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.
Psoriasis affects 2-3% of the world population with no sex predilection. It shows two incidence peaks: ages 15-25 (type I, more severe, associated with HLA-Cw6) and ages 50-60 (type II). The psychosocial impact is profound, with depression and suicidal ideation rates significantly higher than in the general population.
Immune-Mediated Disease
T lymphocytes and the IL23/IL17 axis drive the disease. Psoriasis is neither allergic nor contagious.
Systemic Disease
Increased cardiovascular risk, metabolic syndrome, psoriatic arthritis in 30% of patients, and significant psychological impact.
Epidermal Proliferation
Skin renewal drops from 28 to 3-5 days, causing buildup 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. When the scales are removed, pinpoint bleeding appears (Auspitz sign).
- 02
Pruritus and discomfort
Itching affects 60-90% of patients and ranges from mild to intense. Pain and burning occur 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, heavily scaling plaques that may extend beyond the hairline. Affects 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
Lesions appear in areas of skin trauma (scars, abrasions, sunburns). Important for patient counseling.
CLINICAL FORMS OF PSORIASIS
| FORM | FEATURES | FREQUENCY |
|---|---|---|
| Plaque (vulgaris) | Chronic erythematosquamous plaques on extensors, scalp, lower back | 80-90% |
| Guttate | Small scattered papules, often following 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 can be confused with other inflammatory dermatoses — especially in atypical forms or at special sites such as the scalp and nails.
DIAGNÓSTICO DIFERENCIAL
Differential Diagnosis
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
Read more →- Central face
- Erythema without plaques
- No silvery scale
Lichen Planus: When Biopsy Decides
Lichen planus is a T-lymphocyte-mediated inflammatory disease affecting skin, mucosa, and nails. Polygonal violaceous papules with surface white reticulated striae (Wickham striae) 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 basal-layer (vacuolar) degeneration is the lichen planus pattern, distinct 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 seborrheic dermatitis from 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 no well-demarcated borders; the scalp is the preferred site, along with eyebrows, nostrils, and nasolabial folds. In psoriasis, plaques have sharp borders, silvery scale, and often 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 presents with acute eruption of multiple erythematosquamous papules and small plaques ("droplike") on the trunk and extremities, 2 to 3 weeks after infection. It is often the initial presenting form of psoriasis.
In most cases, guttate psoriasis resolves spontaneously in 2 to 3 months. Antibiotic treatment of the streptococcal infection may accelerate resolution. Some patients progress 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) is an alternative for 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, reduced cutaneous oxidative stress, effects on local microcirculation, and neuroendocrine modulation of stress (a recognized trigger of flares).
In clinical practice, acupuncture is a complementary therapy with potential benefit for 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, incurable disease, but control is excellent in the biologics era. Mild forms respond well to topical therapies. Moderate-to-severe forms, previously hard to control, can now achieve clear or nearly 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 while also 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 and cannot be transmitted by touch, kissing, sexual intercourse, or any other form of contact.
Myth vs. Fact
Psoriasis is just a skin disease.
Psoriasis is a systemic inflammatory disease. Beyond the skin, it can affect joints (psoriatic arthritis in 30%) and is linked to higher cardiovascular risk, type 2 diabetes, depression, and metabolic syndrome.
Myth vs. Fact
Sun always improves psoriasis.
Moderate sun exposure may improve lesions through UVB, but sunburn can trigger the Koebner effect (worsening 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 and completely non-contagious. It is not transmitted by physical contact, shared objects, water, or any other route. Family members face increased risk only through shared susceptibility genes, not through 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 (most frequent), streptococcal infections (especially for guttate psoriasis), physical trauma (Koebner phenomenon), medications (beta-blockers, lithium, NSAIDs, antimalarials), alcohol, smoking, and hormonal variations. Identifying and avoiding individual triggers is an essential part of treatment.
Yes. Psoriasis is a systemic disease linked to important comorbidities: psoriatic arthritis (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 psoriasis patients.
Preliminary clinical studies suggest that acupuncture, as a complementary therapy, may help reduce pruritus, manage stress, and improve quality of life in some patients. Findings on PASI reduction are heterogeneous, and current evidence does not support acupuncture as a substitute for conventional therapies (topicals, phototherapy, conventional systemics, and biologics). Proposed immunomodulation mechanisms (IL-17, IL-23, TNF-alpha) are hypothetical, partially derived from experimental models. The dermatologist and the medical acupuncturist jointly assess appropriateness in each case.
Biologics approved for psoriasis (anti-IL-17: secukinumab, ixekizumab, bimekizumab; anti-IL-23: risankizumab, guselkumab, tildrakizumab; anti-TNF: adalimumab) have an excellent safety profile backed by decades of data. They require screening for latent tuberculosis, hepatitis, and other workup before initiation, and are contraindicated in severe active infections. Regular follow-up with a 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 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 aggravates psoriasis and interferes with hepatotoxic drugs such as methotrexate. Weight loss in obese patients significantly improves therapeutic response.
Pediatric psoriasis — 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 hardest 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 option for severe nail psoriasis. Severe onycholysis is a risk factor for psoriatic arthritis.
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