1.5.1 Psoriasis

None.

• 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.

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.
   

• 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:

    a.    plaque-type
    b.    guttate 
    c.    general pustular psoriasis (GPP)
    d.    erythroderma 
    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. 

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)
• Superinfections
• 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
Avoidance of provocation factors (see above).

Therapy
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:

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.

Systemic treatment:

To qualify for systemic therapy the following criteria according the International Psoriasis Council are recommended :

1. Psoriasis lesions on 10% or more of the body surface, PASI score >10 and Quality of Life >10; or 
2. Psoriasis lesions on sensitive areas of the body (i.e., hands/feet, face, genitals, scalp); or 
3. Topical therapy failed to control symptoms.

1. Methotrexate oral or subcutaneous.
2. Retinoids, i.e. acitretin 
3. Ciclosporin 
4. Fumarates
5. Biologics

The disease basically needs an interdisciplinary approach because of co-morbidities.