An educational, informative presentation on psoriasis. It covers the latest pathogenesis of the disease and treatment guidelines. the differential diagnosis is well defined.

1. Dr. Ayshah Hashimi

2. History about Psoriasis
• It’s a Greek word “Psora” meaning Itchy
• Hkm. Jalinoos (Galen) referred this term to all the epidermopathies with pruritis
• Earlier it was thought that psoriasis was a genetic disease that is triggered by environmental factors
• According to the pathogenesis dermatologist considered it an epidermal disorder in which fundamental
defect resided within Keratinocytes
• Earlier it was believed that decrease epidermal turnover time (10 days) was the main cause that result in
immature hyperproliferation of keratinocytes

3. Introduction to Psoriasis
• Long-lasting or chronic
• Noncontagious or non- infectious
• Inflammatory
• Autoimmune disease
• Characterized by raised areas of abnormal skin due to decrease epidermal turnover time or increase in
production of epidermal cells at a rate that is about six to nine times faster than normal
• These areas are red, or purple on some people with darker skin, dry, itchy, and scaly
• Psoriasis varies in severity from small, localized patches to complete body coverage
• Injury to the skin can trigger psoriatic skin changes at that spot, which is known as the Koebner phenomenon
• Areas of the body most commonly affected are the back of the forearms, shins, navel area, and scalp
• Nails are affected (pits in the nails or changes in nail color)

4. Prevalence
• 1-3% affected but 50% requires instant aggressive treatment
• Common in both the sexes
• Disease exaggerate in winters
• Develop at any age but two peaks are seen
• Early onset:
 Incidence in 3rd decade
 Genetic association observed (HLA-Cw6)
 Positive family history
 More severe
 Presence of arthropathy
• Late onset:
 Peak incidence in 5th decade
 Less frequent family history
 Milder course

5. Etiology/ Provoking factors
• Idiopathic
• Genetic
• Autoimmune reactions
• Infection (streptococcal antigen provokes guttate psoriasis)
• Injury to skin (Kobernization occurs)
• Endocrine factors (puberty and menopause) confirmation required for endocrinological etiologies
• UV rays (favorable in some as they depletes lymphocytes while precipitates in some cases)
• Metabolic syndromes (hyperlipidemias, thyroid dysfunction, DM, obesity) certainly contributes to the
progression of the disease
• Medication (Lithium, β adrenergic blockers, anti-depressants, antimalarials and sudden withdrawal of
corticosteroids)

6. Pathogenesis
• The disease had been considered hyperproliferative disorder and various treatment modalities which were
used for the treatment had antiproliferative actions.
• Molecular techniques have given new views regarding the pathogenesis of the disease
• So, according to the evidences psoriasis is a T-cell mediated inflammatory disease as Both CD4+ and CD8+ t
lymphocytes accumulates in the diseased skin
• Various new treatment modalities are available as the revised pathogenesis is a bit different from the
traditional one
• During genetics screening, 8 loci have been identified which are linked to the pathogenesis of the disease

7. Gene Chromosome locus
PSOR1 (major) 6p21.3
PSOR2 17q
PSOR3 4q
PSOR4 1q
PSOR5 3q
PSOR6 19q
PSOR7 1p
PSOR8 16q
p is short arm while q is long arm of chromosome
PSOR1 is most common of all also its been observed that psoriasis vulgaris
and guttate psoriasis are genetically identical

8. Cardinal features of psoriasis
• Epidermal hyperproliferation with loss of differentiation/ maturation
 Clinical appearance is largely caused by epidermal changes, the disease has traditionally been
considered as a disorder associated with excessive keratinocyte proliferation and abnormal
maturation. It was believed that epidermal turnover time was reduced to approx. 8 folds
 According to recent studies increase proliferation is due to increase in the proliferating cell
compartment in the basal layer. No of cycling cells increase to 7 folds
 Psoriasis is a disease of interfollicular epidermis sparing har follicles
 Several growth factors are present in the lesion e.g. Transforming Growth Factor-α (TGF- α)

9. Cardinal features of psoriasis
• Dilatation and proliferation of dermal blood vessels
 Superficial microvasculature appears dilated and increases by four fold
 Chemokines by activated keratinocytes such as IL-8, TNF- α, vascular endothelial growth factor
(VEGF) are involved in vascular changes
 In addition to vascular proliferation, they also contribute actively in the inflammatory process
through surface expression of molecules to bring leucocyte into the skin
 In lesional skin, e-selectin and intracellular adhesion molecule-1 (ICAM-1) receptors is
upregulated in affected capillaries due to effect of chemokines
 These receptors allow T-Lymphocyte to accumulate within the skin

10. Cardinal features of psoriasis
• Accumulation of inflammatory cells
 Before obvious changes apparent in skin epidermis, numerous lymphocytes appears
 CD+4, CD8+ & Langerhans cells (immature dendritic cell) increases in skin
 Epidermal keratinocytes in psoriatic lesion synthesize Human Leukocyte antigen (HLA)
 Cyclosporine has major inhibitory effect on T cell activation and thus improvement. Also, it has
antiproliferative effect on keratinocytes
 In an experiment, it was observed that injection of T-lymphocytes in normal appearing skin induces
psoriatic lesion
 CD8+ T cells are more in epidermis while CD4+ T cells are abundant in dermis
 Most T cells in skin lesion are memory cells with cutaneous lymphocyte antigen positive
 Dendritic cells produces IL-12 & IL-23 that activates T lymphocyte

11. Pathogenesis
• Any trigger in the skin stresses keratinocytes that releases DNA & RNA which binds with antimicrobial
peptide called as Cathelicin 337 that activates innate immunity i.e. immature Langerhans cells to
mature dendritic cell
• Activated Keratinocytes release IL4,6 and TNF-α
• Mature dendritic cell on activation enters circulation and reaches the draining lymph node and
produces IL12 & IL23
• In the lymph nodes, under the influence of IL-12, T helper cells produces TH1 while IL-23 produces TH17
(activated T lymphocyte)
• T lymphocytes multiplies and enters the circulation and reaches the affected site (infiltration of
lymphocytes)
• TH1 results in progresses inflammatory cascade by releases cytokines (Il-12, interferons etc.) while TH17
causes proliferation of keratinocytes and vascular changes and thus result in development of psoriatic
lesion

12. Classification
• Chronic plaque psoriasis
• Guttate psoriasis
• Pustular psoriasis Chronic plaque psoriasis
Guttate psoriasis
Pustular psoriasis

13. Chronic plaque psoriasis/ Psoriasis vulgaris
• Commonest
• Mild
• Well-demarcated
• Indurated, erythematous (Pink to red plaque often surrounded by a hypopigmented halo called as Ring of
Woronoff)
• Itchy
• Loose (easily detachable), large, lamellar, silvery white scales (minimal in early lesion and absent in
flexures and on glans)
• Discoid but at the site of trauma/scratch linear or irregular
• Size and no. varies
Ring of Woronoff

14. Koebner’s or Isomorphic Phenomenon- Development of psoriatic lesion at the sites of trauma /scratch
Grattage test: Scales in a psoriatic plaque can be accentuated (noticeable) by grating with a glass slide
Au spitz Sign: Appearance of punctate bleeding spots when psoriasis scales are scraped off
• Subdivision according to lesion
 Small plaque psoriasis
 Rupoid psoriasis (heaped-up papules)
• Subdivision according to site
 Flexural psoriasis (more in elderly females, erythematous plaque with minimal scaling)
 Scalp psoriasis (well-defined, indurated, spill beyond hair margin onto forehead and nape of neck)
 Genital psoriasis
 Psoriasis of palm & soles (bilateral, adherent scales)

15. Associated symptoms
• NAILS (30-50%)
 Pitting- deep irregular
 Discoloration of nail plate (yellow-brown)
 Subungual hyperkeratosis
 Onycholysis (separation of distal nail plate from nail bed, characteristically with erythematous proximal
edge)
 Oil spots (salmon patch)
 Hyperkeratotic plaques on knuckles
• Musculoskeletal system
 10% of patients with psoriasis have arthritis
• Metabolic association increase prevalence of hypertension, DM, insulin resistance, obesity, dyslipidaemias,
CAD

16. Guttate psoriasis
• Children and adolescents
• Often precipitated by streptococcal infection
• Several small erythematous lesion with minimal scaling
• Usually present on trunk
Pustular psoriasis
• Triggers due to misused if topical irritant or steroid therapy
Diagnosis
• Exaggerate in winters
• Well-defined, erythematous, indurated, surmounted by loose silvery scales
• Usually present on pressure points, scalp, extensors
• Nail and joint involvement
• Positive grattage test and Auspitz sign

17. Differential Diagnosis
• Dermatitis
• Discoid lupus erythematous
• Pityriasis rosea
• Hand eczema
• Seborrheic dermatitis
• Onychomycosis

18. Features Dermatitis Psoriasis
Morphology of lesion Ill-defined, exudative plaque with crust Well defined, erythematous, indurated, Silvery scales
Itching Severe, oozes on scratch Variable, bleed on scratch
Nail changes Not observed Pitting
Distribution Acral parts Pressure points, scalp, extensors
Dermatitis Psoriasis

19. Features Discoid Lupus Erythematous Psoriasis
Morphology of lesion Annular plaques with scarring & depigmented in center Discoid, no scarring & depigmentation
Scales Adherent Loose
Sign + Carpet tack sign (horny plugs appears on scratch) + Auspitz sign
Distribution Face, ear, scalp Pressure points, scalp, extensors
Cause Exposure to sun No effect of sun exposure

20. Features Pityriasis rosea Psoriasis
Course Self limiting (4-12 weeks) Chronic (on & off)
Onset Large herald patch (80%) Slow progress
Morphology of lesion Annular lesions Discoid
Scales Collarette of scales Loose, silvery scale
Distribution Trunk, parallel to ribs (Christmas tree pattern) Pressure points, scalp, extensors

21. Features Hand Eczema Psoriasis
Itching Severe Variable
Spillage beyond palm Absent Present
Hyperkeratotic plaques on knuckles Absent present
Erythema Less More
Vesicles Frequently present Only if Postular
Psoriasis
Eczema

22. Features Seborrheic Dermatitis Psoriasis
Morphology of lesion Ill-defined Well defined and erythematous
Induration Minimal Present
Spillage Absent Present
Scales Greasy Silvery
Nail changes Not observed Pitting
Itching Severe Moderate

23. Features Onychomycosis Psoriatic Nail
Morphology of lesion Asymmetrical, few nails involved Symmetrical, most of the nails involved
Nail plate Thickened, tunneling Thickened and pitted
Subungual Hyperkeratosis Friable Not friable
KOH mount Positive Negative
Psoriatic Nail
Onychomycosis

24. Treatment
• Counseling
 Its not contagious
 Chronic disease with relapses and remissions
 Treating options are suppressive and not curative
• Topical agents
 Emollients (Vegetable or mineral Oil)- soften skin, hydrate skin (best used after hydration of lesions)
 Coal tar (3-6%)- anti-mitotic, anti-inflammatory (apply and expose to light)
 Dithranol (0.05%) reduces DNA synthesis
 Calcipotriol (0.005%) is antiproliferative, immunosuppressive and promotes differentiation
 Tazarotene(0.05%) is a retinoid which acts as keratolytic and keratoplastic
• Systemic agents are given only in case of severe cases
 Methotrexate 7.5-25mg/ week orally with Folic acid, 5mg after a day
 Acitretin (25-50mg) is an oral retinoid which inhibits cell growth and keratinization
 Cyclosporine 2.5-4mg/kg/day in two divided dose

25. Systemic steroids used in combination, gets instant results but sudden withdrawal causes pustular psoriasis
Topical steroids
• Indications
 Mild to moderate steroids are used incase of lesion on face and genitals
 Potent steroids are used to in case of lesion on trunk and extremities
 Very potent steroid are used to treat lesion on palm and soles
• Advantages
 Effective
 Application and removal is easy
 Non-Irritant
• Disadvantages
 Long term use causes dermal atrophy and tachyphylaxis
 Results in early relapses

26. Phototherapy
• PUVA chambers
• Sun-exposure
• RePUVA (PUVA+ Acitretin)
Biologics (used in severe cases only/ incase of no response/ Intolerance to systemic therapy/ disability
Contraindicated in TB, viral hepatitis, cirrhosis, any life threatening disease, avoid vaccination during and post
6 months therapy)
• TNF-α Inhibitors
 Infliximab 5mg/kg IV at 0 week, 2, 6, 8
 Etanercept 25mg biweekly SC for 24 weeks or 50mg biweekly for 12 weeks
 Adalimumab 80mg at 0 week, 40mg at 1 week
• IL-12/23 Inhibitors
 Ustekinumab 45-90mg SC at 0, 4,12 week (Stelara)
• IL-17 Inhibitors
 Secukinumab 300mg weekly for 4-5 weeks

27. Short synopsis of the Psoriasis
• It is a chronic T-cell mediated inflammatory disease of the skin characterize by erythematous plaques with
loose greyish scales
• Males and females are equally affected
• Cause- Idiopathic but is immune mediated
• Genetic and certain medication (Lithium, β adrenergic blockers, anti-depressants, antimalarials and sudden
withdrawal of corticosteroids) exaggerate the disease
• Pathogenesis confirms involvement of immune cells (Dendrites, T cell, NK cells etc.) and its manifestation
on skin (hyperproliferation of keratinocytes without differentiation and maturation, discoid erythematous
patches with loose silvery white scales)
• Treatment options are topical and systemic agents, photochemotherapy and Biologics

28. Assessment of Psoriasis severity
• According to PASI (Psoriasis Area And Severity Index) score
• According to Body Surface Area (BSA)
 Mild psoriasis <10% of BSA
 Moderate psoriasis 10-30% of BSA
 Severe psoriasis > 30% of BSA
Grading Induration Erythema Scales
No 0 No plaque No erythema No scaling
Minimal 1 0.25mm plaque Faint erythema 5% od lesions have scale
Mild 2 0.5mm plaque Light red Fine scales
Moderate 3 0.75mm plaque Red Course scales
Severe 4 >1mm plaque Dusky red Thick tenacious scales

30. Treatment guidelines for psoriasis
MILD MODERATE SEVERE
Psoriasis vulgaris Topical
agents
Topical agents +
Phototherapy
Topical agent + Systemic agent (no
response observed, Biologics can be
recommended)
Facial Psoriasis Topical Tacrolimus/ Pimecrolimus (Immunosuppressive 0r Immunomodulator)
Palmoplantar
Psoriasis
Topical steroid + Systemic agent
Guttate Psoriasis Antibiotics + Topical agents +/ Phototherapy
Pustular Psoriasis Topical agent + Systemic agent OR Topical steroid + Phototherapy