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Year : 2018  |  Volume : 19  |  Issue : 4  |  Page : 304-307

Allergic contact dermatitis in atopic dermatitis

1 Department of Pediatric Dermatology, Institute of Child Health, Kolkata, West Bengal, India
2 Department of Pediatric Dermatology, Indira Gandhi Institute of Child Health, Bengaluru, Karnataka, India
3 Bajaj Skin Clinic, Allahabad, Uttar Pradesh, India

Date of Web Publication28-Sep-2018

Correspondence Address:
Dr. Sandipan Dhar
Flat 9C, Palazzo, 35, Panditia Road, Kolkata - 700 029, West Bengal
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/ijpd.IJPD_105_18

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Atopic dermatitis (AD) coexisting with allergic contact dermatitis (ACD) is not uncommon. There has been lot of controversies regarding this concept as the prevalence of ACD in AD is similar to that seen in nonatopics. There is increased susceptibility to ACD in AD as AD modulates the exposure to allergens. There is an impaired barrier function that predisposes to the development of ACD in AD. Patch testing is a standard test for detecting allergens in AD.

Keywords: Allergens, allergic contact dermatitis, atopic dermatitis, patch test

How to cite this article:
Dhar S, Srinivas SM, Bajaj AK. Allergic contact dermatitis in atopic dermatitis. Indian J Paediatr Dermatol 2018;19:304-7

How to cite this URL:
Dhar S, Srinivas SM, Bajaj AK. Allergic contact dermatitis in atopic dermatitis. Indian J Paediatr Dermatol [serial online] 2018 [cited 2021 Oct 16];19:304-7. Available from: https://www.ijpd.in/text.asp?2018/19/4/304/242404

  Introduction Top

Atopic dermatitis (AD) is a chronic, inflammatory, relapsing skin disorder with varying degree of pruritus, and inflammation of the skin.[1] AD is a complex interplay of multiple factors that include environmental factors, food, drugs, microbes, behavioral, impaired barrier function, and altered immune mechanisms in a genetically predisposed individual. There is a common cellular mechanism between associations of allergic contact dermatitis (ACD) with AD. Few studies have shown that filaggrin gene mutation has increased the risk of developing ACD.[2] Inflamed skin and disturbed skin barrier in AD predisposes to sensitization of even weak allergens causing contact dermatitis.

  Evolution of Allergic Contact Dermatitis in Atopic Dermatitis Top

Historically, ACD was thought to be uncommon in AD due to the decreased susceptibility; but over the years, it was proven that patients with AD develop mostly irritant dermatitis. In a study by Jones et al., allergic contact sensitivity to Rhus was investigated in 171 humans, out of which 40 individuals had AD. Among them, 3% of atopic individuals had Rhus dermatitis, and 37% of nonatopics had Rhus dermatitis. Survey patch test with Rhus oleoresin has shown positivity in 61% control and 15% in atopics. Patients tested for the second time with Rhus patch testing showed 6% nonsensitive atopics and 31% in nonsensitive control group suggesting that they were sensitized by the first patch test.[3] Experimental studies with dinitrochlorobenzene (DNCB) as contact allergen has shown lower sensitization rate in patients with severe AD.[4] However, subsequent studies with different concentration of DNCB in mild AD have shown unequivocally reduced reactivity.[5]

  Epidemiology of Allergic Contact Dermatitis in Atopic Dermatitis Top

There are few epidemiological studies in literature on association of ACD with AD. Population-based studies have not shown any significant association between AD and contact allergy. The first population-based study was the “Glostrup allergy study,” and the incidence of ACD in this study was higher in patients with AD than nonatopic control.[6] Mortz et al., in the Odense study, with 12 years–6 years old adolescents reported that 37% of AD had ACD while in the whole study sample this proportion was only 21.3%.[7] The KORA allergy study found 28% of the general adult population (25–75 years) was sensitized to at least one standard series allergen.[8]

In a prospective study of 114 children under 16 years presenting with AD, contact allergy was seen in 43%. In this study, patch testing was performed systematically from the European standard series along with tixocortol, pivalate, budesonide, and applied emollient. The most common allergens were metals (19.3%), fragrance (4.4%), balsam of peru (2.6%), lanolin (4.4%), neomycin (2.6%), and emollients (2.6%). Statistically, the analysis demonstrated the risk of developing contact allergy was significantly elevated in children after the age of 5 years. Age of onset or the severity of AD did not affect the development of contact allergy.[9] Girls had significant positive patch testing results to nickel. In another study of 251 patients with moderate-to-severe AD, contact allergy was seen in 11% of children under the age of 2 years, 43% between 7 and 15 years, and 58% in older children.[10] In an Indian study of ACD in AD showed the prevalence of 23%. The most common contact allergen was neomycin followed by gentamycin.[11] Data from the pediatric contact dermatitis registry about the association of ACD with AD were evaluated in 1142 patients. Patch tested children with AD were 1.3 years younger and had a long history of dermatitis. Children with AD had different reaction profiles than those without AD. There was increased frequency to cocamidopropyl betaine, wool alcohol, lanolin, tixocortol pivalate, and parthenolide.[12]

  Pathogenesis of Allergic Contact Dermatitis in Atopic Dermatitis Top

The relationship of ACD with AD is still elusive. Immunological changes associated with AD may facilitate the development of ACD, and this depends on the molecule, type of AD (acute or chronic), skin barrier, immune dysregulation, microbial colonization, and type of potential contact allergen. Allergen (xenobiotic) penetration depends on the chemical properties of the molecule. Small, nonpolar moderately lipophilic substances (haptens with molecular weight >500 D) penetrate more than water-soluble compounds. Inflamed skin and defective barrier in AD lead to penetration of allergen and triggers the immune response.[13] There is increased transepidermal water loss in nonlesional dry skin and active AD lesion which increases the susceptibility of barrier function to irritants.[14] In both AD and ACD, there are activated T cells which are the main effector cell type. There is a dysbalance between Th1 and Th2 response in AD with predominance of Th2 response in acute phase.

Activation of CD4+ and CD8+ T cells in AD produces Th2 cytokines such as IL 4, IL5, and IL 13. In ACD, there is activation of Th1 and Tc1 subsets producing IFN-γ cytokine. Although there is little activation of Th2 cells in ACD, other immunological mechanisms such as increased release of chemokines and cytokines from keratinocytes, high numbers of preactivated dendritic cells releasing chemotactic and proinflammatory mediators, and increased number of activated memory effector and cytotoxic T cells facilitate the development of ACD in AD.[15] ACD to nickel with positive patch testing reactivity has been reported in younger age group with filaggrin mutation carriers than those without mutations.[16] Physical friction is an under-recognized irritant that can contribute to ACD in AD.[17]

  Contact Allergens in Atopic Dermatitis Top

Children with AD can develop ACD to different allergens [Table 1].[18] Children with hand eczema in AD have a strong association between filaggrin mutations and contact sensitization to metals especially nickel. Large number of patients with or without AD is sensitized to neomycin; hence, there is no increased risk of developing contact sensitization. In a study of 71 children with AD using corticosteroids for at least 6 months, patch testing reaction was positive in only one child with tixocortol pivalate, hydrocortisone-17 butyrate 1%.[19] Risk factors for positive patch testing include severe AD, onset before 6 months of age, and IgE mediated sensitization. Compositae allergy is seen more commonly in adults but can be seen in children. A study of 641 consecutive children and adolescents patch testing positivity to composite mixed with 5% petrolatum was seen only in 17 children.[20] Compositae allergy should always be considered in dermatitis exacerbated in summer. Tattoo reactions using temporary black henna containing p-phenylenediamine is being seen in children and adolescents and is unsafe in atopics.[21]
Table 1: Contact allergens

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Eyelid dermatitis is seen more commonly seen with C used in nail polish. ACD to methylisothiazolinone used in diaper wipes, shampoos, moisturizers is very commonly seen in young children with atopics. It is a biocide used to prevent microbial growth in water containing solutions. Methylisothiazolinone in wipes should be considered as a culprit if there is a worsening of diaper dermatitis. Benzoate present in food as preservatives may mimic AD in small children. A retrospective analysis of 79,046 patients in Germany, Switzerland, and Austria has shown that sensitization to sodium benzoate has increased in the studied population by more than 10% between 1996 and 2009 and more common in atopics.[22]

  Sites of Involvement in Allergic Contact Dermatitis with Atopic Dermatitis Top

The most common sites of involvement of ACD in AD are eyelids, perioral region, hands, and flexural areas of the neck.[18] ACD of the eyelid accounts for 55%–63.5% in AD. Allergens causing eyelid dermatitis include fragrances, preservatives, nickel, thiuram, cocamidopropyl betaine, amidoamine, tosylamide, and formaldehyde resins. Perioral dermatitis in children presents with erythematous papules, pustules, or vesicles and is attributed to topical corticosteroid, inhaled systemic glucocorticoids, fluorinated toothpastes, occlusive moisturizers, and rarely from preservatives in food (benzoate) coming in contact with skin. Hand eczema is very common in AD, presents with tiny vesicles, eczematous plaque on fingertips, nail folds, and dorsum of the hands.[23] Patch testing should be considered in hand eczema if there is an alteration in the clinical pattern and recalcitrant lesions. Generalized dermatitis can be precipitated by nickel and balsam of Peru.

  Course of Atopic Dermatitis with Allergic Contact Dermatitis Top

The occurrence of ACD does not change the course of AD as compared to those without sensitization. It does not impair the prognosis of dermatitis in AD. A total of 1053 atopic patients who were studied and patch tested in 1983/84 were sent a questionnaire regarding dermatitis 16 years later (1999). Among them, 801 patients answered and were included in the study. Patients who had one or more positive patch tested in the beginning had no dermatitis in 30.1%, and during follow-up, it had increased to 38.3%. Hand dermatitis and other dermatitis decreased among the contact sensitivity but remained the same without positive patch test reactions.[24]

  Investigations and Management of Allergic Contact Dermatitis in Atopic Dermatitis Top

Skin prick test (SPT) and atopic patch test are the diagnostic tests used to detect ACD. The sensitivity and specificity depend on the allergens. SPT and serum IgE detect immediate-type hypersensitivity whereas atopy patch test detects the delayed type of hypersensitivity reaction.[25],[26] Education and counseling to parents of affected children on allergen avoidance is the mainstay of treatment. Avoidance of food contact with skin is necessary until tolerance is established. Self-feeding in infants with hand eczema should be avoided. Medications devoid of proteinaceous allergens should be used.

  Conclusion Top

AD predisposes to the development of both ACD and irritant contact dermatitis as these conditions share some common mechanisms. The prevalence of ACD is more commonly seen in AD. Chronic recalcitrant dermatitis or any new onset dermatitis should be evaluated and considered for patch testing. Patch testing positivity is more commonly seen in children than adults.

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  References Top

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de Jongh CM, Khrenova L, Verberk MM, Calkoen F, van Dijk FJ, Voss H, et al. Loss-of-function polymorphisms in the filaggrin gene are associated with an increased susceptibility to chronic irritant contact dermatitis: A case-control study. Br J Dermatol 2008;159:621-7.  Back to cited text no. 2
Jones HE, Lewis CW, McMarlin SL. Allergic contact sensitivity in atopic dermatitis. Arch Dermatol 1973;107:217-22.  Back to cited text no. 3
Forsbeck M, Hovmark A, Skog E. Patch testing, tuberculin testing and sensitization with dinitrochlorobenzene and nitrosodimethylanilini of patients with atopic dermatitis. Acta Derm Venereol 1976;56:135-8.  Back to cited text no. 4
Rees J, Friedmann PS, Matthews JN. Contact sensitivity to dinitrochlorobenzene is impaired in atopic subjects. Controversy revisited. Arch Dermatol 1990;126:1173-5.  Back to cited text no. 5
Nielsen NH, Menné T. The relationship between IgE-mediated and cell-mediated hypersensitivities in an unselected Danish population: The Glostrup allergy study, Denmark. Br J Dermatol 1996;134:669-72.  Back to cited text no. 6
Mortz CG, Lauritsen JM, Bindslev-Jensen C, Andersen KE. Prevalence of atopic dermatitis, asthma, allergic rhinitis, and hand and contact dermatitis in adolescents. The Odense adolescence cohort study on atopic diseases and dermatitis. Br J Dermatol 2001;144:523-32.  Back to cited text no. 7
Schäfer T, Böhler E, Ruhdorfer S, Weigl L, Wessner D, Filipiak B, et al. Epidemiology of contact allergy in adults. Allergy 2001;56:1192-6.  Back to cited text no. 8
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Ross-Hansen K, Menné T, Johansen JD, Carlsen BC, Linneberg A, Nielsen NH, et al. Nickel reactivity and filaggrin null mutations – Evaluation of the filaggrin bypass theory in a general population. Contact Dermatitis 2011;64:24-31.  Back to cited text no. 16
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Belloni Fortina A, Romano I, Peserico A. Contact sensitization to compositae mix in children. J Am Acad Dermatol 2005;53:877-80.  Back to cited text no. 20
Corrente S, Moschese V, Chianca M, Graziani S, Iannini R, La Rocca M. Temporary henna tattoo is unsafe in atopic children. Acta Paediatr 2007;96:469-71.  Back to cited text no. 21
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