Psoriasis- Definition,Epidemiology,Clinicalfeatures,Deferential diagnosis and management .

1. PSORIASIS
Diagnosis and management
Dr.Md. Shshidul Islam
Assistant professor
Dermatology & VD, CBMC’B

2. OVERVIEW
5. Case studies
2
4. Managing psoriasis
3. Diagnosing psoriasis
2. Clinical presentation
1. Epidemiology and pathophysiology

3. WHAT IS PSORIASIS?
– Inflammatory and hyperplastic
disease of skin
– Characterised by erythema and
elevated scaly plaques
– Chronic, relapsing condition
– Course of disease often
unpredictable
.
3

4. SYMPTOMS OF PSORIASIS
Adapted from Krueger G et al. Arch Dermatol 2001; 137: 280–4.
4
Most frequently
experienced symptoms

5. SOCIAL IMPACT OF PSORIASIS
40
48
57
0 10 20 30 40 50 60
Percentageofrespondents with severe psoriasis (n = 502)
Adapted from Krueger G et al. Arch Dermatol 2001; 137: 280–4.
5
Psoriasis mistaken for other
disease
Trouble receiving equal
treatment in service
establishments (e.g. hair
salons,
public pools)
Psoriasis mistaken
as contagious

6. PSORIASIS AFFECTS EMOTIONAL STATE 6

7. EPIDEMIOLOGY
• Common skin disorder
• Prevalence variable: ~ 0.3–2.5%
• Prevalence equal in males and females
• Estimated incidence: ~ 60 per 100,000 per year
7

8. AGE OF ONSET
• Mean age: ~ 23–37 years
• Current theory:
2 distinct peaks with possible genetic associations
– Early onset (16–22 years)
• More severe and extensive
• More likely to have affected first-degree family member
– Late onset (57–60 years)
• Milder form
• Affected first-degree family members nearly absent
8

9. GENETIC INFLUENCE
• Evidence suggests strong genetic association
– Studies of monozygotic twins show concordance
for psoriasis (e.g. 64% in a Danish Study)
– Multiple susceptibility loci have been identified
• Disease expression
– likely result of genetic and environmental factors
9

10. COMMON TRIGGER FACTORS FOR PSORIASIS
• Infections (e.g. streptococcal, viral)
• Skin trauma (Koebner phenomenon)
• Psychological stress
• Drugs (e.g. lithium, beta blockers)
• Sunburn
• Metabolic factors (e.g. calcium deficiency)
• Hormonal factors (e.g. pregnancy)
10

11. PSORIASIS IS A T-CELL MEDIATED,
AUTOIMMUNE DISEASE1
Current hypothesis:
– Unknown skin antigens stimulate immune response
• Antigen-specific memory T-cells are primary mediators
• Leads to impaired differentiation and
hyperproliferation of keratinocytes
11

12. CLINICAL PRESENTATION:
CLASSIC PSORIASIS
– Well-defined and
sharply demarcated
– Round/oval-shaped
lesions
– Usually
symmetrical
– Erythematous,
raised plaques
– Covered by white,
silvery scales
12

13. COMMON SITES
AFFECTED BY PSORIASIS
• Can affect any part
of the body –
typically scalp,
elbow, knees and
sacrum
• Extent of disease
varies
1
13

14. TYPES OF PSORIASIS
• Chronic plaque
• Guttate
• Flexural
• Erythrodermic
• Pustular
– Localised and generalised
• Local forms
– Palmoplantar
– Scalp
– Nail (psoriatic
onychodystrophy)
14

15. CHRONIC PLAQUE PSORIASIS
– Most common type – affects
approximately 85%
– Features pink, well-defined
plaques with silvery scale
– Lesions may be single or
numerous
– Plaques may involve large
areas of skin
– Classically affects elbows,
knees, buttocks and scalp
15

16. CHRONIC PLAQUE PSORIASIS 16

17. CHRONIC PLAQUE PSORIASIS 17

18. CHRONIC PLAQUE PSORIASIS 18

19. CHRONIC PLAQUE PSORIASIS 19

20. GUTTATE PSORIASIS
– Numerous and small lesions
– ~ 1 cm diameter
– Pink with less scale than
plaque psoriasis
– Commonly found on trunk
and proximal limbs
– Typically seen in individuals
< 30 years
– Often preceded by an upper
respiratory tract
streptococcal infection
1.
20

21. FLEXURAL PSORIASIS
– Lesions in skin folds
articularly groin,
gluteal cleft, axillae and
submammary regions
– Often minimal or
absent scaling
– May cause diagnostic
difficulty when genital
or perianal region is
affected in isolation
1
21

22. ERYTHRODERMIC PSORIASIS
– Generalised erythema
covering entire skin surface
– May evolve slowly from
chronic plaque psoriasis or
appear as eruptive
phenomenon
– Patients may become febrile,
hypo/hyperthermic and
dehydrated
– Complications include cardiac
failure, infections,
malabsorption and anaemia
– Relatively uncommon
22

23. PUSTULAR PSORIASIS
– Two forms:
• Localised form
• More common
• Presents as deep-seated
lesions with multiple small
pustules on palms and soles
• Generalised form
• Uncommo Associated with
fever and widespread
pustules across the body
• inflamed body surface
23

24. PALMOPLANTAR PSORIASIS
– Can be hyperkeratotic
or pustular
– May mimic dermatitis –
look for psoriatic
manifestations
elsewhere to aid
diagnosis
– Possibly aggravated by
trauma
24

25. SCALP PSORIASIS
– Varies from minor
scaling with erythema
to thick hyperkeratotic
plaques
– May extend beyond
hairline
– Patient scratching may
produce asymmetric
plaques
25

26. NAIL PSORIASIS
– May be present in patients with
any type of psoriasis
– Can take several forms:
• Pitting: discrete, well-
circumscribed depressions on
nail surface
• Subungual hyperkeratosis:
silvery white crusting under
free edge of nail with some
thickening of nail plate
• Onycholysis: nail separates
from nail bed at free edge
• ‘Oil-drop sign’: pink/red colour
change on nail surface
26

27. NAIL PSORIASIS 27

28. NAIL PSORIASIS 28

29. NAIL PSORIASIS 29

30. PSORIATIC ARTHRITIS
– Approximately 5–20%
have associated arthritis
– Five major patterns of
psoriatic arthritis:
• Distal interphalangeal
involvement
• Symmetrical polyarthritis
• Psoriatic spondylarthropathy
• Arthritis mutilans
• Oligoarticular, asymmetrical
arthritis
– Clinical expressions often
overlap
30

31. DIAGNOSING PSORIASIS
• Other dermatological disorders
can resemble psoriasis
• Diagnosed clinically according to appearance,
distribution, history of lesions and family history
• Important to consider non-cutaneous complications
31

32. DIFFERENTIAL DIAGNOSIS
• Localised patches/plaques
– Tinea
– Eczema
– Superficial basal cell
carcinoma and Bowen’s
disease
– Seborrhoeic dermatitis
– Cutaneous T-cell lymphoma
(mycosis fungoides)
• Guttate
– Pityriasis rosea
– Drug eruption
– Secondary syphilis
• Flexural
– Tinea
– Eczema
– Candidiasis
– Seborrhoeic dermatitis
• Erythrodermic
– Eczema
– Cutaneous T-cell lymphoma
– Pityriasis rubra pilaris
– Lichen planus
– Drug
• Palmoplantar
– Tinea
32

33. LOCALISED PATCHES/PLAQUES
Tinea corporis
• Affects body
• Lacks
symmetrical
lesions
• Presence of
peripheral scale
and central
clearing
.
33
Tinea coporis Psoriasis

34. LOCALISED PATCHES/PLAQUES
– Discoid eczema
• Individualised patches
more pruritic than
psoriasis
• Lack silvery scale
• Less vivid colour than
psoriasis
1.
34
Discoid eczema Psoriasis

35. LOCALISED PATCHES/PLAQUES
– Superficial basal
cellcarcinoma/Bowen’
s disease
• Asymmetrical lesions,
either single or few in
number
• Perform biopsy if
lesions resistant to
topical psoriasis
treatment, or to confirm
diagnosis
35
Bowen’s disease Psoriasis

36. LOCALISED PATCHES/PLAQUES
– Seborrhoeic dermatitis
• Characterised by yellowish
scaling and erythema
– Localised to many of the
same areas as psoriasis
• Diffuse scaling differs from
sharply defined psoriasis
plaques
• Affects furrows of face
(facial psoriasis is generally
restricted to hairline)
36
Dermatitis
Psoriasis

37. LOCALISED PATCHES/PLAQUES
– Cutaneous T-cell lymphoma
(mycosis fungoides)
• Red, discoid lesions
• Asymmetrical and less scaly than
psoriasis
• Lesions may present with fine
atrophy and be resistant to
antipsoriatic therapy
• Biopsy to confirm diagnosis
37
Mycosis fungoides
Psoriasis

38. GUTTATE PSORIASIS
– Pityriasis rosea
• Difficult to distinguish from acute
guttate psoriasis
• Presents first as single large patch,
progresses to a truncal rash of
multiple red scaly plaques
(‘Christmas tree’ distribution)
• Resolves over 8–12 weeks
1
38
< Psoriasis ^ Pityriasis rosea

39. GUTTATE PSORIASIS
– Secondary syphilis
• Search for characteristic primary
syphilitic lesion, lymphadenopathy,
and lesions of face, palm and soles
• Conduct serology and skin biopsies
to confirm
1
39
< Psoriasis ^ Secondary syphilis

40. FLEXURAL PSORIASIS
– Tinea cruris
• Affects groin area
• Characterised by central clearing
with advancing edge
• Non-silvery lesion with fine
scale, particularly at periphery
• Lesion frequently extends more
on left side
1
40
< Psoriasis ^ Tinea cruris

41. FLEXURAL PSORIASIS
– Atopic eczema
• Often associated with asthma
and hay fever
• Lacks classic psoriatic nail
involvement and sharply
demarcated scaly plaques
1.
41
< Psoriasis ^ Atopic eczema

42. FLEXURAL PSORIASIS
– Candidiasis
• Characteristic
peripheral pustules and
scaling differ to
psoriasis
• Yeast cultures are
diagnostic
– Seborrhoeic dermatits
1
42
Flexural psoriasis

43. PALMOPLANTAR PSORIASIS
– Tinea manum
• Ringworm of hands
• Fine powdery scale,
particularly involving
palms and palmar
creases
• Usually asymmetrical
1.
43
Tinea corporis Psoriasis

44. PALMOPLANTAR PSORIASIS
– Hand and foot eczema
• Hyperkeratotic forms
difficult to distinguish
from psoriasis
• Biopsies can assist
diagnosis
• Look for history of
atopy, a lack of psoriasis
elsewhere on body, and
evidence of eczema
elsewhere on skin
44
Eczema
Psoriasis

45. PALMOPLANTAR PSORIASIS
– Pompholyx of palms
and soles (dishydrotic
eczema)
• Presents as clear vesicles
– contrast to
white/yellow pustules in
pustular psoriasis
• Accompanied by intense
pruritus
45
Eczema
Psoriasis

46. DETERMINING PSORIASIS SEVERITY
• Psoriasis Area and Severity Index (PASI)
– Score indicates severity of disease at a given time
– Single number that considers severity of lesions and
extent of disease across four major body sites (head,
trunk, upper limbs and lower limbs)
– Score ranges from 0 (no disease) to 72 (maximal
disease)
46

47. MANAGING PSORIASIS
• Before starting treatment
– Establish relationship of trust with patient
– Provide patient with information
• Emphasise benign nature of disease
• Explain that psoriasis tends to be chronic and
recurrent
47

48. MANAGING PSORIASIS
• Determine clinical setting before
selecting treatment, considering
– Disease pattern, severity and extent
– Sites of disease
– Coexistent medical conditions
– Patient’s perception of disease severity
– Time commitments and treatment expense
– Previous treatments for psoriasis
48

49. MANAGING PSORIASIS
• Goals of management
– Tailor management to individual and address both
medical and psychological aspects
– Improve quality of life
– Achieve long-term remission and disease control
– Minimise drug toxicity
– Evaluate and monitor efficacy and suitability of
individual treatments
– Remain flexible and respond to changing needs
49

50. TREATMENT OPTIONS FOR PSORIASIS
• Stepwise approach is advised
• Treatments include:
– General measures and topical therapy
– Phototherapy
– Systemic and biological therapies
• Combination therapies : may
reduce toxicity and improve outcomes
50

51. TREATING PSORIASIS:
GENERAL MEASURES
• Reduce/eliminate potential trigger
factors:
– Stress
– Smoking
– Alcohol
– Trauma
– Drugs
– Infections
1
51

52. TOPICAL THERAPIES
• Approximately 70% of patients with
mild-to-moderate psoriasis can be managed
with topical therapies alone
• Tailor to needs of patient
• Potency, delivery vehicle and patient
motivation may affect compliance
• Application may be time-consuming for patients
52

53. TOPICAL THERAPIES:
EMOLLIENTS
• Include aqueous cream, sorbolene cream, white soft
paraffin and wool fats
• Regular use can:
– alleviate pruritus
– reduce scale
– enhance penetration of concomitant topical therapy
– hydrate dry and cracked skin
• Soap should be avoided
.
53

54. TOPICAL THERAPIES:
KERATOLYTICS
• Over-the-counter products include:
– Salicylic acid
– Urea
• Help dissolve keratin to soften
and lift psoriasis scales
• May enhance penetration of other actives
1
54

55. TOPICAL THERAPIES:
COAL TAR
• Help reduce inflammation and pruritus
• May induce longer remissions
• Use limited by distinctive smell
and ability to stain clothing and skin
• May cause local skin irritation
55

56. TOPICAL THERAPIES:
DITHRANOL
• Anti-proliferative properties
• Particularly effective in thick plaque psoriasis
• Initiate therapy at very low concentrations
– can burn skin
• Not suitable for face, flexures or genitals
• Stains clothes permanently
and skin temporarily
56

57. TOPICAL THERAPIES:
TAZAROTENE
• Topical synthetic retinoid
• For treatment of chronic plaque psoriasis
• Applied once daily in evening
• Commonly causes local irritation
1
57

58. TOPICAL THERAPIES:
CORTICOSTEROIDS
• Possess anti-inflammatory, antiproliferative and
immunomodulatory properties
• Reduce superficial inflammation within plaques
• Potency choice depends on disease severity,
location and patient preference
1
58

59. TOPICAL THERAPIES:
CORTICOSTEROIDS
• Adverse effects associated
with long-term use include:
– Skin atrophy and telangiectasia
– Hypopigmentation
– Striae
– Rapid relapse or rebound on stopping therapy
– Precipitation of pustular psoriasis
– Pituitary-adrenal axis suppression through significant systemic
absorption (rare)
59

60. TOPICAL THERAPIES:
CALCIPOTRIOL (DAIVONEX®
)
• Synthetic vitamin D analogue
• For chronic plaque-type psoriasis
• Reverses abnormal keratinocyte changes by:
– Inducing differentiation
– Suppressing proliferation of keratinocytes
60

61. TOPICAL THERAPIES:
CALCIPOTRIOL (DAIVONEX®
)
• Response may require 4–6 weeks
• Adverse effects include erythema and irritation
61

62. TOPICAL THERAPIES: CALCIPOTRIOL/BETAMETHASONE
DIPROPIONATE OINTMENT (DAIVOBET®
)
• For plaque-type psoriasis
• Combination of calcipotriol and a potent topical
corticosteroid (betamethasone dipropionate)
– Stable formulation for both actives
• Provides rapid, effective psoriasis control
62

63. TOPICAL THERAPIES: CALCIPOTRIOL/BETAMETHASONE
DIPROPIONATE OINTMENT (DAIVOBET®
)
– Combination of calcipotriol and betamethasone dipropionate in
Daivobet is more effective than either active constituent used alone
• 39.2% mean reduction in PASI score after 1 week
.
63

64. TOPICAL THERAPIES: CALCIPOTRIOL/BETAMETHASONE
DIPROPIONATE OINTMENT (DAIVOBET®
)
• Once-daily treatment with the
potential to improve compliance
• Can be used intermittently in 4-weekly cycles with
Daivonex®
used in between for maintenance
• Most common adverse events include pruritus, rash and
burning sensation
1
64

65. TOPICAL THERAPIES: CALCIPOTRIOL/BETAMETHASONE
DIPROPIONATE GEL
• Newly TGA approved product not yet available in
Australia
• Specially formulated for the scalp
• Provides rapid, effective control of scalp psoriasis
– More effective than treatment with individual actives alone
– 53.2% (more than half) of patients had absent or
very mild disease after just two weeks of gel application
• Once-daily formulation may
encourage compliance
65

66. OTHER THERAPIES
• Phototherapy
• Systemic therapies
• Biological agents
66

67. PHOTOTHERAPY
• For psoriasis resistant to topical therapy and covering >
10% of body surface area
• Immunomodulatory and anti-inflammatory effects
• Three main types of phototherapy:
– Broadband UVB
– Narrowband UVB
– PUVA (administration of psoralen before UVA exposure)
• Treatment usually administered 2–3 times/week
1
67

68. SYSTEMIC THERAPIES
• Reserved for patients with widespread
or severe psoriasis
• Potentially serious adverse effects
and drug interactions
• Many require PBS authority
prescription from dermatologist
68

69. SYSTEMIC THERAPIES:
METHOTREXATE
• Most commonly used systemic
treatment for psoriasis
• Slows epidermal cell proliferation
and acts as immunosuppressant
• Closely monitor kidney, liver and
bone-marrow function
• Perform PASI score before starting treatment
69

70. SYSTEMIC THERAPIES:
CYCLOSPORIN
• Immunosuppressive agent
• For patients with severe psoriasis
that is refractory to other treatments
• Requires ongoing monitoring of
blood elements, and renal and liver function
1
70

71. SYSTEMIC THERAPIES:
ACITRETIN
• Oral retinoid
• For treatment of all forms of severe psoriasis
• Once-daily oral therapy
• Teratogenic – pregnancy must be avoided
71

72. BIOLOGICAL AGENTS
• Proteins derived from living organisms that
exert pharmacological actions
• For adults with moderate-to-severe chronic
plaque-type psoriasis who are candidates for
phototherapy or systemic therapy
• Most administered sub-cutaneously
72

73. BIOLOGICAL AGENTS
• Target key parts of immune system
that drive psoriasis
• Biological agents include:
– Tumour necrosis factor-alpha inhibitors
• Etanercept
• Adalimumab
• Infliximab
– Interleukin (IL-12 and IL-32) inhibitor
• Ustekinumab
73

74. CASE STUDY 1
• ((insert image of condition))
• ((insert information under headings below))
• Presentation
• Clinical examination
• Diagnosis
• Management
• ((Diagnosis and management can appear on following
screen as ‘builds’ after audience discussion, if
preferred))
74

75. CASE STUDY 2
• ((insert image of presenting condition))
• ((insert information under headings below))
• Presentation
• Clinical examination
• Diagnosis
• Management
• ((Diagnosis and management can appear on following
screen as ‘builds’ after audience discussion, if
preferred))
75

76. DIAGNOSIS AND MANAGEMENT OF
PSORIASIS: SUMMARY
• Chronic, inflammatory disease of skin
• T-cell mediated disorder
• Classic presentation characterised by red, scaly
plaques
• Management should address both medical and
psychological aspects
• Treatments include topical therapy, phototherapy,
systemic therapy and biological agents
76

77. THANK
YOU
ALL
77