DERMATOLOGICA SINICA 36 (2018) 85e88
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CASE REPORT
Coexistence of adult-onset actinic prurigo and shampoo dermatitis: A case report Tsung-Ju Lee a, Yu-Hung Wu a, b, c, Pa-Fan Hsiao a, b, c, Mei-Eng Tu a, * a
Department of Dermatology, Mackay Memorial Hospital, Taipei, Taiwan Mackay Medicine, Nursing and Management College, Taipei, Taiwan c Department of Medicine, Mackay Medical College, New Taipei City, Taiwan b
a r t i c l e i n f o
a b s t r a c t
Article history: Received: Feb 9, 2017 Revised: Jun 27, 2017 Accepted: Jul 26, 2017
Actinic prurigo is a rare and acquired idiopathic photodermatosis. It usually shows childhood onset and female predominance. Here, we present an unusual case of a male patient with coexistence of adultonset actinic prurigo and shampoo-induced allergic contact dermatitis. He was initially diagnosed with actinic prurigo. However, after detailed examination of the distribution of the rash, careful collection of his history, and interpretation of the results of histopathologic analysis, photo test, patch test, and photopatch test, coexistence of adult-onset actinic prurigo and shampoo-induced allergic contact dermatitis associated with cocamidopropyl betaine was diagnosed. The rash improved after appropriate use of sunscreen and avoidance of shampoo containing this allergen. Dermatologists should be aware of the possibility of concurrent photodermatitis and contact dermatitis. Copyright © 2017, Taiwanese Dermatological Association. Published by Elsevier Taiwan LLC. This is an open access article under the CC BY-NC-ND license (http:// creativecommons.org/licenses/by-nc-nd/4.0/).
Keywords: Actinic prurigo Cocamidopropyl betaine Contact dermatitis Photosensitivity Shampoo dermatitis
Introduction Actinic prurigo (AP) is a rare idiopathic photodermatosis that is more commonly seen in Latin Americans.1,2 AP is rarely found in Caucasian and Asian populations, and it was first reported in Native American populations from Central North and South America.3 It is characterized by familial photodermatosis, childhood onset (younger than 10 years of age), female predilection, strong association with the HLA DR4 allele, intense pruritus, a chronic course (lasting for more than 4 weeks), exacerbation in early spring, and a high incidence of cheilitis and conjunctivitis.1,4,5 AP presents with erythematous papules or nodules on sun-exposed areas, particularly the face, ears, V-neck area, extensor forearms, dorsal hands, and chest. However, covered sites, including the back and buttocks, may be affected occasionally. Adult-onset AP (older than 21 years of age) has been noted in a small number of patients, and these
Conflicts of interest: The authors have no conflict of interest to declare. Prior presentation: No. IRB: Proved by Institutional Review Board of Mackay Memorial Hospital (Number: 15MMHIS199e). * Corresponding author. Department of Dermatology, Mackay Memorial Hospital, 92, Sec. 2, Zhongshan North Road, Taipei, 10449, Taiwan. Fax: þ886 2 25232448. E-mail address:
[email protected] (M.-E. Tu).
patients usually have less severe dermatitis and cheilitis; however, the prognosis is less favorable because the condition can last indefinitely.6 Shampoo-induced allergic contact dermatitis (ACD) shares a similar distribution with AP. Rashes usually involve the scalp, face, neck, shoulders, upper trunk, and hands, where the shampoo may come in contact with the skin.7 Both AP and shampoo-induced ACD may manifest as chronic dermatitis, making clinical distinction difficult. Here, we describe an unusual case of a patient with coexistence of adult-onset AP and shampoo-induced ACD diagnosed after a series of tests. Case report A 50-year-old male driver (phototype IV on the Fitzpatrick scale) presented to our clinic with a 6-month history of pruritic and erythematous rash showing sun-exposed distribution. The skin eruptions began in early spring and were mainly on the sunexposed areas. He felt worse after sun exposure, and facial sunscreen did not result in any improvement. He was healthy and was not using any medicines. He denied a personal history and family history of photosensitivity. Dermatologic examination revealed diffuse desquamated erythema and erosions on the face (sparing submandibular areas), scalp, and ears. Additionally, erythematous
http://dx.doi.org/10.1016/j.dsi.2017.07.004 1027-8117/Copyright © 2017, Taiwanese Dermatological Association. Published by Elsevier Taiwan LLC. This is an open access article under the CC BY-NC-ND license (http:// creativecommons.org/licenses/by-nc-nd/4.0/).
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papules and nodules were present on the nape, lateral neck, Vneck area, extensor forearms, dorsal hands, and bilateral lower legs (Fig. 1aed). Desquamation was also noted on the lips. Laboratory examination showed elevated serum IgE (400 IU/mL, normal range: 10e180) and eosinophil count (450/uL, normal range 0e350). The antinuclear factor was negative and levels of complement (C3 and C4) were within normal range. Biopsy specimens were taken from the forearm and cheek, and histopathological analysis of both specimens showed psoriasiform spongiotic dermatitis. Both specimens showed hyperkeratosis, parakeratosis, irregular acanthosis, and spongiosis. There were perivascular lymphohistiocytic infiltration with some eosinophils in the upper dermis. The findings were consistent with subacute to chronic eczematous dermatitis. Direct immunofluorescent tests, including IgG, IgA, IgM, C3, and fibrinogen, of cheek specimens yielded negative results. The morphology of his cutaneous manifestations and his clinical history indicated the possibility of photodermatosis, especially actinic prurigo. However, the presence of the rash on the post-
auricular area, scalp, distal dorsal fingers, nail folds, and thumb thenar area was not consistent with photodermatitis (Fig. 1e). Detailed clinical history taking revealed that he used sunscreen on his face occasionally and anti-dandruff shampoo daily. Hence, contact or photocontact dermatitis associated with sunscreen or shampoo use was suspected. Two months later, photo test, patch test and photopatch tests were performed after the skin rash had subsided. A photo test was performed for the non-sun-exposed abdomen. His minimal erythema doses (MEDs) of ultraviolet A (UVA) and ultraviolet B (UVB) were decreased to 10 J/cm2 and 20 mJ/cm,2 respectively. A patch test was performed using the European standard series, common shampoo allergens (Chemotechnique Diagnostics, Malmo, Sweden), personal shampoo A and shampoo B (2% and 5% aq.), and personal sunscreen. Photopatch tests were performed with the last three items and irradiation with UVA (7 J/cm2). Assessments were performed at 48 h, 72 h, and 1 week after the tests according to the International Contact Dermatitis Research Group recommendation.
Fig. 1 Before treatment. (a,b,d,e) Erythematous papules and nodules on the cheek, V-neck area, extensor forearms, dorsal hands (c) Rashes on the scalp and nape.
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The patch tests showed positive reactions to several shampoo allergens, including cocamidopropyl betaine (CAPB), captan, 4chloro-3-cresol, miconazole, and econazole nitrate, and personal shampoo A and shampoo B (both containing CAPB). The reaction to sunscreen was negative (Table 1). The photopatch test showed no photoallergic reaction to personal shampoo A and shampoo B or sunscreen. According to the results of the patch and photopatch tests, it was more likely that the patient had ACD induced by CAPB in shampoo, whereas contact or photocontact dermatitis due to sunscreen was less likely. The overall clinical features, histopathology findings, patch test results, and photopatch test results confirmed the diagnosis of concurrent adult-onset AP and shampoo-induced ACD. Broad-spectrum sunscreens, rigorous photoprotection, and alternative shampoos without CAPB or other allergic ingredients were suggested. A systemic oral steroid, oral antihistamine, and strong topical steroid were prescribed during the acute exacerbation stage, and these were later changed to 1% pimecrolimus cream. After treatment for 2 months, his skin lesions improved drastically and only some residual papulonodules eruptions were present on the dorsal hands, nape and V-neck (Fig. 2aec). After 1 year, he had only a few episodes of acute exacerbations soon after sun exposure, and large nodules did not occur again. Discussion This case demonstrated the importance of careful interpretation of the distribution of skin rash, careful history taking, and appropriate skin tests, including photo, patch, and photopatch tests, for patients suspected of having photodermatitis. Most AP patients have reduced MEDs. In a previous study of 53 British AP patients undergoing photo tests, 40 (75.5%) patients had abnormal results, with 17, 5, and 18 patients having an abnormal action spectrum in the UVB range alone, in the UVA range alone, and in the combined UVA/UVB range, respectively.5 In 2002, a case series conducted in Australia indicated that 60% of patients showed reduced MEDs of UVA in photo tests.3,4 Case series performed in Asia, including Singapore and Thailand, showed variable ratios of reduced MED (either UVA or mixed UVA/UVB) from 17% to 100%.2,6,8 Our patient also showed decreased MED of UVA and UVB. Therefore, photo tests should be performed using both UVA and UVB for all patients suspected to have AP.2,3 A photo test is valuable for determining the
Table 1 Patch test result. Item
Conc./Veh
PTy
Shampoo allergens Cl þ Me-isothiazolinone (MCI/MI) Paraben mix Formaldehyde Resorcinol Choloroacetamide Cocamidopropyl betaine 2-Bromo-2-nitropropane-1,3-diol Captan 4-Chloro-3-cresol (PCMC) 4-Choloro-3,5-xylenol (PCMX) Imidazolidinyl urea (Germall 115) Zinc pyrithione (Zinc omadine) Diazolidnylurea (Germall II) Miconazole Econazole nitrate Personal shampoo Aa Personal shampoo Ba Personal sunscreen
0.01% aq. 16.0% pet. 1.0% aq. 1.0% pet. 0.2% pet. 1.0% aq. 0.25% pet. 0.5% pet. 1.0% pet. 0.5% pet. 2.0% pet. 1.0% pet. 2.0% pet. 1.0% alc. 1.0% alc. 2%, 5% aq. 2%, 5% aq. As is
e e e e e þ e þ þ e e e e þ þ þ þ e
PTy: patch test. a Negative in five healthy volunteer controls.
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action spectrum of individual patients and subsequently may be beneficial for planning treatment strategies. AP is less commonly seen in Asia, and this may be attributed to two reasons. The first is the photoprotective effects of pigmented skin types in Asia, and the second is skin hardening that results from year-round sun exposure in tropical countries.2 In Asia, adultonset AP is more common than childhood-onset AP, and the characteristics differ. In two studies performed in Singapore, most of the AP patients were Chinese.2,8 A previous study reported that all patients were adults with a mean onset age of 60 years (range, 44e76 years) and male predominance, which differs from the characteristics of childhood-onset AP. Additionally, the symptoms of AP may persist throughout the year.2,6,8 The pathogenesis of AP remains unclear. Some researchers believe that AP is a type of autoimmune disease in which epidermal proteins are transformed to antigens with irradiation of UV light. Under normal circumstances, the number of Langerhans cells in the skin decreases on exposure to UV irradiation.4 However, in AP patients, the number of Langerhans cells do not decrease, which results in the continuous manifestation of UV-induced antigens, thus inducing or augmenting the inflammatory response.4 Previous dermatitis, hand dermatitis, or AP in our patient may have caused damage to the skin barrier, making it easier for allergens to enter the body through the skin, which might have resulted in ACD. However, in reality, we were unable to clearly differentiate the order of onset between AP and contact dermatitis. It is also possible that the concurrent onset of both conditions was merely a coincidence. There are 10e30 ingredients in shampoo, including surfactants, conditioners, fragrance, preservatives, and other additives. The most commonly reported allergens in shampoo are fragrance, CAPB, and preservatives.9 CAPB is an amphoteric surface agent frequently used in cosmetics and personal hygiene products. The allergic potential of CAPB is still controversial. According to Schnuch et al., CAPB is an irritant, and the patch test results are often considered to be false positive.10 Careful interpretation and clinical correlation are required to confirm the diagnosis. The actual sensitizers may be impurities during synthesis of CAPB, such as 3dimethylaminopropylamine and amidoamine.10 With regard to the treatment of AP, spontaneous remission may occur in adolescence, particularly in patients with childhood onset; however, persistence or recurrence is common. Adult-onset AP may have a chronic course lasting for more than 5 years.6 The firstline treatment for AP is the use of sunscreen and emollient, which are sometimes combined with topical and intra-lesional injections of corticosteroids. Sun exposure restriction is ultimately the best treatment; however, it is not a realistic option for most patients. In severe cases, oral therapeutic agents, such as prednisolone, thalidomide, and azathioprine, should be considered.8 PUVA therapy can also be considered.8 Topical tacrolimus has been used as an alternative treatment for plaque lesions, with good responses in some cases.6 Our patient switched to CAPB-free shampoo and used sunscreen. Oral and topical steroids were used to control the acute stage. After the acute stage, 1% pimecrolimus cream was effective. In conclusion, all clinical findings should be carefully assessed to reach an accurate diagnosis. A single patient might have many different skin diseases, such as photodermatitis and contact dermatitis. The diagnosis of adult-onset AP should be based on the clinical features and results of photo tests. The possibility of another concurrent disease should be considered if additional rashes are noted on the covered areas or shadow areas. Dermatologists should be aware of the possibility of concurrent photodermatitis and contact dermatitis. Comprehensive tests, including patch, photo, and photopatch tests, should be performed to achieve an accurate diagnosis.
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Fig. 2 After treatment for 2 months. (aee) Skin lesions improved drastically and only some papulonodular eruptions on the dorsal hands.
Funding sources This article has no funding source.
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