What Is Psoriasis?
Psoriasis is a chronic, immune-mediated inflammatory disease that primarily affects the skin and joints. It is characterized by well-demarcated erythematous (reddish) plaques, covered by silvery scales, the result of accelerated epidermal proliferation and chronic inflammation.
Psoriasis is currently recognized as a systemic disease, not just cutaneous. It is associated with a higher risk of cardiovascular disease, metabolic syndrome, type 2 diabetes, depression, and psoriatic arthritis. This understanding has radically changed the therapeutic approach.
It affects 2-3% of the world population, with no sex predilection. It presents two peaks of incidence: between 15-25 years (type I, more severe, associated with HLA-Cw6) and between 50-60 years (type II). The psychosocial impact is profound, with rates of depression and suicidal ideation significantly higher than in the general population.
Immune-Mediated Disease
T lymphocytes and the IL23/IL17 axis are the protagonists. It is not an allergic disease nor contagious.
Systemic Disease
Increased cardiovascular risk, metabolic syndrome, psoriatic arthritis in 30% of patients, and significant psychological impact.
Epidermal Proliferation
The skin renewal cycle drops from 28 to 3-5 days, causing accumulation of immature keratinocytes — the characteristic scales.
Pathophysiology
Psoriasis is driven by the IL-23/IL-17 axis. Activated dendritic cells produce IL-23, which stimulates Th17 lymphocytes to secrete IL-17A, IL-17F, and IL-22. IL-17 induces production of chemokines, antimicrobial peptides, and pro-inflammatory cytokines in keratinocytes, creating a feedback loop.
IL-22 stimulates keratinocyte hyperproliferation and inhibits their terminal differentiation. The result is epidermal thickening (acanthosis) and parakeratosis (nucleated keratinocytes at the surface) that form the scales. TNF-alpha amplifies inflammation and promotes angiogenesis — the dilated and tortuous vessels of the papillary dermis cause the erythema.
Genetic predisposition is strong: 70% concordance in identical twins. The main susceptibility gene is HLA-Cw6 (chromosome 6p), associated with early-onset type I. Environmental factors such as streptococcal infections, stress, smoking, alcohol, and medications (lithium, beta-blockers) can trigger or exacerbate the disease.
Symptoms
The most common form is plaque psoriasis (vulgaris), representing 80-90% of cases. The plaques are well demarcated, erythematous, with adherent silvery scales. They are preferentially located on the scalp, elbows, knees, lower back, and nails.
Manifestations of Psoriasis
- 01
Erythematosquamous plaques
Reddish, well-demarcated plaques covered by silvery scales. On removal of the scales, points of bleeding appear (Auspitz sign).
- 02
Pruritus and discomfort
Itching present in 60-90% of patients. May be mild to intense. Pain and burning in plaque fissures.
- 03
Nail involvement
Pinpoint depressions (pitting), onycholysis (detachment), subungual hyperkeratosis, "oil-drop" spots. Present in 50% of patients with cutaneous psoriasis.
- 04
Scalp involvement
Thick plaques with intense scaling that may extend beyond the hairline. Present in 50-80% of patients.
- 05
Psoriatic arthritis
Joint pain, swelling, and stiffness. May affect peripheral joints and/or spine (spondylitis). Active screening is recommended.
- 06
Koebner phenomenon
Appearance of lesions in areas of skin trauma (scars, abrasions, sunburns). Important for patient guidance.
CLINICAL FORMS OF PSORIASIS
| FORM | FEATURES | FREQUENCY |
|---|---|---|
| Plaque (vulgaris) | Chronic erythematosquamous plaques on extensors, scalp, lower back | 80-90% |
| Guttate | Small disseminated papules, often post-streptococcal infection | 2-10% |
| Inverse | Smooth erythema without scales in folds (axillary, inguinal, submammary) | 3-7% |
| Pustular | Sterile pustules on an erythematous base; may be localized (palmoplantar) or generalized | 1-3% |
| Erythrodermic | Generalized erythema (>90% of body surface). Dermatologic emergency | <1% |
Diagnosis
The diagnosis is clinical in the great majority of cases. Skin biopsy is reserved for atypical presentations. Evaluation should include determination of severity (PASI, BSA, DLQI), screening for psoriatic arthritis, and assessment of metabolic and cardiovascular comorbidities.
The PASI (Psoriasis Area and Severity Index) assesses the extent and severity of plaques in four body regions. The DLQI (Dermatology Life Quality Index) measures the impact on quality of life. The combination of PASI ≥10 or BSA ≥10 or DLQI ≥10 defines moderate-to-severe disease, with indication for systemic therapy.
Differential Diagnosis
Psoriasis is recognized by its erythematous plaques with silvery scale, but it can be confused with other inflammatory dermatoses — especially in atypical forms or in special locations such as the scalp and nails.
DIAGNÓSTICO DIFERENCIAL
Diagnóstico Diferencial
Seborrheic Dermatitis
- Scalp and face
- Yellowish greasy scale
- No thick plaques
Lichen Planus
- Violaceous papules
- Wickham striae
- Oral mucosa
Testes Diagnósticos
- Biopsy
Guttate Psoriasis
- Drop-shaped lesions after streptococcal infection
- Young patients
- Sudden onset
Rosacea
Leia mais →- Central face
- Erythema without plaques
- No silvery scale
Lichen Planus: When Biopsy Decides
Lichen planus is an inflammatory disease mediated by T lymphocytes that affects skin, mucosa, and nails. Polygonal violaceous papules with white reticulated striae (Wickham striae) on the surface and oral mucosal involvement (white reticular pattern) are highly characteristic. However, hypertrophic lichen planus on the lower limbs may mimic psoriasis with thick plaques.
Histologic biopsy is definitive: the band-like lymphocytic infiltrate at the dermoepidermal junction with degeneration of the basal layer (vacuolar degeneration) is the lichen planus pattern, differing from the acanthosis with parakeratosis and Munro microabscesses of psoriasis. Treatment of lichen planus — especially the erosive oral form — requires potent topical or systemic corticosteroids.
Seborrheic Dermatitis vs. Scalp Psoriasis
Distinguishing between seborrheic dermatitis and scalp psoriasis is one of the most frequent diagnostic challenges in dermatology. In seborrheic dermatitis, the scale is yellowish and greasy, with diffuse erythema and without well-demarcated borders; the scalp is the preferential location, together with eyebrows, nostrils, and nasolabial fold. In psoriasis, plaques have sharp borders, silvery scale, and frequently extend beyond the hairline.
"Sebopsoriasis" — overlap of seborrheic dermatitis and psoriasis — is a recognized entity, especially in individuals with genetic predisposition for psoriasis. Treatment of sebopsoriasis combines antifungals (for the Malassezia component) with topical corticosteroids and, eventually, vitamin D analogues.
Guttate Psoriasis: Infectious Trigger and Course
Guttate psoriasis is triggered by streptococcal throat infections (pharyngotonsillitis) in genetically susceptible individuals, typically children and young adults. It manifests with acute eruption of multiple erythematosquamous papules and small plaques ("droplike") on the trunk and extremities, 2 to 3 weeks after the infection. It is frequently the initial presenting form of psoriasis.
In most cases, guttate psoriasis resolves spontaneously in 2 to 3 months. Treatment of the streptococcal infection with antibiotics may accelerate resolution. A portion of patients progresses to chronic plaque psoriasis. UVB phototherapy is highly effective in persistent cases.
Treatment
Treatment is tiered according to severity. Topical therapies for mild forms, phototherapy for moderate forms, and systemic therapies (biologics and small molecules) for moderate-to-severe forms. The anti-IL-17 and anti-IL-23 biologics represent the greatest advance, with unprecedented PASI 90-100 rates.
Mild: Topical Therapy
First lineTopical corticosteroids (foundation of topical treatment), vitamin D analogues (calcipotriene), corticosteroid + calcipotriene combination (more effective). Calcineurin inhibitors for face and folds. Emollients always.
Moderate: Phototherapy
Narrowband UVB, 2-3x/weekNarrowband UVB phototherapy: induces apoptosis of pathogenic T lymphocytes and immunomodulation. Effective in 60-70% of patients. PUVA (psoralen + UVA) as alternative in thick plaques.
Moderate to Severe: Conventional Systemics
When phototherapy is inadequateMethotrexate: standard for decades, also effective in psoriatic arthritis. Cyclosporine: rapid action, use limited to 1-2 years. Acitretin: for pustular and palmoplantar psoriasis.
Moderate to Severe: Biologics
Targeted treatmentAnti-TNF (adalimumab, infliximab). Anti-IL-17 (secukinumab, ixekizumab): PASI 90 in 60-70%. Anti-IL-23 (guselkumab, risankizumab): PASI 90 in 70-85%, convenient dosing. JAK/TYK2 inhibitors (deucravacitinib): oral.
Acupuncture as Treatment
Acupuncture has been studied in psoriasis with a focus on its immunomodulatory effects, particularly modulation of the Th17 response and reduction of pro-inflammatory cytokines such as TNF-alpha and IL-17. Experimental studies demonstrate that acupuncture may reduce keratinocyte proliferation and dermal angiogenesis in animal models.
Hypothesized mechanisms — still without robust clinical validation in human psoriasis — include possible modulation of the hypothalamic-pituitary-adrenal axis, reduction of cutaneous oxidative stress, effects on local microcirculation, and neuroendocrine modulation of stress (a recognized triggering factor of flares).
In clinical practice, acupuncture is considered a complementary therapy, with potential benefit in pruritus control, stress reduction, and quality-of-life improvement. It does not replace conventional dermatologic or biologic therapies in moderate-to-severe forms.
Prognosis
Psoriasis is a chronic disease without cure, but with excellent control in the era of biologics. Mild forms respond well to topical therapies. Moderate-to-severe forms, previously difficult to control, can now achieve clear or almost clear skin with biologics.
The main long-term risk is cardiovascular. Patients with severe psoriasis have a 3-fold higher risk of myocardial infarction and a 5-year shorter life expectancy than the general population. Adequate control of systemic inflammation with biologics may reduce this cardiovascular risk, in addition to improving the skin.
Myths and Facts
Myth vs. Fact
Psoriasis is contagious.
Psoriasis is not contagious in any way. It is an autoimmune/immune-mediated disease with a genetic basis. It cannot be transmitted by touch, kissing, sexual intercourse, or any form of contact.
Myth vs. Fact
Psoriasis is just a skin disease.
Psoriasis is a systemic inflammatory disease. In addition to skin, it can affect joints (psoriatic arthritis in 30%) and is associated with higher cardiovascular risk, type 2 diabetes, depression, and metabolic syndrome.
Myth vs. Fact
Sun always improves psoriasis.
Moderate sun exposure may improve lesions through the action of UVB, but sunburn may cause the Koebner effect (worsening of lesions). Exposure should be gradual and controlled, never excessive.
When to Seek Help
Frequently Asked Questions
Frequently Asked Questions
No. Psoriasis is a genetic autoimmune disease, completely non-contagious. It is not transmitted by physical contact, sharing of objects, water, or any other route. Family members have increased risk only by sharing susceptibility genes, not by contagion.
There is no cure for psoriasis, but modern treatments — especially biologics — allow prolonged complete remission in most patients with moderate-to-severe disease. Many patients achieve "clear skin" (PASI 100) with anti-IL-17 or anti-IL-23 biologics, maintaining remission for years of continued treatment.
The most common triggers include: emotional stress (the most frequent), streptococcal infections (especially for guttate psoriasis), physical trauma (Koebner phenomenon), medications (beta-blockers, lithium, NSAIDs, antimalarials), alcohol consumption, smoking, and hormonal variations. Identifying and avoiding individual triggers is an essential part of treatment.
Yes. Psoriasis is a systemic disease associated with important comorbidities: psoriatic arthritis (in 20-30% of patients), metabolic syndrome, type 2 diabetes, cardiovascular disease, inflammatory bowel disease, depression, and anxiety. Active screening for these comorbidities is recommended in all patients with psoriasis.
Preliminary clinical studies suggest that acupuncture, as a complementary therapy, may contribute to reduction of pruritus, stress management, and improvement in quality of life in some patients. Findings on PASI reduction are heterogeneous, and current evidence does not support the use of acupuncture as a substitute for conventional therapies (topicals, phototherapy, conventional systemics, and biologics). Mechanisms regarding immunomodulation (IL-17, IL-23, TNF-alpha) are hypothetical, partially derived from experimental models. The dermatologist and the medical acupuncturist evaluate together the appropriateness in each case.
The biologics approved for psoriasis (anti-IL-17: secukinumab, ixekizumab, bimekizumab; anti-IL-23: risankizumab, guselkumab, tildrakizumab; anti-TNF: adalimumab) have an excellent safety profile with decades of data. They require screening for latent tuberculosis, hepatitis, and other tests before initiation. They are contraindicated in severe active infections. Regular follow-up with the dermatologist is essential.
Psoriatic arthritis should be suspected in patients with psoriasis who present: joint pain and stiffness (especially morning), dactylitis ("sausage finger"), enthesitis (tendon pain, especially at the heel), inflammatory low back pain (worse with rest, better with exercise), and extensive nail changes. Early diagnosis is crucial to prevent permanent joint damage.
Evidence suggests that the Mediterranean diet (rich in omega-3, fruits, vegetables, and olive oil) may reduce systemic inflammation and complement treatment. Obesity is a recognized risk factor for more severe psoriasis and worsens response to biologics. Alcohol worsens psoriasis and interferes with hepatotoxic medications such as methotrexate. Weight loss in obese patients significantly improves therapeutic response.
Pediatric psoriasis — which represents 30% of cases — is treated with topical corticosteroids of adequate potency, topical vitamin D analogues, and, for moderate-to-severe disease, UVB phototherapy. Several biologics (secukinumab, etanercept, adalimumab) already have pediatric approval. The psychological impact at school and in social relationships should be actively assessed and addressed.
Nail psoriasis — with pitting, onycholysis, oil-drop spot, and subungual hyperkeratosis — is the most difficult manifestation to treat. Intralesional corticosteroids and vitamin D analogues (injected into the nail matrix) have moderate efficacy. Systemic biologics, especially anti-IL-17, are the most effective for severe nail psoriasis. The presence of severe onycholysis is a risk factor for psoriatic arthritis.
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