PSORIASIS

• DEFINITION :• A GREEK WORD MEANING “ITCHY

CONDITION”{PSORA”ITCH”+SIS”CONDITION”}• IT IS A NON CONTAGIOUS, IMMUNE–

MEDIATED INFLAMMATORY SKIN DISEASE CHARACTERISED BY WELL CIRCUMSCRIBED ,ERYTHEMATOUS,DRY SCALING PLAQUES COMMONLY FOUND ON THE EXTENSOR SURFACE.

•Basal Keratinocytes: Proliferate

• Basal keratinocytes migrate upwards to differentiate into

• Stratum spinosum

• Stratum granulosum

• stratum corneum

Epidermal layers: Proliferate and Differentiate

Differentiation

Normal cycle of proliferation and differentiation takes in 28-30 days

T cell

Disturbed Immune System

Keratinocytes Replicate at Faster Rate: 3 to 5 days

PSORIASIS

LOSS OFGRANULAR LAYER

INFLAMMATION

SCALES

PROLIFERATION KERATINOCYTE

EPIDEMIOLOGY• Equal frequency in both sexes• Mean age is 27 but can occur from neonatal

period to 70• In pregnancy there may be a temporary

improvement or even disappearance of lesions however its manifestation differs from one pregnant women to another

• Lymphoma and coeliac disease is highly associated with psoriasis

INHERITANCE Inheritance is multifactorial Incidence increases in succesive generationsLinked to MHC 1 and 2 on chromosome 6 5% of first degree relatives are susceptibleChance of a sibling inheriting the disease is 16% if one

parent has psoriasis and 50% if both the parents have. If one twin has psoriasis ,the other twin is affected in

20% of dizygotic pairs and 73% in monozygotic pairs indicating that environmental factors control gene expression.

TYPE 1 PSORIASIS early onset predominantly involve Cw6 ,DR7,B57TYPE 2 PSORIASIS late onset predominantly involve Cw2Genetic loci PSORS1 on chromosome 6 and PSORS2 on chromosome 17qB13 and B17 are increased in guttate and erythodermic psoriasisB27 in pustular psoriasisHLA typing is of limited value in assesing an individual

TYPES OF PSORIASIS

PLAGUE PSORIASIS- 1.most common type 2.characterised by erythematous plaques covered by silvery micaceous scalesGUTTATE PSORIASIS- 1.small drop like psoriatic papules and plaques 2.seen in association with streptococcal pharyngitis

PUSTULAR PSORIASIS 1.appear as small sterile fluid filled blisters that contain W.B.C 2. Types are: Generalised pustular psoriasis(pustular psoriasis of von zumbusch) Pustulosis palmaris et plantaris(pustular psoriasis of barber type) Annular pustular psoriasis Acroderamatitis continua Impetigo herpetiformis

INVERSE PSORIASIS 1. genitcalymmatobacteriun granulomatisLipoid granuloma- xanthomaLipophagic granuloma-granuloma associated with loss of subcutaneous fatSarcoid granuloma-seen in sarcoidosisSwimming pool granuloma-caused by mycobacterium balnei

INVERSE PSORIASIS 1.found on flexural surface like arm pits , groins 2.devoid of scales

ERYTHODERMIC PSORIASIS 1.develops over large area of body 2.skin is red with excess shedding of scales 3.usually after the abrupt withdrawal of systemic treatment and is fatal

NAIL PSORIASIS 1.nail changes like pitting, discolouration,thickening and loosening of nail 2.oil-drop appearance seen

PSORIATIC ARTHRITIS 1.most common asymmetric monoarthritis of fingers and toes 2.result in sausage shape swelling of toes and fingers(dactylitis) 3.symmetrical polyarthritis mimics rhuematoid arthritis but devoid of RA factor

4.can involve spine(spondylitis) mimicking idiopathic ankylosing spondilitis 5.severe form called “arthritis mutilans” present as subluxation, shortening of digits

OTHER TYPESDrug induced psoriasisNapkin psoriasisSeborrheic_like psoriasisScalp psoriasis

CHIEF FEATURES

1.KOEBNER PHENOMENON2.AUSPITZ SIGN3.RECURRENCE4.PERSISTENCE5.WORNOFF RING- often the first sign that the patient is responding to phototherapy

AGGRAVATING FACTORS

• STRESS• ANXIETY • DRUGS• INFECTION• SUDDEN STOPPAGE OF SYSTEMIC

STEROIDS(REBOUND PHENOMENON)

Langerhans cell take up & process antigens to form APC

APC presents

the antigen

to T cells to

form activated

T cells

Activated T cells

proliferate & migrate

to epidermis

Psoriasis: Pathophysiology

Activated T cells release

cytokines like IL -8

Induces inflammation

& hyper proliferation

Psoriasis : Activation of cells

Hyperproliferation

Release inflammatory IL-8 cytokine

Induces inflammation

Act on Keratinocyte Act on T Lymphocyte

Improper differentiation

DIFFERENTIAL DIAGNOSIS

• SEBORRHEIC DERMATITIS• PITYRIASIS ROSEA• LUPUS ERYTHEMATOUS• LICHEN PLANUS• ECZEMA• PSORIASIFORM SYPHILID• DERMATOMYOSITIS

TREATMENT

Psoriasis severity chart

2 2

Psoriasis Area and Severity Index( PASI)

• Estimates severity and extent of psoriasis• Takes into account – Size of the area involved–Redness–Thickness– Scaling

• Mild to moderate Psoriasis: –PASI Score of < 10

Systemic

Phototherapy

UVBPUVA

TopicalCorticosteroids

Vitamin D3 AnalogsSalicylic acid

Retinol

Mild

Mod

erat

e

Seve

re

Psoriasis Severity : Treatment

Reduces hyperprolifer

ation & induces

differentiation

Exerts immuno

modulatory action

Safe for long term use

Achieves &

maintains remission

Goals of Therapy

Vitamin D3 Analog : Acts on all stages of Psoriasis

Topical Corticosteroids

Vitamin D3 Analogs

Inhibits Hyperproliferation

++++ ++++

Keratinocyte differentiation

Nil ++++

Immunomodulatory action

++++ +++

Vitamin D3 Analog : First Line choice

Calcipotriol: MOA

InhibitsHyperproliferation

Induces Differentiation

Release Anti-inflammatory IL-10 cytokine

Reduces inflammation

Calcipotriol binds to VDR

Vitamin D3 Analog

VDR receptor

Act on Keratinocyte Act on T Lymphocyte

•Long-term use of topical calcipotriol in chronic Plaque Psoriasis•Dermatology 1994:189:260-264

Maintains remission for 12 months

well tolerated for 52 weeks

Achieves Remission 2 month

Maintains Remission 12 month

First line in combination with other anti psoriatics

In combination with UVB, PUVA therapy, Topical corticosteroids

Indication and Dosage

In adults: 100gm/ week

In children over 12 years: 75gm/ week

•Applied once or twice daily on the affected area

In children over 6 -12 years: 50gm/ week

Dosage

Indication

Chronic stable Plaque Psoriasis in Adults and Children

Advantages of CALCIPOTRIOL

Only Topical agent • Checks hyperproliferation• Induces differentiation• Exerts immunomodulatory action

Can be used in combination

with potent TCS

Effective in combination with UVB &

PUVA

Well tolerated and safe in adults and

children

Main stay • Clearance

• Transition

• Maintenance

OTHER TOPICAL MODALITIES

• TARS• TAZAROTENE

retinoic acid receptor specific retinoid modulates keratinocyte proliferation and

reduces inflammation• MACROLACTAMS Topical tacrolimus and pimecrolimus Helpful for thin lesion in areas prone to

atrophy or steroid acne

• SALICYLIC ACID keratolytic agent widespread use leads to salicylate toxicity•ULTRAVIOLET LIGHT narrow band UVB more effective response rate is close to PUVA therapy•GOECKERMANN TECHNIQUE•INGRAM TECHNIQUE•PUVA THERAPY UVA radiation given 2 hr after 8-methoxypsoralen most clear by 20-25 treatments but maintenance treatment is needed polyethylene sheet bath is another alternative to oral psoralen

• Risk of cataract, melanoma and squamous cell carcinoma of skin and genitalia• SURGICAL TREATMENT• tonsillectomy for streptococcci pharyngitis• HYPERTHERMIA• OCCLUSIVE TREATMENT

SYSTEMIC TREATMENT

• CORTICOSTEROID generally avoided due to rebound reaction given in impetigo herpetiformis• METHOTREXATE psoriatic arthritis psoriatic erythroderma acute pustular psoriasis widespread body surface involvement

•CYCLOSPORIN•DIET fish oil rich in polyunsaturated fatty acids•ANTIMICROBIAL THERAPY for infection with streptococcal pharyngitis•RETINOIDS•BIOLOGIC AGENTS infliximab adalimumab etanercept ustekinumab

COMBINATION THERAPY

• Combination of PUVA and retinoids is called RE-PUVA

• Combination therapy has the potential to reduce the overall toxicity if the toxicities of each agent is different

• Methotrexate is combined with infliximab to reduce the incidence of neutralising antibodies

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