 30 million people live with psoriasis, yet stigma and misinformation cause many to delay treatment for years. DermaVue dermatologists use a stepwise approach — combining topical therapy, phototherapy, systemic agents, and biologics — tailored to disease severity, body surface area, and each patient's quality-of-life impact.

Psoriasis vulgaris (ICD-10: L40.0) is a chronic, immune-mediated inflammatory dermatosis characterised by well-demarcated, erythematous plaques with silvery-white micaceous scale, reflecting accelerated epidermal turnover from a normal 28-day cycle to 3–5 days. Pathogenesis centres on dysregulated Th1/Th17 axis activation — IL-17A, IL-23, and TNF-α drive keratinocyte hyperproliferation, angiogenesis, and neutrophilic infiltration forming Munro microabscesses.[1] The Auspitz sign (pinpoint bleeding on scale removal) and Koebner phenomenon (lesions at trauma sites) are pathognomonic clinical features. Comorbidity burden is significant: psoriatic arthritis (up to 30%), metabolic syndrome, cardiovascular disease, and depression require integrated management. Indian Fitzpatrick IV–VI phototypes frequently present with post-inflammatory hyper- or hypopigmentation at resolving plaques, complicating cosmetic outcomes.

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

What does Psoriasis look like?

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

Red Scaly Plaques
Well-defined, raised, erythematous patches covered with silvery-white scale — most commonly on elbows, knees, scalp, and lower back.
Mod. Severe
Intense Itching & Burning
Pruritus ranges from mild to severe and worsens with dryness, stress, and sweating. Scratching triggers the Koebner response, spreading lesions.
Moderate
Scalp Involvement
Thick plaques on the scalp extending beyond the hairline, often mistaken for severe dandruff. May cause temporary hair thinning at plaque sites.
Moderate
Nail Changes
Pitting, onycholysis (nail lifting), subungual hyperkeratosis, and oil-drop discolouration — present in up to 50% of psoriasis patients.
Moderate
Skin Cracking & Bleeding
Dry plaques fissure and bleed, especially over joints. Auspitz sign — pinpoint bleeding on scale removal — is a clinical hallmark.
Mod. Severe
Joint Pain & Stiffness
Up to 30% of psoriasis patients develop psoriatic arthritis — pain, swelling, and stiffness in fingers, toes, or larger joints. Early detection is critical.
Mod. Severe
Post-Inflammatory Pigment Changes
Resolving plaques in Indian skin (Fitzpatrick IV–VI) frequently leave hyper- or hypopigmented macules that persist for months after disease control.
Moderate
Emotional & Social Impact
Visible plaques cause significant psychological distress — social avoidance, depression, and anxiety. Stigma in Indian society compounds the burden.
Severe
Root Causes

What actually causes Psoriasis?

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

🧬
Genetic Predisposition
Family history is the strongest risk factor — over 40 susceptibility loci identified, with HLA-Cw6 being the primary risk allele. If one parent has psoriasis, a child has a 15–20% risk; if both, 50–75%.
Immune Dysregulation (Th17/IL-23)
Overactivation of the Th1/Th17 pathway releases TNF-α, IL-17A, and IL-23, driving keratinocyte hyperproliferation and chronic inflammation — the central mechanism in plaque psoriasis.
Stress & Psychological Triggers
Acute and chronic stress elevate cortisol and neuropeptides that amplify Th17 responses — making stress the most commonly reported flare trigger in Indian psoriasis patients.
🦠
Infections (Streptococcal & Viral)
Streptococcal pharyngitis is a well-established trigger for guttate psoriasis, particularly in children and young adults. COVID-19 has also been linked to new-onset and flare episodes.
🍚
Obesity & Metabolic Syndrome
Visceral adiposity produces pro-inflammatory adipokines that worsen psoriasis severity. India's rising metabolic syndrome prevalence directly correlates with psoriasis burden.
🧴
Medications & External Triggers
Lithium, beta-blockers, antimalarials, and rapid corticosteroid withdrawal are known triggers. Self-prescribed topical steroids — extremely common in India — cause rebound flares.
Kerala-Specific Climate Factors
While moderate sun exposure helps psoriasis, Kerala's high humidity increases sweat-related irritation at flexural sites. Monsoon dampness promotes secondary fungal infections on compromised plaques.
Who gets psoriasis in India?
  • 2–3% of India's population — over 30 million people — live with psoriasis, yet fewer than 40% receive dermatologist-led care
  • Bimodal age onset: early-onset (16–22 years, HLA-Cw6+) and late-onset (55–60 years) — early-onset tends to be more severe and familial
  • Men and women are equally affected, but women report greater quality-of-life impact due to cosmetic and social stigma in South India
  • Kerala & South India show higher reported prevalence partly due to better dermatology access — but monsoon humidity and stress are genuine aggravators
  • Fitzpatrick IV–VI skin types develop prominent post-inflammatory hyperpigmentation at resolving plaques, creating a cosmetic burden even after disease control
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 Examination & PASI Scoring
Dermatologist evaluates plaque morphology, distribution, and severity using the Psoriasis Area and Severity Index (PASI). Auspitz sign and Koebner phenomenon assessed. Baseline photography taken.
02
Nail & Joint Assessment
Systematic examination of all 20 nails for pitting, onycholysis, and oil-drop sign. Joint screening with CASPAR criteria to detect psoriatic arthritis early — critical in Indian patients who often present late.
03
Differential Diagnosis Workup
Ruling out fungal infections (common in Kerala's humid climate), eczema, seborrheic dermatitis, lichen planus, and secondary syphilis. KOH mount and skin biopsy performed when diagnosis is uncertain.
04
Comorbidity & Metabolic Screening
Blood glucose, lipid profile, liver function, uric acid, and BMI assessment — screening for metabolic syndrome, fatty liver, and cardiovascular risk factors that co-occur with moderate–severe psoriasis.
05
Personalised Treatment Protocol
A severity-matched, written treatment plan based on PASI score, body surface area, nail/joint involvement, comorbidities, and patient preference — from topical-only for mild disease to biologics for severe recalcitrant psoriasis.
Available at DermaVue

Psoriasis treatments we offer

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

Topical Therapy
Prescription-strength corticosteroids, calcipotriol (vitamin D analogue), coal tar preparations, and calcineurin inhibitors applied directly to plaques. First-line for mild psoriasis covering less than 5% body surface area.
Mild plaque psoriasis (BSA < 5%)
Narrowband UVB Phototherapy
311 nm ultraviolet B light delivered in controlled doses 2–3 times weekly. Induces T-cell apoptosis and reduces keratinocyte proliferation. Highly effective with minimal systemic side effects.
Moderate psoriasis, widespread thin plaques
Systemic Medications
Methotrexate, cyclosporine, acitretin, or apremilast prescribed based on disease severity, comorbidities, and reproductive status. Regular blood monitoring ensures safety during long-term use.
Moderate–severe psoriasis, psoriatic arthritis
Biologic Therapy
Targeted biologics (anti-TNF, anti-IL-17, anti-IL-23) for patients with moderate–severe psoriasis unresponsive to conventional systemics. PASI 75–90 clearance achievable in 12–16 weeks.
Severe recalcitrant psoriasis, biologic-eligible patients
Excimer Laser (308 nm)
Targeted UVB laser delivers high-intensity light precisely to individual plaques without affecting surrounding skin. Fewer sessions than whole-body phototherapy for localised disease.
Localised stubborn plaques, scalp psoriasis
PRP & Adjunctive Therapies
Platelet-rich plasma and intralesional therapies for recalcitrant plaques and scalp psoriasis. Used alongside primary treatment to accelerate plaque resolution and reduce relapse rates.
Recalcitrant scalp psoriasis, localised plaques
Chemical Peels for Residual PIH
After disease control, glycolic and lactic acid peels address post-inflammatory hyperpigmentation left by resolved plaques — a significant cosmetic concern in Indian skin types.
Post-psoriatic hyperpigmentation (Fitzpatrick IV–VI)
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Treatment Journey

Your Psoriasis treatment timeline

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

Week 1
Consultation, PASI scoring, baseline photography, and comorbidity screening. Joint assessment completed. Treatment plan initiated.
Topical therapy prescribed. Phototherapy schedule begins if indicated. Steroid tapering plan if prior misuse identified.
Month 1–2
Active treatment phase — topical therapy, phototherapy sessions (2–3×/week), or systemic medication initiated. Early plaque thinning observed.
Scale reduction and itch relief typically begin within 2–4 weeks. Lab monitoring for systemic agents started.
Month 3–4
Significant plaque clearance expected. PASI 50–75 achieved in most patients on appropriate regimen. Residual pigment changes becoming visible.
Phototherapy frequency may be reduced. Systemic dose adjustment based on response. Comorbidity management ongoing.
Month 5–6
Disease control phase — PASI 75+ achievable. Focus shifts to maintenance therapy and relapse prevention. PIH treatment can begin.
Biologic patients often reach PASI 90 by this stage. Transition to maintenance dosing and extended treatment intervals.
Month 6+
Long-term management plan established. Quarterly dermatologist review, comorbidity monitoring, and trigger avoidance strategy in place.
Psoriasis is chronic — ongoing management prevents relapse. Most patients maintain clearance with step-down maintenance protocols.
FAQ

Frequently asked questions about Psoriasis

No, psoriasis is absolutely not contagious. It cannot be transmitted by touching, sharing clothes, swimming together, or any form of physical contact. Psoriasis is an autoimmune condition driven by genetic and immune factors — not by any bacteria, virus, or fungus. The widespread misconception in Indian society that it spreads by touch causes significant social stigma and must be corrected.

Psoriasis is a chronic condition — there is currently no permanent cure. However, modern treatments including biologics, phototherapy, and systemic agents can achieve near-complete clearance (PASI 90–100) and sustained remission for extended periods. With proper dermatologist-led management, most patients achieve excellent disease control and quality of life. Flares can be minimised through trigger avoidance, stress management, and maintenance therapy.

Common triggers in Kerala include monsoon humidity causing sweat irritation at flexural sites, stress — the most frequently reported trigger — streptococcal throat infections (especially in children), abrupt withdrawal of self-prescribed steroid creams, alcohol consumption, and weight gain. Kerala's climate is a double-edged sword: moderate sun exposure helps psoriasis, but high humidity and monsoon dampness can worsen flexural and intertriginous involvement.

DermaVue consultation fee is ₹300 at most branches. Topical treatment costs ₹500–2,000 monthly depending on medications prescribed. Narrowband UVB phototherapy sessions range ₹800–1,500 per session. Systemic medications like methotrexate are affordable at ₹200–500 monthly; biologics are significantly more expensive. Complete cost transparency is provided at your first consultation — treatment plans are matched to both disease severity and budget.

Up to 30% of psoriasis patients develop psoriatic arthritis — inflammatory joint disease causing pain, stiffness, and swelling in fingers, toes, spine, or larger joints. Nail psoriasis is a strong predictor of future joint involvement. Early detection through screening at every dermatology visit is critical because untreated psoriatic arthritis can cause irreversible joint damage. DermaVue dermatologists screen for joint symptoms at every review.

While some Ayurvedic formulations may offer symptomatic relief, there is no high-quality clinical evidence supporting long-term disease modification with alternative therapies alone. The risk is that patients delay evidence-based treatment, allowing disease progression and joint damage. DermaVue dermatologists recommend an evidence-based primary treatment plan, and patients may use complementary approaches alongside — not instead of — proven therapies.

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