Summary / Overview
- Psoriasis is a chronic, relapsing, immune-mediated inflammatory disease that mainly affects the skin, nails, and sometimes joints.
Etiology
- The exact cause is not fully understood.
- Psoriasis occurs in genetically susceptible individuals under the influence of immune dysregulation and environmental triggers.
- Important triggers may include infection, trauma, stress, obesity, and certain drugs.
- Family history is common, but absence of heredity does not exclude the disease.
Pathogenesis
- Psoriasis is driven by abnormal interaction between keratinocytes, dendritic cells, and T cells, leading to chronic cutaneous inflammation.
- The strongest classic genetic association is with HLA-C*06:02, an allele of the HLA-C gene.
- The central immune pathway is the IL-23 / Th17 / IL-17 axis, with contribution from TNF-related inflammatory signaling.
- These inflammatory signals drive keratinocyte hyperproliferation, abnormal epidermal differentiation, vascular change, and plaque formation.
- In psoriatic arthritis and more extensive disease, the inflammatory process extends beyond skin to joints and entheses.
Symptoms
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Signs
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Investigations
- There is no specific blood test to diagnose psoriasis.
- Diagnosis is usually clinical and may be supported by exclusion of other dermatoses.
- CBC, eosinophil count, and total IgE may help when eczema / allergic dermatitis is suspected.
- Skin scraping/KOH may help exclude fungal infection.
- Biopsy is reserved for atypical, modified, or diagnostically difficult cases.
- CBC, liver function, renal function, hepatitis serology, PPD, and pregnancy test are mainly baseline investigations before systemic treatment.
The exact cause is not fully understood.
Psoriasis occurs in genetically susceptible individuals under the influence of immune dysregulation and environmental triggers.
Important triggers may include infection, trauma, stress, obesity, and certain drugs.
Family history is common, but absence of heredity does not exclude the disease.
References
PDF
Allergy& Immunology
2026-05-13 10:59:32
PDF
elsevier
2026-05-13 10:57:57
PDF
NCBI
2026-05-13 10:54:22
There is no specific blood test to diagnose psoriasis.
Diagnosis is usually clinical and may be supported by exclusion of other dermatoses.
CBC, eosinophil count, and total IgE may help when eczema / allergic dermatitis is suspected.
Skin scraping/KOH may help exclude fungal infection.
Biopsy is reserved for atypical, modified, or diagnostically difficult cases.
CBC, liver function, renal function, hepatitis serology, PPD, and pregnancy test are mainly baseline investigations before systemic treatment.
Psoriasis is driven by abnormal interaction between keratinocytes, dendritic cells, and T cells, leading to chronic cutaneous inflammation.
The strongest classic genetic association is with HLA-C*06:02, an allele of the HLA-C gene.
The central immune pathway is the IL-23 / Th17 / IL-17 axis, with contribution from TNF-related inflammatory signaling.
These inflammatory signals drive keratinocyte hyperproliferation, abnormal epidermal differentiation, vascular change, and plaque formation.
In psoriatic arthritis and more extensive disease, the inflammatory process extends beyond skin to joints and entheses.
* Well-demarcated erythematous plaques
* Silvery-white scaling over plaques
* Predilection for extensor surfaces such as elbows and knees
* Scalp involvement with adherent scaling
* Lumbosacral / sacral plaque lesions
* Nail pitting
* Onycholysis / subungual hyperkeratosis in some cases
* Auspitz sign (pinpoint bleeding points seen after removal of scales)
* Koebner phenomenon (new lesions appearing at sites of trauma)
* In modified or treated cases, classical scale may be reduced or absent
Psoriasis is a chronic, relapsing, immune-mediated inflammatory disease that mainly affects the skin, nails, and sometimes joints.
* It typically presents with well-demarcated erythematous plaques covered by silvery scale, often on the scalp, elbows, knees, and lumbosacral region.
* The disease may be limited to the skin or be associated with nail changes, psoriatic arthritis, and systemic/metabolic comorbidity.
* Diagnosis is mainly clinical, though partially treated lesions may lose their classical appearance.
* Management depends on severity and may include topical therapy, phototherapy, systemic drugs, or biologics.
Cutaneous symptoms
* Dry scaling lesions
* Mild or moderate itching
* Burning / irritation
* Soreness when plaques crack
Associated symptoms
* Scalp flaking
* Nail roughness or deformity noticed by patient
* Joint pain / morning stiffness if arthritis is present
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