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Psoriasis-The best Presentation
The document discusses psoriasis, including its epidemiology, pathophysiology, clinical presentations, diagnosis, differential diagnosis, and management. Psoriasis is a chronic, inflammatory skin condition characterized by red scaly plaques. It has a genetic component and can be triggered by various environmental factors. Clinical diagnosis is usually based on appearance of lesions. Topical therapies are first-line treatment for mild-moderate disease, while phototherapy and systemic therapies may be used for more severe cases. Proper management requires a tailored approach based on individual disease characteristics and goals of improving quality of life and long-term disease control.
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Psoriasis-The best Presentation
- 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 Adaptedfrom Krueger G et al. Arch Dermatol 2001; 137: 280–4. 4 Most frequently experienced symptoms
- 5. SOCIAL IMPACT OFPSORIASIS 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 EMOTIONALSTATE 6
- 7. EPIDEMIOLOGY • Common skindisorder • 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 • Evidencesuggests 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 FACTORSFOR 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 AT-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 BYPSORIASIS • 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
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- 20. GUTTATE PSORIASIS – Numerousand 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 – Lesionsin 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 – Generalisederythema 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 – Twoforms: • 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 – Canbe hyperkeratotic or pustular – May mimic dermatitis – look for psoriatic manifestations elsewhere to aid diagnosis – Possibly aggravated by trauma 24
- 25. SCALP PSORIASIS – Variesfrom minor scaling with erythema to thick hyperkeratotic plaques – May extend beyond hairline – Patient scratching may produce asymmetric plaques 25
- 26. NAIL PSORIASIS – Maybe 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
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- 30. PSORIATIC ARTHRITIS – Approximately5–20% 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 • Otherdermatological 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 • Localisedpatches/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 – Discoideczema • Individualised patches more pruritic than psoriasis • Lack silvery scale • Less vivid colour than psoriasis 1. 34 Discoid eczema Psoriasis
- 35. LOCALISED PATCHES/PLAQUES – Superficialbasal 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 – Seborrhoeicdermatitis • 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 – CutaneousT-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 – Pityriasisrosea • 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 – Secondarysyphilis • 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 – Tineacruris • 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 – Atopiceczema • 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 – Tineamanum • Ringworm of hands • Fine powdery scale, particularly involving palms and palmar creases • Usually asymmetrical 1. 43 Tinea corporis Psoriasis
- 44. PALMOPLANTAR PSORIASIS – Handand 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 – Pompholyxof 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 • Beforestarting 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 • Determineclinical 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 • Goalsof 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 FORPSORIASIS • 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 • Approximately70% 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 • Includeaqueous 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-counterproducts 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-proliferativeproperties • 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 • Topicalsynthetic retinoid • For treatment of chronic plaque psoriasis • Applied once daily in evening • Commonly causes local irritation 1 57
- 58. TOPICAL THERAPIES: CORTICOSTEROIDS • Possessanti-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 • Adverseeffects 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 DIPROPIONATEOINTMENT (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 DIPROPIONATEOINTMENT (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 DIPROPIONATEOINTMENT (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 DIPROPIONATEGEL • 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 psoriasisresistant 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 • Reservedfor 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 • Mostcommonly 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 • Immunosuppressiveagent • 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 • Oralretinoid • For treatment of all forms of severe psoriasis • Once-daily oral therapy • Teratogenic – pregnancy must be avoided 71
- 72. BIOLOGICAL AGENTS • Proteinsderived 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 • Targetkey 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 MANAGEMENTOF 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
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Editor's Notes
- #5 Additional information1 Results based on 4-page, self-administered questionnaire mailed in 1998 to entire membership of United States National Psoriasis Foundation (n = 40,350) Questionnaire returned by 17,488 respondents Questionnaire was followed by a telephone survey of selected respondents with severe psoriasis (n = 502) 1. Krueger G et al. Arch Dermatol 2001; 137: 280–4.
- #6 Additional information1 Of respondents with severe psoriasis: 57% reported that others have mistaken their condition as contagious 48% reported that their psoriasis had been mistaken for a different disease or condition, typically poison ivy and occasionally AIDS 40% had had trouble receiving equal service or treatment in various establishments: 24% in hair salons or barbershops 19% in public pools 11% in health clubs Study responses indicate that patients believe that physicians do not always fully appreciate the severity and lifestyle repercussions of psoriasis 1. Krueger G et al. Arch Dermatol 2001; 137: 280–4.
- #7 Additional information1 The youngest group of patients with severe psoriasis (18 to 34 years) was most likely to report emotional suffering due to the disease It is important to note that 10% of questionnaire respondents (aged 18 to 34 years) reported having contemplated suicide 1. Krueger G et al. Arch Dermatol 2001; 137: 280–4.
- #8 Additional notes Prevalence (0.3-2.5%) – derived from estimates of psoriasis prevalence made in cross-sectional studies1. Prevalence varies according to race and geographical location2. 60 per 100,000 incidence rate (sex and age adjusted) was reported from a four-year population based study conducted in Rochester, Minnesota3. 1. Plunkett A et al. Australas J Dermatol 1998; 39: 225–232. 2. Barker J. Clin Exp Dermatol 2001;26(4):321-5. 3. Bell LM et al. Arch Dermatol 1991; 127: 1184–7.
- #11 Additional information1 Other drugs which may act as a trigger for psoriasis include chloroquine, hydroxychloroquine, interferon alfa and the abrupt withdrawal of systemic and potent topical corticosteroids 1. Dermatology Expert Group. Therapeutic guidelines: dermatology. Version 3. Melbourne: Therapeutic Guidelines Limited, 2009.
- #14 Additional information1 The extent of psoriasis can range from minor inflammation at one or two sites, to total skin involvement with pustulation and constitutional symptoms 1. Dermatology Expert Group. Therapeutic guidelines: dermatology. Version 3. Melbourne: Therapeutic Guidelines Limited, 2009.
- #27 Additional information1 Pitting Depressions about 1 mm in diameter on nail surface May involve only a few fingernails, or may involve the majority of the fingernails May also involve the toenails, although to a lesser degree Onycholysis Produces white to yellow discolouration of distal nail plate Discolouration may range from 1–2 mm at the distal free edge to involvement of entire nail ‘Oil-drop sign’ Well-demarcated, usually circular colour change Separate and distinct from onycholysis 1. Menter A et al. Fast facts: psoriasis. 2nd ed. Oxford: Health Press, 2004.
- #31 Additional information Distal interphalangeal involvement1 Most classical form of psoriatic arthritis – up to 50%2 Patients often have concomitant nail disease Menter A et al. Fast facts: psoriasis. 2nd ed. Oxford: Health Press, 2004. Van de Kerkhof P, ed. Textbook of psoriasis. 2nd edition. Melbourne: Blackwell Publishing 2003
- #47 Additional information1 For each of the four body sites, the severity of plaques is assessed based on following characteristics: degree of redness amount of scale or flakiness thickness of plaque 1. Dubertret L. Psoriasis from clinic to therapy. France: Med’com, 2005.
- #51 Additional information Combination therapies1,2 As psoriasis is a chronic disease, treatment is often long term, which gives rise to issues with cumulative treatment toxicity Combination therapies can possibly reduce toxicity risk by enabling lower therapy dosages to be used Therapeutic outcome may be improved by using treatments in combination Combination therapies can involve combinations of: two topical agents phototherapy with a topical or systemic agent systemic therapy with a topical agent Rotational therapy is also an option, whereby treatments are rotated before significant individual drug toxicity occurs 1. Menter A et al. Fast facts: psoriasis. 2nd ed. Oxford: Health Press, 2004. 2. Rossi S, ed. Australian Medicines Handbook. Adelaide: AMH, 2010.
- #59 Additional information1 Anti-inflammatory activity of topical corticosteroids varies Topical corticosteroids are categorised as mild, moderate, potent or very potent 1. Menter A et al. Fast facts: psoriasis. 2nd ed. Oxford: Health Press, 2004.
- #60 Additional information1 Although complications are possible with long-term use, corticosteroids remain an important part of topical therapy Adverse effects can be minimised while retaining therapeutic efficacy by: using the least potent corticosteroid required to maintain control giving intermittent pulses of therapy after achieving remission 1. Menter A et al. Fast facts: psoriasis. 2nd ed. Oxford: Health Press, 2004.
- #66 Currently waiting for PBAC approval Results for speed of onset based on efficacy data from two randomised, double blind, 8-week clinical studies. At week 2 calcipotriol/betamethasone dipropionate gel was shown to be statistically significantly more effective than calcipotriol in gel vehicle, betamethasone in gel vehicle and gel vehicle used alone.1 1. Daivobet Gel Product Information, 14 July 2010