Therapeutics in Dermatology
A reference textbook in dermatology
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Allergic contact dermatitis

9 May 2012, by TENNSTEDT D. & BAECK M.

Allergic contact dermatitis (also known as contact dermatitis or allergic contact eczema) occurs following either direct application of, or airborne contact with, an exogenous substance that acts as a hapten (transforming into a complete allergen in the epidermis after binding with a protein) and elicits a delayed-type cell-mediated hypersensitivity reaction (type IV according to the Gell and Coombs classification). Allergic contact dermatitis usually develops in 7 to 10 days after the first contact with the allergen (induction phase) and after 24 to 72 hours following a later contact (elicitation phase). It is very important to remember that, in the vast majority of cases, allergic contact dermatitis does not necessarily develop at the first contact. This kind of allergic reaction can occur after several months or even, less commonly, several years of tolerance. “People are not born with allergies, they become allergic”. The prevalence of contact dermatitis in the general population is somewhere around 2 to 10% according to the studies. However, this is likely to be an underestimate given that it does not account for the significant number of people who know that they are sensitised to an allergen (such as nickel or perfume) and so they have never been tested!



The clinical features of allergic contact dermatitis vary considerably depending on its topography and chronology. At onset, there is acute eczema combining erythema, wheals and vesicles. Considerable pruritus is often present. The lesions classically have poorly defined borders with flaking edges. There is erythema and possibly oedema to the skin and on top of this, numerous vesicles (or even bullae) that are more or less translucent develop, and these slowly seep fluid that quickly leads to small areas of crusting. At this stage, it is possible for a superinfection to develop (impetiginisation).

The “dry” type of allergic contact dermatitis can be present from onset or arise further to an acute episode. The lesions are erythematous, slightly scaly, always have poorly defined borders and are pruriginous. There may be desquamation and possibly some skin cracking. If dry eczema progresses, patients can develop lichenified eczema, which is highly pruriginous and often chronic. Scratching plays a role in encouraging lesions to persist. The skin becomes thickened and purplish with strips of keratosis running across and forming a grid.

In some cases, patients only report a diffuse pruritus while no clinically visible lesion is found.

The distinction between allergic contact dermatitis and irritant contact dermatitis is not always clear-cut, especially where the hands and feet are concerned.

It is imperative that the clinical diagnosis of allergic contact dermatitis rests on two criteria: the history of the illness and carrying out patch tests and additional variations to them.

The highly detailed interview (history of the illness), possibly to be repeated, remains the first step in the aetiological diagnosis of allergic contact dermatitis. All of the following must be covered: chronology of the development of dermatitis, localisation, the features indicating progression in multiple outbreaks and the mode of spread. It is important to use a real “detective” style interview technique, ideally following a pre-established protocol for history taking, and not to ignore any potential clue. Clinicians must as a matter of course explore all potential sources of contact encountered in the patient’s occupation (looking into work tasks, products used at work, preventive steps or cleansing methods etc.), in clothing (type of fabric, shoes, clothing accessories etc.), and in cosmetics and medicines (local topical treatments used recently or in the past).

It is clear that a thorough history can only provide clues in order to make assumptions. It is imperative that this investigation is completed by patch testing to confirm any suspicions.

Patch tests form the second cornerstone of the clinical diagnosis of allergic contact dermatitis; they aim to identify the allergen responsible by reproducing allergic contact dermatitis in miniature.

In other words, confirmation by patch testing is an essential step in the overall management of a patient suspected of having allergic contact dermatitis. In principle, testing should only be carried out after the eczema has resolved. However, it is not feasible to begin taking action to remove an allergen before it has been identified. It is reasonable to carry out at least the standard European battery of tests (Table I) proposed by the European Environmental and Contact Dermatitis Research Group (EECDRG) and the European Society of Contact Dermatitis (ESCD), adopted in France by the Groupe d’Etudes et de Recherches en Dermato-Allergologie (GERDA – Dermatology and Allergology Research and Study Group). In some cases, it may be crucial to carry out further tests: additional series, topical medicines, cosmetics, chemical products handled by the patient, chemical products in the environment or various objects encountered in daily life. The decision to carry out additional series will be made based on the patient’s profession, the topography of the dermatitis and the results from the standard battery of tests (table II).

There are additional methods of investigation that are recent innovations and they complete the confirmation: open tests, semi-open tests, repeated open application tests (ROAT), usage tests etc.

Even if the test results are negative this does not always mean that allergic contact dermatitis can be excluded. A highly detailed retrospective history can, in the light of early observations, help the clinician in proceeding to discover what the allergen(s) responsible may be. Furthermore, an understanding of allergen cross-reactivity and/or an awareness of any concomitant allergies will enable the clinician to put forward their appraisal in response to the problem presented by the patient. The next essential step, which is based on the history, the clinical examination and the results of patch tests, is to look into the relevance of the results to the patient considering both past and present contact. This process is key to proposing an empirical (or certain) diagnosis in the exploration of allergic contact dermatitis. It is critical to establish a link between the test results and the clinical manifestations presented by the patient. This involves a degree of investigation that is sometimes complex but indispensable. The removal of the allergen(s) and therefore the resolution of allergic contact eczema depends on this process.

The very foundation for the treatment of allergic contact dermatitis rests on the essential knowledge of which allergen(s) is/are causing it.

It is essential to be aware of potential cross-reactivity because the clinician can then predict which other substances might elicit further allergic reactions (for example: paraphenylenediamine and benzocaine, octocrylene and ketoprofen etc.).


The histopathology features, as with other types of eczema, are those of spongiotic dermatitis.

At the acute stage, the most characteristic lesion on histology is epidermal spongiosis. This corresponds to an intercellular oedema that varies in intensity and causes keratinocytes to be pulled apart. The intercellular bridges are stretched. There is most significant spongiosis in the lower layers of the epidermis. This can result in vesicle formation (spongiotic vesicles). Inflammatory cells, essentially lymphocytes and less crucially neutrophils and eosinophils, migrate and build up in the spongiotic vesicles (exocytosis). When spongiotic vesicles rupture this leads to the formation of true epidermal perforations. The superficial dermis is the site of significant oedema, which can separate the dermal papillae. The lymph capillaries can become dilated. An intense and interstitial perivascular infiltrate, broadly made up of lymphocytes and histiocytes, is present within the dermis.

At the chronic stage, only residual spongiosis remains. The thickness of the epidermis has increased significantly: acanthosis, lengthened epidermal ridges, and hyperkeratosis alternating with ortho- or parakeratosis.


Laboratory testing does not contribute to the diagnosis of allergic contact dermatitis. Sometimes a patient may present eosinophilia. IgE are not raised, except when there is underlying atopic dermatitis.


Allergic contact dermatitis has a considerable physical and psychological impact on the patient. Since pruritus is often violent, this condition must be considered to be a dermatological emergency in the acute phase and it requires swift management that aims to relieve the patient’s symptoms as quickly as possible.

In the acute phase, the physical impact concerns both the pruritus and the extent of the lesions. Patients experience the greatest psychological impact when the onset is sudden and the clinical expression is striking, and above all when the face or hands are affected.

In chronic illness, therapeutic management must still be suitably conducted in order to avoid the patient feeling discouraged or fatalistic. Of course, aetiological investigation is fundamental because “simple” symptomatic treatment is insufficient.

Furthermore, the socioprofessional consequences in cases of occupational allergic contact dermatitis can be so significant that it is crucial to make a declaration to the local sickness insurance fund for employees subscribing to a general scheme or to an agricultural sickness insurance fund, where relevant. This declaration must be completed in triplicate (by the patient, the employer and the doctor). Various tables of work-related illness can be consulted in cases of “eczema-type lesions recurring after further exposure to risks or confirmed by a positive patch test to the handled product”. The doctor from the sickness insurance fund will make an appraisal and must then make sure either that the patient is offered a new post within the company, or they are transferred. However, it must be recognised that these options sometimes work better in theory than in practice.

In this case, since many patients end up continuing with their occupation or remaining in contact with the allergen, individual (or collective) measures of prevention take on prime importance in reducing contact with the responsible allergen(s) to a strict minimum.


Given that the progression of allergic contact dermatitis involves fluctuating clinical severity, it is clear that it is especially important to monitor this condition attentively because each stage that it progresses through could involve changes to the treatment approach.



This is a crucial and indispensible phase in the treatment of allergic contact dermatitis. Removal of the allergen is obviously not possible unless it has been identified. A symptomatic approach to treatment is doomed to fail more or less entirely if steps to remove the allergen are not taken. Whether removal is simple or challenging depends on what the allergen is. It may be difficult because the allergen is ubiquitous (nickel, for example); removing occupational allergens is also a challenge. Where there is hypothetical or incomplete removal only, collective and individual preventive measures (gloves, appropriate clothing, suitable shoes etc.) take on major importance. With occupational allergens, it is often crucial to work closely with an occupational health officer.


It is crucial to inform the patient about the various sources of exposure that they may be faced with, based on identification of the responsible allergen(s) and, above all, confirmation of its role in the development of symptoms. It may be useful to provide the patient with specific leaflets concerning the sources, exposure and usage of allergens as long as they are explained in a suitable way and relevant to the patient, in accordance with the way in which their eczema presents as well as the various circumstances in which he/she could come across the allergen. Blindly handing out extensive and off-putting lists without comment would not only be useless but also a source of anxiety or discouragement for the patient who will feel as though they are drowning in a flood of unusable information!


Table I Standard European battery of tests proposed by the EECDRG (1) (adopted in France by GERDA).



Test concentration in %


1. Potassium dichromate 

0.5 % (vaseline)

2. Paraphenylenediamine (free base)

1 % (vaseline)

3. Thiuram mix

1 % (vaseline)

4. Neomycin sulfate 

20 % (vaseline)

5. Cobalt chloride 

1 % (vaseline)

6. Benzocaine

5 % (vaseline)

7. Nickel sulfate 

5 % (vaseline)

8. Clioquinol

5 % (vaseline)

9. Colophony

20 % (vaseline)

10. Parabens mix (methyl, ethyl, propyl, butyl-hydroxybenzoate)

16 % (vaseline)

11. N-isopropyl-N’-phenyl-paraphenylenediamine 

0.1 % (vaseline)

12. Wool alcohols (lanolin)

30 % (vaseline)

13. Mercapto mix

2 % (vaseline)

14. Epoxy resins

1 % (vaseline)

15. Balsam of Peru (Myroxylon pereirae)

25 % (vaseline)

16. Paratertiary butylphenol formaldehyde resin

1 % (vaseline)

17. Mercaptobenzothiazole

2 % (vaseline)

18. Formaldehyde

1 % (water)

19. Fragrance mix I (evernia prunastri (oakmoss absolute), eugenol, isoeugenol, hydroxycitronellal, cinnamyc alcohol, cinnamic aldehyde, geraniol, amyl cinnamaldehyde)

8 % (vaseline)

20. Sesquiterpene lactones

0.1 % (vaseline)

21. Quaternium 15 (Dowicil 200)

1 % (vaseline)

22. Primin

0.01 % (vaseline)

23. Chloromethylisothiazolinone / methylisothiazolinone 

0.01 % (water)

24. Budesonide

0.01 % (vaseline)

25. Tixocortol Pivalate

0.1 % (vaseline)

26. Methyldibromo glutaronitrile

0.5 % (vaseline)

27. Fragrance mix II (Lyral®, citral, farnesol, citronellol, hexylcinnamic aldehyde, coumarin)

14 % (vaseline)

28. Hydroxyisohexyl 3-cyclohexene carboxaldehyde (ou Lyral ®)

5 % (vaseline)

(1) EECDRG : European Environmental and Contact Dermatitis Research Group


Table II Examples of additional series.
AcrylatesFragrance mix I : version containing eight substances 
Rubber additivesFragrance mix II : version containing six substances
Flavourings and spicesSunscreen
Baked goodsIndustrial oils
Hair products Medications
Glues and plasticsMercury
Clothing dyesPesticides
CorticosteroidsPhotographic products

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