The classic presentation of ACD is a pruritic, eczematous dermatitis initially localized to the primary site of allergen exposure. Geometric or linear patterns or involvement of focal skin areas, may also be suggestive of an exogenous etiology (Fig. 12-4B). A linear or streaky array on the extremities, for example, often represents ACD from poison ivy, poison oak, or poison sumac. Occasionally, the actual sensitizing substance in these plants, an oleoresin named urushiol may be aerolized when the plants are burned, leading to a more generalized and severe eruption on exposed areas such as the face and arms. Transfer of the resin from sources other than directly from the plant (such as clothes, pets, or hands) may result in rashes on unexpected sites (i.e., genital involvement in a patient with poison ivy). Thus, relevant historic data gathered from thoughtful questioning may prove as useful as the distribution of the lesions.
It is important to note that lesions of ACD will vary morphologically depending on the stage of the disease. For example, during the acute phase, lesions are marked by edema, erythema, and vesicle formation. As the vesicles rupture, oozing ensues and papules and plaques appear. Stronger allergens often result in vesicle formation, whereas weaker allergens often lead to papular lesion morphology, with surrounding erythema and edema. Subacute ACD on the other hand, will present with erythema, scaly juicy papules and weeping; whereas chronic ACD can present with scaling, fissuring, and lichenification. A key symptom for allergy is pruritus, which seems to occur more typically with allergy, than a complaint of burning.47 Moreover, there are some noneczematous clinical variants of ACD that are infrequently observed.48 These include among others:
- Purpuric ACD is mainly observed on the lower legs and/or feet and has been reported with a wide variety of allergens including textile dyes.
- Lichenoid ACD is considered a rare variant. Clinical features mimic lichen planus and has been associated with metallic dyes in tattoos. Oral lichenoid ACD from dental amalgams can resemble typical oral lichen planus.
- Pigmented ACD has been mainly described in populations from Asian ethnicity.
- Lymphomatoid ACD is based only on histopathological criteria (presence of significant dermal infiltrate displaying features of pseudolymphoma). Clinical signs which are nonspecific include erythematous plaques, sometimes very infiltrated, at the site of application of the contact allergen. Some examples include allergy to metal, allergy to hair dye, and to dimethylfumarate, a mold inhibitor found in sachets within some furniture implicated in causing a severe epidemic of ACD.
Dermatitis distribution is usually the single most important clue to the diagnosis of ACD. Typically, the area of greatest eczematous dermatitis is the area of greatest contact with the offending allergen(s). Location, in fact, can be one of the most valuable clues as to which chemical might be the culprit of a patient's ACD. For instance, an eczematous dermatitis in the peri/infraumbilical area suggests contact allergy to metal snaps in jeans and belt buckles, whereas eczema distributed around the hairline and behind the ears suggests contact allergy to an ingredient(s) in hair products (hair dyes, shampoo, conditioners, styling products) (Fig. 13-4). Using the same rationale, eczema on the dorsum of the feet suggests contact allergy to products used to make shoe uppers like leather, rubber, or dyes, while eczematous dermatitis on the weight-bearing surfaces of the feet suggests contact allergy to products used to make insoles/soles like rubber and adhesive materials. Notably, facial, eyelid, lip, and neck patterns of dermatitis should always raise suspicion of a cosmetic-related contact allergy. However, for all of these presentations, correct identification of the culprit chemical(s) will still require patch testing, since even the most astute and experienced clinician is, for the most part, unable to properly surmise the positive allergen(s) prior to testing. The pattern of dermatitis should be mainly used in determining whether or not to patch test, and which allergens and screening series to test.
ACD to para-phenylenediamine. A. Notice the eczema on the distribution of the hairline and behind the ears. B. Dermatitis on the forehead where the bangs came in contact with the skin of the same patient. C. para-Phenylenediamine, the most frequent relevant allergen in hair dye, is a strong sensitizer. It will darken the patch-test site. There is a strong edematous and vesicular reaction that is spreading, a 3+ reaction to this patch test.
Occasionally, the topographic approach does not hold, and the distribution can actually be misleading. This mainly refers to cases of ectopic ACD or airborne ACD. Ectopic ACD can follow two circumstances: Auto transfer, in which the allergen is inconspicuously transferred to other body sites by the fingers—the classical example being nail lacquer dermatitis located on the eyelids or lateral aspects of the neck; and heterotransfer, in which the offending allergen is transferred to the patient by someone else (spouse, parent, etc.); this is described in the literature as connubial or consort ACD.
A discussion of allergens in the context of common patterns of presentation is briefly detailed below.
The face is a common site for ACD. Among patients with facial dermatitis, women are more commonly affected than men, particularly by cosmetic-associated allergens such as fragrances, PPD, preservatives, and lanolin alcohols (eFig. 13-4.1).49 Allergens can be applied to the face directly but can also be indirectly transferred from airborne or hand-to-face exposure. In addition to allergens found as ingredients in cosmetics, products used to apply them—such as cosmetic sponges, have also been reported to produce facial dermatitis in rubber-sensitive patients.50 A similar situation is seen with nickel-plated objects used on the hair, such as bobby pins and curlers that may produce scalp and facial dermatitis in nickel-sensitive patients.
Facial dermatitis in a patient with multiple positive patch-test reactions to formaldehyde releasing preservatives.
Allergens applied to the scalp most often produce patterns of dermatitis on the forehead and lateral aspect of the face, eyelids, ears, neck, and hands; whereas the scalp remains uninvolved, suggesting that the scalp is particularly “resistant” to contact dermatitis. Nevertheless, patients exquisitely sensitive to certain ingredients in hair products such as PPD or glyceryl monothioglycolate may show a marked scalp reaction with edema and crusting. PPD is one of the most potent sensitizers known and is widely used as an ingredient in hair dyes. In general, PPD sensitization manifests on the face and scalp of female adult patients who had contact with a hair dye.51–54 Glyceryl thioglycolate (GMT), on the other hand, is a chemical substance used in permanent wave solutions. Allergic sensitivity to GMT can manifest as intense scalp reactions with scaling, edema, and crusting.55
The eyelids are one of the most sensitive skin areas, and are highly susceptible to irritants and allergens perhaps due to the thinness of the eyelid skin, as compared with the rest of the skin, and perhaps because they can accumulate the offending chemical in the skin folds. Transfer of small amounts of allergens used on the scalp, face, or hands can be enough to cause an eczematous reaction of the eyelids, while the primary sites of contact remain unaltered (eFig. 13-4.2). Similarly, volatile agents may affect the eyelids first and exclusively, causing airborne eyelid contact dermatitis. Sources of contact dermatitis of the eyelids include cosmetics such as mascara, eyeliners and eye shadows, adhesive in fake eyelashes, and nickel and rubber in eyelash curlers. Furthermore, marked edema of the eyelids is often a feature of hair-dye dermatitis.56 As mentioned earlier in this chapter, eyelids are also known for being a typical site for “ectopic contact dermatitis” caused by ingredients found in nail lacquer, such as tosylamide formaldehyde resin (TSFR), the chemical added to nail varnish to facilitate adhesion of the varnish to the nail and epoxy resin, also added to some nail polishes. Topical antibiotics (like bacitracin and neomycin) and certain metals such as gold57 can also cause eyelid contact dermatitis. In fact, in the 2007 NACDG analysis of contact allergens associated with eyelid dermatitis,58 gold was the most common allergen accounting for pure eyelid dermatitis. Notably, it has been observed that upon contact with hard particles such as titanium dioxide (used to opacify facial cosmetics, and in sunscreens as a physical blocker of ultraviolet light), gold found in jewelry may abrade, resulting in the release of gold particles that can then make contact with facial and eyelid skin, causing dermatitis.59 Aside from gold, fragrances and preservatives have been found to be the main cosmetic allergens to cause dermatitis limited to the eyelids.60
Classical appearance of allergic eyelid dermatitis. Culprit allergens may include gold, fragrances, and preservatives.
According to an NACDG study, approximately one-third of patients with cheilitis—without other areas of dermatitis—are typically found to have an allergen as a contributing factor.61,62 Allergic contact cheilitis (ACC) has been reported to result from the use of a wide array of products including cosmetics such as lip balms, lipsticks, lip glosses, moisturizers, sunscreens, nail products, and oral hygiene products (mouthwashes, toothpastes, dental floss) (Fig. 13-5).63–65 ACC has a marked female predominance, with most studies reporting a range of 70.7%–90% female patients.66 This is likely explained by the assumption that women wear more cosmetics and lip products than men. Most studies have reported fragrance allergens [such as fragrance mix and Myroxylon pereirae (Balsam of Peru)] as the most common cause of contact allergy in patch-tested patients with cheilitis.67 Of note, some uncommonly reported allergens, namely, benzophenone-3 and gallates, may be relevant to a dermatitis localized to the lips. Benzophenone-3, a major constituent of many sunscreens, is also a common ingredient in many lip products and is increasingly reported as a culprit for ACC.68,69 Gallates are antioxidants used in waxy or oily products such as lip balms, lipsticks, and lip glosses.70
Allergic Contact Cheilitis. Fragrances and flavorings are top among the most common causes of contact allergy in patch-tested patients with cheilitis.
The neck is also a highly reactive site for ACD. Cosmetics applied to the face, scalp, or hair often initially affect the neck. Nail-polish ingredients (tosylamide formaldehyde resin and epoxy resin) are common culprits in this region.71 Furthermore, as a cultural practice, perfumes are sprayed on the neck. In a fragrance-sensitized individual, the practice of repeated application of fragrances to the anterior neck may result in the appearance of a dermatitic plaque on the neck, which has been coined the “atomizer sign.”72 Also, in this topographic area, metal allergy can manifest as chronic eczematous dermatitis from exposure to necklaces and jewelry clasps that contain nickel and/or cobalt.
The torso can encounter fragrances, preservatives, surfactants, and other chemicals from the use of personal care products; yet it is also susceptible to allergens found in textiles. Textile-associated allergens include disperse dyes (azoanilines) and formaldehyde-releasers used as durable press chemical finishes (DPCF). In the past, finishes used to contain large amounts of free formaldehyde, which led to many cases of allergic contact dermatitis to clothing in the 1950s and 1960s. However, currently most finishes are based on modified dimethylol dihydroxyethyleneurea, which releases less formaldehyde. Importantly, recent studies have shown that the amount of free formaldehyde in most garments will likely be below the threshold for the elicitation of dermatitis for all but the most sensitive patients, and that the amount of free cyclized urea in clothes is unlikely to be high enough to cause sensitization.73
Heat, humidity, and friction of the axillary fold may contribute to the leaching of textile resins and dyes and dermatitis accentuation in these areas.74 The axillary region is also uniquely exposed to deodorants and antiperspirants. These products contain most notably the contact allergens fragrances and preservatives (formaldehyde releasers, parabens, etc.). A commonly observed effect with the use of these products is the sparing of the axillary vault, mainly secondary to perspiration diluting the allergens. Aerosolized exposure of the allergens through antiperspirant/deodorants in spray, may lead to scattering of the allergen and the resulting picture may be that of scattered satellite papules.
Hand dermatitis has a particularly high incidence secondary to the fact that the hands are the main means of interaction with the environment, with increased possibility for numerous allergen exposures. Hand dermatitis accounts for as much as 80% of the occupationally related skin diseases, especially in certain “wet work” occupations such as health care workers, food handlers, etc.75 Thus, careful consideration should be given to occupation-specific exposures in the evaluation of patients with hand dermatitis. As an example, a hairdresser may be sensitized to ingredients in hair-care products such as PPD, glyceryl monothioglycolate, or cocamidopropyl betaine (a surfactant-detergent, commonly found in shampoos), whereas a construction worker may become allergic to chromium through exposure to wet cement. Clinical clues that should raise a higher index of suspicion of ACD include the involvement of the finger web spaces and the dorsal hands, as well as the predominance of pruritus as a symptom. Still the multifactorial etiology of hand dermatitis (irritant exposure, atopy, pompholyx or chronic vesicular hand eczema, psoriasis, dermatophyte infection, among others) adds to the complexity of both diagnosing and treating these patients. Chronic hand dermatitis is an indication for patch testing, as causal or contributing allergy can result in improvement or resolution of the problem. Similarly, the evaluation of foot dermatitis should include patch testing with the allergens most commonly associated with this condition. These include, rubber-related chemicals (such as mercaptobenzothiazole, carba mix, thiuram mix, mercapto mix, black rubber mix, and mixed dialkyl thioureas) potentially present as components of shoes and insoles; glues and adhesives used in shoe manufacturing like 4-tert-butylphenol formaldehyde resin; and potassium dichromate found in tanned leather-made shoes. Testing materials should also include topical antibiotics, corticosteroids, or antifungal medications (both over-the-counter and prescription) that may have been used by the patient to treat the affected area.
Other topographic areas affected by ACD include the oral mucosa, which may present with contact stomatitis from dental metals and the perianal area, which may react to sensitizing chemicals in proctologic preparations such as benzocaine.
Scattered Generalized Dermatitis
Patients with scattered generalized dermatitis (SGD) usually present a difficult diagnostic and therapeutic challenge. Patch testing can be a strategy for evaluating ACD as a potential relevant factor. In 2008, Zug and NACDG colleagues 76 examined the yield of patch testing as well as the relevant allergens in patients with SGD referred for patch testing. Of 10,061 patients studied during a period of 4 years, 14.9% had SGD. Men and patients with a history of atopic eczema were more likely to have dermatitis in this distribution. Of the total of patients presenting with SGD, 49% had at least one relevant positive patch-test reaction. Preservatives, fragrances, propylene glycol, cocamidopropyl betaine, ethyleneurea melamine formaldehyde, and corticosteroids were among the more frequently relevant positive allergens.
Systemic Contact Dermatitis
In 2001, members of the International Contact Dermatitis Research Group (ICDRG) developed the concept of the allergic contact dermatitis syndrome (ACDS).77 This concept considers the various facets of contact allergy, including morphological aspects and staging by symptomatology. ACDS has three stages that can be defined (Table 13-1) and with many causes (Table 13-2).
Table 13-1 Stages of the Allergic Contact Dermatitis Syndrome ||Download (.pdf)
Table 13-1 Stages of the Allergic Contact Dermatitis Syndrome
The skin symptoms are limited to the site (s) of application of contact allergen(s).
There is a regional dissemination of symptoms (via lymphatic vessels), extending from the site of application of allergen(s).
Can be further subdivided in
Stage 3A: Corresponds to hematogenous dissemination of ACD at a distance.
Stage 3B: Corresponds to systemic reactivation of ACD (nontopical trigger)
Table 13-2 Systemic Drugs that Can Cause Systemic Reactivation of ACD ||Download (.pdf)
Table 13-2 Systemic Drugs that Can Cause Systemic Reactivation of ACD
Related Drug with Potential to Cause Systemic Reactivation of ACD
Ethylenediamine dihydrochloride (stabilizer infrequently found in skin care products)
Piperazine antihistamines: hydroxyzine, cetirizine, levocetirizine and meclizine
Thiuram (rubber antioxidant)
Tetraethyl thiuram disulfide (generic name: disulfiram)
Thimerosal (mercury-derived preservative)
Systemic contact dermatitis describes a systemic reactivation of allergic contact dermatitis; in other words, a cutaneous eruption in response to systemic (nontopical) exposure to an allergen.78 In considering the chains of events resulting in the development of systemic reactivation of ACD, the ICDRG has suggested that the occurrence of some successive steps is necessary. Initially, direct skin contact with an allergen results in sensitization. Second, in some relatively uncommon cases, weeks or even years after that first episode of ACD, the patient is systemically exposed to exactly the same allergen, or to a related substance that is chemically closely related to it (cross-sensitization), elicitating a systemic reactivation of ACD. There are multiple routes of exposure for the elicitation of systemic contact dermatitis—subcutaneous, intravenous, intramuscular, inhalation, and oral ingestion. It is important then to note, that by definition, in systemic contact dermatitis, there is no occurrence of topical skin contact to the allergen. Clinically, systemic contact dermatitis has a wide spectrum of presentation, from a recall reaction (dermatitis at the site of prior topical sensitization), to widespread dermatitis and erythroderma. Other patterns that have been associated with systemic contact dermatitis include axillary vaults, upper inner thighs, and buttocks—sometimes described as “baboon syndrome,”79 which has been associated with some internally ingested allergens, i.e., cashew nut shell oil causing a cross-reaction to the allergen urushiol. Dyshidrotic hand eczema/pompholyx are conditions in which oral challenges with nickel, and Myroxylon pereirae have demonstrated flaring of this type of hand eczema in some studies (eFig. 13-5.1).80 Of particular notoriety is the allergen Myroxylon pereirae also known as balsam of Peru, a substance derived from Myroxolon balsamum, a tree that is native to the country of El Salvador. Because the main components of Myroxylon pereirae (cinnamic acid, cinnamyl cinnamate, benzyl benzoate, benzoic acid, benzyl alcohol, and esterified polymers of coniferyl alcohol) are naturally derived, they have a significant number of natural cross-reactors. Certain foods, such as tomatoes and tomato-containing products, citrus fruit peel/zest, chocolate, ice cream, wine, beer, vermouth, dark colored sodas, and spices such as cinnamon, cloves, curry, and vanilla, have chemical ingredients related to balsam of Peru.81 Consumption of these foods may result in a systemic reactivation of ACD in some patients allergic to balsam of Peru. Salam and Fowler drew attention to this ability of orally ingested balsam-related substances to induce systemic contact dermatitis, and reported that, in their study, remarkably almost half of the subjects with a positive patch test to Myroxylon pereirae who followed a balsam of Peru-reduction diet, had a significant to complete improvement of their dermatitis. Finally, some oral or IV medications may cause systemic reactivation of ACD in patients previously sensitized to related allergens by direct skin contact82–85 (Table 13-2).
Chronic vesicular hand eczema has been associated with nickel allergy and in some cases will improve with a low-nickel diet.
Because “frequent is frequent,” the approach to a patient with suspected ACD can also be done taking into account the most likely culprits based on frequency data of a given region, and the patient's occupation or other individual exposures. This approach should not replace by any means actual patch testing; nevertheless, a working knowledge of the most common allergens can prove to be useful when evaluating a patient with suspected ACD. Next is a brief description of the most frequently patch-test positive allergens in North America.
Nickel is a ubiquitous metal used in a wide range of products including those that have a prolonged contact with the skin (costume jewelry, suspenders, zippers, button snaps, belt buckles, eyeglasses frames, cell phones, nickel-containing coins, keys, among many others). There is a well-documented rising incidence of nickel allergy in the United States and elsewhere, with high nickel sensitization rates documented in children.86 Ear piercing at an early age, in addition to the trend of a greater number of other body piercings, are consistently linked to the rise in nickel sensitization in the recent decade.87,88 Currently, nickel allergy is the most common cause of contact dermatitis in the industrial world, particularly affecting females.89 Several studies have examined the striking discrepancy of sensitization incidence to nickel in females versus males and have associated this with ear piercing.90,91 Classically, nickel contact dermatitis presents as an eruption on the earlobes, the neckline, the wristband, or the periumbilical area since those are common areas for exposure to nickel-containing jewelry or button snaps, zippers, and belt buckles. Facial dermatitis caused by nickel has also been reported to musical instruments and more recently to cell phones.92 Furthermore, the presence of nickel in implantable medical devices and potential complications derived from nickel allergy is a rising subject of discussion. The relevance of nickel allergy in the failure of metal orthopedic implants and cardiac devices is not clear. Documented cases of joint replacement failure associated with nickel or other metal sensitivity are clearly rare, and arthroplasty prostheses rarely cause a problem in the nickel sensitive individual. Existing publications are largely retrospective and thus can only suggest a possible association of nickel allergy with implant failure rather than determine causation.93 Similarly, eczematous reactions temporally related to joint replacement or implantation of other orthopedic devices (i.e., metallic plates and screws) although reported, are infrequent (eFig. 13-5.2). More studies are needed in this area.
A. Localized eczematous dermatitis in the skin overlying an orthopedic metal plate containing nickel. B. Positive patch-test reaction to nickel in the same patient.
In an attempt to prevent the development of nickel sensitivity, Denmark in 1990, and the rest of the European Union in 1994, have regulated the amount on nickel that may be released from objects with direct and prolonged skin contact (≤0.5 μg nickel/cm2/week; revision for 2004: ≤0.2 μg nickel/cm2/week for items inserted into pierced parts of the body). Recent evidence indicates that the prevalence of nickel allergy is decreasing among young Danish females from 27.6% in 1985 to 16.8% in 2007.94 The American Academy of Dermatology and the American Contact Dermatitis Society favor enacting similar legislation in the United States.
Fragrances are aromatic compounds that impart a smell or odor. They can be natural (from botanical or animal products) or synthetic in origin. It has been estimated that between 1% and 4% of the general population is allergic to fragrances.95,96 Fragrance allergy is one of the two top causes of contact allergy to personal care products; the typical sites of involvement include the face and hands, as well as behind the ears, neck, and axillae, in addition to a scattered generalized distribution of eczematous dermatitis.97,98 Two of the main substances used by most patch-test groups for screening are among the top ten allergens in North America. The first is fragrance mix I, which is a mixture of eight fragrance allergens, and the second is Myroxylon pereirae (MP) also known as balsam of Peru (BOP), whose main components are fragrance ingredients.99 MP is considered to be a good marker for fragrance allergy, able to identify approximately 50% of fragrance allergic individuals.100 MP-related substances can be found in products such as cosmetics, perfumes, pharmaceutical preparations, toothpastes and mouthwashes, as well as in scents and flavorings for foods and drinks. Similarly, certain foods, such as the ones mentioned earlier in the chapter, contain chemical ingredients related to MP. Surgical adhesives used postprocedure to secure dressings also may cross-react and produce dermatitis in individuals sensitive to MP.
Neomycin belongs to the aminoglycoside family of antibiotics commonly used in topical formulations for the prevention and treatment of superficial skin, ear, and eye infections. The frequency of neomycin sensitization in the general population is 1.1%,101 while reported sensitization rates in selected patient populations referred for patch testing vary from as low as 1.1102 to as high as 10%, the latter reported by the NACDG.103 This high rate of sensitization in North America may be due to the availability of this antibiotic in numerous over-the-counter preparations, especially “triple antibiotic” creams and ointments.104 Subgroups at higher risk include patients with stasis dermatitis and leg ulcers, anogenital dermatitis, and otitis externa. Because antibiotic preparations are applied to already damaged skin, ACD from neomycin is not always easily recognized. It often presents as persistence or worsening of a preexisting dermatitis.105 Additionally, it may mimic cellulitis; the clue for contact allergy is itching rather than pain. An intensification of itch and the progression of lesions beyond the initial site of involvement may offer clues to the correct diagnosis. Occupational dermatitis involving the hands can occur in nurses, physicians, pharmacists, dentists, and veterinarians.106
Formaldehyde and Formaldehyde-Releasing Preservatives
Formaldehyde is a colorless gas with preservative and disinfectant properties. Although there is a wide range of uses for formaldehyde-like cleansing products, glues, biocides, and photographic developers, currently it is rarely used as-is in personal care because it has demonstrated to be a frequent sensitizer.107 Therefore, many manufacturers have replaced the use of formaldehyde with formaldehyde-releasing preservatives (FRPs) to preserve personal care products.108 FRPs include quaternium-15, imidazolidinyl urea (Germall), diazolidinyl urea (Germall II), DMDM hydantoin (Glydant), 2-bromo-2-nitropropane-1, 3-diol (Bronopol), and tris nitromethane (Tris Nitro).109 Of these, Quaternium-15 is the most common cosmetic preservative allergen (Figs. 13-6 and 13-7).110–112
This eczematous dermatitis was caused by the most frequent preservative allergen, quaternium-15, which was present in the patient's moisturizer.
An example of a weak, 1+ reaction to quaternium-15.
Cobalt is a metal which is often added to other metals to increase overall strength. Cobalt is commonly a contaminant present in nickel ores and is frequently a minor element in nickel compounds.113 As with nickel, a majority of sensitization exposures result from contact with jewelry, clothing snaps, buckles, coins, keys, and other metal objects. Furthermore, it can also be found in prosthetic joint replacements, dental alloys, ceramics, paints, tattoo dyes, cement (mostly in Europe), and multivitamins containing vitamin B12 (cobalt is a main component of vitamin B12, Cyanocobalamine).114 Concomitant allergy to nickel and cobalt is often observed among patients with dermatitis, probably as a result of cosensitization. In general, the best way of avoiding contact with metallic cobalt is by avoiding contact with nickel-plated objects that come in direct contact with the skin.
Bacitracin is a topical antibiotic frequently used for postoperative and general wound care by both the medical profession and the general public since it is readily available in over-the-counter preparations. Bacitracin is known to be a common sensitizer and can cause not only allergic contact dermatitis but also urticarial reactions and even, rarely, anaphylaxis.115 It is important to note that despite its high prevalence, bacitracin is not included as a screening allergen in the currently available T.R.U.E. Test series, which will be further discussed briefly in this chapter. Interestingly, patients often show simultaneous sensitivity to bacitracin and neomycin, although the two substances are not chemically related, meaning there is coreactivity but not cross-reactivity between both substances. Independent sensitization probably occurs to both antibiotics, which are often used simultaneously in over-the-counter combinations.116
Methyldibromoglutaronitrile/Phenoxyethanol (MDGN/PE) is a preservative combination also known as Euxyl K400. It has become an increasingly important sensitizing agent,117 resulting in a ban on use in Europe, first from stay-on cosmetics in 2005, and later from rinse-off cosmetics in 2007, in an attempt to decrease the rates of contact allergy.118 The use of MDGN/PE is not banned in cosmetics produced outside the European Union, and therefore toiletries sold elsewhere may contain MDGN/PE, albeit at a lesser concentration than had been allowed European formulations. Most allergic reactions to MDGN/PE are due to the use of personal care products containing the allergen, especially creams, lotions, wet wipes, and liquid soaps.
PPD is an oxidizing agent used as a permanent hair dye. Both consumers and hairdressers alike are at risk for sensitization. As mentioned earlier in this chapter, contact allergy to PPD often presents as facial dermatitis near the hairline, but it may also involve the eyelids and the neck, while the scalp may or may not be spared.119 Once oxidized, PPD is no longer allergenic, thus, dyed hair itself does not pose further risk of allergic stimulation. This is in contrast to permed hair, in which the allergen, glyceryl monothioglycolate, retains ability to further stimulate dermatitis in the allergic individual (i.e., an allergic hairdresser cutting the hair of a client who has had GMT permanent waving applied to the hair weeks ago). PPD has the potential to cross-react with other para-amino group chemicals such as para-aminobenzoic acid (PABA), sulfonylureas, hydrochlorothiazide, benzocaine, procainamide, and certain azo and aniline dyes.120,121 Additionally, PPD has gained notoriety for its use in adulterating natural henna to make “black henna,” a substance increasingly used to make temporary tattoos.122,123