© The Authors • Journal compilation © Blackwell Verlag GmbH, Berlin • JDDG • 1610-0379/2010/0803 JDDG | 3˙2010 (Band 8)

JDDG; 2010 • 8:159–165 Submitted: 4.6.2009 | Accepted: 26.6.2009

Keywords• periocular eczema• periorbital dermatitis• risk factors• allergic contact dermatitis• irritant contact dermatitis• atopic dermatitis

SummaryPeriorbital dermatitis is common and frequently difficult to treat. Patients withperiorbital dermatitis often suffer severely because their disease is in such a vis-ible location. Because of the variety of clinical appearance, the differential diag-nostic considerations are often difficult. We examined the causes of periorbitaldermatitis and compared the data of 88 patients from the Department ofDermatology, University Hospital Erlangen to those of the German IVDK(Information Network of the Departments of Dermatology). Between 1999 and2004, predominant causes of periorbital dermatitis were allergic contact der-matitis (Erlangen 44 %, IVDK 32 %), atopic eczema (Erlangen 25 %, IVDK 14 %),airborne contact dermatitis (Erlangen 10 %, IVDK 2 %) and irritant contact der-matitis (Erlangen 9 %, IVDK 8 %). Less frequent causes for secondary eczema-tous periocular skin lesions were periorbital rosacea, allergic conjunctivitis orpsoriasis vulgaris. Female gender, atopic skin diathesis and age of 40 years andolder were identified as risk factors for periocular dermatitis. Common elicitorsof periorbital allergic contact dermatitis were leave-on cosmetic products (facecream, eye shadow) and eye drops with the usual allergens being fragrances,preservatives and drugs. Exact identification of relevant contact allergens andallergen elimination are essential for successful treatment. Calcineurininhibitors are the first-line therapy for facial atopic eczema. They may be alsoeffective in periocular eczematous lesions of other origins although they arenot approved for such use.

Periorbital dermatitis: Causes, differential diagnosesand therapyAlexandra Feser, Vera MahlerDepartment of Dermatology, University Hospital of Erlangen, Friedrich-Alexander University, Erlangen-Nürnberg, Germany

IntroductionPeriorbital dermatitis is a commonly occurring dermatological disorder that isoften resistant to therapy. A recent studyat the Department of Dermatology, University Hospital of Erlangen (Ger-many) and the Information Network ofDepartments of Dermatology (Informa-tionsverband Dermatologischer Kliniken,IVDK) suggests that the incidence of periorbital dermatitis is 4.8 % and 3.9 % respectively [1]. There are no re-cent epidemiological data on the preva-

lence in the general population in the literature.Because of the visible involvement of theface, most patients with periorbital der-matitis are highly distressed [2]. The dis-order is usually persistent and patientsoften undergo repeated therapies withtopical corticosteroids, which tend to failto achieve lasting improvement or reso-lution of the dermatitis and can also in-volve steroid-induced side effects (skinatrophy, telangiectasias, rebound phe-nomenon) [3].

Periocular dermatitis may be caused byallergic or irritant contact dermatitis,protein contact dermatitis, secondaryeczematous periocular rosacea and furtherskin disorders of another origin. Patho-genesis can also be multifactorial.

Epidemiology of perioculardermatitisIn 1989 Nethercott and colleagues re-ported that in 79 patients with periocu-lar dermatitis (total sample: n = 1 091)there was a clear preponderance of

DOI: 10.1111/j.1610-0387.2009.07216.x Review Article 159

women at 89 %, with a slightly higheraverage age of 41.4 years compared withthe total sample (40.5 years) [4]. Theseresults were confirmed by subsequentepidemiological studies on perioculardermatitis: In a study conducted from1994 to 1998, Cooper and Shaw re-ported a significantly higher prevalenceof periocular dermatitis among women,at 84.9 % of 232 patients (total sample:n = 3 11 of a patch tests clinic) [5]. In astudy from 1990-1994, Ockenfels andcolleagues reported a predominance ofwomen of 81 % among 609 patientswith periorbital dermatitis (total sample:n = 30 690) [6]. Herbst and colleaguesfound that women made up 80.3 % of1,641 patients with periocular dermatitisout of a total of 49,256 patients testedbetween 1995–1999 [7].Epidemiological studies on patients withperiocular dermatitis from 1999–2004have confirmed that female sex (Erlan-gen 73.9 %, IVDK 78.8 %) is a risk fac-tor (Table 1), although for the first timeof a proportion below 80 % [1]. Thehigh prevalence of women among patients with periorbital dermatitis hasbeen attributed to the more frequent useof cosmetic products [5].There is an increased frequency of atopicskin diathesis in patients with perioculardermatitis (1995–1999) (28.2 % vs.16.2 % of total sample) [7]. Atopic skindiathesis was recently confirmed as a riskfactor for the development of perioculardermatitis (1999–2004): in one study,44.3 % of patients with periocular der-matitis had a history of atopic dermatitiscompared with 29.2 % in the entire sam-ple of all patients (n = 1 827) who hadundergone a patch test from 1999–2004at the Department of Dermatology ofthe University Hospital of Erlangen(Table 1) [1]. Among patients with peri-ocular dermatitis in the IVDK sample(1999–2004), a higher proportion had ahistory of atopic eczema also (22.9 % periocular dermatitis vs. 16.2 % of totalsample) [1]. An average atopy score [8] of 10.5 points(assessment: atopic skin diathesis) hasbeen reported in patients with perior-bital dermatitis [1]. Patients with perioc-ular atopic dermatitis had an averageover 12 points (assessment: atopic skindiathesis), patients with periorbital aller-gic contact dermatitis had an average of9.7 points (assessment: atopic skindiathesis), patients with irritant contact

dermatitis had an average 4.4 points (as-sessment: no atopic skin diathesis). Theperiocular region is a predilection site foratopic dermatitis and can be irritated byaeroallergens (e.g., pollen, house dustmites) [9]. Abnormal skin barrier func-tion can promote the development ofsensitization [10, 11]. Age (≥40 years) has also been identifiedas a risk factor in periocular dermatitis[1]. In the Erlangen and IVDK samples, more than 70 % of patients with periorbital dermatitis were over 40 years of age (Table 1), which is ahigher average age than in the totalsample. In the Erlangen sample, therewas an increased frequency of periocu-lar dermatitis in patients aged 50 yearsand older (Figure 1) [1]. Another studyfound that the age of patients with al-lergic periocular dermatitis was higherthan in patients with “non-allergic pe-riocular dermatitis” [7]. This is attrib-uted in part to the more common useof ophthalmologic medications becauseof a higher prevalence of ophthalmo-logical disease (e.g., glaucoma) in olderpatients [12].

Differential diagnosis and clinicalexaminationThe clinical appearance of various differ-ential diagnoses in periocular eczema issometimes uncharacteristic and is not di-agnostically conclusive (Figure 2a–g).

The most commonly reported cause ofperiocular dermatitis is contact allergy at54 % (44 % due to direct contact;10.2 % due to airborne contact dermati-tis) [1]. Other causes of eczematoid peri-ocular skin lesions include atopic der-matitis (25 %), irritant contact dermatitis(9.1 %), and secondary eczematous skinlesions in periorbital rosacea (4.5 %), pe-riorbital psoriasis vulgaris, and allergicconjunctivitis at 2.1 % each [1].In a retrospective study conducted from1997–2003 at the University of Arkansas(USA) on 203 patients with perioculardermatitis, a clinically manifest allergiccontact dermatitis was reported in 74 %of patients (n = 151), protein contactdermatitis in 23 %, and in less than 1 %irritant contact dermatitis was identifiedas the sole trigger [13]. Differences in thefrequencies of the various causes of peri-ocular dermatitis are due partly to differ-ent exposures and partly to differences inselection criteria of the studies.

Allergic contact dermatitisPeriocular dermatitis is most oftencaused by an allergic reaction. In onestudy, an allergic or airborne allergic con-tact dermatitis was identified as the re-sponsible trigger in 54% of patients; anon-allergic cause was found in the re-maining 46 % [1]. When diagnosing allergic contact der-matitis, a specific medical history should

160 Review Article Periorbital dermatitis

JDDG | 3˙2010 (Band 8) © The Authors • Journal compilation © Blackwell Verlag GmbH, Berlin • JDDG • 1610-0379/2010/0803

Table 1: The MOAHLFA-index is an instrument to characterize differenttest populations for concise interpretation of patch test study results. TheMOAHLFA-index of all patch-tested patients in Erlangen and in the IVDK-collective (excluding Erlangen) is displayed and compared with theMOAHLFA-index of patients with periorbital dermatitis in Erlangen and inthe IVDK-collective (excluding Erlangen) between 1999 and 2004.

Total Periocular

Erlangen (n = 1 827)

IVDK (n = 52 580)

Erlangen (n = 88)

IVDK (n = 2 035)

M Male 40.5 % 38.0 % 26.1 % 21.2 %

O Occupational 14.7 % 14.3 % 5.7 % 2.7 %

A Atopic dermatitis 29.2 % 16.2 % 44.3 % 22.9 %

H Hand dermatitis 27.4 % 26.8 % 0 % 0 %

L Leg dermatitis 6.1 % 11.3 % 0 % 0 %

F Facial dermatitis 13.5 % 14.0 % 100 % 100 %

A Age ≥ 40 61.1 % 65.7 % 71.6 % 70.3 %

be taken and appropriate patch testsshould be performed. The reader is re-ferred to the guidelines of the GermanSociety of Dermatology on “ContactDermatitis” [14] and “Performing apatch test with contact allergens” [15]. Type IV hypersensitivity to nickel (II)sulfate is the most prevalent sensitizationin the general population and is alsocommonly associated with perioculardermatitis, regardless of whether it is rel-evant [15] to the dermatitis in question(Valsecchi et al.: 52 % periocular versus25.5 % of total sample; Cooper & Shaw:17.2 % periocular versus 15.9 % of totalsample; Nethercott et al.: 13.5 % periocu-lar versus 10.2 % total sample) [4, 5, 16]. At least one large study (n = 49,256) hasfound, however, that positive patch teststo nickel (II) sulfate were no more com-mon in patients with allergic periorbitaldermatitis than among patients withnon-allergic periorbital dermatitis [7].Although nickel (II) sulfate was the mostcommonly associated type IV allergy(19.5 %), it was only rarely (< 1 %) be-lieved to be a clinically relevant cause ofperiocular dermatitis in a case-related as-sessment of relevance [1].Nickel has been identified in cosmeticproducts used around the eyes such asmascara [17], make-up base [18], eyeshadow [19], contact lens solution [20],and Kajal pencils [21]. Because thenickel is inadvertently incorporated dur-ing the manufacturing process, it is notlisted as an ingredient in such products[13]. In a sample of patients studiedfrom1999–2004, fragrance mix and bal-sam of Peru were identified in 19 % and10 % as the relevant contact allergens intriggering periocular dermatitis [1]. Therelevance of fragrances in triggering peri-ocular dermatitis varies depending on ex-posure and period in time. Cooper andShaw reported a fragrance allergy in 6 %of patients with eyelid dermatitis (vs.7.4 % in the total sample) [5]. In 1992Valsecchi and colleagues reported fra-grance allergies as the cause of perioculardermatitis in 8 % of patients (vs. 4.56 %in non-periocular dermatitis) [16]. Bal-sam of Peru is a mixture of natural ingre-dients consisting of more than 200 components, many of which are used inthe fragrance and aroma industries [22].The suitability of using balsam of Peru as a marker for fragrance allergy has been controversially discussed [22]. The

Periorbital dermatitis Review Article 161

© The Authors • Journal compilation © Blackwell Verlag GmbH, Berlin • JDDG • 1610-0379/2010/0803 JDDG | 3˙2010 (Band 8)

Figure 1: Age distribution of patients with periorbital dermatitis (n = 88) compared with all patch-tested patients (n = 1 827) in Erlangen 1999–2004: the normal curve of distribution is shifted to anage ≥ 50 years.

Figure 2: Periorbital atopic eczema (a, b), periorbital allergic contact dermatitis (c, d), periorbitalrosacea (e, f ), periorbital psoriasis (g).

IVDK data showed an association be-tween the presence of an allergy to bal-sam of Peru allergy and contact allergy tothe patient’s own personal products con-taining fragrance. Perfumes and cos-metic products now use extracts and dis-tillates of balsam of Peru, which animalstudies have shown to be less sensitizingthan balsam of Peru itself [23]. Casestudies have occasionally reported an as-sociation between oral administration ofbalsam of Peru (e.g., chocolate, marzi-pan, colas) and persistent allergic contactdermatitis [24]. Balsam of Peru is nolonger used as an additive in medications(Red List 2009).The preservatives thimerosal (10 %),phenylmercuric acetate (8 %) and thetopical antibiotic neomycin sulfate (8 %)were shown in a study from 1999-2004to be relevant triggers of periocular der-matitis [1]. Thimerosal was formerlyused as a preservative in medicationssuch as eye drops, ointments usedaround the eyes, nasal sprays, injectionsolutions, vaccines, in cosmetic prod-ucts, make-up base, eye make-up re-mover, and in contact lens solutions forcleansing and storage. As of 2008,thimerosal was included as an additive in5 different medications (2 types of eyedrops and 3 vaccines), and by 2009 itwas in 4 different medications (1 eyedrops and 3 vaccines) (Red List 2008,2009). Thimerosal is now only rarelyfound in contact lens solutions and cos-metic products. Due to decreased expo-sure, thimerosal is presumably less likelyto be a current triggering factor in clini-cally apparent periocular dermatitis.In one study, in 31 % of patients withperiocular allergic or airborne contactdermatitis, the patients’ personal prod-ucts (face cream 20 %, eye shadow 20 %,ophthalmologic medications 20 %, nailpolish 13 %, make-up 13 %, mascara 7 %, glue 7 %) were identified as the relevant contact allergen source [1] (Figure 3). In 12.5 % of patients with allergic or airborne allergic contact dermatitis, the triggers could only be diagnosed by conducting tests using the patients’ own personal products, and notby patch testing of commercial selectedseries based on the patient’s medical his-tory. Possible contact allergens includepreservatives and fragrances (includingthose which must be listed as well asthose which are exempt) [25]. If patchtesting with the patient’s own personal

products is positive, individual sub-stances should be tested; this requireswritten communication between thetreating dermatologist and the manufac-turer directly (which may be compli-cated by company confidentiality policy)or with the involvement of the Informa-tion and Documentation Center forContact Allergy (Informations- undDokumentationsstelle für Kontaktal-lergien, IDOK) [26] of the IVDK.If the manufacturer does provide indi-vidual substances, the procedure is usu-ally blinded. To determine scientificallysound, suitable patch test dilutions [27],the IDOK offers its support as an inde-pendent entity to manufacturers of cos-metics and body care products who pro-vide the IDOK with complete andconfidential information (which is notmade available to the public) on thepreparation in question. After blind test-ing of the substances, the treating derma-tologist reports the results to IDOK.This procedure also helps improve prod-uct safety by standardized documenta-tion and assessment.Other potential triggers of airborne con-tact dermatitis include air fresheners andpreservatives (e.g., chloromethylisothia-zolinone in dispersion paints), nail pol-ish (toluene sulfonamide-formaldehyderesin) and glues [1, 13, 28] (Figure 3).Numerous other causes of airborne con-tact dermatitis (e.g., plants, wood andnatural resin, synthetic materials, metals,

pharmaceutical products, pesticides, andothers) have also been reported in casestudies [28].

Atopic dermatitisIn patients with periocular atopic der-matitis, it is helpful to collect informa-tion about minor signs of atopic skindiathesis (e.g., with the Erlangen AtopyScore [8]) to support the diagnosis. It iswise to rule out an additional sensitiza-tion to topical agents and exogenoustriggers (e.g., through contact with pro-teins such as house dust mite allergens).

Protein contact dermatitisProtein contact dermatitis (= IgE-medi-ated contact dermatitis) is an allergicskin reaction induced by plant or animalproteins. The reaction occurs with a de-lay after contact with the responsibleprotein. The clinical appearance ischronic dermatitis, the pathogenesis ofwhich is attributed to IgE-mediated acti-vation and allergen presentation ofLangerhans cells and infiltration by Tlymphocytes [29, 30]. Prior atopic or ir-ritant damage of the skin barrier appearsto be a relevant factor in the manifesta-tion of protein contact dermatitis [30].In patients with atopic dermatitis, pro-tein contact sensitization has mostlybeen shown to plant or animal proteins(pollen, house dust mites, animal hair,foodstuffs, latex); it may occur after con-tact with the sensitive periocular region

162 Review Article Periorbital dermatitis

JDDG | 3˙2010 (Band 8) © The Authors • Journal compilation © Blackwell Verlag GmbH, Berlin • JDDG • 1610-0379/2010/0803

Figure 3: Hit list of consumers´ products, which were elicitors for periorbital allergic contact dermati-tis or airborne dermatitis (Department of Dermatology, University Hospital Erlangen 1999–2004):facial cream, eye shadow, ophthalmologic medications, nail polish, make-up, mascara, glue.

[30]. Depending on the source of the al-lergen, diagnosis of IgE-mediated con-tact dermatitis includes avoidance of theallergen, an atopy patch test, patch test-ing, skin prick testing with native mate-rials, and measurement of specific serumIgE [9, 30, 31]. The specificity of anatopy patch test can be higher, at64–92 %, depending on the tested (aero)allergens than skin prick testing andserum IgE measurements (33–71 %),while sensitivity is lower [32]. Scratchchamber methods (patch test on ascratch test) are sometimes used (e.g.,with native foods), but are not well stan-dardized. In a sample of patients with pe-riocular dermatitis who participated in astudy from 1999–2004, protein contactdermatitis (as a main diagnosis) playedonly a minor role [1]. Nineteen patients(48.7 %) out of 39 patients with a posi-tive atopy patch test to house dust mites(out of n = 150 patients who underwentatopy patch testing) had eczematous skinlesions on the face or neck. In these pa-tients, protein contact dermatitis was asecondary diagnosis along with pre-exist-ing atopic dermatitis (n = 14) or allergiccontact dermatitis (n = 5).

Irritant contact dermatitisIrritant contact dermatitis is much lesscommon at periocular sites than on thehands where various (especially occupa-tional) irritant exposures are possible [1,33]. Dust, fumes, and mechanical factorscan have an irritating effect on facial skinand should be considered as potentialtriggers in patients with periocular der-matitis. A history of exposures andavoidance of allergens as well as the ex-clusion of allergic and atopic co-factorscan aid diagnosis.

Periocular rosaceaThe presence of multiple erythematouspapules may be a sign of periocularrosacea. The diagnosis may be aided bythe presence of pustules and telangiec-tasias around the mouth and/or eyes, although they are not always present. Patients often report a burning andstinging sensation [34]. Since rosaceacan coexist with contact allergy, per-forming a patch test in patients with severe erythema and scaling may be wiseto rule out an additional contact allergy[35]. In one study type IV hypersensitiv-ity to propolis was shown to be signifi-cantly more common in patients with

rosacea compared with the total sample[35]. The same was shown in anotherstudy on type IV sensitivity to gentam-icin sulfate, a result which is attributedto the increased use of topical antibioticsin rosacea patients [36].

Other differential diagnosesRare triggers of periocular dermatitisare secondarily eczematous skin disor-ders of other origins such as eczematousperiorbital psoriasis vulgaris and conjunctivitis allergica (Erlangen study: 2.1 % each), drug intolerance(IVDK 1.8 %), and seborrheic dermati-tis (IVDK 1999–2004: 0.9 %) [1].Predilection sites for seborrheic der-matitis on the face are the nasolabialfolds and the forehead, including theeyebrow region (T zone). The majorpathophysiologic causes are thought to be excessive sebum production aswell as abnormal colonization withMalassezia yeasts and the subsequent in-flammatory reaction [37]. Periocularinvolvement is rare. Photoallergic andphototoxic triggers are rare and werenot identified in the IDVK sample [1].

TherapyIf a contact allergy has been establishedas the cause of periorbital dermatitis, thetreatment of choice is to avoid the aller-gen. The patient should be given conciseinformation on the relevant contact al-lergens and should be given a formaldocumentation (in Germany an “allergypassport” is issued) listing the respectivetype IV allergens (possibly with addi-tional information concerning potentialsources) [15, 38]. It is also important toprovide information on the InternationalNomenclature of Cosmetic Ingredients(INCI) declaration, which is used forlisting cosmetics ingredients given thatthe abbreviations sometimes differ fromthose commonly used for contact allergens (e.g., oak moss absolute = Evernia prunastri extract [INCI], tree moss = Evernia furfuracea extract[INCI], Lyral® = hydroxyisohexyl-3-cyclohexene carboxaldehyde [INCI], di-bromdicyanobutane = methyldibromog-lutaronitrile [INCI]). The InternationalNomenclature of Cosmetic Ingredientswas introduced on 1 January 1997 as a European regulation (96/335/EG)aimed at creating a standardized nomen-clature for ingredients in cosmetic prod-ucts [39, 40].

Symptoms may be treated with cal-cineurin inhibitors, the treatment ofchoice in atopic dermatitis affecting theperiocular region [41]. Calcineurin in-hibitors do not have any atrophogenicproperties [3]. Numerous studies havedemonstrated their efficacy in atopicdermatitis [42]. A recent systematic re-view recently provided evidence-basedconfirmation of the safety of topical cal-cineurin inhibitors in the treatment ofatopic dermatitis involving the face[43]. The 2007 Cochrane review “topi-cal pimecrolimus for eczema” including31 studies (n = 8 019 patients) showedthat pimecrolimus was superior inshort-term (≤ 6 weeks) and long-termstudies (≥ 6 months) for the treatmentof atopic dermatitis in reducing eczema-tous skin lesions (n = 9 long-term stud-ies, n = 3 091 patients, RR 1.47, 95 %,confidence interval of 1.32 to 1.64 after 6 months) and improving quality of lifecompared with vehicle [44]. Pime-crolimus was significantly less effective,however, than moderately or highly potenttopical corticosteroids (triamcinoloneacetonide 0.1 %, betamethasone valerate0.1 %) or 0.1 % tacrolimus [44].The only approved indication for cal-cineurin inhibitors is treatment of atopicdermatitis. Nevertheless, a number ofplacebo-controlled and open studieshave shown the effectiveness of topicalcalcineurin inhibitors in the treatment ofperiorbital contact dermatitis, irritantcontact dermatitis, seborrheic dermatitis,rosacea, facial, and intertriginous psoria-sis vulgaris [37, 45–48]. The use in aller-gic contact dermatitis, seborrheic der-matitis, protein contact dermatitis,eczematous psoriasis vulgaris, rosacea,and other diagnoses is off-label (and thusinvolves potential liability issues andpossible insurance claims). For off-labeluse, the patient must be thoroughly in-formed, and, if necessary, written con-sent should be obtained.Animal studies have shown increasedUV-induced carcinogenesis after topicalapplication of calcineurin inhibitors;this has not been confirmed in humanshowever, protective measures againstexposure to sunlight in accordance withthe pertinent guidelines are recom-mended [49]. If calcineurin inhibitor therapy fails toachieve a significant effect, short-termuse of newer topical corticosteroids witha good therapeutic index (TIX; the ratio

Periorbital dermatitis Review Article 163

© The Authors • Journal compilation © Blackwell Verlag GmbH, Berlin • JDDG • 1610-0379/2010/0803 JDDG | 3˙2010 (Band 8)

between objectively measured desired ef-fects [anti-eczema effect, vasoconstric-tion] and undesirable effects [skin atro-phy, adrenal cortex suppression,allergenic potential]) [50]. The topicalcorticosteroids methylprednisolone ace-ponate (substance class II, Advantan®)and prednicarbate (substance class II,Dermatop®), mometasone furoate (sub-stance class III, Ecural®) for examplehave a TIX of 2.0 and thus a good effi-cacy/side effect profile [50]. Corticos-teroids are not suitable for long-termtherapy of periorbital dermatitis, and pa-tients should be informed of this. Experience has also shown positive effects of using facial masks with softzinc paste (Pasta zinc mollis sine lanolinGerman Pharmacopoeia (DAB) [NewGerman Formulary 11.21])/Unguentumleniens (DAB 10) (1: 1) and astringentblack tea dressings.

ConclusionRisk factors for periorbital dermatitis in-clude female sex, age ≥ 40 years, andatopic skin diathesis. The most commoncause is allergic contact dermatitis. Othercommon causes and differentials are peri-ocular atopic dermatitis, periocular air-borne contact dermatitis, irritant contactdermatitis, and periocular rosacea. Raretriggers include seborrheic dermatitis,secondarily eczematous conjunctivitis al-lergica, and periorbital psoriasis vulgaris.Diagnosis of allergic periocular dermati-tis should be done with patch tests usingcommercial test series as well the pa-tient’s own personal care products –more than 10 % of cases of allergic con-tact dermatitis involving the periorbitalregion can only be diagnosed by patch testing of patients’ own products, not bycommercial series. Relevant test series in Germany for the diagnosis of perioculardermatitis, based on the patient’s med-ical history, include the German ContactDermatitis Group (DKG) standard,DKG topical agent ingredients, DKGpreservatives, DKG ophthalmologicagents, and DKG medications. The treatment of choice in periorbitalatopic dermatitis are calcineurin inhibitors(tacrolimus and pimecrolimus) [41] whichmay also be effective in the treatment ofperiocular dermatitis of causes other thanthose approved for prescription use. <<<

Conflict of interestNone.

Correspondence to

Priv.-Doz. Dr. med. Vera MahlerHautklinik Universitätsklinikum ErlangenHartmannstraße 14D-91052 ErlangenTel.: +49-9131-853-3161Fax: +49-9131-853-2724E-mail: vera.mahler@uk-erlangen.de

References1 Feser A, Plaza T, Vogelgsang L, Mahler

V. Periorbital dermatitis – a recal-citrant disease: Causes and differentialdiagnoses. Br J Dermatol 2008; 159:858–63.

2 Davies E, Patel C, Salek MS, Finlay AY.Does ad hoc quality-of-life discussionin inflammatory skin disease consulta-tions reflect standardized patient-repor-ted outcomes? Clin Exp Dermatol2008; 33: 16–21.

3 Murrell DF, Calvieri S, Ortonne JP, HoVC, Weise-Riccardi S, Barbier N, PaulCF. A randomized controlled trial of pi-mecrolimus cream 1 % in adolescentsand adults with head and neck atopicdermatitis and intolerant of, or depen-dent on, topical corticosteroids. Br JDermatol 2007; 157: 954–9.

4 Nethercott JR, Nield G, Holness DL. Areview of 79 cases of eyelid dermatitis. JAm Acad Dermatol 1989; 21: 223–30.

5 Cooper SM, Shaw S. Eyelid dermatitis:an evaluation of 232 patch test patientsover 5 years. Contact Dermatitis 2000;42: 291–3.

6 Ockenfels HM, Seemann U, Goos M.Contact allergy in patients with perior-bital eczema: an analysis of allergens.Data recorded by the Information Net-work of Departments of Dermatology.Dermatology 1997; 195: 119–24.

7 Herbst RA, Uter W, Pirker C, Geier J,Frosch PJ. Allergic and non-allergic pe-riorbital dermatitis: patch test results ofthe Information Network of the Departments of Dermatology during a5-year period. Contact Dermatitis2004; 51: 13–9.

8 Diepgen TL, Fartasch M, HornsteinOP. Kriterien zur Beurteilung der ato-pischen Hautdiathese. DermatologieBeruf Umwelt 1991; 39: 79–83.

9 Czarnecka-Operacz M, Bator-WegnerM, Silny W. Atopy patch test reactionto airborne allergens in the diagnosis ofatopic dermatitis. Acta Dermatovene-reol Croat 2005; 13: 3–16.

10 Vickery BP. Skin barrier function inatopic dermatitis. Curr Opin Pediatr2007; 19: 89–93.

11 McLean WH, Hull PR. Breach deli-very: increased solute uptake points to adefective skin barrier in atopic dermati-tis. J Invest Dermatol 2007; 127: 8–10.

12 Rein DB, Zhang P, Wirth KE, Lee PP,Hoerger TJ, McCall N, Klein R,Tielsch JM, Vijan S, Saaddine J. Theeconomic burden of major adult visualdisorders in the United States. ArchOphthalmol 2006; 124: 1754–60.

13 Guin JD. Eyelid dermatitis: experiencein 203 cases. J Am Acad Dermatol2002; 47: 755–65.

14 Brasch J, Becker D, Aberer W, BircherA, Kränke B, Denzer-Fürst S, SchnuchA. AWMF-Leitlinie: Kontaktekzem. JDtsch Dermatol Ges 2007; 5: 943–52.

15 Schnuch A, Aberer W, Agathos M,Becker D, Brasch J, Elsner P, Frosch PJ,Fuchs T, Geier J, Hillen U, Löffler H,Mahler V, Richter G, Szliska C.AWMF-Leitlinie: Durchführung desEpikutantests mit Kontakt-Allergenen.J Dtsch Dermatol Ges 2008; 6: 770–5.

16 Valsecchi R, Imberti G, Martino D,Cainelli T. Eyelid dermatitis: an evalua-tion of 150 patients. Contact Dermati-tis 1992; 27: 143–7.

17 Brandrup F. Nickel eyelid dermatitisfrom an eyelash curler. Contact Derma-titis 1991; 25: 77.

18 Karlberg AT, Liden C, Ehrin E. Colo-phony in mascara as a cause of eyeliddermatitis. Chemical analyses andpatch testing. Acta Derm Venereol1991; 71: 445–7.

19 Van Ketel WG, Liem DH. Eyelid dermatitis from nickel contaminatedcosmetics. Contact Dermatitis 1981; 7:217.

20 Vilaplana J, Romaguera C, Grimalt F.Contact dermatitis from nickel and co-balt in a contact lens cleaning solution.Contact Dermatitis 1991; 24: 232–3.

21 Zemba C, Romaguera C, Vilaplana J.Allergic contact dermatitis from nickelin an eye pencil. Contact Dermatitis1992; 27: 116.

164 Review Article Periorbital dermatitis

JDDG | 3˙2010 (Band 8) © The Authors • Journal compilation © Blackwell Verlag GmbH, Berlin • JDDG • 1610-0379/2010/0803

22 Johansen JD, Andersen TF, Veien N,Avnstorp C, Andersen KE, Menné T.Patch testing with markers of fragrancecontact allergy. Acta Derm Venereol1997; 77: 149–53.

23 Api MA. Only Peru Balsam extracts ordistillates are used in perfumery.Contact Dermatitis 2006; 54: 179.

24 Hausen BM. Rauchen, Süßigkeiten,Perubalsam – ein Circulus vitiosus? AktDermatol 2001; 27: 136–43.

25 Schnuch A, Szlisha C, Uter W. Allergi-sches Gesichtsekzem. Auswertungendes IVDK und Literaturübersicht.Hautarzt 2009; 60: 13–21.

26 Uter W, Geier J, Schnuch A, Arnold R. Konzept einer Informations- und Dokumentationsstelle für Kontaktall-ergien (IDOK) des Informationsver-bundes Dermatologischer Kliniken(IVDK). Version 26.03.2003.

27 De Groot AC. Patch testing. Patch testconcentrations and vehicles for 4 350Chemicals. 3d Edition, Acdegroot pu-blishing, HV Wapserveen, 2008.

28 Santos R, Goossens A. An update onairborne contact dermatitis: 2001–2006. Contact Dermatitis 2007; 57:353–60.

29 Stingl G, Maurer D. IgE-mediated all-ergen presentation via Fc epsilon RI onantigen-presenting cells. Int Arch All-ergy Immunol 1997; 113: 24–9.

30 Levin C, Warshaw E. Protein contactdermatitis: allergens, pathogenesis, andmanagement. Dermatitis 2008; 19:241–51.

31 Darsow U, Laifaoui J, Kerschenlohr K,Wollenberg A, Przybilla B, WüthrichB, Borelli S Jr, Giusti F, Seidenari S,Drzimalla K, Simon D, Disch R, Bo-relli S, Devillers AC, Oranje AP, De Ra-eve L, Hachem JP, Dangoisse C, Blon-deel A, Song M, Breuer K, Wulf A,Werfel T, Roul S, Taieb A, Bolhaar S,Bruijnzeel-Koomen C, BrönnimannM, Braathen LR, Didierlaurent A,André C, Ring J. The prevalence of po-sitive reactions in the atopy patch testwith aeroallergens and food allergens insubjects with atopic eczema: a Euro-

pean multicenter study. Allergy 2004;59: 1318–25.

32 Darsow U, Ring J. Atopie-Patch-Testmit Aeroallergenen und Nahrungsmit-teln. Hautarzt 2005; 56: 1133–40.

33 Dickel H, Kuss O, Schmidt A, Kretz J,Diepgen TL. Importance of irritantcontact dermatitis in occupational skindisease. Am J Clin Dermatol 2002; 3:283–9.

34 Lonne-Rahm SB, Fischer T, Berg M.Stinging and rosacea. Acta Derm Vene-reol 1999; 79: 460–1.

35 Jappe U, Schnuch A, Uter W. Rosaceaand contact allergy to cosmetics and to-pical medicaments – retrospective ana-lysis of multicentre surveillance data1995–2002. Contact dermatitis 2005;52: 96–101.

36 Jappe U, Schäfer T, Schnuch A, UterW. Contact allergy in patients with ro-sacea: a clinic-based, prospective epide-miological study. J Eur Acad DermatolVenereol 2008; 22: 1208–14.

37 Cook BA, Warshaw EM. Role of topical calcineurin inhibitors in the treatment of seborrheic dermatitis: a review of pathophysiology, safety, andefficacy. Am J Clin Dermatol 2009; 10:103–18.

38 Worm M, Sterry W. Periokuläre Kon-taktekzeme. Klin Monatsbl Augen-heilkd 2005; 853–5.

39 De Groot AC, van Ginkel CJ, WeijlandJW. Statement of ingredients of cosme-tics. Ned Tijdschr Geneeskd 1997;141:1747–8.

40 De Groot AC, Weijland JW. Conver-sion of common names of cosmetic allergens to the INCI nomenclature.Contact Dermatitis 1997; 37: 145–50.

41 Werfel T, Aberer W, Augustin M, Biedermann T, Fölster-Holst R, Friedrichs F, Gieler U, Heratizadeh A,Kapp A, Przybilla B, Rietschel E, Schlaeger M, Schmid-Grendelmeier P,Sitter H, Staab D, Szczepanski R, VielufD, Voigtmann I, Worm M. AWMF-Leitlinie: Neurodermitis. 04/2008. http://www.uni-duesseldorf.de/AWMF/ll/013-027.htm.

42 Hultsch T, Kapp A, Spergel J. Immun-omodulation and safety of topical calci-neurin inhibitors for the treatment ofatopic dermatitis. Dermatology 2005;211: 174–87.

43 Callen J, Chamlin S, Eichenfield LF,Ellis C, Girardi M, Goldfarb M, Hanifin J, Lee P, Margolis D, Paller AS,Piacquadio D, Peterson W, KaulbackK, Fennerty M, Wintroub BU. A syste-matic review of the safety of topical therapies for atopic dermatitis. Br JDermatol 2007; 156: 203–21.

44 Ashcroft DM, Chen LC, Garside R,Stein K, Williams HC. Topical pimecrolimus for eczema. CochraneDatabase Syst Rev 2007; Issue 4. Art.No.: CD005500. DOI: 10.1002/14651858.CD005500.pub2. Publ. online Okt 17, 2007.

45 Day I, Lin AN. Use of pimecrolimuscream in disorders other than atopicdermatitis. J Cutan Med Surg 2008;12: 17–26.

46 Luger T, Paul C. Potential new indicati-ons of topical calcineurin inhibitors.Dermatology 2007; 215: 45–54.

47 Mensing CO, Mensing CH, MensingH. Treatment with pimecrolimuscream 1 % clears irritant dermatitis ofthe periocular region, face and neck. IntJ Dermatol 2008; 47: 960–4.

48 Jacobi A, Braeutigam M, Mahler V,Schultz E, Hertl M. Pimecrolimus 1 %cream in the treatment of facial psoria-sis: a 16-week open-label study. Derma-tology 2008; 216: 133–6.

49 Langley RGB, Luger TA, Cork MJ,Schneider D, Paul C. An Update on theSafety and Tolerability of PimecrolimusCream 1 %: Evidence from ClinicalTrials and Post-Marketing Surveillance.Dermatology 2007; 215 (Suppl 1):27–44.

50 Luger T, Loske KD, Elsner P, Kapp A,Kerscher M, Korting HC, Krutmann J,Niedner R, Röcken M, Ruzicka T,Schwarz T. AWMF-Leitlinie: TopischeDermatotherapie mit Glukokortikoi-den – Therapeutischer Index. J DtschDermatol Ges 2004; 2: 629–34.

Periorbital dermatitis Review Article 165

© The Authors • Journal compilation © Blackwell Verlag GmbH, Berlin • JDDG • 1610-0379/2010/0803 JDDG | 3˙2010 (Band 8)