PSORIASIS

 A common chronic , inflammatory &

proliferation condition of the skin
- Polygenic predisposition
- Erythrosquamous lesions
sharply demarcated silvery scaly lesion- most
common form of psoriasis
- Distributed over knee , elbow, scalp ,gluteal &
genital area
Incidence
- Universal in occurrence
- In US, ~ 2 % of the population, 150000 new
cases/year
- Age
-Onset any age
-most 10 - 30 year old
 Sex
 M=F
- Strong genetic basis
- Alteration in
. epidermal growth & differentiation
. immunological
. vascular
Genetic predisposition
 Family history
-common among first & second degree relatives
-35-73% concordance MZ twins
 HLA association
Trigger factors :
 Infections
-streptococcal( group A  Haemolytic)
-onset or exacerbation
-after 1-2 wks of acute strep infection
-Acute guttate or guttate flare up
-HIV
-HIV patients often develop aggressive psoriasis
 Physical trauma
- scratching (koebner’s reaction)
-incidence of lesions in 40% of pts
-all-or none

 Drugs - lithium, beta blockers, antimalarias

 Stress neuropeptides / Hormonal
 Smoking
- ≥15 cigarettes /day
-has more association with palmoplantar
pustular psoriasis
 Alcohol
 Obesity
 Ultraviolet radiation
-summer exacerbation in exposed
areas
Epidermal proliferation
Vascular changes
Immunology and inflammation
 History
 age at onset and Family Hx
 younger age of onset and (+)Family Hx.
 more widespread and recurrent disease
 prior course of the disease-“acute” and
“chronic”
 persist unchanged for months or even years
 sudden outbreak of lesions within a short time (days).
• Relapses Hx
– frequent relapses (wkly/ mthly) Vs. stable
(occasional recurrence)
• frequently relapsing ->
– more severe ,rapidly enlarging ,significant portions
of the body surface
– more rigorous treatment
• Hx. of medication
– Certain medications may worsen psoriasis
• Hx. of Joint complaints
– osteoarthritis-> common and can coexist with
psoriasis
– onset of joint symptoms < 4th decade
– warm, swollen joints
 psoriatic arthritis
 Cutaneous Lesions
 Classic lesion:
 Well demarcated, raised, red plaque with a white
scale -skin has a glossy homogeneous erythema, and
bleeding points by rubbing ( Auspitz sign)
 Size: pinpoint papules to plaques
 Symmetric eruption[Unilateral, can occur]
 Koebner phenomenon ( isomorphic response) :
 Traumatic induction of psoriasis on nonlesional skin
 More frequently during flares
 The Koebner reaction:
 7 to 14 days after injury, and
 ≈ 25 % of patients
 lifetime prevalence rise as high as 76%
 infection, emotional stress, and drug reactions
 not specific for psoriasis but helpful in making
the diagnosis
PSORIASIS VULGARIS, CHRONIC STATIONARY
PSORIASIS, PLAQUE-TYPE PSORIASIS
– most common; ≈ 90 %
– Red, scaly, symmetrically distributed plaques
– extensor aspects of the extremities
(elbows/knees), along with scalp, lower
lumbosacral, buttocks, and genitalia
• umbilicus and the intergluteal cleft
– Constant production of large amounts of scale
– Single small lesions confluent = psoriasis
geographica (land map)
– Confluence of several plaques = psoriasis gyrata
– partial central clearing = annular psoriasis
(ringlike)
• Associated with lesional clearing and good prognosis
 Small (0.5 to 1.5 cm ) papules [upper trunk &
proximal ext.
 Early age onset - young adults
 Strongest ass. to
 HLA-Cw6
 Strept. throat infection [precedes/concomitant]
 Abc Rx. :- not beneficial to shorten the disease course
 Resembles guttate psoriasis clinically
 Onset in older patients ;Chronic
 Larger lesions (1 to 2 cm); thicker and scalier
 Common adult-onset presentation of psoriasis in
Korea and other Asian countries
 Localized in the major skin folds
 axillae, the genito-crural region, and the neck
 Scale:minimal or absent
 Lesions: glossy sharply demarcated erythema
 localized to areas of skin-to-skin contact
 Sweating is impaired in affected areas
• Generalized form (all body sites)
– face, hands, feet, nails, trunk, and
extremities
– erythema is the most prominent feature
– superficial scaling Vs. thick, adherent,
white scale
– Hypothermia - generalized vasodilatation
– Hypohidrotic - occlusion of the sweat ducts
• risk of hyperthermia in warm climates
– Lower extremity edema: vasodilatation and
loss of protein
– High output cardiac failure and impaired
hepatic and renal function
• Several clinical variants:
– Generalized :
• generalized pustular psoriasis (von Zumbusch )
• exanthematic Pustular Psoriasis
• annular pustular psoriasis
• impetigo herpetiformis
– Localized :
• Pustulosis palmaris et plantaris
• Acrodermatitis continua [H]
 Acute ; 3rd tri; Erythematous patchs, margins studded in sub
corneal pustules
 Flexural areas spreads centrifugally
 Subungual lesion-onycholysis
 Mucous membrane: rarely painful erosions
 Face , palms, & soles : speared
• May be Pruritic/painful
• Onset may be ass. with constitutional
symptom
– Fever ,chills , malaise , diarrhea, nausea &
arthralgia
• No family Hx.; abrupt resolution of sxs after
delivery & tendency to recur only in
subsequent pregnancy
• Absence of triggering factors
– Infection , drugs , discontinuation of steroid
 Ischronic pustular dermatosis
 Palms &soles
 Treatment resistant; high recurrence rate
 Histology - intraepidermal vesicles filled with
neutrophils
 F>M ; 20-60yrs
• Pustules (2-4mm), arise within few hrs
• Palms & sole, symmetrical
• Surrounded by erythematous ring
• Extends to dorsa of fingers, feet or volar
aspect of wrists
• Yellow to dark brown
• Itching & burning sensation
– Sever eruptions- pain & inability to walk, stand
• Remission:-
– Erythematus, hyperkeratotic skin confusing with
eczema
– Lasts days, wks or months
• Begins at tips of 1/2 fingers(less often toes)
• Trauma plays triggering factor
• 1st sign:-
– Pustules with erythematus, shiny area
– Coalesce to form polycyclic lakes of pus
• Pustulation of nail bed & matrix
• Sever onychodytrophy ; anonychia
• Skin:
– Shiny , severely atrophic [distal phalanx]
• Spreads proximally (hand, dorsum of forearm/foot)
– Or confined to original site
• Common clinical entity ; Erythematous plaques
+ greasy scales
• Localized to seborrheic areas(not beyond
border)
• Distinction from SD is difficult
– In the absence of typical findings of psoriasis
elsewhere,
• May represent a modification of SD/genetic
background of psoriasis
• Relatively resistant to treatment
• Etiologic role of Pityrosporum remains
unproven
– But antifungal agents may be useful
• NAIL CHANGES IN PSORIASIS
– Frequently seen (up to 40 %)
– rare in the absence of skin disease elsewhere.
– Nail involvement increases with
• Age , duration and extent , presence of psoriatic
arthritis.
– Nail pitting:
• One of the commonest, involving the fingers > the
toes
• Pits range from 0.5 to 2.0 mm in size and can be
single or multiple.
• Pitting is due to defective keratinization.
• Also seen in alopecia areata and other disorders
– Other alterations
• Onychodystrophy , leukonychia, and oil spots
 Idiopathic inflammatory disorder; local loss
of filiform papillae
 Asymptomatic erythematous patches +
serpiginous borders (map)
 Common condition and is seen in many non-
psoriatic individuals
 Arthritis
is a common extra-cutaneous
manifestation of psoriasis
 up to 40 % of patients
 It has a strong genetic component
Severity of psoriasis:

Mild psoriasis
- ‹10% BSA
Moderate psoriasis
- >10% BSA
Severe psoriasis
- > 30% BSA
• Histopathologic examination: helpful in
difficult cases.
• Guttate and chronic plaque psoriasis:
– Initial Lesion
• Upper dermis: marked edema, and mononuclear cell
infiltrates
• Epidermis : spongiotic + focal loss of the granular
layer
– Developing Lesion
• ≈ 50 % increase in epidermal thickening
• large increase in the metabolic activity of epidermal
– DNA synthesis, mast cells + degranulation and dermal
macrophages
• ↑ numbers of dermal T cells and DCs
• Rete ridges begin to develop in the marginal zone
• Mature Lesion:
• uniform elongation of rete ridges + thinning of the
epidermis
• Parakeratosis, loss of the granular layer, may
alternate with orthokeratosis
• lymphocytes are observed in the epidermis
• Spongiosis more uniform than of eczematous skin
lesions
• Pustular psoriasis:
• epidermis: slightly acanthotic (In early lesions)
• psoriasiform hyperplasia (in older and persistent
lesions)
• Neutrophils
– SC = Munro’s microabscesses
– Spinous layer = spongiform pustules of Kogoj
• Increased morbidity from cardiovascular
events:
– severe and long duration
– Risk of MI= ↑in younger patients with severe
psoriasis
• Increased relative risk of lymphoma [severe
disease]
• Emotionally disabling with significant
psychosocial difficulties
• Psychological aspects can modify the course of
illness;
 Feeling stigmatized:
 treatment noncompliance and worsening of
psoriasis
 Psychological stress:-depression and anxiety
 suicidal ideation and depression > other medical
conditions & general pop.
 Significantly impair quality of life.
 recent survey:79 % (severe psoriasis) reported a
negative impact on their lives
- Corticosteroids
.mild to moderate psoriasis
.flexural and genital areas
.high potency
.daily bases for 2 – 4 weeks
- Vitamine D3 analogues
.bind VD receptor & regulate cell growth,
differentiation,immune function
.inhibit cytokine production(IL-2,IFN-ᵧ )
.Calcipotriene,tacalcitol,maxacalcitol
.combined with steroids
- Anthralin
.Dithranol(1,8-dihydroxy-9-anthrone)
.for resistant plaque p
.can be combined with UVB(Ingram-
regimen)
.decreases keratinocyte & T-cell
proliferation
.stains clothes,may have irritant effect
.0.05 – 0.1%,use with petrolium or zinc
paste,
or SA
- Coal tar
.suppress DNA-synthesis,anti inflammatory
.good effect when combined with SA(2-5%)
.combined with UVB(Geockerman-regimen)
- Tazarotene
.inhibits epidermal cell proliferation &
differentiation- binding RAR.
.reduces scaling & plaque thickness
.combine with steroids, UVB
- Calcinuerin inhibitors
.binds immunophilin, then inhibit calcineurin
(blocks T-lymphocyte signal transduction &
IL-2 transcription)
.inverse and facial psoriasis
.Tacrolimus, Pimecrolimus

- Bland Emollients
- Intralesional corticosteroids
-Induce epidermal T-cell apoptosis
-Shift from Th1 to Th2-cell response

 UVB
-290 – 320 nm, NBUVB(312-13) is better
-moderate to severe plaque p
-3-5 times per week, start with 50-75%of
MED
-combination has better out come
 PUVA
-is best, methoxsalen(8-methoxypsoralen)
+
UVA(320-400nm)
-for more extensive disease
 Excimer laser
-supra-erythemogenic fluences of UVB & A
-deliver high dose light to limited plaques
-for stable recalcitrant plaques
 MTX
-inhibits keratinocyte & lymphocyte prolife
-by inhibition of DHFR and purine metabolism
-used for severe p, nail p, resistant ones
-has BM suppression, hepatorenal toxicity,
teratogenicity
-2.5 – 5.0mg test dose, then 15- 25mg per wk
-leucovorin calcium is antidote
 Cyclosporine =CsA
-inhibits T-cell activation & IL-2 translocation
-from fungus-Tolypocladium inflatum gams
-2 – 5mg/kg/day-(solutions, capsules)
-for plaque p, nail p & is pregn category B
-nephrotoxicity, HTN, neurologic effect, SCC
-phenytoin compete for plasma protein
binding
 Acitretin
-second generation retinoid
-initial dose: 0.25mg/kg/day-erythrodermic p
1.0mg/kg/day-pustular p
-cheilitis, teratogenicity, paronychia, hair loss
-combine with phototherapy,VD3
 Fumeric acid easters
-shift Th1 to Th2 response
-Three types-1-recombinant human cytokines
2-fusion proteins
3-monoclonal antibodies
-For severe psoriasis, unresponsive to MTX
 Patient education
-chronicity of the illness
-long-term therapy, side effect
-what to avoid