Dermatology disorders

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Overview of Common Dermatology Disorders: In-Depth Clinical Detail

1. Atopic Dermatitis (Eczema)

Definition & Pathophysiology Eczema is a reaction pattern defined by the histologic finding of spongiosis (intercellular epidermal edema). Atopic dermatitis (AD) is the most common form - the cutaneous expression of the atopic state. Prevalence is increasing worldwide. When both parents are affected, >80% of children develop it; when only one parent is affected, prevalence drops to >50%.

A key defect is impaired epidermal barrier - many patients have a mutation in the gene encoding filaggrin, a structural protein of the stratum corneum. Immunologically, AD shows:

Increased IgE synthesis and elevated serum IgE
Impaired delayed-type hypersensitivity reactions
Th2-predominant inflammation

Clinical Features (age-dependent)

Infants (onset in first year of life, 50% of cases; 80% present by age 5): weeping, inflammatory patches and crusted plaques on face, neck, and extensor surfaces
Children/adolescents: flexural dermatitis - especially antecubital and popliteal fossae
Adults: may persist as lichen simplex chronicus or hand eczema

Diagnostic features include: pruritus and scratching, exacerbations and remissions, personal/family history of atopy (asthma, allergic rhinitis, food allergies), dry skin, lichenification, and course >6 weeks.

Cutaneous stigmata include perioral pallor, Dennie-Morgan folds (extra skin fold under lower eyelid), and increased palmar skin markings.

About 40% of children with AD will have dermatitis in adult life; ~80% co-express allergic rhinitis or asthma.

Treatment

Avoid irritants; daily lukewarm bathing followed immediately by topical agents
Topical glucocorticoids (low-to-mid potency) are the mainstay. Low-potency agents for face/intertriginous areas to avoid atrophy
Non-steroid topical agents: tacrolimus ointment (calcineurin inhibitor), pimecrolimus cream (calcineurin inhibitor), crisaborole ointment (PDE-4 inhibitor), ruxolitinib cream (JAK inhibitor) - none cause skin atrophy or HPA suppression
Pruritus control: topical anti-inflammatories; sedating antihistamines for sleep
Secondary infections: culture lesions; treat S. aureus with penicillinase-resistant penicillins or cephalosporins (dicloxacillin or cephalexin 250 mg QID x 7-10 days). For CA-MRSA: TMP-SMX, minocycline, doxycycline, or clindamycin. Adjuncts: dilute bleach baths (0.005% hypochlorite) and nasal mupirocin
Systemic biologics (dupilumab - IL-4Rα antagonist) for moderate-to-severe refractory disease

2. Seborrheic Dermatitis

Features: Chronic, relapsing dermatitis in sebaceous gland-rich areas (scalp, face, central chest). Characterized by erythema with greasy, yellowish scale. Associated with Malassezia (Pityrosporum) yeast.

Treatment:

Low-potency topical glucocorticoids + topical antifungal (ketoconazole or ciclopirox cream)
Scalp: antidandruff shampoos (leave on 3-5 min); severe scalp involvement responds to high-potency steroid solutions (betamethasone or clobetasol)
Avoid high-potency steroids on the face - risk of steroid-induced rosacea or atrophy

3. Psoriasis

Definition & Epidemiology Psoriasis affects up to 2% of the world's population. It is an immune-mediated, systemic inflammatory disease. Now understood as a systemic disease where skin inflammation is dramatically evident, not merely a skin-limited condition.

Histology: Thickened hyperproliferative epidermis, markedly reduced basal keratinocyte transit time, abnormal keratinocyte differentiation, neutrophilic and lymphocytic inflammation, and prominent capillary loops extending into the superficial dermis.

Pathogenesis

Driven by T lymphocytes (especially Th17 cells producing IL-17)
Dermal dendritic cells produce IL-23 (required for Th17 development) and TNF-alpha
IL-17 promotes neutrophil-predominant inflammation and antimicrobial peptide production; TNF-alpha augments IL-17 effects on keratinocytes
Triggers: infections (streptococcal), stress, lithium, beta-blockers, antimalarial drugs
Koebner (isomorphic) phenomenon: lesions develop at trauma sites

Clinical Variants

Type	Features
Plaque (most common)	Erythematous, sharply demarcated plaques with silvery micaceous scale; elbows, knees, gluteal cleft, scalp; symmetric
Guttate (eruptive)	Common in children/young adults; small papules after streptococcal upper respiratory infection; DDx: pityriasis rosea, secondary syphilis
Pustular	Sterile pustules on erythematous base; fever (39-40°C), recurrent episodes; can generalize to erythroderma
Inverse	Affects intertriginous areas (axilla, groin, submammary, navel); moist plaques without scale
Nail	Pitting, onycholysis, oil spots
Psoriatic arthritis	Can co-occur or occur in absence of skin lesions

Treatment

Topical: high-potency glucocorticoids, vitamin D analogs (calcipotriol), retinoids, coal tar
Phototherapy: UVB or PUVA (psoralen + UVA); both have antiproliferative and immunomodulatory effects
Systemic (moderate-severe): methotrexate (antimetabolite), cyclosporine (calcineurin inhibitor - targets lymphocytes)
Biologics (severe/refractory): anti-TNF-alpha (infliximab, adalimumab, etanercept); anti-IL-12/23 (ustekinumab); anti-IL-17 (secukinumab, ixekizumab); anti-IL-23 (guselkumab, risankizumab)

4. Acne Vulgaris

Pathogenesis Self-limited disorder primarily of teenagers and young adults; 10-20% of adults continue to experience it. The permissive factor is increased sebum production at puberty. Sequence:

Follicular orifice blockage by retained keratinous material + sebum → comedone formation
Cutibacterium acnes (formerly Propionibacterium acnes) in comedones releases free fatty acids
Inflammation within cyst → cyst wall rupture
Foreign-body inflammatory reaction to extruded oily/keratinous debris

Clinical Features

Closed comedone (whitehead): 1-2 mm pebbly white papule; precursor of inflammatory lesions; contents not easily expressed
Open comedone (blackhead): dilated follicular orifice; oxidized, darkened, oily content; rarely causes inflammatory acne
Inflammatory lesions: papules, pustules, nodules
Distribution: face (earliest on forehead in adolescence, then cheeks/nose/chin), chest, back
Severe nodulocystic acne can result in significant scarring

Aggravating Factors: friction/trauma (helmets, straps), comedogenic cosmetics, glucocorticoids (topical or systemic), progestin-only contraception, lithium, isoniazid, androgenic steroids, halogens, phenytoin, phenobarbital, polycystic ovary syndrome

Treatment (stepwise)

Mild-moderate (topical): retinoic acid, benzoyl peroxide, salicylic acid (normalize desquamation, prevent comedones); topical antibacterials (benzoyl peroxide, azelaic acid, erythromycin, clindamycin, dapsone) - always combine topical antibiotics with benzoyl peroxide to prevent bacterial resistance; clascoterone cream (topical antiandrogen receptor agent - FDA approved)
Moderate-severe (systemic): minocycline or doxycycline 100 mg BID (anti-inflammatory + antibacterial); duration 3 months
Hormonal (females): FDA-approved oral contraceptives; spironolactone (antiandrogen - safe, effective, durable)
Severe nodulocystic (isotretinoin): synthetic retinoid; weight-based, cumulative dosing; excellent results; highly teratogenic - requires enrollment in iPLEDGE program, two negative pregnancy tests before initiation, monthly negative tests. Side effects: dry skin, cheilitis; severe extracutaneous effects are rare

5. Acne Rosacea

Features: Inflammatory disorder predominantly of the central face. Primarily affects Caucasians of northern European background; seen almost exclusively in adults >30 years old; more common in women, but more severely affected in men.

Characterized by: erythema, telangiectasias, and superficial pustules. No comedones (key distinction from acne vulgaris). Rarely involves chest or back.

Often begins as pronounced facial flushing reactions, triggered by hot drinks, spicy foods, alcohol, and UV exposure.

Treatment: Topical metronidazole, azelaic acid, ivermectin; oral tetracyclines (doxycycline) for inflammatory disease; laser/light therapy for telangiectasias; brimonidine gel for persistent erythema

6. Bullous (Blistering) Disorders

Pemphigus Vulgaris (PV)

Autoantigen: IgG autoantibodies against desmoglein 3 (Dsg3) (initial), followed by anti-Dsg1
Dsg3 is expressed in lower epidermal layers and oral/esophageal mucosae → oral and cutaneous blistering
Acantholysis: intraepidermal blister (suprabasal)
Oral mucosa is often the first site affected
Treatment: high-dose systemic corticosteroids + rituximab or other immunosuppressants

Bullous Pemphigoid (BP)

Autoantigen: IgG autoantibodies against collagen XVII (BP180/COL17) and BP230 - components of hemidesmosomes
COL17 expressed on cell surfaces (major antigen); BP230 is intracellular
Subepidermal (not intraepidermal) blistering
Related variants: Pemphigoid gestationis (identical to BP, occurs in pregnancy), mucous membrane pemphigoid, epidermolysis bullosa acquisita (anti-collagen VII antibodies)

7. Erythroderma

When the majority of skin surface is erythematous. Can cause severe systemic consequences: fever, chills, hypothermia, reactive lymphadenopathy, peripheral edema, hypoalbuminemia, high-output cardiac failure.

Major Causes:

Cutaneous diseases: psoriasis, dermatitis (atopic > contact > stasis/seborrheic)
Drug reactions: penicillin, sulfonamides, aromatic anticonvulsants (carbamazepine, phenytoin), allopurinol - can cause DRESS syndrome (drug reaction with eosinophilia and systemic symptoms)
Systemic diseases: cutaneous T-cell lymphoma (Sezary syndrome, erythrodermic mycosis fungoides), other lymphomas
Idiopathic (usually older men)

Quick Reference Table

Disorder	Key Morphology	Distribution	Pathogen/Mechanism	First-Line Treatment
Atopic Dermatitis	Spongiotic patches, lichenification	Flexures (antecubital, popliteal)	Filaggrin mutation, Th2	Topical steroids, emollients
Seborrheic Dermatitis	Greasy yellow scale + erythema	Scalp, face, central chest	Malassezia	Low-potency steroid + antifungal
Psoriasis	Silvery micaceous scale on plaques	Elbows, knees, scalp	Th17/IL-17/TNF-alpha	Topical steroids + vitamin D; biologics for severe
Acne Vulgaris	Comedones, papules, pustules	Face, chest, back	C. acnes + sebum	Topical retinoids + benzoyl peroxide
Rosacea	Erythema, telangiectasias, pustules (no comedones)	Central face	Vascular dysregulation	Topical metronidazole; oral doxycycline
Pemphigus Vulgaris	Flaccid bullae, erosions	Mucosa first, then skin	Anti-Dsg3 IgG	Systemic corticosteroids + rituximab
Bullous Pemphigoid	Tense bullae on erythematous base	Trunk, extremities	Anti-COL17/BP230 IgG	Topical/systemic corticosteroids

Sources: Harrison's Principles of Internal Medicine 22E (2025), Fitzpatrick's Dermatology 5e, Andrews' Diseases of the Skin Clinical Dermatology

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