Psoriasis Vulgaris (Plaque Psoriasis): Chronic Inflammatory Skin Disease
Overview
Psoriasis vulgaris, also known as chronic plaque psoriasis or chronic stationary psoriasis, is the most common form of psoriasis and accounts for up to 90% of cases. It is a chronic, immune-mediated inflammatory skin disorder characterized by the presence of well-defined, red, scaly plaques that can affect various parts of the body. These plaques often have a silvery-white surface due to hyperproliferation and defective maturation of keratinocytes.
Although not life-threatening, psoriasis significantly impairs quality of life due to its visible symptoms, pruritus, and potential systemic associations. It often follows a relapsing-remitting course and may be triggered or exacerbated by a variety of environmental and internal factors.
Epidemiology
Psoriasis affects approximately 1–2% of the population worldwide and occurs with equal frequency in men and women. While it can present at any age, two peaks are observed:
- Type I (early-onset): Appears before the age of 40, usually between 20 and 30 years; often associated with a familial history and more severe disease;
- Type II (late-onset): Appears after the age of 50 and is generally not hereditary.
Etiology and Triggering Factors
Psoriasis has a multifactorial origin, with contributions from genetic, environmental, and immunological mechanisms. While there is often a genetic predisposition, environmental triggers are typically required to initiate or exacerbate the disease.
Key factors include:
- Genetic susceptibility: Polygenic inheritance; HLA-Cw6 gene is strongly associated with Type I psoriasis;
- Immune dysfunction: Activation of Th1 and Th17 immune responses, leading to cytokine overproduction (IL-17, TNF-α);
- Physical trauma (Koebner phenomenon);
- Infections: Particularly streptococcal infections (in guttate psoriasis), and upper respiratory tract infections;
- Drugs: Beta-blockers, lithium, NSAIDs, antimalarials, interferons, and withdrawal of systemic corticosteroids;
- Alcohol and tobacco use;
- Obesity and metabolic syndrome;
- Psychological stress;
- Climatic factors: Cold and dry environments may worsen symptoms.
Clinical Features
Psoriasis vulgaris typically presents with erythematous plaques covered by thick, white or silvery scales. The lesions are sharply demarcated, elevated, and may vary in size and distribution.
Common sites of involvement:
- Extensor surfaces of the elbows and knees;
- Scalp (including hairline and behind the ears);
- Trunk (especially lower back and umbilical region);
- Face (including eyelids and auditory canal);
- Palms and soles;
- Genital area;
- Nails (psoriatic onychodystrophy): Pitting, onycholysis, subungual hyperkeratosis, dystrophic thickening.
Pruritus is reported in approximately 60% of patients and may range from mild to severe. During exacerbations, lesions may multiply, enlarge, and become more inflamed. Periods of remission may last weeks to months or longer, depending on individual disease control.
Diagnostics
The diagnosis of psoriasis vulgaris is primarily clinical. A dermatologist can typically recognize the condition based on the characteristic appearance and distribution of lesions.
Diagnostic steps include:
- Physical examination: Identification of sharply demarcated plaques with silvery scaling, especially in typical areas (elbows, knees, scalp);
- Psoriatic triad (Auspitz signs):
- Stearin spot phenomenon: Scales are easily removed in layers;
- Terminal film: A shiny red surface appears under removed scales;
- Point bleeding: After scraping, pinpoint bleeding appears from capillaries.
- Skin biopsy: Used in atypical cases or for confirmation. Histology reveals acanthosis, parakeratosis, Munro abscesses, and elongated rete ridges;
- PASI score (Psoriasis Area and Severity Index): A standardized measure to assess extent and severity. PASI ≤10 is mild, >10 is moderate to severe.
Differential Diagnosis
Psoriasis vulgaris may mimic or overlap with other inflammatory dermatoses. Differential diagnosis should consider:
- Lichen planus;
- Atopic dermatitis;
- Chronic eczema;
- Pityriasis rubra pilaris;
- Pink lichen (pityriasis rosea);
- Seborrheic dermatitis (especially on scalp);
- Drug-induced dermatoses (e.g., lithium or antimalarial reactions);
- Cutaneous T-cell lymphoma (early mycosis fungoides);
- Ichthyosis, particularly in widespread scaling cases.
Treatment
The main goal of psoriasis treatment is to control symptoms, reduce inflammation, normalize keratinocyte turnover, and improve the patient’s quality of life. Treatment is guided by the extent of skin involvement, severity of symptoms, and presence of comorbidities.
Topical therapy (PASI ≤10):
- Keratolytic agents: Urea, salicylic acid, and lactic acid to remove scaling;
- Topical corticosteroids: Low to high potency depending on location;
- Vitamin D analogs (e.g., calcipotriol): Normalize epidermal proliferation;
- Calcineurin inhibitors: Useful on sensitive areas (face, groin);
- Topical retinoids: Tazarotene for plaque reduction.
Systemic and advanced therapy (PASI >10 or refractory cases):
- Oral retinoids: Acitretin;
- Immunosuppressants: Methotrexate, cyclosporine;
- Fumaric acid esters;
- Biologic agents: Targeted therapies such as TNF-α inhibitors (adalimumab, etanercept), IL-12/23 inhibitors (ustekinumab), IL-17 inhibitors (secukinumab), PDE-4 inhibitors (apremilast);
- Phototherapy: UVB narrowband or PUVA therapy in moderate cases.
Complications
Although psoriasis vulgaris is not life-threatening, it can be associated with multiple systemic complications, especially in severe and long-standing disease:
- Cardiovascular disease: Increased risk of hypertension, ischemic heart disease, and stroke;
- Metabolic syndrome: Obesity, insulin resistance, and dyslipidemia are more common in patients with moderate to severe psoriasis;
- Psoriatic arthritis: Joint pain, swelling, and progressive damage in up to 30% of cases;
- Psychosocial impact: Depression, anxiety, social isolation due to visible skin lesions and chronicity of the disease.
Prevention and Lifestyle Recommendations
Psoriasis cannot be completely prevented due to its genetic basis, but the frequency and severity of flares can be reduced through lifestyle and environmental modifications:
- Avoid known triggers (infections, trauma, smoking, stress, alcohol);
- Use emollients daily to maintain skin hydration and barrier function;
- Protect the skin from injury (Koebner phenomenon);
- Monitor for side effects if on long-term systemic therapy;
- Manage associated comorbidities, especially cardiovascular and metabolic risk factors;
- Follow regular dermatologic evaluations to monitor disease progression and response to treatment.
Conclusion
Psoriasis vulgaris is a common, chronic inflammatory skin disease with a significant impact on patients’ physical and emotional well-being. While it is currently incurable, advancements in topical, systemic, and biologic therapies allow for effective symptom control and improvement in quality of life.
Early diagnosis, personalized treatment, and patient education remain essential components of comprehensive care in patients with psoriasis vulgaris.
