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Volume 14 Number 5

Chronic actinic dermatitis Alexandria V Booth MD, Stephanie Mengden MD, Nicholas A Soter MD, David Cohen MD, MPH Dermatology Online Journal 14 (5): 25 Department of Dermatology, New York University

Abstract

A 71-year-old man presented with a six-year history of a pruritic, erythematous, blistering eruption of the face, chest, and arms. Clinical findings, histopathologic features, and phototests were consistent with a diagnosis of chronic actinic dermatitis. The patient also had contact allergy and photocontact allergy to multiple allergens. A discussion of chronic actinic dermatitis is presented.

Clinical synopsis

A 71-year-old Albanian man was referred to the Charles C. Harris Skin and Cancer Pavilion Allergy/Contact Dermatitis Section with a 6-year history of an intermittently pruritic, paroxysmally flaring eruption over the face, chest, arms, and legs. It typically begins as pruritus and edema with subsequent blisters and desquamation over a 3-week period. It initially affected his face but began to involve his entire body 4 years later. He felt that the eruption was worse after sun exposure and during the Spring. He noted temporary improvement with the use of systemic glucocorticoids. Past medical history included allergic rhinitis, cervical spondylitis, arthritis, and hypercholesterolemia. His only medication is diphenhydramine for pruritus. Allergy history included contact allergy to iodine, grass, and synthetic clothing as a child. He is a retired otolaryngologist, and his hobbies include watercolor painting, walking, and working on his computer.

Physical Examination

Confluent erythema was present on the face and V-area of the upper chest with sparing below the chin. Erythema with scattered erosions and lichenification was noted over the dorsal aspects of the arms and hands, with demarcation at the mid-portion of the upper arms and sparing of the proximal areas.

Figure 1

Figure 2

A complete blood count with differential analysis and comprehensive metabolic panel were normal. Antinuclear, anti-Ro, and anti-La antibodies were negative.

Phototests showed no immediate response to ultraviolet A, ultraviolet B or visible light; MEDa was low at 15 J/cm2, and MEDb was low at 5mJ/cm2.

Photopatch test reactions were positive to promethazine and chlorpromazine. Patch test reactions were positive to formaldehyde, quaternium-15, imidazolidinyl urea, diazolidinyl urea, ethyleneurea melamine formaldehyde, thiuram mix, carba mix, propylene glycol, methylchloroisothiazolone methylisothiazolone, and methylbibromoglutoaronitrile.

Histopathology

There is mild acanthosis, focal parakeratosis, and a few, necrotic keratinocytes within a spongiotic epidermis. Within the superficial and mid-to-deep dermis, there is a perivascular and periadnexal predominantly lymphocytic infiltrate with some exocytosis of lymphocytes. The inflammatory infiltrate is also composed of a few neutrophils and macrophages containing melanin.

Comment

Chronic actinic dermatitis (CAD) is the term first proposed in 1979 by Hawk and Magnus [1] to unify the conditions known as persistent light reactivity described by Wilkinson [2] in 1961, actinic reticuloid described by Ive et al. [3] in 1969, photosensitive eczema described by Ramsay and Black [4] in 1973, and photosensitivity dermatitis described by Frain-Bell et al. [5] in 1974. The three main criteria of CAD are reduction in the minimal erythema dose to UVA, UVB and/or visible light; a persistent eczematous eruption that predominantly affects sun-exposed skin and sometimes extends to covered areas; and histopathologic changes consistent with chronic eczema with or without cutaneous lymphoma-like changes [6].

Chronic actinic dermatitis has been reported in Caucasians, Latin Americans, Blacks, Japanese, and Indians and is most common in temperate climates [7, 8]. The condition is typically seen in elderly men and is rare in women [7]. It may or occur after endogenous eczema, photoallergic or allergic contact dermatitis, oral drug photosensitivity, occasionally polymorphic light eruption, or rarely human immunodeficiency virus infection [8].

The initial symptom is usually persistent erythema of the face, with subsequent development of an eczematous, patchy or diffuse, pruritic, often lichenified eruption in sun-exposed areas, particularly the face, scalp, V-area of chest, back and sides of neck, and dorsal aspects of hands

and forearms, often with sharp demarcation at lines of clothing [8]. After some time, and often rapidly, non-sun-exposed areas also become involved [7]. Palmar and plantar eczema is also possible as well as loss of eyebrow and scalp hair that develops after scratching; erythroderma occasionally may develop [8]. Affected individuals with CAD may not complain of abnormal reactions to sunlight because they may be so sensitive to UVA and visible wavelengths, which penetrate window glass, that no relationship to sunlight exposure is noticed [9].

The histopathologic changes are characterized by epidermal spongiosis and acanthosis, sometimes with hyperplasia, along usually with a deep dermal, predominantly perivascular, frequently dense, mononuclear-cell infiltrate and not infrequently large hyperchromatic convoluted nuclei and mitotic figures. There also may be macrophages, eosinophils, and plasma cells; in some instances, the disorder may be difficult to differentiate from cutaneous T-cell lymphoma (CTCL) [8]. Chronic actinic dermatitis has a characteristic immunophenotype distinct from most cases of CTCL, with CD8 cells in the epidermis and discordance between BF1 (chain constant region of T-cell receptor) cells and CD3 expression in CAD [10].

Phototests to ultraviolet and often visible irradiation may show erythematous or eczematous responses, normally at doses much lower than the normal minimal erythema dose. The reaction peaks between seven and 24 hours after exposure. The provoking wavelengths are ultraviolet B (UVB) (280-320 nm) in virtually all patients, ultraviolet A (UVA) (320-400 nm) in most patients, and visible light or UVA alone in a few patients [9, 8].

Allergic and/or photallergic contact dermatitis commonly coexist with CAD and often precedes the onset of photosensitivity [6]. In 1 study of 89 patients with CAD, 74 percent had positive patch or photopatch tests. Of patch tests 36 percent were positive to sesquiterpene lactone mix, 21 percent to fragrance compounds, 20 percent to colophony, and 14 percent to rubber chemicals. In 1 photopatch test study, 6 percent were positive to musk ambrette, 7 percent to sunscreens, and 1 to both [11].

Other tests to consider are ANA and anti-Ro and anti-La antibodies [8].

The pathogenisis of CAD is not completely understood, but the histologic and immunohistochemical features of CAD, along with increased ICAM-1 expression and a dermal infiltrate of predominantly CB8+ T cells mimic the delayed-type hypersensitivity response

observed in contact dermatitis [8, 6]. One theory has proposed that during an initial photoallergic reaction, a normal skin constituent is altered to become antigenic. Induction begins with UVAdependent covalent binding of hapten to an endogenous protein and is followed by a delayedtype hypersensitivity response. As the disease progresses to CAD, UVB and UVA alone may trigger the immune response without the hapten by continuing to form the antigenic photoproduct from the endogenous carrier protein [6]. There has been theoretical support for this mechanism using an in vitro model with the photosensitizer tetrachlorosalicylanilide, which demonstrated phototoxic oxidation of histidine with modification of the carrier albumin into a weak antigen [12].

The mainstay of treatment is sunlight avoidance and, when applicable, allergen avoidance. Sunlight avoidance includes wearing protective clothing, application of non-irritating broadspectrum sunscreens, and application of filters to home and car windows. Topical and/or oral glucocorticoids with emollients are usually necessary [8]. Topical tacrolimus ointment has been shown to be beneficial in case reports [13, 14]. Treatments for resistant disease include low-dose PUVA photochemotherapy, narrow-band UVB phototherapy, cyclosporine, azathioprine, and mycophenolate mofetil alone or in combination [8, 15].

Resolution of photosensitivity in 1 study of CAD occurred in 20 percent in 10 years; severe abnormal UVB photosensitivity and positive patch tests to 2 or more unrelated patch test batteries to be predictors of a poorer prognosis [16]. There is usually persistence of the allergic contact allergy even with clinical improvement in the photosensitivity [17]. References 1. Hawk JLM, Magnus IA. Chronic actinic dermatitis-an idiopathic photosensitivity syndrome including actinic reticuloid and photosensitive eczema. Br J Dermatol 1979;101(Suppl 17):24

2. Wilkinson DS. Photodermatitis due to tetrachlorosalicylanilide. Br J Dermatol 1961;73:213

3. Ive FA, et al. 'Actinic Reticuloid'; a chronic dermatosis associated with severe photosensitivity and the histological resemblance to lymphoma. Br J Dermatol 1969;81:469

4. Ramsay CA, Black A. Photosensitive eczema. Trans St. John's Hosp Derm Soc 1973;59:152

5. Fain-Bell W, et al. The syndrome of chronic photosensitivity dermatitis and actinic reticuloid. Br J Dermatol 1974;91:617

6. Somani VK. Chronic actinic dermatitis-a study of clinical features. Indian J Dermatol Venereol Leprol 2005;71:409

7. Roelandts R. Chronic actinic dermatitis. J Am Acad Dermatol 1993;28:240

8. Hawk JLM. Chronic actinic dermatitis. Photodermatol Photoimmunol Photomed 2004;20:312

9. Dawe R. Chronic actinic dermatitis in the elderly. Drugs Aging 2005;22:201

10. Heller P, et al. Chronic actinic dermatitis: an immunochemical study of its T-cell antigenic profile, with comparison to cutaneous T-cell lymphoma. Am J Dermatopathol 1994;16:510

11. Menage H, et al. Contact and photocontact sensitization in chronic actinic dermatitis: sesquiterpene lactone mix is an important allergen. Br J Dermatol 1995;132:543

12. Kochevar IE, Harber LC. Photoreactions of 3,3',4',5-tetrachlorosalicylanilide with proteins. J Invest Dermatol 1977;68:151

13. Schuster C, et al. Successful treatment of recalcitrant chronic actinic dermatitis with tacrolimus. Dermatology 2004;209:325

14. Baldo A, et al. A case of chronic actinic dermatitis treated with topical tacrolimus. J Derm Treat 2005;16:245

15. Nousari HC, et al. Mycophenolate in psoralen-UV-A desensitization therapy for chronic actinic dermatitis. Arch Dermatol 1999;135:1128

16. Dawe RS, et al. The natural history of chronic actinic dermatitis. Arch Dermatol 2000;136:1215

17. Addo HA, Frain-Bell W. Persistence of allergic contact sensitivity in subjects with photosensitivity dermatitis and actinic reticuloid syndrome. B J Dermatol 1987;117:555

2008 Dermatology Online Journal

DOJ Isi

Volume 14 Nomor 5 Kronis actinic dermatitis Alexandria V Booth MD, Stephanie Mengden MD, Nicholas A MD Soter, David Cohen MD, MPH Dermatology Online Journal 14 (5): 25 Departemen Dermatology, New York University

Abstrak Seorang pria 71 tahun dengan riwayat enam tahun dari eritematosa, pruritus, letusan terik wajah, dada, dan lengan. Temuan klinis, gambaran histopatologis, dan phototests yang konsisten dengan diagnosis dermatitis actinic kronis. Pasien juga memiliki alergi kontak dan alergi terhadap alergen photocontact beberapa. Sebuah diskusi tentang dermatitis actinic kronis disajikan. Klinis sinopsis Seorang pria 71-tahun Albania dirujuk ke Skin C. Charles Harris dan Kanker Pavilion Alergi / Contact Bagian Dermatitis dengan sejarah 6 tahun dari pruritus sebentar-sebentar, paroxysmally pembakaran letusan atas wajah, dada, lengan, dan kaki. Ini biasanya dimulai sebagai pruritus dan edema dengan lepuh berikutnya dan deskuamasi selama periode 3-minggu. Ini awalnya terpengaruh wajahnya, tetapi mulai melibatkan seluruh tubuhnya 4 tahun kemudian. Dia merasa bahwa letusan lebih buruk setelah paparan sinar matahari dan selama musim semi. Dia mencatat perbaikan sementara dengan penggunaan glukokortikoid sistemik. Riwayat medis masa lalu termasuk rhinitis alergi, spondilitis serviks, arthritis, dan hiperkolesterolemia. Obat satu-satunya adalah diphenhydramine untuk pruritus. Riwayat alergi termasuk alergi kontak terhadap yodium, rumput, dan pakaian sintetik sebagai seorang anak. Dia adalah seorang otolaryngologist pensiunan, dan hobinya meliputi lukisan cat air, berjalan, dan bekerja di komputernya. Pemeriksaan Fisik

Eritema konfluen hadir pada wajah dan V-daerah dada bagian atas dengan hemat bawah dagu. Eritema dengan erosi tersebar dan lichenifikasi tercatat atas aspek dorsal lengan dan tangan, dengan batas di bagian tengah-dari lengan atas dan hemat dari daerah proksimal.

Gambar 1 Gambar 2 Hitung darah lengkap dengan diferensial dan analisis yang komprehensif panel metabolisme normal. Antibodi antinuklear, anti-Ro, anti-La dan negatif. Phototests menunjukkan tidak segera menanggapi ultraviolet A, ultraviolet atau cahaya tampak, Meda rendah pada 15 J/cm2, dan MEDB rendah pada 5mJ/cm2. Reaksi uji patch yang positif promethazine dan klorpromazin. Patch reaksi tes yang positif terhadap formaldehida, quaternium-15, imidazolidinyl urea, diazolidinyl urea, melamin formaldehid ethyleneurea, thiuram campuran, carba campuran, propilen glikol, methylisothiazolone methylchloroisothiazolone, dan methylbibromoglutoaronitrile. Histopatologi Ada acanthosis ringan, parakeratosis fokal, dan, beberapa keratinosit nekrotik dalam epidermis spongiotic. Dalam dermis superfisial dan pertengahan-ke-dalam, ada perivaskular dan periadnexal didominasi limfositik menyusup dengan beberapa exocytosis limfosit. Yang infiltrat inflammatory juga terdiri dari neutrofil dan makrofag yang mengandung beberapa melanin. Komentar Dermatitis aktinik kronis (CAD) adalah istilah yang pertama kali diusulkan pada tahun 1979 oleh Hawk dan Magnus [1] untuk menyatukan kondisi yang dikenal sebagai reaktivitas cahaya persisten dijelaskan oleh Wilkinson [2] pada tahun 1961, actinic retikuloid dijelaskan oleh Ive et al. [3] pada tahun 1969, eksim fotosensitif dijelaskan oleh Ramsay dan Black [4] pada tahun 1973, dan dermatitis fotosensitivitas dijelaskan oleh Frain-Bell et al. [5] pada tahun 1974. Tiga kriteria utama CAD adalah pengurangan dosis eritema minimal untuk UVA, UVB dan / atau cahaya tampak, letusan eczematous gigih yang dominan mempengaruhi terkena sinar matahari kulit dan kadang-kadang meluas ke daerah tertutup, dan perubahan histopatologi konsisten dengan eksim kronis dengan atau tanpa kulit limfoma-seperti perubahan [6]. Dermatitis aktinik kronis telah dilaporkan di Kaukasia, Amerika Latin, kulit hitam, Jepang, dan India, dan paling sering terjadi pada daerah beriklim [7, 8]. Kondisi ini biasanya terlihat pada

pria tua dan jarang terjadi pada wanita [7]. Ini mungkin atau terjadi setelah eksim endogen, dermatitis kontak fotoalergi atau alergi, photosensitivity obat oral, letusan ringan sesekali polimorfik, atau infeksi virus human immunodeficiency jarang [8]. Gejala awal biasanya eritema persisten dari wajah, dengan perkembangan selanjutnya dari eczematous, merata atau difus, pruritus, letusan sering lichenified di daerah terkena sinar matahari, terutama wajah, kulit kepala, V-daerah dada, belakang dan samping leher , dan aspek dorsal tangan dan lengan bawah, seringkali dengan batas tajam di lini pakaian [8]. Setelah beberapa waktu, dan sering cepat, non-terkena sinar matahari daerah juga terlibat [7]. Palmar dan eksim plantar juga mungkin serta hilangnya alis dan rambut kulit kepala yang berkembang setelah menggaruk, eritroderma terkadang dapat mengembangkan [8]. Individu yang terkena dengan CAD mungkin tidak mengeluhkan reaksi abnormal terhadap sinar matahari karena mereka mungkin begitu sensitif terhadap UVA dan panjang gelombang terlihat, yang menembus kaca jendela, bahwa tidak ada hubungan dengan paparan sinar matahari yang melihat [9]. Perubahan histopatologi ditandai dengan spongiosis epidermal dan acanthosis, kadang-kadang dengan hiperplasia, bersama biasanya dengan kulit dalam, terutama perivaskular, sering padat, mononuklear-sel menyusup dan tak jarang besar inti berbelit-belit hyperchromatic dan mitosis angka. Ada juga mungkin makrofag, eosinofil, dan sel plasma, dalam beberapa kasus, gangguan tersebut mungkin sulit untuk membedakan dari kulit T-sel limfoma (CTCL) [8]. Dermatitis aktinik kronis memiliki karakteristik yang berbeda dari imunofenotipe sebagian besar kasus CTCL, dengan CD8 sel di epidermis dan kejanggalan antara BF1 (-rantai wilayah konstan T-sel reseptor) sel dan CD3 ekspresi dalam CAD [10]. Phototests untuk ultraviolet dan iradiasi sering terlihat dapat menunjukkan eritematosa atau tanggapan eczematous, biasanya pada dosis yang lebih rendah dari dosis eritema minimal yang normal. Puncak Reaksi antara tujuh dan 24 jam setelah paparan. Panjang gelombang ultraviolet B yang memprovokasi (UVB) (280-320 nm) di hampir semua pasien, ultraviolet A (UVA) (320400 nm) pada kebanyakan pasien, dan cahaya tampak atau UVA sendirian di beberapa pasien [9, 8] . Dermatitis kontak alergi dan / atau photallergic umumnya hidup berdampingan dengan CAD dan sering mendahului terjadinya fotosensitifitas [6]. Dalam 1 studi dari 89 pasien dengan CAD, 74 persen memiliki patch yang positif atau tes patch. Dari uji patch 36 persen positif untuk seskuiterpen lakton campuran, 21 persen untuk senyawa aroma, 20 persen menjadi colophony, dan 14 persen untuk bahan kimia karet. Dalam 1 studi uji patch, 6 persen positif musk ambrette, 7 persen menjadi tabir surya, dan 1 untuk kedua [11]. Pemeriksaan lainnya yang perlu dipertimbangkan adalah ANA dan anti-Ro dan anti-La antibodi [8].

The pathogenisis CAD tidak sepenuhnya dipahami, tetapi fitur histologis dan imunohistokimia dari CAD, bersama dengan peningkatan ICAM-1 ekspresi dan dermal infiltrat didominasi CB8 + T sel meniru respon tertunda-jenis hipersensitivitas diamati pada dermatitis kontak [8, 6] . Salah satu teori yang telah mengusulkan bahwa selama reaksi fotoalergi awal, konstituen kulit normal diubah menjadi antigenik. Induksi dimulai dengan UVA-dependent pengikatan kovalen dari hapten ke protein endogen dan diikuti dengan respon hipersensitivitas tertunda-jenis. Sebagai penyakit berlangsung untuk CAD, UVB dan UVA saja dapat memicu respon imun tanpa hapten dengan terus membentuk photoproduct antigenik dari protein pembawa endogen [6]. Telah ada dukungan teoretis untuk mekanisme menggunakan model in vitro dengan tetrachlorosalicylanilide fotosensitizer, yang menunjukkan oksidasi fototoksik dari histidin dengan modifikasi pembawa albumin menjadi antigen yang lemah [12]. Andalan pengobatan sinar matahari dan menghindari, jika memungkinkan, menghindari alergen. Menghindari sinar matahari termasuk pakaian memakai aplikasi, pelindung non-menjengkelkan spektrum luas tabir surya, dan aplikasi filter untuk jendela rumah dan mobil. Glukokortikoid topikal dan / atau lisan dengan emolien biasanya diperlukan [8]. Topikal tacrolimus salep telah terbukti bermanfaat dalam laporan kasus [, 13 14]. Pengobatan untuk penyakit tahan termasuk dosis rendah PUVA fotokemoterapi, sempit-band UVB fototerapi, cyclosporine, azathioprine, dan mycophenolate mofetil sendiri atau dalam kombinasi [8, 15]. Resolusi fotosensitifitas pada 1 studi CAD terjadi pada 20 persen dalam 10 tahun, photosensitivity UVB parah abnormal dan uji patch positif terhadap 2 atau lebih baterai uji tempel terkait untuk menjadi prediktor prognosis yang lebih buruk [16]. Biasanya ada kegigihan dari alergi kontak alergi bahkan dengan perbaikan klinis dalam photosensitivity [17]. Referensi 1. Hawk JLM, Magnus IA. Kronis actinic dermatitis-sindrom fotosensitifitas idiopatik termasuk retikuloid actinic dan eksim fotosensitif. Br J Dermatol 1979, 101 (Suppl 17): 24 2. Wilkinson DS. Karena tetrachlorosalicylanilide Photodermatitis. Br J Dermatol 1961; 73:213 3. Ive FA, et al. 'Actinic retikuloid', sebuah dermatosis kronis yang berhubungan dengan photosensitivity parah dan kemiripan histologis untuk limfoma. Br J Dermatol 1969; 81:469 4. Ramsay CA, Black A. eksim fotosensitif. Trans St John Hosp Derm Soc 1973; 59:152 5. Fain-Bell W, et al. Sindrom dermatitis fotosensitivitas kronis dan retikuloid actinic. Br J Dermatol 1974; 91:617 6. Somani VK. Dermatitis-a actinic kronis studi klinis. India J Dermatol Venereol Leprol 2005;

71:409 7. Roelandts R. dermatitis actinic kronis. J Am Acad Dermatol 1993; 28:240 8. Elang JLM. Kronis actinic dermatitis. Photodermatol Photoimmunol Photomed 2004; 20:312 9. Dawe R. dermatitis actinic kronis pada orang tua. Obat Aging 2005; 22:201 10. Heller P, et al. Dermatitis aktinik kronis: sebuah studi immunochemical dari T-sel profil antigenik, dengan dibandingkan dengan kulit T-sel limfoma. Am J Dermatopathol 1994; 16:510 11. Menage H, et al. Kontak dan sensitisasi photocontact dalam dermatitis actinic kronis: seskuiterpen lakton mix merupakan alergen penting. Br J Dermatol 1995; 132:543 12. Kochevar IE, Harber LC. Photoreactions dari 3,3 ', 4' ,5-tetrachlorosalicylanilide dengan protein. J Invest Dermatol 1977; 68:151 13. Schuster C, et al. Sukses pengobatan dermatitis actinic bandel kronis dengan tacrolimus. Dermatologi 2004; 209:325 14. Baldo A, et al. Sebuah kasus dermatitis actinic kronis diobati dengan tacrolimus topikal. J Derm Treat 2005; 16:245 15. Nousari HC, et al. Mofetil di psoralen-UV-A terapi desensitisasi untuk dermatitis actinic kronis. Arch Dermatol 1999; 135:1128 16. Dawe RS, et al. Riwayat alami dermatitis actinic kronis. Arch Dermatol 2000; 136:1215 17. Addo HA, Frain-Bell W. Kegigihan sensitivitas kontak alergi pada subyek dengan dermatitis photosensitivity dan sindrom retikuloid actinic. B J Dermatol 1987; 117:555 2008 Jurnal online Dermatology