This document defines psoriasis as a chronic, immune-mediated inflammatory skin disease characterized by well-circumscribed erythematous scaly plaques. It disrupts the normal cycle of skin cell proliferation and differentiation, causing keratinocytes to replicate rapidly within days rather than weeks. Psoriasis has no cure, but can be managed with topical therapies like vitamin D analogs, phototherapy, or systemic drugs when widespread. Calcipotriol is a first-line topical therapy that exerts immunomodulatory and anti-proliferative effects on keratinocytes and T cells to reduce inflammation and hyperplasia.

1. 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.

2. Epidermal layers: Proliferate and Differentiate
•Basal Keratinocytes:
Proliferate
Differentiation
• Basal keratinocytes
migrate upwards to
differentiate into
•
Stratum spinosum
•
Stratum granulosum
•
stratum corneum
T cell
Normal cycle of proliferation and differentiation takes in 28-30 days

3. Disturbed Immune System
PSORIASIS
SCALES
INFLAMMATION
LOSS OF
GRANULAR LAYER
PROLIFERATION
KERATINOCYTE
Keratinocytes Replicate at
Faster Rate: 3 to 5 days

4. 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

5. INHERITANCE
 Inheritance is multifactorial
 Incidence increases in succesive generations
 Linked to MHC 1 and 2 on chromosome 6
 5% of first degree relatives are susceptible
 Chance 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.

6. TYPE 1 PSORIASIS
early onset
predominantly involve Cw6 ,DR7,B57
TYPE 2 PSORIASIS
late onset
predominantly involve Cw2
Genetic loci PSORS1 on chromosome 6 and PSORS2 on
chromosome 17q
B13 and B17 are increased in guttate and
erythodermic psoriasis
B27 in pustular psoriasis
HLA typing is of limited value in assesing an individual

7. TYPES OF PSORIASIS
PLAGUE PSORIASIS-
1.most common type
2.characterised by erythematous
plaques covered by silvery micaceous scales
GUTTATE PSORIASIS1.small drop like psoriatic papules and
plaques
2.seen in association with
streptococcal pharyngitis

8. 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

9. 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

10. 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

11.  4.can involve spine(spondylitis) mimicking
idiopathic ankylosing spondilitis
 5.severe form called “arthritis mutilans”
present as subluxation, shortening of digits
OTHER TYPES
Drug induced psoriasis
Napkin psoriasis
Seborrheic_like psoriasis
Scalp psoriasis

12. CHIEF FEATURES
1.KOEBNER PHENOMENON
2.AUSPITZ SIGN
3.RECURRENCE
4.PERSISTENCE
5.WORNOFF RING- often the first sign
that the patient is responding to
phototherapy

13. AGGRAVATING FACTORS
•
•
•
•
•
STRESS
ANXIETY
DRUGS
INFECTION
SUDDEN STOPPAGE OF SYSTEMIC
STEROIDS(REBOUND PHENOMENON)

14. Psoriasis: Pathophysiology
Langerhans
cell take up
& process
antigens to
form APC
APC
presents
the antigen
to T cells
to form
activated T
cells
Induces
inflammation &
hyper
proliferation
Activated T
cells
proliferate &
migrate to
epidermis
Activated T
cells release
cytokines like
IL -8

15. Psoriasis : Activation of cells
Act on Keratinocyte
Act on T Lymphocyte
Release inflammatory
IL-8 cytokine
Hyperproliferation
Improper
differentiation
Induces inflammation

16. DIFFERENTIAL DIAGNOSIS
•
•
•
•
•
•
•
SEBORRHEIC DERMATITIS
PITYRIASIS ROSEA
LUPUS ERYTHEMATOUS
LICHEN PLANUS
ECZEMA
PSORIASIFORM SYPHILID
DERMATOMYOSITIS

18. Psoriasis severity chart
2
2

19. 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

20. Psoriasis Severity : Treatment
Systemic
Phototherapy
UVB
PUVA
Topical
Corticosteroids
Vitamin D3 Analogs
Salicylic acid
Retinol

21. Goals of Therapy
Reduces
hyperprolifer
ation &
induces
differentiatio
n
Exerts
immuno
modulator
y action
Achieves
&
maintains
remission
Safe for long
term use

22. Vitamin D3 Analog : Acts on all stages of Psoriasis
Topical
Corticosteroids
Inhibits
Vitamin D3
Analogs
++++
++++
Nil
++++
++++
+++
Hyperproliferation
Keratinocyte
differentiation
Immunomodulatory
action
Vitamin D3 Analog : First Line choice

23. Calcipotriol: MOA
Calcipotriol
binds to VDR
Act on Keratinocyte
Act on T Lymphocyte
Vitamin D3 Analog
VDR receptor
Release Anti-inflammatory
IL-10 cytokine
Inhibits
Hyperproliferation
Induces
Differentiation
Reduces inflammation

24. Maintains remission for 12 months
•Long-term use of topical calcipotriol in chronic Plaque Psoriasis
•Dermatology 1994:189:260-264
Maintains Remission
12 month
Achieves Remission
2 month
well tolerated for 52 weeks

25. First line in combination with other anti psoriatics
In combination with UVB, PUVA therapy, Topical corticosteroids

26. Indication and Dosage
Indication
Chronic stable Plaque Psoriasis in Adults and Children
Dosage
•Applied once or twice daily on the affected area
In adults:
100gm/ week
In children over 12 years
: 75gm/ week
In children over 6 -12 years
: 50gm/ week

27. 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

28. 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

29. • 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

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

31. 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

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

33. 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

34. THANK YOU