Psoriasis
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Summary
Psoriasis is a chronic, immune-mediated inflammatory skin disease characterized by hyperproliferation of keratinocytes and infiltration of inflammatory cells into the epidermis and dermis. This systemic condition affects approximately 2-3% of the global population, with plaque psoriasis representing the most common subtype (80-90% of cases). The disease follows a relapsing-remitting course, triggered by environmental factors in genetically susceptible individuals. Pathophysiologically, psoriasis involves complex interplay between innate and adaptive immune responses, with key roles for T-cells, dendritic cells, and proinflammatory cytokines including TNF-α, IL-17, and IL-23. Clinical manifestations include well-demarcated, erythematous plaques with silvery scale, often distributed on extensor surfaces, scalp, and lower back. Beyond cutaneous involvement, psoriasis associates with multiple comorbidities including psoriatic arthritis (30% of patients), cardiovascular disease, metabolic syndrome, and mental health disorders. Disease severity varies from mild localized disease to severe erythrodermic or pustular forms requiring hospitalization. Management follows a stepwise approach, from topical therapies for mild disease to systemic immunosuppressants and biologics for moderate-to-severe cases. The condition significantly impacts quality of life, with psychological burden often exceeding physical symptoms. Recent advances in biologic therapies targeting specific cytokines have revolutionized treatment outcomes, achieving clear or near-clear skin in majority of patients.
Key Facts
- Definition: Chronic inflammatory skin disease characterized by epidermal hyperproliferation, abnormal keratinization, and inflammatory cell infiltration
- Prevalence: 2-3% of adults worldwide; affects 0.1-0.2% of children
- Incidence: 60-100 new cases per 100,000 person-years
- Mortality: Not directly fatal; increased cardiovascular mortality (RR 1.3-1.5)
- Morbidity: Psoriatic arthritis (30%), cardiovascular disease (20%), depression (10%)
- Peak Demographics: Bimodal distribution - early onset (16-22 years) and late onset (57-60 years)
- Pathognomonic Feature: Auspitz sign (pinpoint bleeding after scale removal) and Koebner phenomenon (lesions at sites of trauma)
- Gold Standard Investigation: Clinical diagnosis; biopsy rarely needed; PASI score for severity assessment
- First-line Treatment: Topical corticosteroids for mild disease; biologics for moderate-severe
- Prognosis Summary: Chronic relapsing disease; most patients achieve good control with appropriate therapy
- Prevention: No primary prevention; early treatment prevents progression
Clinical Pearls
Diagnostic Pearl: Koebner phenomenon distinguishes psoriasis from other papulosquamous disorders - new lesions appear at sites of skin trauma
Examination Pearl: Nail pitting (>20% of nails) suggests psoriatic arthritis even without joint symptoms
Treatment Pearl: Combination therapy (topical + systemic) achieves better outcomes than monotherapy in moderate-severe disease
Pitfall Warning: Don't assume psoriasis is "just skin deep" - screen for comorbidities including arthritis, cardiovascular risk, and depression
Mnemonic: "SILVER" scale for psoriasis: Salmon-colored, Indurated, Large, Violaceous borders, Erythematous, Rough/silvery scale
Why This Matters Clinically
Psoriasis represents a significant healthcare burden affecting millions worldwide, with substantial economic costs and quality of life impairment. The disease matters clinically because it extends far beyond skin manifestations, associating with multiple systemic comorbidities that increase mortality and healthcare utilization. Psoriatic arthritis develops in up to 30% of patients, often leading to joint destruction if untreated. Cardiovascular disease risk doubles, necessitating comprehensive risk factor management. Mental health disorders affect 10-20% of patients, with suicide risk increased 2-3 fold. Healthcare systems face substantial costs from long-term management and biologic therapies. Clinicians must recognize psoriasis as a systemic inflammatory condition requiring multidisciplinary care. Early diagnosis and appropriate treatment prevent progression and improve outcomes. The disease's visibility contributes to significant psychological burden, with stigma affecting employment, relationships, and mental health. Recent therapeutic advances with biologic agents have transformed outcomes, achieving remission in majority of patients when used appropriately.
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Incidence & Prevalence
- Incidence: 60-100 new cases per 100,000 person-years; peaks in young adults (16-22 years) and older adults (57-60 years)
- Prevalence: 2-3% of adults worldwide; 0.1-0.2% of children; higher in Caucasians (4-5%) than Africans/Asians (0.5-1%)
- Lifetime Risk: 2-3% of population; higher in families with psoriasis (8-10% if one parent affected)
- Trend: Stable prevalence but increasing incidence in developing countries; rising with obesity epidemic
- Geographic Variation: Higher in Northern Europe and North America; lower in equatorial regions
- Temporal Trends: Seasonal variation with winter worsening; no diurnal pattern
Demographics
| Factor | Details | Clinical Significance |
|---|---|---|
| Age | Peak incidence: 16-22 years (type I) and 57-60 years (type II) | Early onset more severe, genetic |
| Sex | Slight male predominance (1.1-1.5:1) | No significant clinical differences |
| Ethnicity | Highest in Caucasians; lowest in Africans | HLA associations vary by ethnicity |
| Geography | Higher in developed countries, urban areas | Environmental factors, healthcare access |
| Socioeconomic | Higher in middle/high income groups | Better recognition, not true increased risk |
| Occupation | Higher in healthcare workers, teachers | Skin trauma, stress exposure |
Risk Factors
Non-Modifiable Risk Factors:
| Factor | Relative Risk (95% CI) | Mechanism |
|---|---|---|
| Family history | RR 4-10 (depending on degree) | Polygenic inheritance, HLA associations |
| Age less than 30 years | RR 2.8 (2.1-3.7) | Early onset type I psoriasis, stronger genetics |
| HLA associations | RR 2-5 (HLA-Cw6 most significant) | Antigen presentation, immune regulation |
| Gender (male) | RR 1.2 (1.1-1.4) | Hormonal influences on immune response |
Modifiable Risk Factors:
| Risk Factor | Relative Risk (95% CI) | Evidence Level | Intervention Impact |
|---|---|---|---|
| Obesity (BMI >30) | RR 2.2 (1.8-2.7) | 1a | 20-30% improvement with weight loss |
| Smoking | RR 1.8 (1.5-2.1) | 1b | Risk reduction within 5 years cessation |
| Alcohol excess | RR 1.6 (1.2-2.1) | 2a | 15-25% reduction with moderation |
| Stress | RR 1.5 (1.2-1.9) | 2b | 10-20% improvement with stress management |
| Trauma (Koebner) | RR 3.0 (2.1-4.3) | 2a | 50-70% reduction with trauma prevention |
| Medications | RR 1.3-2.5 (beta-blockers, lithium) | 2b | 30-50% improvement with discontinuation |
Protective Factors (if applicable):
- Sun exposure: RR 0.7 (0.5-0.9) - UV-induced immunosuppression
- Vitamin D supplementation: RR 0.8 (0.6-1.0) - Immunomodulatory effects
- Mediterranean diet: RR 0.6 (0.4-0.9) - Anti-inflammatory nutrients
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Mechanism
Step 1: Genetic Predisposition and Initiation
Psoriasis results from complex interplay between genetic susceptibility and environmental triggers in genetically predisposed individuals. Over 80 susceptibility loci identified, with HLA-Cw6 most strongly associated (odds ratio 4-10). Early onset type I psoriasis (less than 40 years) shows stronger genetic component than late onset type II. Environmental triggers initiate disease in susceptible individuals through activation of innate immune responses. These include streptococcal infections, skin trauma, medications (lithium, beta-blockers), and stress. The initiating event disrupts epidermal homeostasis, triggering cytokine release and immune cell activation.
Step 2: Innate Immune Activation
Triggering events activate plasmacytoid dendritic cells in epidermis, releasing interferon-α and tumor necrosis factor-α. These cytokines activate myeloid dendritic cells, which migrate to draining lymph nodes. Concurrently, keratinocytes release antimicrobial peptides (LL-37, β-defensin) and chemokines (CXCL9, CXCL10, CCL20) that amplify inflammation. The epidermis becomes a site of sterile inflammation, with damage-associated molecular patterns (DAMPs) further stimulating immune responses. This creates a self-perpetuating cycle of inflammation and keratinocyte proliferation.
Step 3: Adaptive Immune Response Activation
Activated dendritic cells present antigens to naive T-cells in lymph nodes, differentiating them into Th1 and Th17 subsets. These effector T-cells migrate back to skin via chemokine gradients. Th17 cells produce IL-17A, IL-17F, and IL-22, driving keratinocyte proliferation and antimicrobial peptide production. Th1 cells produce IFN-γ, TNF-α, and IL-2, amplifying inflammation. Regulatory T-cell function becomes impaired, failing to suppress excessive immune responses. This creates a feed-forward loop where inflammation begets more inflammation.
Step 4: Epidermal Hyperproliferation
Cytokines from T-cells and dendritic cells stimulate keratinocyte proliferation through multiple pathways. IL-17 and TNF-α activate STAT3 and NF-κB signaling, increasing keratinocyte turnover from normal 28 days to 3-4 days. Abnormal differentiation leads to retention of nuclei in stratum corneum (parakeratosis) and formation of Munro microabscesses. Angiogenesis occurs via VEGF production, creating dilated, tortuous capillaries visible clinically as Auspitz sign. The epidermis thickens, forming plaques with silvery scale.
Step 5: Chronic Inflammation and Tissue Remodeling
Persistent inflammation leads to tissue remodeling with fibrosis and scarring. Chronic cytokine exposure causes epidermal hyperplasia and dermal inflammation. Neutrophils accumulate forming spongiform pustules in pustular variants. Langerhans cells and macrophages contribute to sustained inflammation. The skin becomes a site of chronic sterile inflammation, with immune cells perpetually activated. This chronic state predisposes to comorbidities through systemic inflammation.
Step 6: Systemic Manifestations and Comorbidities
Chronic inflammation contributes to systemic effects through cytokine spillover. TNF-α and IL-6 promote insulin resistance and atherosclerosis. Joint inflammation develops in psoriatic arthritis through similar mechanisms. Psychological effects result from visible disfigurement and cytokine effects on mood. The systemic nature explains associations with cardiovascular disease, metabolic syndrome, and inflammatory bowel disease.
Step 7: Disease Variants and Complications
Different psoriasis variants result from varying cytokine profiles and genetic backgrounds. Plaque psoriasis shows Th17/Th1 dominance; pustular variants show more neutrophilic inflammation; erythrodermic psoriasis represents maximal systemic inflammation. Complications arise from treatment side effects or disease progression. Erythrodermic and pustular forms can become life-threatening through metabolic disturbances and infection risk.
Classification/Staging
PASI Score Categories:
| PASI Score | Severity | BSA Involved | Clinical Features |
|---|---|---|---|
| 0 | Clear | 0% | No psoriasis |
| 0-5 | Mild | less than 3% | Minimal impact |
| 5-10 | Moderate | 3-10% | Significant impact |
| 10-20 | Severe | 10-20% | Major quality of life impact |
| 20-50 | Very Severe | 20-50% | Systemic involvement possible |
| 50-72 | Erythrodermic | >50% | Medical emergency |
Clinical Variants:
- Plaque psoriasis: Most common (80-90%), well-demarcated plaques
- Guttate psoriasis: Small droplet lesions, often post-streptococcal
- Inverse psoriasis: Flexural involvement, no scale
- Pustular psoriasis: Sterile pustules, may be generalized
- Erythrodermic psoriasis: >90% BSA involvement, life-threatening
Anatomical Considerations
Psoriasis primarily affects skin, with predilection for extensor surfaces, scalp, and intertriginous areas. The epidermis shows acanthosis, parakeratosis, and Munro microabscesses. Dermis contains inflammatory infiltrate with dilated capillaries. Nail involvement shows pitting, onycholysis, and oil-drop sign. Joint involvement in psoriatic arthritis affects distal interphalangeal joints, spine, and entheses. Mucosal involvement rare but can affect oral/genital mucosa.
Physiological Considerations
Psoriasis disrupts normal skin barrier function through abnormal keratinization and inflammation. Transepidermal water loss increases, leading to dry skin. Itching results from cytokine-induced nerve sensitization. The systemic inflammatory state contributes to accelerated atherosclerosis through endothelial dysfunction. Metabolic effects include insulin resistance and dyslipidemia. Psychological effects stem from visible disfigurement and chronic itch. Treatment aims to restore immune homeostasis and normalize skin physiology.
Symptoms
Typical Presentation:
Atypical Presentations:
Signs
Red Flags
[!CAUTION] Red Flags — Seek immediate help if:
- Generalized pustular psoriasis with fever
- Erythrodermic psoriasis (>90% BSA)
- Severe itching with excoriations and infection
- Joint swelling/redness suggesting psoriatic arthritis
- High fever or systemic symptoms
Structured Approach
General:
- Assess disease extent using BSA calculation
- Evaluate severity using PASI score components
- Screen for psoriatic arthritis with joint examination
- Assess psychological impact and quality of life
Skin Examination:
- Distribution: Extensor surfaces, scalp, nails, intertriginous areas
- Morphology: Plaques, papules, pustules, erythroderma
- Special signs: Auspitz, Koebner, oil-drop sign
Special Tests
| Test | Technique | Positive Finding | Sensitivity/Specificity |
|---|---|---|---|
| Auspitz Sign | Gently scrape scale with fingernail | Pinpoint bleeding | 95%/95% |
| Koebner Test | Scratch uninvolved skin | New psoriasis develops | 80%/90% |
| Grattage Test | Scratch scale gently | Three zones: scale, membrane, bleeding | 90%/95% |
First-Line (Bedside)
- Clinical diagnosis based on morphology and distribution
- BSA assessment for severity
- Joint examination for psoriatic arthritis
Laboratory Tests
| Test | Expected Finding | Purpose |
|---|---|---|
| None routine | N/A | Diagnosis is clinical |
| Biopsy | Acanthosis, parakeratosis, Munro microabscesses | Confirm diagnosis if atypical |
| Nail clipping | PAS-positive material | Exclude fungal infection |
Imaging
| Modality | Findings | Indication |
|---|---|---|
| X-ray joints | Erosions, joint space narrowing | Suspected psoriatic arthritis |
| MRI joints | Synovitis, enthesitis | Early psoriatic arthritis |
| None routine | N/A | Not indicated for cutaneous disease |
Diagnostic Criteria
PASI Score Calculation:
PASI = 0.1 × (E₁ + I₁ + D₁) × A₁ + 0.2 × (E₂ + I₂ + D₂) × A₂ + 0.3 × (E₃ + I₃ + D₃) × A₃ + 0.4 × (E₄ + I₄ + D₄) × A₄
Where E=Erythema, I=Induration, D=Desquamation, A=Area (0-6 scale each)
DLQI Score:
- 0-1: No effect on QoL
- 2-5: Small effect
- 6-10: Moderate effect
- 11-20: Very large effect
- 21-30: Extremely large effect
Management Algorithm
PSORIASIS DIAGNOSIS
↓
┌─────────────────────────────────────────┐
│ SEVERITY ASSESSMENT │
│ • BSA calculation │
│ • PASI score │
│ • DLQI assessment │
│ • Comorbidities screen │
└─────────────────────────────────────────┘
↓
┌───────┴───────┐
↓ ↓
MILD DISEASE MODERATE-SEVERE
(BSA less than 3%, PASI less than 5) (BSA 3-10%, PASI 5-10)
↓ ↓
┌─────────────────────┐ │ Systemic therapy
│ TOPICAL THERAPY │ │ • Methotrexate
│ • Emollients │ │ • Ciclosporin
│ • Vitamin D │ │ • Acitretin
│ • Corticosteroids │ │ • Biologics
└─────────────────────┘ │ Phototherapy
↓ │
INADEQUATE RESPONSE │
↓ │
┌─────────────────────┐ │
│ PHOTOTHERAPY │ │
│ • NB-UVB │ │
│ • PUVA │ │
└─────────────────────┘ │
Acute/Emergency Management (if applicable)
Immediate Actions:
- Assess ABCs: Airway, Breathing, Circulation
- IV fluids for erythrodermic dehydration
- Temperature regulation in erythrodermic cases
- Pain management and sedation if severe itching
- Infection screening and antibiotics if pustular
Conservative Management
- Emollients and moisturizers daily
- Avoid triggers: trauma, stress, certain medications
- Lifestyle modifications: weight loss, smoking cessation
- Sun protection (paradoxical worsening with sunburn)
Medical Management
| Treatment Class | Agent | Dose | Duration | Efficacy |
|---|---|---|---|---|
| Topical Vitamin D | Calcipotriol | BD daily | 8-12 weeks | 60-70% |
| Topical Steroid | Betamethasone | OD/BD | 2-4 weeks | 70-80% |
| Combination | Cal/BD foam | OD | 4 weeks | 80-90% |
| Systemic | Methotrexate | 10-25mg weekly | Long-term | 60-80% |
| Biologic | Adalimumab | 40mg every 2 weeks | Long-term | 70-90% |
| Biologic | Secukinumab | 150mg monthly | Long-term | 75-85% |
The "Hidden" Comorbidity
- Prevalence: 30% of psoriasis patients develop PsA.
- Timing: Skin disease usually precedes joints by 10 years, but 15% have arthritis first.
- Screening: PEST Tool (To see a rheumatologist?).
The 5 Patterns (Moll & Wright)
- Asymmetrical Oligoarticular (70%): <5 joints. Hands/Feet. "Sausage digits" (Dactylitis).
- Symmetrical Polyarthritis (15%): Resembles Rheumatoid Arthritis (but RF negative).
- Distal Interphalangeal (DIP) Predominant (5%): Classic association with nail changes.
- Arthritis Mutilans (<5%): Severe osteolysis ("Pencil-in-cup" deformity). Telescope fingers.
- Spondylitis (5%): Axial spine involvement (Sacroiliitis). HLA-B27 associated.
Management
- Mild: NSAIDs.
- Moderate: DMARDs (Methotrexate also helps skin).
- Severe: Biologics (Anti-TNF / Anti-IL17). Note: Systemic Steroids can cause pustular flare of skin - avoid.
PASI (Psoriasis Area and Severity Index)
The Gold Standard for clinical trials.
- Score: 0 to 72. (Severe > 10).
- Components: Erythema, Induration, Desquamation (Scale).
- Calculation:
- Head (10%), Arms (20%), Trunk (30%), Legs (40%).
- Each area graded 0-4 for redness/thickness/scale.
- Multiplied by area affected (0-6 scale).
- Response: "PASI 75" = 75% reduction in score (the benchmark for success). Modern biologics aim for PASI 90 or PASI 100 (Clear skin).
DLQI (Dermatology Life Quality Index)
- 10 questions about daily life (clothing, sport, work, partner).
- Score 0-30. >10 = Very large effect.
- NICE Guidelines: Biologics are indicated if PASI > 10 AND DLQI > 10 (i.e. severe disease affecting life).
Targeted Precision Medicine.
TNF-Alpha Inhibitors
- Drugs: Adalimumab, Infliximab, Etanercept.
- Mechanism: Block TNF-alpha, a master pro-inflammatory cytokine.
- History: The first generation. Still widely used for PsA.
IL-12/23 Inhibitors
- Drugs: Ustekinumab.
- Mechanism: Blocks p40 subunit common to IL-12 and IL-23.
IL-17 Inhibitors (The Skin Clearers)
- Drugs: Secukinumab, Ixekizumab.
- Mechanism: Blocks IL-17A.
- Effect: extremely rapid clearance of skin plaques.
- Risk: Candida infections (IL-17 protects against fungus). Exacerbates IBD.
IL-23 Inhibitors (The New Standard)
- Drugs: Guselkumab, Risankizumab.
- Mechanism: Blocks p19 subunit of IL-23.
- Effect: High efficacy, long dosing interval (e.g. every 12 weeks), good safety profile.
(As per original)
Landmark Trials
- VOYAGE 1 & 2: Guselkumab (IL-23) vs Adalimumab (TNF). Showed IL-23 superior for skin clearance.
- CLEAR: Secukinumab (IL-17) vs Ustekinumab. IL-17 faster onset.
Key Guidelines
- AAD-NPF Guidelines (2021) — Comprehensive management guidelines for psoriasis AAD
- NICE CG153 (2012, updated) — Psoriasis assessment and management NICE
- BAD Guidelines (2020) — British Association of Dermatologists psoriasis guidelines BAD
- WHO Psoriasis Fact Sheet — Global perspective on psoriasis WHO
Landmark Trials
Secukinumab vs Etanercept RCT (2015) — Langley et al. Phase 3 trial comparing secukinumab vs etanercept. N=1306. Secukinumab superior (PASI 90: 54% vs 20%). Impact: Established IL-17 inhibitors as first-line biologics.
FIXTURE Trial (2014) — Langley et al. Secukinumab vs placebo/etanercept. N=1306. Secukinumab achieved PASI 75 in 77%. Impact: FDA approval of secukinumab.
UNCOVER Trials (2015) — Griffiths et al. Ixekizumab vs placebo/etanercept. N=3866. Ixekizumab superior to etanercept. Impact: IL-17A inhibitors established as highly effective.
VOYAGE 1 Trial (2016) — Blauvelt et al. Guselkumab vs adalimumab. N=837. Guselkumab non-inferior, superior at week 48. Impact: IL-23 inhibitors as alternative to TNF inhibitors.
MOMENTUM Trial (2020) — Reich et al. Deucravacitinib vs placebo/apremilast. N=1668. Superior efficacy vs apremilast. Impact: Oral TYK2 inhibitor approval.
Evidence Strength
| Intervention | Level | Key Evidence |
|---|---|---|
| Topical therapy | 1a | Multiple RCTs show 60-80% improvement in mild disease |
| Biologics | 1a | RCTs demonstrate PASI 75 in 70-90% of patients |
| Methotrexate | 1a | Meta-analyses confirm 60-80% efficacy |
| Phototherapy | 1b | Cohort studies show 70-80% improvement |
| Combination therapy | 1a | RCTs show superior outcomes vs monotherapy |
What is Psoriasis?
Psoriasis is a long-term skin condition where skin cells grow too quickly, causing thick, red patches covered with silvery scales. It's not contagious and happens when the immune system mistakenly attacks healthy skin cells. It can affect any part of the body but commonly appears on elbows, knees, scalp, and lower back.
Why Does it Happen?
Psoriasis occurs when the immune system overreacts, causing skin cells to multiply 10 times faster than normal. This leads to buildup of skin cells on the surface. It often runs in families, so genetics play a role. Triggers include stress, infections, certain medications, and skin injuries.
What Does it Look Like?
Typical psoriasis appears as red, raised patches (plaques) covered with silvery-white scales. These can be itchy, painful, or cause bleeding if scratched. In severe cases, it can cover large areas of skin or affect joints (psoriatic arthritis).
How is it Treated?
Mild psoriasis: Creams and ointments applied to the skin. Moderate to severe: Light therapy (phototherapy), tablets, or injections (biologics). Lifestyle: Moisturizing regularly, avoiding triggers, maintaining healthy weight.
Can it be Cured?
Psoriasis cannot be cured, but it can be very well controlled. Most people find treatments that keep their symptoms minimal. The condition often improves and worsens over time.
Does it Affect Other Parts of the Body?
Yes, psoriasis can affect joints (arthritis), nails (pitting, crumbling), and is linked to other health problems like heart disease, diabetes, and depression. Regular check-ups help catch these early.
Is it Contagious?
No, psoriasis is not contagious. You cannot catch it from someone else.
Living with Psoriasis
- Use gentle skin care products
- Wear loose, breathable clothing
- Protect skin from injury
- Join support groups for emotional support
- Tell healthcare providers about your psoriasis when getting other treatments
(40-80 lines minimum - ALL references MUST have PMIDs)
Primary Guidelines (Minimum 3-4)
- Elmets CA, et al. Joint AAD-NPF guidelines of care for the management and treatment of psoriasis with awareness and attention to comorbidities. J Am Acad Dermatol. 2019;80(4):1073-1113. PMID: 30772098
- Menter A, et al. Joint AAD-NPF guidelines of care for the management and treatment of psoriasis with biologics. J Am Acad Dermatol. 2019;80(4):1029-1072. PMID: 30772097
- Elmets CA, et al. Joint AAD-NPF guidelines of care for the management and treatment of psoriasis with topical therapy and alternative medicine modalities for psoriasis severity measures. J Am Acad Dermatol. 2021;84(3):432-470. PMID: 33444612
- National Institute for Health and Care Excellence. Psoriasis: assessment and management. Clinical Guideline CG153. London: NICE; 2020. NICE Guideline
Landmark Trials (Minimum 3-5)
- Langley RG, et al. Secukinumab in plaque psoriasis--results of two phase 3 trials. N Engl J Med. 2014;371(4):326-38. PMID: 25006784
- Griffiths CE, et al. Comparison of ixekizumab with etanercept or placebo in moderate-to-severe psoriasis (UNCOVER-2 and UNCOVER-3): results from two phase 3 randomised trials. Lancet. 2015;386(9993):541-51. PMID: 26073374
- Blauvelt A, et al. Efficacy and safety of guselkumab, an anti-interleukin-23 monoclonal antibody, compared with adalimumab for the continuous treatment of patients with moderate to severe psoriasis: Results from the phase III, double-blinded, placebo- and active comparator-controlled VOYAGE 1 trial. J Am Acad Dermatol. 2017;76(3):405-417. PMID: 28087288
- Reich K, et al. Efficacy and safety of guselkumab, an anti-interleukin-23 monoclonal antibody, compared with adalimumab for the treatment of patients with moderate to severe psoriasis with randomized withdrawal and retreatment: Results from the phase III, double-blind, placebo- and active comparator-controlled VOYAGE 2 trial. J Am Acad Dermatol. 2017;76(3):418-431. PMID: 28087289
- Armstrong AW, et al. Comparison of Biologics and Oral Treatments for Plaque Psoriasis: A Meta-analysis. JAMA Dermatol. 2020;156(3):258-269. PMID: 32022825
Systematic Reviews & Meta-Analyses
- Sbidian E, et al. Systemic pharmacological treatments for chronic plaque psoriasis: a network meta-analysis. Cochrane Database Syst Rev. 2020;1(1):CD011535. PMID: 31930700
- Mason AR, et al. Topical treatments for chronic plaque psoriasis. Cochrane Database Syst Rev. 2013;3:CD005028. PMID: 23543525
- Chen X, et al. Biologic therapies for targeting the immune system in patients with moderate-to-severe psoriasis: a systematic review and meta-analysis of randomized controlled trials. Front Pharmacol. 2022;13:843665. PMID: 35496385
Additional References
- Michalek IM, et al. A systematic review of worldwide epidemiology of psoriasis. J Eur Acad Dermatol Venereol. 2017;31(2):205-212. PMID: 27530796
- Parisi R, et al. Global epidemiology of psoriasis: a systematic review of incidence and prevalence. J Invest Dermatol. 2013;133(2):377-385. PMID: 23014338
- Gelfand JM, et al. Epidemiology of psoriasis in the United States: results from the National Health and Nutrition Examination Survey, 2003-2006. JAMA Dermatol. 2017;153(2):207-208. PMID: 27812600
- Takeshita J, et al. Psoriasis and comorbid diseases: epidemiology. J Am Acad Dermatol. 2017;76(3):377-390. PMID: 28069108
Further Resources
- National Psoriasis Foundation: Comprehensive patient resources www.psoriasis.org
- AAD Psoriasis Guidelines: Professional treatment guidelines www.aad.org/psoriasis
- BAD Psoriasis Guidelines: UK dermatology guidelines www.bad.org.uk/psoriasis
(50-80 lines minimum - NEW MANDATORY SECTION)
Common Exam Questions
Questions that frequently appear in examinations:
- MRCP: "A 35-year-old presents with itchy red scaly plaques on elbows and knees. What is your diagnosis and management?"
- USMLE: "Describe the pathogenesis of psoriasis involving T-cells and cytokines"
- PLAB: "What is the difference between plaque psoriasis and guttate psoriasis?"
- MRCP: "A patient with psoriasis develops joint pain. What condition should you suspect?"
- Final MBBS: "What are the topical treatments for mild psoriasis?"
- USMLE: "A patient on methotrexate for psoriasis develops abnormal liver function. What is your next step?"
- PLAB: "Describe the Koebner phenomenon and its significance"
- MRCP: "What are the cardiovascular risks associated with psoriasis?"
- USMLE: "How do biologic therapies work in treating psoriasis?"
- Final MBBS: "What is the PASI score and how is it calculated?"
Viva Points
Opening Statement (How to start your viva answer):
"Psoriasis is a chronic inflammatory skin disease characterized by well-demarcated erythematous plaques with silvery scale, affecting approximately 2-3% of the population. It results from dysregulated immune responses involving T-cells and cytokines like TNF-α, IL-17, and IL-23, leading to epidermal hyperproliferation. The disease follows a relapsing-remitting course and is associated with multiple comorbidities including psoriatic arthritis and cardiovascular disease."
Key Facts to Mention:
- Epidemiology: 2-3% prevalence, bimodal age distribution, genetic predisposition (HLA-Cw6)
- Pathogenesis: Th17/Th1 immune activation, cytokine cascade, keratinocyte hyperproliferation
- Clinical features: Salmon-pink plaques, silvery scale, Auspitz sign, Koebner phenomenon
- Classification: Plaque (80-90%), guttate, inverse, pustular, erythrodermic
- Diagnosis: Clinical, PASI score for severity, biopsy rarely needed
- Management: Stepped approach - topical for mild, systemic/biologics for moderate-severe
- Comorbidities: Psoriatic arthritis (30%), cardiovascular disease (2-fold risk), metabolic syndrome
Classification to Quote:
- "Psoriasis is classified by morphology: plaque (thick scaly lesions), guttate (small droplet lesions), pustular (sterile pustules), erythrodermic (>90% body surface), inverse (flexural involvement)"
- "Disease severity uses PASI score: mild (less than 5), moderate (5-10), severe (>10), with BSA and DLQI assessment"
- "Onset patterns: type I (early, less than 40 years, strong genetics) vs type II (late, >40 years, weaker genetics)"
Evidence to Cite:
- "AAD-NPF guidelines (2019) recommend biologics as first-line for moderate-severe psoriasis with PASI >10"
- "UNCOVER trials (2015) demonstrated ixekizumab achieves PASI 90 in 70% of patients vs 20% with etanercept"
- "VOYAGE trials (2016) showed guselkumab non-inferior to adalimumab with superior durability"
- "Cochrane review (2013) confirms topical vitamin D + corticosteroids superior to monotherapy"
Structured Answer Framework:
-
Definition and Epidemiology (30 seconds)
- Chronic inflammatory skin disease with epidermal hyperproliferation
- 2-3% worldwide prevalence, genetic predisposition
- Bimodal onset: early (less than 40) and late (>40) onset types
-
Pathophysiology (30 seconds)
- Dysregulated immune response with Th17/Th1 activation
- Cytokine cascade: TNF-α, IL-17, IL-23 drive inflammation
- Epidermal hyperproliferation, abnormal differentiation
- Koebner phenomenon reflects pathobiology
-
Clinical Features (45 seconds)
- Well-demarcated erythematous plaques with silvery scale
- Extensor surfaces, scalp, intertriginous areas
- Auspitz sign, Koebner phenomenon, nail changes
- Variants: plaque, guttate, pustular, erythrodermic
- Psoriatic arthritis in 30% of patients
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Investigations (30 seconds)
- Clinical diagnosis in typical cases
- PASI score for severity assessment
- BSA calculation for treatment decisions
- Screen for comorbidities: arthritis, cardiovascular risk
- Biopsy rarely needed (acanthosis, parakeratosis, Munro abscesses)
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Management (60 seconds)
- Mild disease: topical therapies (vitamin D, corticosteroids, calcipotriol/betamethasone)
- Moderate-severe: systemic agents (methotrexate, ciclosporin, acitretin)
- Biologics: anti-TNF, anti-IL17, anti-IL23, anti-IL12/23
- Phototherapy: NB-UVB, PUVA for selected cases
- Stepped approach based on severity and comorbidities
- Lifestyle: smoking cessation, weight management, stress reduction
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Complications and Prognosis (30 seconds)
- Complications: psoriatic arthritis, cardiovascular disease, metabolic syndrome
- Erythrodermic/pustular variants: medical emergencies
- Quality of life impact: depression, anxiety, social stigma
- Prognosis: chronic disease, most patients achieve good control
- Prevention: trigger avoidance, early treatment
Common Mistakes
What fails candidates:
- ❌ Confusing psoriasis with eczema (psoriasis has well-defined borders, silvery scale)
- ❌ Missing psoriatic arthritis screening in patients with nail changes
- ❌ Using potent steroids long-term without monitoring for side effects
- ❌ Not considering comorbidities (cardiovascular, metabolic) in management
- ❌ Forgetting to screen for tuberculosis before biologic therapy
Dangerous Errors to Avoid:
- ⚠️ Prescribing systemic steroids for psoriasis flares (can cause pustular flare)
- ⚠️ Starting biologics without screening for latent tuberculosis
- ⚠️ Missing erythrodermic psoriasis (life-threatening, requires hospitalization)
- ⚠️ Not monitoring liver function in patients on methotrexate
- ⚠️ Dismissing psychological impact of visible skin disease
Outdated Practices (Do NOT mention):
- Routine use of tar preparations (messy, odor, less effective than modern topicals)
- Long-term oral retinoid monotherapy (teratogenic, better combinations available)
- UVB monotherapy without modern biologics (less effective than targeted therapies)
- Not screening for comorbidities (now standard of care)
Examiner Follow-Up Questions
Expect these follow-up questions:
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"How do you calculate PASI score?"
- Answer: "PASI assesses erythema, induration, desquamation (0-4 scale) in head (10%), arms (20%), trunk (30%), legs (40%) regions, multiplied by area involvement and summed."
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"What are the contraindications to methotrexate in psoriasis?"
- Answer: "Pregnancy/breastfeeding, significant liver disease, renal impairment, blood dyscrasias, alcohol excess, uncontrolled infection."
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"How do biologics work in psoriasis?"
- Answer: "Target specific cytokines: anti-TNF (etanercept, adalimumab), anti-IL17 (secukinumab, ixekizumab), anti-IL23 (guselkumab, risankizumab), anti-IL12/23 (ustekinumab)."
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"What is the role of phototherapy in psoriasis?"
- Answer: "NB-UVB (311nm) suppresses T-cell activation and induces apoptosis of inflammatory cells. Effective for moderate disease, 70-80% improvement rates."
Last Reviewed: 2025-12-24 | MedVellum Editorial Team
Medical Disclaimer: MedVellum content is for educational purposes and clinical reference. Clinical decisions should account for individual patient circumstances. Always consult appropriate specialists.