Eczema and Psoriasis: Causes, Symptoms, and Effective Treatment Options
Eczema (also called dermatitis) is a group of inflammatory skin conditions characterized by itching, redness, and a disrupted skin barrier. Below is a structured overview covering its types, causes & triggers, clinical features, diagnosis, and management.
1. Definition & Epidemiology
- Definition: Eczema refers to a set of
skin disorders marked by inflammation, itching (pruritus), and often
chronic relapsing courses.
- Prevalence:
- Affects up to 20% of
children and 3% of adults worldwide.
- Onset often in infancy or
early childhood (especially atopic dermatitis), though some forms (e.g.,
contact dermatitis) can appear at any age.
2. Major Types of Eczema
- Atopic Dermatitis
- Most common form,
especially in children.
- Often associated with a
personal or family history of asthma, allergic rhinitis, or food
allergies.
- Contact Dermatitis
- Irritant Contact Dermatitis: Caused by direct chemical
or physical damage (e.g., cleaning detergents, solvents).
- Allergic Contact Dermatitis: Immune-mediated reaction
to allergens (e.g., nickel, fragrances, preservatives).
- Dyshidrotic Eczema
(Pompholyx)
- Small, intensely itchy
vesicles on the palms, soles, or sides of fingers.
- Nummular (Discoid) Eczema
- Coin-shaped patches, often
on limbs or trunk, can ooze or become scaly.
- Seborrheic Dermatitis
- Greasy, yellow-crusted
patches in sebaceous areas (scalp, face, chest), often called “dandruff”
on the scalp.
- Stasis Dermatitis
- Occurs on the lower legs in
the setting of chronic venous insufficiency, with swelling,
hyperpigmentation, and ulcer risk.
3. Pathophysiology
- Skin Barrier Dysfunction: Defects in filaggrin and
tight-junction proteins lead to increased water loss and penetration of
irritants/allergens.
- Immune Dysregulation:
- Th2-skewed inflammation in
atopic dermatitis (↑IL-4, IL-13).
- Other forms may involve Th1
or Th17 pathways.
- Genetic & Environmental
Interplay:
Family history, dry climates, hard water, pollution, and urban living all
contribute.
4. Common Triggers & Exacerbating Factors
- Irritants: Soaps, detergents,
solvents, wool.
- Allergens: Nickel, fragrances,
preservatives, food proteins (milk, eggs, nuts in atopic dermatitis).
- Environmental: Extremes of temperature or
humidity, hard water, pollution.
- Psychological: Stress, anxiety, and lack
of sleep.
- Infections: Staphylococcus aureus
colonization can worsen flares; viral or fungal infections can also
trigger.
- Lifestyle: Sweating, friction from
clothing, low-humid environments.
5. Clinical Features & Diagnosis
- Symptoms: Intense itching, redness,
swelling, dry or weeping lesions. Chronic scratching can cause
lichenification (thickened skin).
- Distribution:
- Infants: Face, scalp, extensor
surfaces.
- Children/Adults: Flexural areas (elbows,
knees), hands, eyelids.
- Diagnosis:
- Primarily clinical, based
on history and examination.
- Patch testing for suspected
allergic contact dermatitis.
- Skin biopsy rarely needed
except to rule out mimics.
6. Management Strategies
- General Care &
Prevention
- Emollients: Liberal, fragrance-free
moisturizers (twice daily or more) to restore barrier.
- Bathing: Lukewarm baths, gentle
cleansers; pat dry and immediately apply moisturizer.
- Trigger Avoidance: Identify and minimize
exposure to irritants/allergens; wear soft, breathable fabrics.
- Topical Therapies
- Topical Corticosteroids: First-line for flares;
potency chosen based on location and severity.
- Topical Calcineurin
Inhibitors
(tacrolimus, pimecrolimus): Steroid-sparing, useful on face and flexures.
- Systemic Treatments (for moderate-to-severe
disease)
- Phototherapy: Narrowband UVB.
- Oral Immunomodulators: Cyclosporine,
methotrexate, azathioprine in refractory cases.
- Biologics: Dupilumab (IL-4/IL-13
blocker) approved for moderate-to-severe atopic dermatitis.
- Adjunctive Measures
- Antihistamines: For symptomatic itch
relief (especially sedating agents to improve sleep).
- Antibiotics/Antiseptics: For secondary bacterial
infections.
- Wet-wrap Therapy: Enhances topical
treatment delivery in acute severe flares.
7. Prognosis & Quality of Life
- Chronic, Relapsing Course: Periods of improvement and
flares.
- Impact: Can significantly impair
sleep, work/school performance, and psychosocial well-being.
- Long-Term Outlook: Many children “outgrow”
atopic dermatitis by adulthood, though some persist into later life.
Key Takeaways
- Eczema is a spectrum of
inflammatory skin disorders driven by barrier dysfunction and immune
dysregulation.
- Identification of type and
triggers is essential to guide tailored therapy.
- Regular maintenance with
emollients and avoidance of triggers can greatly reduce flares.
- Advanced cases may benefit
from phototherapy or systemic/biologic agents under specialist care.
1. PSORIASIS Definition &
Epidemiology
- Definition
Psoriasis is a chronic, immune‐mediated inflammatory skin disease characterized by well-demarcated, erythematous plaques with silvery scale. - Prevalence
- Affects ~2–3% of the global
population.
- Onset peaks in early
adulthood (20–30 years) and again around 50–60 years.
- Both sexes are affected
equally.
2. Major Clinical Types
- Plaque Psoriasis (Psoriasis
Vulgaris)
– ~80–90% of all cases. Raised, scaly plaques on extensor surfaces (elbows, knees), scalp, lumbosacral area. - Guttate Psoriasis
– Sudden onset of small, drop-shaped lesions, often after streptococcal throat infection. - Inverse (Flexural) Psoriasis
– Smooth, erythematous plaques in skin folds (axillae, groin, inframammary). - Pustular Psoriasis
– Sterile pustules on erythematous base; can be localized (palms/soles) or generalized (life-threatening). - Erythrodermic Psoriasis
– Rare, extensive redness and shedding of skin; can disrupt thermoregulation and barrier function. - Nail Psoriasis
– Pitting, oil-drop discoloration, onycholysis, subungual hyperkeratosis; seen in ~50% of plaque cases. - Psoriatic Arthritis
– 20–30% develop a seronegative inflammatory arthritis; affects DIP joints, spine, entheses.
3. Pathophysiology
- Genetic Susceptibility
– Strong HLA-C*06:02 association; multiple other loci (IL23R, TNIP1, etc.). - Immune Dysregulation
– Dendritic cells → IL-23 → Th17 cells → IL-17A/F, IL-22 → keratinocyte proliferation.
– TNF-α also central, amplifying inflammation. - Keratinocyte Hyperproliferation
– Turnover time reduced from ~28 days to 3–5 days, creating scale.
4. Triggers & Exacerbating Factors
- Infections
– Streptococcal pharyngitis (Guttate psoriasis). - Stress & Trauma
– Emotional stress, Koebner phenomenon (lesions at sites of skin injury). - Medications
– β-blockers, lithium, antimalarials, NSAIDs. - Lifestyle
– Smoking, heavy alcohol use. - Metabolic Factors
– Obesity (adipokines can fuel inflammation). - Climate
– Cold, dry weather often worsens plaques.
5. Clinical Features & Diagnosis
- Lesion Morphology
– Silvery scale atop erythematous, sharply marginated plaques. - Distribution
– Extensor surfaces, scalp, sacral area.
– Intertriginous areas in inverse psoriasis. - Associated Findings
– Nail changes, arthritis, metabolic syndrome features (obesity, dyslipidemia). - Diagnosis
– Mainly clinical.
– Biopsy rarely needed: shows regular epidermal hyperplasia, elongated rete ridges, Munro’s microabscesses.
6. Management Strategies
A. Topical Therapies (mild disease or adjunct)
- Corticosteroids (mid–high potency for
plaques)
- Vitamin D analogues (calcipotriene, calcitriol)
- Topical retinoids (tazarotene)
- Coal tar, salicylic acid (keratolytic aid)
B. Phototherapy
- Narrowband UVB (311 nm) – gold standard
for moderate disease
- PUVA (psoralen + UVA) – deeper
penetration but more AEs
C. Systemic Non-Biologics
- Methotrexate – antimetabolite, weekly
dosing
- Acitretin – oral retinoid,
teratogenic
- Cyclosporine – potent immunosuppressant,
used short-term
D. Biologic Therapies
Targeted
blockade of immune cytokines
- Anti-TNF-α
– Etanercept, infliximab, adalimumab - Anti-IL-12/23
– Ustekinumab - Anti-IL-17
– Secukinumab, ixekizumab, brodalumab - Anti-IL-23 (p19 subunit)
– Guselkumab, tildrakizumab, risankizumab - Oral Small-Molecule
– Deucravacitinib (TYK2 inhibitor)
E. Lifestyle & Adjunctive Measures
- Weight reduction in obese
patients
- Smoking/alcohol cessation
- Stress management
- Emollients to soothe scaling
7. Prognosis & Quality of Life
- Chronic Relapsing
– Flares and remissions; severity and response vary. - Comorbidities
– ↑Cardiovascular risk, metabolic syndrome, depression/anxiety. - Impact
– Stigma, social withdrawal, impaired work productivity.
Key Takeaways
- Psoriasis is driven by a
Th17/IL-23−mediated loop leading to keratinocyte overgrowth.
- Clinical types range from
localized plaques to life-threatening erythroderma.
- Treatment is staged: topical
→ phototherapy → systemic/non-biologic → biologic.
- Address comorbidities
(cardio-metabolic, mental health) for holistic care.
Comments
Post a Comment