Psoriasis

Psoriasis is a chronic, immune-mediated inflammatory disease that primarily affects the skin, characterized by periods of exacerbation and remission. It is not simply a skin condition; it is a systemic disease that manifests most visibly on the skin and can also impact joints (psoriatic arthritis) and other organ systems.

Psoriasis is a chronic non contagious auto immune disease of the skin in which the epidermal cells are produced at an abnormal rate.

• Chronic: This means it is a lifelong condition with no known cure. Patients will experience flare-ups (worsening of symptoms) and periods of remission (improvement or resolution of symptoms), but the underlying predisposition remains.
• Immune-Mediated: Psoriasis is driven by an overactive immune system. Specifically, certain immune cells (particularly T-cells) become overactive and trigger an inflammatory response in the skin. This abnormal immune activity leads to the rapid growth of skin cells.
• Inflammatory: The affected skin areas exhibit signs of inflammation, such as redness (erythema), swelling, and heat. This inflammation is a direct result of the immune system's attack on healthy skin cells.
• Skin Disease: The most prominent and characteristic signs of psoriasis appear on the skin. These manifestations are typically well-demarcated, erythematous (red), scaly plaques, often covered with silvery scales. While skin is the primary target, nails and joints can also be affected.
• Accelerated Keratinocyte Turnover: In healthy skin, keratinocytes (the main cells of the epidermis) mature and shed over approximately 28-30 days. In psoriasis, this process is dramatically accelerated, occurring in as little as 3-7 days. This rapid turnover leads to the accumulation of immature skin cells on the surface, forming the characteristic thick, silvery scales.

Understanding the epidemiology and risk factors of psoriasis helps us appreciate its global impact and identify individuals who may be more susceptible to the disease.

• Prevalence: Psoriasis is a common chronic inflammatory disease, affecting approximately 2-3% of the global population .
• Prevalence varies geographically, with higher rates observed in Northern European and Scandinavian populations (e.g., up to 11% in some studies) and lower rates in East Asian and African populations.
• It affects males and females equally .
• Age of Onset: Psoriasis can occur at any age, from infancy to old age.
• There are typically two peaks of onset : Early-onset (Type I): Occurs between 15 and 30 years of age (peak in the early 20s). This type is often associated with a stronger genetic predisposition and is usually more severe.
• Late-onset (Type II): Occurs between 50 and 60 years of age. This type is generally less severe and has a weaker genetic link.
• Approximately one-third of psoriasis cases begin in childhood or adolescence.

Psoriasis is a multifactorial disease, meaning it results from a complex interplay of genetic, immunological, and environmental factors.

• This is the strongest risk factor . Psoriasis often runs in families.
• Having a first-degree relative (parent, sibling) with psoriasis significantly increases an individual's risk. If one parent has psoriasis, the risk for a child is about 10-25%.
• If both parents have psoriasis, the risk for a child can be as high as 50-70%.
• Numerous genes are associated with psoriasis, with the HLA-Cw6 allele on chromosome 6 being the most strongly linked, particularly with early-onset plaque psoriasis. Other genes involved in immune regulation (e.g., those related to IL-23, IL-12, TNF-alpha pathways) also play a significant role.
• While genetics provide the predisposition, environmental factors often act as "triggers" that initiate or exacerbate the disease in susceptible individuals.
• Infections: Streptococcal infections (e.g., strep throat): A common trigger for guttate psoriasis, especially in children and young adults.
• Other infections (e.g., HIV) can also exacerbate psoriasis.
• Trauma to the Skin (Koebner Phenomenon): Physical injury to the skin (e.g., cuts, scrapes, burns, insect bites, surgical incisions, even aggressive scratching) can induce psoriatic lesions in that area. This phenomenon is highly characteristic of psoriasis.
• Stress: Psychological stress is a well-recognized trigger for psoriasis flares in many individuals. The exact mechanisms are still being researched but involve neuro-immune interactions.
• Medications: Certain drugs can induce or worsen psoriasis. Common culprits include: Beta-blockers (used for hypertension, heart disease)
• Lithium (used for bipolar disorder)
• Antimalarials (e.g., chloroquine, hydroxychloroquine)
• NSAIDs (Nonsteroidal Anti-inflammatory Drugs)
• Systemic corticosteroids (withdrawal of systemic steroids can trigger severe flares, especially pustular or erythrodermic psoriasis).
• Interferon
• Smoking: Cigarette smoking is an independent risk factor for psoriasis development and can also worsen existing disease. It's thought to be related to its effects on the immune system and inflammation.
• Alcohol Consumption: Heavy alcohol intake, particularly in men, is associated with an increased risk and severity of psoriasis, and can also interfere with treatment efficacy.
• Obesity: Obesity is strongly linked to an increased risk of developing psoriasis and can exacerbate its severity. It's also associated with a poorer response to treatment and a higher risk of psoriatic comorbidities. Adipose tissue is metabolically active and can contribute to systemic inflammation.
• Vitamin D Deficiency: While not a primary cause, low vitamin D levels have been observed in psoriasis patients, and vitamin D analogues are a common treatment.

The pathophysiology of psoriasis is complex, involving a dysregulation of the immune system that leads to chronic inflammation and rapid turnover of skin cells. It's primarily considered a T-cell mediated autoimmune disease .

The central players in psoriatic inflammation are a type of white blood cell called T-lymphocytes (T-cells) and various cytokines (signaling proteins) they produce.

• Initiation by Antigen-Presenting Cells (APCs): It is hypothesized that initial triggers (e.g., genetic predisposition, environmental factors like trauma or infection) activate resident dendritic cells (a type of APC) in the skin.
• These activated dendritic cells produce inflammatory cytokines, particularly IL-12 and IL-23 .
• Activation and Differentiation of T-cells: IL-12 and IL-23 act on naive T-cells, promoting their differentiation into specific types of effector T-cells: Th1 cells (T-helper 1): Stimulated by IL-12, they produce cytokines like interferon-gamma (IFN-γ) and TNF-alpha .
• Th17 cells (T-helper 17): Stimulated by IL-23 (and IL-6), they are considered key drivers in psoriasis. Th17 cells produce a range of inflammatory cytokines, notably IL-17A, IL-17F, IL-22, and TNF-alpha .
• Resident memory T-cells (Trm): These T-cells, which "remember" previous inflammation, are found in psoriatic plaques and can quickly reactivate the inflammatory cascade upon re-exposure to triggers.
• Cytokine Cascade: The activated Th1 and Th17 cells, along with other immune cells (e.g., macrophages, neutrophils), release a cascade of pro-inflammatory cytokines into the skin.
• Key Pro-inflammatory Cytokines: TNF-alpha (Tumor Necrosis Factor-alpha): A central inflammatory mediator involved in many chronic inflammatory diseases. It promotes inflammation, activates keratinocytes, and attracts other immune cells.
• IL-17 (Interleukin-17): A potent cytokine that plays a crucial role in psoriasis. It directly stimulates keratinocyte proliferation and the release of further inflammatory mediators.
• IL-22 (Interleukin-22): Also directly stimulates keratinocyte proliferation and contributes to epidermal hyperplasia.
• IL-23 (Interleukin-23): Essential for the survival and expansion of Th17 cells, thus sustaining the inflammatory cycle.

The constant bombardment of keratinocytes by these inflammatory cytokines (especially IL-17, IL-22, TNF-alpha) leads to the hallmark features of psoriatic plaques:

• Accelerated Keratinocyte Proliferation (Epidermal Hyperplasia): Normal keratinocyte turnover is about 28-30 days. In psoriasis, it's reduced to 3-7 days.
• This rapid proliferation leads to a massive accumulation of immature keratinocytes, forming thickened epidermis (acanthosis) and the characteristic silvery scales.
• Abnormal Keratinocyte Differentiation: The rapid cell division means keratinocytes don't have enough time to mature properly.
• They retain their nuclei in the stratum corneum (parakeratosis), which contributes to the silvery, flaky appearance of the scales.
• There is a loss of the granular layer of the epidermis.
• Inflammation and Angiogenesis: The inflammatory environment leads to the dilation and proliferation of blood vessels in the upper dermis (angiogenesis). This contributes to the redness (erythema) of the psoriatic plaques and accounts for the Auspitz sign (pinpoint bleeding when scales are removed, due to thin epidermis over dilated capillaries).
• Inflammatory cells (neutrophils, T-cells) infiltrate the epidermis and dermis. Neutrophils can aggregate to form sterile microabscesses (Munro's microabscesses) in the stratum corneum, particularly visible in pustular psoriasis.
• Genetic factors (e.g., HLA-Cw6, genes related to IL-23R/IL-12B, TNF-alpha) predispose individuals by influencing the immune system's responsiveness and regulation. These genetic variants can lead to a more easily triggered and sustained inflammatory response.

The pathophysiology of psoriasis can be visualized as a vicious cycle:

• Genetic predisposition + Environmental trigger (e.g., trauma, infection, stress).
• Activation of APCs in the skin.
• APCs release IL-12 and IL-23 .
• These cytokines activate and differentiate T-cells (Th1, Th17).
• Activated T-cells release a cascade of pro-inflammatory cytokines (e.g., TNF-alpha, IL-17, IL-22 ).
• These cytokines drive keratinocyte hyperproliferation and abnormal differentiation , as well as inflammation and angiogenesis .
• The resulting skin changes perpetuate the inflammatory environment, creating a chronic cycle.

Psoriasis can manifest in several distinct clinical types, each characterized by specific lesion morphology, distribution, and associated features. It's also important to recognize associated conditions like nail psoriasis and psoriatic arthritis.

• Plaque Psoriasis (Psoriasis Vulgaris): Most Common Type: Accounts for approximately 80-90% of all cases.
• Appearance: Characterized by well-demarcated, erythematous (red) plaques covered with silvery-white scales. The plaques can vary in size from small to large, often coalescing to form larger patches.
• Texture: Lesions are typically raised, thickened, and often feel rough.
• Location: Commonly found on the extensor surfaces of the body (e.g., elbows, knees, scalp, lower back, sacral area). However, it can appear anywhere.
• Symptoms: Often itchy (pruritic), and can be painful, especially if the skin cracks or bleeds.
• Auspitz Sign: When the silvery scales are gently scraped, pinpoint bleeding occurs due due to the thinning of the epidermis over dilated capillaries.
• Koebner Phenomenon: New psoriatic lesions can appear at sites of skin trauma (e.g., scratches, cuts, surgical scars).
• Guttate Psoriasis: Appearance: Characterized by numerous small (0.5-1.5 cm diameter), salmon-pink, drop-like lesions with fine scales.
• Location: Often appears suddenly and widely over the trunk and proximal extremities.
• Trigger: Frequently triggered by a preceding streptococcal infection (e.g., strep throat) 1-3 weeks prior to onset, especially in children and young adults.
• Course: Can resolve spontaneously, but some cases may progress to chronic plaque psoriasis.
• Inverse Psoriasis (Flexural Psoriasis): Appearance: Presents as smooth, shiny, erythematous plaques without significant scaling. The moist environment prevents the typical scale formation.
• Location: Found in skin folds (intertriginous areas) such as the armpits (axillae), groin, under the breasts, in the belly button, and in the gluteal cleft.
• Symptoms: Often exacerbated by friction, sweating, and often accompanied by itching and pain. Can be challenging to differentiate from fungal infections.
• Pustular Psoriasis: Appearance: Characterized by sterile pustules (small, pus-filled blisters) on red, inflamed skin. The pustules are not infectious.
• Types: Generalized Pustular Psoriasis (GPP / Von Zumbusch Psoriasis): A rare, severe, and potentially life-threatening form. Presents with widespread pustules, high fever, malaise, extreme fatigue, and often requires hospitalization. Can be triggered by abrupt withdrawal of systemic corticosteroids, infection, or certain medications.
• Localized Pustular Psoriasis (e.g., Palmoplantar Pustulosis): Affects specific areas, most commonly the palms and soles. Characterized by crops of sterile pustules on a red, thickened background. Often chronic and difficult to treat, and not typically associated with systemic symptoms.
• Erythrodermic Psoriasis: Rarest and Most Severe Form: Affects almost the entire body surface (over 90% BSA), causing widespread redness, scaling, and shedding of skin.
• Symptoms: Patients often experience severe itching, pain, swelling, and systemic symptoms like fever, chills, malaise, and fluid loss.
• Complications: Can lead to serious complications such as dehydration, hypothermia or hyperthermia (due to impaired skin barrier), fluid and electrolyte imbalance, and high-output cardiac failure. Requires immediate medical attention and often hospitalization.
• Triggers: Can develop gradually from chronic plaque psoriasis or be triggered by systemic corticosteroid withdrawal, severe sunburn, infection, or certain medications.
• Nail Psoriasis (Psoriatic Onychodystrophy): Affects approximately 50% of psoriasis patients and up to 80% of those with psoriatic arthritis.
• Appearance: Can manifest as: Pitting: Small depressions in the nail plate.
• Onycholysis: Separation of the nail plate from the nail bed.
• Oil spots (salmon patches): Translucent, reddish-yellow discoloration under the nail plate.
• Subungual hyperkeratosis: Thickening of the nail bed, accumulation of scales under the nail.
• Crumbing: Disintegration of the nail plate.
• Impact: Can be painful, functionally impairing, and aesthetically distressing.
• Psoriatic Arthritis (PsA): Definition: A chronic inflammatory arthritis associated with psoriasis, affecting up to 30% of psoriasis patients.
• Onset: Can precede, coincide with, or (most commonly) follow the onset of skin psoriasis.
• Symptoms: Joint Pain and Swelling: Can affect peripheral joints (fingers, toes, knees, ankles) and/or axial skeleton (spine, sacroiliac joints).
• Dactylitis ("Sausage Fingers/Toes"): Inflammation of an entire digit.
• Enthesitis: Inflammation at sites where tendons or ligaments attach to bone (e.g., Achilles tendon).
• Morning Stiffness: Joint stiffness that is worse in the morning and improves with activity.
• Fatigue.
• Subtypes: Can be symmetrical, asymmetrical, distal (DIP joint dominant), spondylitis, or arthritis mutilans (a severe, deforming type).
• Diagnosis: Clinical, often supported by imaging (X-rays, MRI) and exclusion of other arthropathies.
• Oral Psoriasis: Very rare, can appear as white or grey lesions, fissured tongue, or geographic tongue.
• Psoriasis of the Eyes: Can cause conjunctivitis, blepharitis, or uveitis.

Diagnosing psoriasis typically relies heavily on the characteristic clinical appearance of the lesions. However, in atypical cases or when differentiation from other skin conditions is necessary, additional diagnostic tools may be employed.

• Patient History: Onset and Duration: When did the lesions first appear? How long have they been present?
• Progression: Have they spread? Have they changed in appearance?
• Symptoms: Are they itchy (pruritic)? Painful? Burning?
• Precipitating Factors: Has the patient identified any triggers (stress, infection, trauma, medications)?
• Family History: Is there a family history of psoriasis or psoriatic arthritis?
• Medical History: Past medical conditions, current medications (including over-the-counter drugs and supplements), alcohol and tobacco use.
• Systemic Symptoms: Ask about joint pain, stiffness, swelling (to screen for psoriatic arthritis); fever, malaise (for severe forms like erythrodermic or generalized pustular psoriasis).
• Impact on Quality of Life: Assess the psychological and social impact of the disease.
• Physical Examination: Skin Inspection: Lesion Morphology: Carefully observe the size, shape, color, and texture of the lesions (e.g., well-demarcated erythematous plaques with silvery scales are classic for plaque psoriasis).
• Distribution: Note the location of the lesions (extensor surfaces, scalp, lower back, flexural areas, palms/soles, nails).
• Auspitz Sign: Gently scrape a scale to check for pinpoint bleeding. (Often done cautiously as it can irritate the skin).
• Koebner Phenomenon: Look for lesions in areas of trauma or scarring.
• Nail Examination: Inspect for signs of nail psoriasis (pitting, oil spots, onycholysis, subungual hyperkeratosis).
• Joint Examination: Palpate joints for tenderness, swelling, and warmth.
• Assess range of motion.
• Look for dactylitis (sausage digits) or enthesitis. (Crucial for screening for psoriatic arthritis).
• Mucous Membranes: Examine mouth, genitals for inverse psoriasis (less common).
• When Indicated: A skin biopsy is generally not required for typical cases of psoriasis where the clinical presentation is classic. However, it is invaluable in: Atypical presentations.
• When the diagnosis is uncertain and needs to be differentiated from other inflammatory dermatoses (e.g., eczema, seborrheic dermatitis, lichen planus, cutaneous T-cell lymphoma, tinea infections).
• Suspected drug-induced eruptions.
• Histopathological Findings: Epidermal Hyperplasia (Acanthosis): Marked thickening of the epidermis.
• Parakeratosis: Retention of nuclei in the stratum corneum (outermost layer), which is normally anucleated. This correlates with the silvery scales.
• Elongated Rete Ridges: Downward projections of the epidermis are elongated and thickened.
• Dilated Blood Vessels: In the dermal papillae, close to the epidermis.
• Inflammatory Infiltrate: Lymphocytes and neutrophils in the upper dermis and epidermis.
• Munro's Microabscesses: Collections of neutrophils in the stratum corneum (especially in pustular forms).
• Spongiform Pustules of Kogoj: Intraepidermal collections of neutrophils (especially in pustular forms).

It's important to consider other conditions that may resemble psoriasis, especially in its atypical forms:

• Seborrheic Dermatitis: Can overlap with psoriasis (sebopsoriasis), but typically less erythematous, greasier scales, and predilection for face, scalp, chest.
• Atopic Dermatitis (Eczema): Often more poorly demarcated, intense pruritus, and usually affects flexural surfaces (though inverse psoriasis affects flexural surfaces, its appearance is different).
• Lichen Planus: Characterized by purple, polygonal, pruritic papules and plaques, often with Wickham's striae.
• Pityriasis Rosea: Oval, erythematous, fine-scaling patches, often following skin cleavage lines, usually preceded by a "herald patch."
• Tinea (Fungal Infections): Can mimic plaque or inverse psoriasis; usually unilateral, often with active border; potassium hydroxide (KOH) examination or fungal culture helps differentiate.
• Cutaneous T-cell Lymphoma (Mycosis Fungoides): Can appear as erythematous, scaly patches and plaques, requiring biopsy for differentiation.
• Drug Eruptions: Many drugs can cause psoriasiform rashes.
• Generally not used for diagnosis of skin psoriasis.
• May be ordered to: Rule out other conditions (e.g., antistreptolysin O (ASO) titer for guttate psoriasis triggered by strep infection).
• Monitor for comorbidities (e.g., lipids, glucose for metabolic syndrome).
• Baseline monitoring for systemic therapies (e.g., complete blood count, liver and kidney function tests for methotrexate).
• Screen for psoriatic arthritis (e.g., inflammatory markers like ESR, CRP, though not specific for PsA; rheumatoid factor and anti-CCP antibodies are typically negative in PsA, helping differentiate from rheumatoid arthritis).

Assessing the severity of psoriasis is crucial for determining the appropriate treatment strategy, monitoring treatment effectiveness, and evaluating the overall impact of the disease on a patient's life. Severity assessment typically involves a combination of objective measures of skin involvement and subjective measures of patient well-being.

These scales quantify the extent and characteristics of psoriatic lesions.

• Psoriasis Area and Severity Index (PASI): Description: The most widely used and validated tool for assessing the severity of plaque psoriasis in clinical trials and often in clinical practice. It considers the area of involvement and the severity of erythema (redness), induration (thickness), and desquamation (scaling).
• Calculation: The body is divided into four regions: head (10%), upper extremities (20%), trunk (30%), and lower extremities (40%).
• For each region, the area of involvement (A) is estimated on a scale from 0 to 6 (0=none, 1=<10%, 2=10-29%, 3=30-49%, 4=50-69%, 5=70-89%, 6=90-100%).
• The severity of erythema (E), induration (I), and desquamation (D) for the affected areas within each region is rated on a scale from 0 to 4 (0=none, 1=mild, 2=moderate, 3=severe, 4=very severe).
• The PASI score is calculated using a complex formula: PASI = 0.1(H(E h +I h +D h ) + 0.2(U(E u +I u +D u ) + 0.3(T(E t +I t +D t ) + 0.4(L(E l +I l +D l )
• The final PASI score ranges from 0 to 72.
• Interpretation: Mild Psoriasis: PASI < 10
• Moderate Psoriasis: PASI 10-20
• Severe Psoriasis: PASI > 20
• Limitation: Can be time-consuming to calculate and requires training, making it less practical for routine clinical use by general practitioners.
• Body Surface Area (BSA): Description: A simpler and quicker measure. It estimates the percentage of the total body surface area affected by psoriasis.
• Calculation: Often estimated using the "rule of palms," where the patient's palm (including fingers) represents approximately 1% of their total BSA.
• Interpretation: Mild Psoriasis: < 3% BSA
• Moderate Psoriasis: 3-10% BSA
• Severe Psoriasis: > 10% BSA
• Limitation: Does not account for the redness, thickness, or scaling of the lesions, nor does it consider involvement of critical areas (e.g., face, genitals, palms/soles) which can significantly impair quality of life even with small BSA.
• Physician's Global Assessment (PGA) or Static Physician's Global Assessment (sPGA): Description: A subjective assessment by the clinician, providing an overall evaluation of the patient's psoriasis severity.
• Scale: Typically a 5- or 6-point scale ranging from clear/almost clear to severe/very severe, based on the physician's holistic judgment of erythema, induration, and desquamation.
• Advantage: Quick and easy to use.
• Limitation: More subjective and less quantitative than PASI.

These tools evaluate how psoriasis affects a patient's daily life, which is critical for defining severity, especially if it affects critical areas or causes significant distress.

• Dermatology Life Quality Index (DLQI): Description: A widely used, 10-item questionnaire completed by the patient. It assesses the impact of skin disease on various aspects of daily life over the past week.
• Score: Ranges from 0 (no impact) to 30 (extremely large impact).
• Interpretation: 0-1: No effect on patient's life
• 2-5: Small effect
• 6-10: Moderate effect
• 11-20: Very large effect
• 21-30: Extremely large effect
• Importance: A high DLQI score, even with a low BSA, can indicate severe disease from the patient's perspective, warranting systemic treatment.
• Psoriasis Disability Index (PDI): Similar to DLQI but specific to psoriasis.

Based on a combination of these measures, psoriasis is often categorized for treatment planning:

• Mild Psoriasis: BSA < 3% to 5%
• PASI < 5-10
• DLQI < 5
• No involvement of critical areas (e.g., face, palms, soles, genitals, nails) causing significant functional or psychological impairment.
• Moderate to Severe Psoriasis: BSA > 5% to 10%
• PASI > 10
• DLQI > 5
• OR significant involvement of critical areas, even if BSA is low, due to profound impact on quality of life, function, or psychological well-being.
• OR failure of topical treatments.
• OR presence of psoriatic arthritis.
• Treatment Selection: Guides the choice between topical therapies, phototherapy, systemic medications (oral or injectable biologics). More severe disease often necessitates more aggressive systemic treatments.
• Monitoring: Allows clinicians to objectively track a patient's response to treatment over time (e.g., PASI 75 - 75% improvement in PASI score is a common endpoint in clinical trials).
• Research: Standardizes patient populations for clinical studies.
• Communication: Provides a common language for healthcare providers.
• Patient Advocacy: Helps justify access to more expensive systemic therapies for patients with severe disease.

The management of psoriasis is highly individualized, depending on the type and severity of psoriasis, the presence of comorbidities, patient preferences, and response to previous treatments. It often follows a "step-up" approach, starting with less intensive therapies for mild disease and progressing to more potent systemic treatments for moderate to severe cases.

• Patient Education: Crucial for adherence, self-management, and coping.
• Identification and Avoidance of Triggers: Stress reduction, managing infections, avoiding certain medications, cessation of smoking and alcohol.
• Addressing Comorbidities: Managing associated conditions like psoriatic arthritis, cardiovascular disease, obesity, and mental health issues.
• Psychosocial Support: Psoriasis can significantly impact mental health; support groups and counseling can be beneficial.

These are applied directly to the skin.

• Corticosteroids (Topical): Mechanism: Anti-inflammatory, antiproliferative, vasoconstrictive.
• Forms: Creams, ointments, lotions, gels, foams, sprays. Potency varies (low, medium, high, super high).
• Use: Often first-line for localized plaques. High potency for thick plaques on trunk/extremities, lower potency for face/intertriginous areas.
• Side Effects: Skin atrophy, telangiectasias, striae, hypopigmentation, folliculitis. Systemic absorption can occur with extensive use of high-potency steroids. Tachyphylaxis (decreasing response over time) can occur. Intermittent use or pulse therapy helps mitigate side effects.
• Vitamin D Analogues: Agents: Calcipotriene (calcipotriol), calcitriol.
• Mechanism: Regulate keratinocyte proliferation and differentiation, reduce inflammation.
• Use: Effective for mild to moderate plaque psoriasis, often used in combination with topical corticosteroids.
• Side Effects: Skin irritation, burning, itching. Minimal risk of hypercalcemia with appropriate use.
• Topical Retinoids: Agent: Tazarotene.
• Mechanism: Normalizes keratinocyte differentiation, anti-inflammatory.
• Use: Mild to moderate plaque psoriasis. Often used with corticosteroids to reduce irritation.
• Side Effects: Irritation, redness, burning, photosensitivity. Contraindicated in pregnancy.
• Calcineurin Inhibitors: Agents: Tacrolimus, pimecrolimus.
• Mechanism: Immunomodulatory, suppress T-cell activation.
• Use: Off-label for inverse psoriasis, facial psoriasis, or areas where steroids are contraindicated due to risk of atrophy.
• Side Effects: Burning, itching (especially initially). No risk of skin atrophy.
• Coal Tar: Mechanism: Antiproliferative, anti-inflammatory.
• Use: Available in various concentrations, often in shampoos, creams, and lotions. Less frequently used due to odor, staining, and messiness.
• Side Effects: Folliculitis, photosensitivity, skin irritation.
• Anthralin: Mechanism: Reduces keratinocyte proliferation.
• Use: Short-contact therapy for chronic plaques.