Contact allergy: dermatitis, causes and treatment

Contact allergy is a delayed-type immune reaction of the skin to low-molecular chemicals that have previously sensitized the body. Clinically, it manifests as allergic contact dermatitis: itching, erythema, edema, papules and vesicles, and, in chronic cases, lichenification and cracking. It is important to distinguish allergy from irritant contact dermatitis, where direct skin injury causes a similar picture without the involvement of immune memory. Accurate differentiation is crucial to the entire process, from diagnosis to treatment. [1]

Contact allergens surround us at home and at work: metals (nickel), fragrances and their oxidized products, preservatives (isothiazolinones), para-phenylenediamine in dyes, acrylates in gel varnishes and dental/printing materials, biocides, rubber chemicals in gloves, cosmetics and ophthalmic products. The picture of the disease develops differently in different people: in some, the eyelids are involved (cosmetics and ophthalmology), in others - the hands (wet work, gloves, acrylates), in others - the feet and torso (shoes, textiles, professional contacts). [2]

Modern diagnostics are based on epicutaneous patch testing with standardized allergens, with correct timing and assessment of clinical relevance. If photoallergy is suspected, a photopatch test is used: a dual set of allergens, one of which is irradiated with ultraviolet A, which helps confirm a photoinduced reaction. This approach is reproducible and forms the basis for personalized treatment. [3]

Prevention is equally important: regulatory measures and public awareness are making a real difference in epidemiology. In Europe, following restrictions on nickel in consumer products, the prevalence of sensitization decreased, and following restrictions on methylisothiazolinone, the proportion of related allergies decreased. This demonstrates that effective exposure control strategies are effective and should accompany each individual treatment. [4]

Code according to ICD-10 and ICD-11

In the International Classification of Diseases, Tenth Revision, allergic contact dermatitis is coded in block L23 (with details on causes: metals, cosmetics, adhesives, etc.), irritant contact dermatitis in L24, and "unspecified" contact dermatitis in L25. Photoinduced contact reactions are classified in block L56: photocontact dermatitis and drug-induced photoallergic reactions. This allows coding of both the mechanism and the presumed source. [5]

In the International Classification of Diseases, Eleventh Revision, allergic contact dermatitis is classified under skin diseases under code EK00, with detailed subcodes (cosmetics and fragrances, hair products, food additives on skin, disinfectants, etc.). Photoallergic contact dermatitis (EK01) and irritant contact dermatitis (EK02) are coded separately. This level of detail helps better identify clinically significant triggers and plan preventive measures. [6]

Table 1. Frequently used codes for contact dermatitis

Clinical situation	ICD-10	ICD-11
Allergic contact dermatitis	L23.*	EK00 (subcodes by source, for example EK00.1 - fragrances/cosmetics) [7]
Irritant contact dermatitis	L24.*	EK02
Contact dermatitis, unspecified	L25.*	use EK00/EK02 for clarification
Photocontact dermatitis	L56.2, L56.1 (drug photoallergy)	EK01 (photoallergic contact dermatitis) [8]

Epidemiology

Contact sensitization is very common in the general population. A meta-analysis of population studies found that at least 20% of people are sensitized to common contact allergens when tested. This does not mean everyone has symptoms, but "immune readiness" is high. [9]

Data from patients at specialized centers demonstrate a high proportion of positive patch tests and a diversity of significant allergens. A modern review reported that in a sample of 3,119 European patients, the frequency of at least one positive patch test was 27%, and the clinical diagnosis of allergic contact dermatitis was 8.2%. These figures are consistent with the daily practice of large dermatology clinics. [10]

The composition of "leading allergens" changes over time. In North America, according to the North American Contact Dermatitis Group, a high proportion of positive reactions to fragrances, isothiazolinones, and nickel is noted, although the methylisothiazolinone "epidemic" there is declining later than in Europe. The European trend in recent years has been a decline in isothiazolinones following restrictions and an increase in the proportion of sensitization to oxidized terpenes of fragrances (limonene, linalool). [11]

Regulations are working: after the "nickel directive" in the European Union, the prevalence of nickel sensitization in young women decreased significantly; data for methylisothiazolinone show similar trends. This is an argument in favor of prevention at the policy and industry level, and not just for individual patients. [12]

Table 2. Epidemiological landmarks

Indicator	Grade
Proportion of people with contact sensitization in the population	≥20% [13]
Positive patch tests in a European clinical cohort (3119 individuals)	27% [14]
Diagnosis of allergic contact dermatitis in the same cohort	8.2% [15]
Isothiazolinone trends in Europe (post-restriction)	Decrease [16]

Reasons

Allergic contact dermatitis is caused by haptens—small molecules that bind to skin proteins and are recognized by the immune system as foreign. Typical sources include metals (nickel, cobalt), fragrances and their oxidized products (limonene, linalool), preservatives (methylisothiazolinone, methylchloroisothiazolinone, benzisothiazolinone), para-phenylenediamine in dyes, acrylates in the nail industry and dentistry, formaldehyde-releasing agents, biocides, and disinfectants. [17]

The composition of "major" allergens is changing under the influence of the market and regulations: for example, the restriction of methylisothiazolinone in cosmetics reduced the proportion of related reactions in Europe, while in North America the decline occurred later. Separately, it is worth noting the increasing diagnostic significance of oxidized terpenes in fragrances. [18]

Photoallergic reactions are most often associated with sunscreen components and photosensitizing medications; they are confirmed by photopatch testing. Mineral UV filters (titanium dioxide, zinc oxide) very rarely cause true allergies, while organic filters and fragrances may be involved. [19]

In professional settings, wet work, frequent disinfection, dyes, and acrylates play a significant role in hairdressers and nail technicians, as do cleaning agents and biocides in cleaners and healthcare workers. Hands often exhibit a combination of irritant and allergic mechanisms. [20]

Table 3. Common allergens and where they “hide”

Allergen	Typical sources
Nickel	Costume jewelry, clasps, techniques, tools
Flavors (including oxidized limonene/linalool)	Cosmetics, household chemicals, “aromatized” goods [21]
Isothiazolinones (MI, MCI/MI, BIT)	Cosmetics, paints, adhesives, detergents [22]
Para-phenylenediamine	Hair, eyebrow, and eyelash dyes
Acrylates	Gel polishes, dentistry, 3D printing; gloves allow some acrylates to pass through
Preservatives/biocides	Disinfection products, household chemicals

Risk factors

Key factors include wet work and frequent contact with detergents, occupational exposures, penetration of allergens through a damaged skin barrier, and multiple microdoses of allergens in everyday cosmetics. Piercings and contact with nickel increase the risk of nickel allergy, especially in young women. [23]

Hair and nail technicians are at high risk due to dyes, bleaches, and acrylates; healthcare workers are at high risk due to gloves, antiseptics, disinfectants, and wet hygiene. Proper glove selection and glove changing practices, skin care, and training reduce the risk but do not eliminate the need for patch testing if symptoms occur. [24]

Atopic dermatitis, as a background condition, does not "protect" against contact allergies: on the contrary, the barrier defect increases skin permeability and the likelihood of sensitization. This is especially noticeable on the eyelids and hands, where the skin is thin and frequently comes into contact with potential allergens. [25]

Regional and regulatory factors are also important: where restrictions on nickel release and preservatives are in place, the sensitization pattern changes and the risk to the population is reduced. [26]

Table 4. Risk factors and what to do about them

Factor	What increases the risk	What helps?
Wet work, frequent washing	Irritation, penetration of haptens	Barrier creams, warm water, mild detergents, cotton gloves
Professional chemicals	Dyes, acrylates, biocides	Glove selection, training, task rotation, ventilation
Damaged barrier	Atopic background, cracks	Daily emollients, barrier repair, early treatment of flare-ups
Piercing, nickel	Long exposure	Nickel-free jewelry, test kits, and replacement sources

Pathogenesis

Allergic contact dermatitis is a delayed-type immune reaction. A hapten molecule binds to skin proteins, forming a neoantigen. Langerhans cells present it to T lymphocytes, forming a memory pool. Upon repeated contact, T cells trigger inflammation with the release of cytokines and the recruitment of effector cells, resulting in clinical manifestations. [27]

Some haptens, such as nickel, directly activate the innate immune system (including through danger recognition receptors), which enhances sensitization. Low doses, repeated many times, can "train" the immune system more powerfully than a single, intense exposure. [28]

In the photoallergic variant, ultraviolet A energy is required: the molecule is transformed by light and becomes a fully functional hapten; this is confirmed by a photopatch test with irradiation of one of the series. It is important not to confuse photoallergy with phototoxicity, where there is no immune memory. [29]

Finally, irritant dermatitis is predominantly a direct barrier injury and an inflammatory reaction without immune memory, but in practice both mechanisms often coexist, especially on the hands, complicating the presentation and treatment. [30]

Symptoms

Acute course: itching, redness, swelling, small blisters and "serous wells," often with oozing. Subacute forms produce scaling and cracking. Chronic course is characterized by thickening of the skin, lichenification, painful cracks, sleep disturbances, and disruption of daily activity. Localization often "hints" at the source (eyelids, hands, ears, feet). [31]

The eyelids are a "litmus test" for contact allergies to cosmetics, ophthalmic drops, fragrances, and nickel (hand-transferred). Even minimal contact can cause a pronounced reaction. The primary source may not be the eyelids, but, for example, nail polish or shampoo. [32]

Hands suffer from wet work, contact with detergents, biocides, cosmetics, and acrylates. Irritant and allergic mechanisms often combine here, and the damage can become chronic and difficult to treat. [33]

Photoallergic reactions occur on exposed skin, are aggravated by sunlight, and are confirmed by photopatch testing. Unlike photoallergy, phototoxicity symptoms appear more quickly and affect more people with similar exposure. [34]

Table 5. Site Hints and Probable Triggers

Localization	Common causes
eyelids	Cosmetics, ophthalmic preparations, fragrances, nickel (transfer) [35]
Brushes	Wet work, disinfectants, gloves, acrylates, biocides [36]
Neck, ears	Jewelry, perfume, hair dyes
Dorsal foot	Shoe materials, adhesives, rubber chemicals
Open areas	Photoallergens in sunscreens/medications [37]

Classification, forms and stages

Based on the mechanism, allergic and irritant contact dermatitis are distinguished; based on the influence of light, photoallergic and phototoxic variants are distinguished. For the allergic variant, proof is a positive patch test with clinical relevance; for the photoallergic variant, a photopatch test is used. [38]

By duration - acute, subacute and chronic. Chronic is more common on the hands with mixed mechanisms and requires a separate treatment and prevention strategy. [39]

By localization - “eyelid eczema”, “hand eczema”, “shoe dermatitis”, etc. This linkage facilitates the search for sources, since the set of allergens in each “zone” is predictably different. [40]

Severity ranges from mild, limited to severe, refractory, requiring systemic therapy. For chronic hand eczema, there are detailed European guidelines with step-by-step therapy algorithms. [41]

Table 6. Key forms of contact dermatitis

Form	The difference	Diagnostic test
Allergic	Immune memory, delay 24-72 hours	Patch test
Irritable	Direct damage to the barrier	Clinical and anamnestic assessment
Photoallergic	Requires ultraviolet A	Photopatch test
Phototoxic	Without immune memory, many	History + exception

Complications and consequences

Without addressing the underlying causes, chronic inflammation leads to persistent itching, pain, cracks, secondary infection, sleep loss, and decreased productivity. In the hands, this directly impacts professional performance. [42]

Occupational forms of contact eczema are one of the most common causes of occupational skin diseases. Unrecognized allergies lead to lengthy sick leave, job changes, and financial losses. [43]

In the eyelids, prolonged inflammation worsens the quality of life, interferes with wearing contact lenses and requires a thorough revision of ophthalmological care and treatment. [44]

Finally, “secondary chronification” due to the addition of an irritant mechanism against the background of a damaged barrier makes therapy more complex and requires more comprehensive tactics. [45]

When to see a doctor

If rash, itching, and redness recur in the same areas after contact with cosmetics, jewelry, household chemicals, gloves, nail polish, or sunscreen, this is a reason to undergo a specialist examination and schedule patch tests.

If the eyelids or hands are affected, or there are signs of photo-dependence (worse after sun exposure), it is better not to delay: the sooner the allergen is identified, the easier the remission. [46]

In severe exacerbations with extensive oozing, cracks, pain and sleep disturbances, with signs of secondary infection (pus, yellow crusts, fever), an in-person examination and correction of therapy are required.

In cases of chronic hand eczema that interferes with work, it is important to involve an occupational health specialist/occupational safety service to select gloves, organize “dry” periods and provide training. [47]

Diagnostics

Step 1. A detailed interview and "allergy map." I find out what exactly has come into contact with the skin in the last 7-10 days, which areas are affected, and whether there is a connection with the sun, work, cosmetics, manicures, hair dyes, jewelry, or new home remedies. This will narrow the list down to a few candidates.

Step 2. Epicutaneous patch testing. Standardized patches containing the European core series of allergens are applied to the back, along with additional panels (fragrances, acrylates, gloves, and the patient's own products), as indicated. Readings are taken at approximately 48 hours and 72-96 hours, assessing the strength of the reaction and its relevance to symptoms. [48]

Step 3. If photoallergy is suspected, perform a photopatch test. Two identical series of allergens are applied; one is irradiated with ultraviolet A light after 48 hours, while the other is left unirradiated. Comparing the reactions confirms or refutes the photoallergic mechanism. [49]

Step 4. Localized tests and provocations. In questionable cases, testing with "own products" is used, sometimes open tests on a small area are used. For hand eczema and doubts about a mixed mechanism, the role of irritants (frequency of washing, disinfection, gloves) is assessed. The result is a personalized list of allergens and an elimination plan. [50]

Table 7. Diagnostic methods: what, when, why

Method	What does it give?	When especially needed
Patch test with base series	Search for the "main" allergens	Primary diagnosis in most patients [51]
Advanced panels	Clarification "under profession/hobby"	Nail industry, hairdressers, dentistry, cleaning
Test "own products"	Checking household triggers	Varnishes, creams, sun protection, hygiene products
Photopatch test	Confirmation of photoallergy	Suspected sunscreens, photosensitizing drugs [52]

Differential diagnosis

The main "double" is irritant contact dermatitis. It develops in many people with strong irritants, develops more quickly, often stings more than itches, and does not require sensitization. However, both mechanisms often coexist, especially on the hands. [53]

Contact allergies must be distinguished from atopic dermatitis, seborrheic dermatitis, psoriasis, dermatophytosis, perioral dermatitis, and contact urticaria (immediate mechanism). Regarding eyelids, be aware of ophthalmic drops and topical antibiotics as sources of sensitization. [54]

In photoinduced rashes, photoallergy and phototoxicity, as well as other photodermatoses, are differentiated. The exposure history and photopatch testing are decisive here. [55]

Finally, systemic rashes that coincide with medication intake may mask contact allergies or coexist with them. If in doubt, refer the patient to a dermatologist-allergist and review the entire drug therapy.

Table 8. How to distinguish the main conditions

State	Start	Itching/burning	A test that helps
Allergic contact dermatitis	24-72 hours after contact	Itching is predominant	Patch test
Irritant contact dermatitis	Hours-days, often from the first contact	Burning, pain	History + exception
Photoallergy	After sun on "blurred" areas	Itching, erythema +	Photopatch test
Contact urticaria	Minutes	Blisters, burning	Immediate reaction tests

Treatment

Allergen education and elimination. The key to success is eliminating the cause. I'll help you create a personalized list of allergens and sources, teach you how to read ingredients, and choose alternatives. For work, establish a rotation of wet tasks, use cotton undergloves, change gloves regularly, and protect your skin during household chores. Avoiding strong fragrances and "hourly antiseptics" without medical advice dramatically reduces flare-ups. [56]

Restoring the barrier. Daily emollients with urea or glycerin, gentle, fragrance-free cleansers, and good hygiene habits (warm, not hot, water; patting dry with a towel; applying creams "immediately after washing") are not cosmetics, but therapy. For hands, "oily" creams applied overnight under cotton gloves are helpful. The better the barrier, the less likely it is to become sensitized again. [57]

Topical corticosteroids remain the first-line therapy for flare-ups: moderate to strong doses on the trunk and extremities, and weak, short-course doses on the face and eyelids. The "finger rule" and strict duration limits reduce the risk of side effects. After the inflammation has subsided, we switch to maintenance emollients and a "proactive" regimen if relapses are likely. [58]

Calcineurin inhibitors for sensitive areas. Tacrolimus and pimecrolimus are suitable for the eyelids, face, and groin folds, where long-term use of corticosteroids is undesirable. They are also suitable for maintaining remission during frequent relapses. This is especially relevant in "cosmetic" forms in adults. [59]

Acute, severe flare-ups. For extensive oozing and rashes, systemic corticosteroids can be prescribed briefly, followed by rapid dose reduction and strict allergen elimination to prevent rebound. If signs of secondary infection appear, antiseptics or antibiotics are added as indicated. After relief, we always return to topical anti-inflammatory therapy and barrier care. [60]

Phototherapy for chronic forms. Narrowband ultraviolet light therapy or ultraviolet A1 can help with chronic hand eczema when topical therapy is insufficient. However, if photoallergy or phototoxicity is suspected, this method is contraindicated—diagnostic testing should first be performed using a photopatch test. [61]

Systemic immunomodulators for chronic hand eczema. In countries where alitretinoin (an oral retinoid) is available, it is considered for severe cases resistant to topical therapy; cyclosporine, methotrexate, or azathioprine are also used depending on the patient's profile. These strategies are outlined in European and national guidelines for hand eczema. [62]

New option: delgocitinib (topical Janus kinase inhibitor). Since 2024, delgocitinib 2% cream has been approved in the European Union for adults with moderate-to-severe chronic hand eczema when corticosteroids are insufficient or inappropriate. In Phase 3 studies, the drug improved all primary endpoints at 16 weeks and showed minimal systemic exposure; in 2025, superiority over alitretinoin in a head-to-head comparison for efficacy and tolerability was reported. This is not an “anti-allergy shot,” but a powerful anti-inflammatory tool for complex hand eczema. [63]

Special situations: eyelids and ophthalmology. For eyelids, avoid high-potency corticosteroids; use short courses of weak corticosteroids and/or calcineurin inhibitors. Review eye drops, their preservatives, eye makeup, and makeup removers; consult an ophthalmologist if necessary. [64]

Workplaces and relapse prevention. Occupational health and safety services should be involved: glove selection (some acrylates penetrate latex—nitrile is better and changes should be more frequent), dry break protocols, dispensers for mild products and barrier creams, and an exposure checklist. We provide the patient with a written plan, a list of "prohibited" and "permitted" alternatives, and training in reading labels. [65]

Table 9. Choice of therapy by situations

Situation	Base	Escalation
eyelids	Calcineurin inhibitors, short courses of weak corticosteroids	Eliminate ophthalmic preservatives and cosmetics, patch test with your own drops [66]
Hands, chronic course	Elimination + strong local corticosteroids in courses + barrier	Phototherapy; systemic (alitretinoin/immunosuppressants); delgocitinib 2% cream (European Union) [67]
Suspected photoallergy	Avoiding sun and triggers until verification	Photopatch test, then targeted elimination [68]

Prevention

The main strategy is to reduce exposure. Choose "fragrance-free" and "isothiazolinone-free" products, use simple care products, and avoid harsh cleaning products without gloves. Nickel-free jewelry and fittings actually reduce the risk of sensitization. [69]

At work, manage wet loads: regulate washing frequency, use proper gloves and change them regularly, wear cotton undergloves, apply barrier creams at all sinks, and train employees. This reduces both irritant and allergic reactions. [70]

If you're prone to "cosmetic" reactions, keep a diary, introduce new products one at a time, and have your products patch-tested by a doctor. For sunscreen, choose fragrance-free products and perform photopatch testing if necessary. [71]

Regulatory measures have proven effective: the reduction in nickel and isothiazoline sensitization in Europe is a result of these restrictions. At the family level, this means that informed product choices work. [72]

Forecast

By identifying and eliminating allergens, most patients achieve sustained remission. The contribution of the irritant mechanism decreases with barrier restoration and habit modification.

In the hands, the prognosis depends on occupation and the willingness to follow dry work and care protocols. Involvement of an occupational therapist and updated treatment options (including delgocitinib in the European Union) improve long-term outcomes. [73]

On the eyelids, the prognosis is favorable with a correct revision of all products, including ophthalmic drops and decorative cosmetics: even a small “hidden” exposure can maintain inflammation. [74]

Population-wide trends show that prevention at the government and industry levels is working. This reinforces the idea that personalized elimination strategies and "smart" drug selection are an investment in a relapse-free future. [75]

FAQ

Is it possible to "relieve allergies" permanently with medication?
There are no pills that will "rewrite" the immune system's memory to contact haptens. The real tactic is to find the allergen and eliminate it, restore the barrier, and use anti-inflammatory medications during flare-ups.

How reliable are patch tests?
They are a clinical standard: a properly selected series, readings at 48 and 72-96 hours, and relevance assessment provide high diagnostic accuracy. If photoallergy is suspected, a photopatch test is necessary. [76]

Do antihistamines interfere with patch testing?
Patch testing is a delayed-type reaction, and antihistamines affect immediate reactions. They generally don't interfere with patch testing results, but it's best to discuss this with your doctor: topical and systemic corticosteroids, as well as intense ultraviolet light, can affect readings. [77]

What's new in the treatment of chronic hand eczema?
Delgocitinib 2% cream has been available in the European Union since 2024 for adults when corticosteroids are ineffective or unsuitable; studies have shown significant efficacy and minimal systemic exposure. Alitretinoin is available in some countries for severe cases; phototherapy and systemic immunosuppressants are also used. [78]

Is nickel "no longer a problem" after the directives?
The problem is lessened, but it hasn't disappeared. In susceptible individuals, even small doses in jewelry and fittings trigger relapses, so choosing certified products remains important. [79]