Contact dermatitis (allergic and irritant)

Contact dermatitis is among the most common skin diseases encountered in clinic, occupational medicine, and general practice. ICD accounts for ~80% of contact dermatitis; ACD ~20%. Occupational distribution is heavy — healthcare, hairdressing, construction, food service, cleaning. Common sensitizers shift over time; current high-prevalence allergens include nickel (most common worldwide), methylisothiazolinone (preservative epidemic over past decade), fragrance mix, paraphenylenediamine (PPD, hair dyes and henna), and neomycin.

ACD — type IV (delayed) hypersensitivity:

• Sensitization phase: hapten (small molecule that binds protein) encounters skin, processed by Langerhans cells, presented to naive T cells in lymph node → memory T cells. Takes 10–14 days minimum; may be years of asymptomatic exposure before clinical reaction.
• Elicitation phase: on re-exposure, memory T cells activate within 12–72 hours → clinical dermatitis.

ICD — non-immune chemical/physical damage:

• Direct disruption of barrier lipids or keratinocytes by detergents, solvents, acids, alkalis, friction, prolonged moisture.
• No sensitization required; dose-dependent; occurs in anyone given sufficient exposure.

Some conditions combine both (e.g., chronic hand dermatitis often begins as ICD and is complicated by secondary ACD to glove or topical medication).

Acute ACD: pruritic, erythematous plaques with vesicles or bullae, often weeping. Geometry/linearity matches the contactant (linear streaks from plant contact; square from a patch test; circular from a button or watchband).

Chronic ACD or ICD: lichenified, fissured, scaly plaques, often on hands. Wet-work and cumulative irritation dominate.

Distribution is the diagnostic clue:

• Periumbilical: nickel (belt buckle, jean stud).
• Eyelid: transferred from hands (nail polish, shampoo, fragrance). Eyelid dermatitis is often ACD to something not touched directly to the eye.
• Scalp/hairline/ears: hair dye (PPD), shampoo (methylisothiazolinone), rubber in helmets.
• Face (airborne): fragrances, plant resins; characteristic sparing of submental/retroauricular areas.
• Hands (dorsal > palmar): occupational wet work, glove rubber, soaps; dishpan hands.
• Feet: rubber in shoes (mercaptobenzothiazole), dichromate in leather.
• Linear streaks (extremity): plant contact (poison ivy, poison oak, poison sumac — Toxicodendron/urushiol).
• Anogenital: preservatives in wipes, topical anesthetics (benzocaine), latex condom.

Id reaction (autosensitization): symmetric papulovesicular eruption on trunk/extremities remote from the primary site, especially in stasis dermatitis or chronic hand/foot ACD.

• Erythema is often subtle or absent in Fitzpatrick V–VI. The diagnostic features are geometric/pattern-matched distribution, intense pruritus, vesiculation (when present), and post-inflammatory dyspigmentation (hyper- more often than hypo-).
• Lichenification and PIH dominate chronic contact dermatitis in darker skin; acute vesiculation is still visible.
• Hair dye ACD (PPD) is common and clinically important in SoC adults — severe scalp edema, oozing, involvement of ears and posterior neck can occur.
• Hydroquinone and skin-lightening products can cause contact dermatitis and exogenous ochronosis (blue-grey macular hyperpigmentation from prolonged use) — ask about OTC/imported lightening creams.
• Cosmetic/hair-product allergens are particular relevant in SoC dermatology: PPD in dyes and henna, fragrance, cocamidopropyl betaine, propylene glycol, shea butter (rare but documented).
• Perilabial and perioral ACD from toothpaste (cinnamon), fluoride, lip balm ingredients — commonly missed.

• Phytophotodermatitis — contact with furocoumarins (lime juice, celery, parsley) + UV → bizarre streaky hyperpigmentation. Common 'margarita dermatitis.' Not true ACD — it's a phototoxic reaction. Pigment persists months.
• Systemic contact dermatitis — sensitized patient ingests/absorbs the allergen systemically; diffuse dermatitis, 'baboon syndrome' (erythema in flexures, buttocks). Nickel in food (chocolate, soy, legumes, shellfish), balsam of Peru in spices, mercury from dental amalgam — rare.
• Protein contact dermatitis — type I + type IV to proteins (latex, food handlers). Combined urticarial + eczematous response.
• Photoallergic contact dermatitis — ACD requiring UV activation. Sunscreens (older benzophenones, octocrylene), topical NSAIDs (ketoprofen).

• Atopic dermatitis — ill-defined, flexural, atopic history; often coexists with ACD.
• Psoriasis — well-demarcated, silvery scale, extensor, nail changes.
• Seborrheic dermatitis — greasy scale, nasolabial/scalp/chest distribution.
• Tinea — annular, central clearing, KOH positive; consider whenever ACD is atypical.
• Drug eruption (morbilliform) — symmetric, trunk-predominant, temporally related to a new drug.
• Cellulitis — unilateral, warm, tender, febrile; ACD can mimic but lacks systemic features.
• Stasis dermatitis — lower legs in older adults, varicosities, hemosiderin; often with secondary ACD to neomycin or other topicals applied over it.
• Cutaneous T-cell lymphoma — adult eczema refractory to therapy; biopsy.

Most cases clinical + empiric avoidance. When ACD is suspected and persists after avoiding obvious culprits:

• Patch testing — gold standard for ACD. Standardized allergen panels (T.R.U.E. Test for broad screen; NACDG or EU standard series for comprehensive panel; supplemental panels for specific exposures — hairdresser, dental, photographic). Read at 48 hours and 72–96 hours (sometimes 7 days for metals and neomycin).
• Avoid patch testing during active dermatitis on the test site (back), during systemic corticosteroid >10 mg/day, or recent UV exposure of the back.
• KOH: rule out tinea in atypical or annular cases.
• Biopsy: rarely diagnostic for ACD vs. other eczematous disorders but useful to exclude mimickers (CTCL).
• Photo-patch testing: for suspected photoallergic contact dermatitis.
• Document occupation, hobbies, skincare routine, OTC products in detail — the history IS the test.

• Identify and avoid the allergen/irritant. This is curative for ACD; management for ICD.
• Barrier protection — gloves for wet work (cotton liner beneath rubber to reduce rubber sensitization), emollients (ceramide-based, petrolatum) several times daily.
• Gentle skin care — non-soap cleansers, avoidance of fragrance, lukewarm water.
• Topical corticosteroids — matched to site and severity. Class I (clobetasol 0.05%) short courses for thick hand/body plaques; low-potency for face/eyelid/intertriginous; taper over 1–2 weeks as tolerated.
• Topical calcineurin inhibitors (tacrolimus 0.1%, pimecrolimus 1%) — steroid-sparing for eyelid, face, intertriginous, chronic maintenance. No atrophy.
• Wet compresses for acute weeping ACD, followed by topical steroid.
• Oral antihistamines — minimal evidence for itch in ACD; sedating antihistamines at bedtime can help sleep.

• Systemic corticosteroids — severe, widespread ACD (classic extensive poison ivy). Prednisone taper over 2–3 weeks (e.g., 40–60 mg/day x 5 days, then taper) — shorter courses rebound.
• Phototherapy (nbUVB or PUVA) — for chronic contact dermatitis not controlled by topicals/avoidance.
• Systemic immunosuppressives (methotrexate, cyclosporine, azathioprine, mycophenolate) — chronic refractory disease after patch testing has excluded ongoing exposure.
• Dupilumab — off-label for chronic hand ACD; emerging evidence.
• JAK inhibitors — topical ruxolitinib, oral upadacitinib/abrocitinib — evolving evidence in chronic eczematous disease.

Excellent when allergen/irritant is identified and avoided. Occupational hand ACD has the worst prognosis because exposure often continues. ACD is lifelong once sensitized — patch test results matter forever. Chronic unavoidable exposure (certain jobs) may require job modification.

• Distribution is diagnostic. Periumbilical → nickel; eyelid → transferred (think nail polish, shampoo, fragrance); linear streaks → plant.
• Eyelid dermatitis is usually ACD to something fingers carry — examine hands + detailed product history.
• Treatments themselves can sensitize. Neomycin is among the most common allergens we prescribe. Consider mupirocin or plain petrolatum instead.
• Preservatives in 'hypoallergenic' or 'natural' products (methylisothiazolinone, formaldehyde releasers) are leading allergens — patients may need specialized patch testing to identify.
• Short (6-day) prednisone packs rebound for poison ivy — use 2–3 week taper.
• Patch testing > scratch testing for ACD. Prick/scratch tests are for IgE-mediated (type I) allergies.
• Persistent post-patch-testing reaction >3 months in one reading position — consider ongoing low-level exposure or flare from product reintroduction.
• 'Toilet seat dermatitis' — formaldehyde in public toilet seats or disinfectants; peculiar pattern on posterior thighs in children.

Contact dermatitis means your skin is reacting to something you've touched. Finding and avoiding that thing is the cure. I may send you for patch testing to identify allergens — you'll wear patches on your back for two days, then come in twice to have them read. In the meantime: avoid fragrance, use gentle soap and moisturizer, and apply the prescribed cream. If widespread (poison ivy etc.), oral steroids for 2–3 weeks will be needed to prevent rebound. Once we identify your allergens, you'll need to check product ingredient labels for life — I'll give you a list of safe alternatives. Eyelid rashes are usually from something your hands are carrying, like nail polish or shampoo.