Grading & Level of Importance: B
- About 125 million people worldwide affected ( 2%–4% of the population in Western countries)
- Different degrees of clinical manifestation depending on genetic background, age and geographic as well as environmental factors.
- Adults (from 0.9 % to 8.5%) more frequently affected than children (from 0% to 2.1%)
- Dual peak of incidence: 30–39 years ( type I ) and > 40 years of age (type II).
- About 20% of psoriatic patients develop sero-negative arthritis.
- Systemic, chronic auto-inflammatory and auto-immune skin disease with a spectrum of clinical phenotypes, frequently associated with co-morbidities psychological, metabolic, arthritic, and cardiovascular co-morbidities .
- Interplay of genetic, epigenetic, environmental, and immunological factors.
Aetiology & Pathogenesis
Susceptibility to psoriasis involving both adaptive and innate immune system. While adaptive immune responses predominate in chronic plaque psoriasis, innate and auto-inflammatory responses dominate in pustular forms of psoriasis.
- Psoriasis shows polygenic inheritance. Genome-wide association studies report that the histocompatibility complex HLA-C*06:02 (previously known as HLA-Cw6) is associated with early-onset psoriasis and guttate psoriasis.
- Genotype and exogenous factors (e.g. local effects like Köbner's phenomenon or systemic ones) are responsible for phenotypic expression.
- Psoriasis is multifactorial and an immune-mediated inflammatory disease (IMID). Pathological mechanisms : Th17 cells play a key rolewith interleukin IL-23 mainly produced by dendritic cells. Null-Th17 cells produce various cytokines, including IL-17A, IL-17F and IL-22. IL-17A and IL-22 induce not only keratinocyte proliferation, but also tumor necrosis factor (TNF)-a. TNF-a accelerates the infiltration of inflammatory cells, including lymphocytes, monocytes and neutrophils.
- Provocation and maintaining factors: physical, chemical, metabolic, certain inflammatory diseases (dermatoses), drugs (lithium, chloroquine, beta-blockers, interferon-alpha), infections (streptococci, HIV), alcohol, nicotine, fatty food, and stress.
Signs & Symptoms
- Circumscribed erythematous plaques bordering silvery scales of different size and thickness ranging from guttate to large geographic like lesions.
- Pustules may appear on site of lesions or primarily ( pustular psoriasis )
- Dystrophic or pitted nails or yellowish discolouring (oil patch)
- Palmo-plantar hyperkeratosis
- Sometimes gyrate pattern on the tongue, lips or glans penis
- When scales are very thick: Intense itch, pain and scaly skin lesions that can crack and bleed.
- Koebner’s sign; Candle sign: production of candle-grease-like scale when scraping a plaque with curette.
- Auspitz sign: punctate bleeding when psoriasis scales are scraped away, due to a thin layer of suprapapillary epidermis.
Sites of predilection: extensor surfaces (knees, elbows), scalp, retroauricular, sacral, gluteal cleft, umbilicus, genital, intertriginous (psoriasis inversa), palmo-plantar.
The recent last classifications of the acute and chronic types proposed by the International Psoriasis Council identifies four main forms of psoriasis:
c. general pustular psoriasis (GPP)
e. In addition several further subphenotypes according to distribution (localized vs. widespread), anatomical localization (flexural, scalp, palms/soles/nail), size (large vs. small) and thickness (thick vs. thin) of plaques and scales, onset (early vs. late),and disease activity (active vs. stable)
- Psoriatic arthritis (HLA-B27): different sub-phenotypes with localization at vertebrae, cervical, iliosacral, distal joints or fingers.
Laboratory & other workups
No specific blood test for psoriasis, sometimes HLA- C6 can help in differentiating Type I, Type II.
- Laboratory workup for co-morbidities (CRP, blood count, kidney-, liver- and lipid values can be examined).
- A skin biopsy should be taken if uncertain type of lesions occur or other differential diagnoses have to be excluded.
- Confluent parakeratosis and hyperkeratosis
- Intracorneal neutrophils (Munro microabscesses)
- Acanthosis is thickening of the rete ridges or reduced layers above papilla.
- Elongation and widening of the papillary spiral-like formed capillaries.
- A strong lympho-mononuclear inflammatory infiltrate mixed with neutrophilic granulocytes in the dermis
In general, the course is chronic-recurrent or chronic-persistent. Acute eruptions such as the guttate forms sometimes clear with complete resolution (streptococcal infection, drug cessation). Chronic plaque-like types may suddenly show exacerbations with disseminated guttate lesions or becoming more inflammatory and growing in size.
- Co-morbidities (see above)
- Reduced quality of life and reduced life span.
- Disabling features (nails, joints)
- Non-melanoma skin cancer in patients with long-term photo- or photochemotherapy or therapy with cytotoxic agents.
- Incidence of lung cancer and CTCL type of lymphoma may be increased, but not colon-,breast-or prostate cancer.
Clinical features and histopathology in unclear cases.
- Pityriasiform or guttate like lesions such as in secondary syphilis, pityriasis rosea, in those of the parapsoriasis group, in pityriasis rubra pilaris and in cutaneous T-cell lymphoma
- Chronic nummular eczema
- Hypertrophic lichen planus
- Tinea corporis, pemphigus foliaceus, glucagonoma syndrome
- Chronic and subacute lupus erythematosus
- Seborrhoeic dermatitis, especially on the head and neck area
Prevention & Therapy
Avoidance of provocation factors (see above).
In general, the type of psoriasis, acute or non acute, localisation,age and profession, adherence and quality of life, co-morbidities and additional arthritis, all have in each patient individually to be considered.
Topical therapy is indicated when less than 10 % of body surface or PASI score is < 10. Certain localisations such as face, scalp, nails and hands need combined therapies.
-Salicylic acid in varying concentrations (5-10%) depending on localisation and age (cave resorption in childhood)
-Dithranol 0.03-2% in vaseline or zinc paste (overnight or minute therapy).
-Topical corticosteroids, especially higher potency.
-Vitamin D3 and its analogues (calcipotriol, tacalcitol).
-Combination of betamethasone and calcipotriol.
-Vitamin-A acid derivatives (tazarotene gel).
-Crisaborole (PDE 4 inhibitor)
-UV light therapy regimen such as photo bath therapy 15% NaCl + UVB.
Phototherapy (UVA +) UVB/narrow band UVB 311 nm.
Photochemotherapy: 8-(5-) MOP + UVA (PUVA) via local cream, via full skin surface bathing (bath PUVA ) or systemic oral application.
To qualify for systemic therapy the following criteria according the International Psoriasis Council are recommended :
- Psoriasis lesions on 10% or more of the body surface, PASI score >10 and Quality of Life >10; or
- Psoriasis lesions on sensitive areas of the body (i.e., hands/feet, face, genitals, scalp); or
- Topical therapy failed to control symptoms.
- Methotrexate oral or subcutaneous.
- Retinoids, i.e. acitretin
The disease basically needs an interdisciplinary approach because of co-morbidities.
- Statement 1 Systemic therapy is always preferred in treating psoriasis
- Statement 1 Tinea corporis must be excluded in the differential diagnosis of psoriasis
- Which of these treatments frequently shows a rebound effect when stopped, and is thus less than desirable in psoriasis?
- Which statements about the etiology and pathogenesis of psoriasis are true?
- Which of these diseases falls into the differential diagnostic consideration for psoriasis?
- A psoriatic lesions typically shows:
- Which statements about psoriasis are correct?
- The above photomicrograph is typical for psoriasis. Which descriptions are correct?
- One of the following is not a known trigger for psoriasis of appropriate genotypes. Find the incorrect answer.
Further Images / DOIA
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