Successful Treatment of Chronic Actinic Dermatitis with Tofacitinib.

We present the case of a 58-year-old male patient who presented with pruritic skin plaques and papules on the scalp, face, back, and back of the hands for over a year. The symptoms worsened upon exposure to sunlight and improved on cloudy days. Despite previous attempts at treatment with glucocorticoid ointment and antihistamine drugs, the patient experienced progressive aggravation of symptoms. Physical examination revealed hypertrophic and infiltrating nodules, with significant scratches and local exudation. Skin biopsy confirmed the diagnosis of sun-induced dermatosis. The patient was initiated on tofacitinib, an oral Janus Kinase inhibitor, along with a halometasone ointment, oral ebastine tablets, and strict sun protection. Over the course of four revisits spanning four months, the patient experienced a significant improvement in symptoms, with the rash almost disappearing and pruritus subsiding. The treatment was well tolerated and no adverse effects were observed. Follow-up for six months post-treatment showed no recurrence of symptoms. This case highlights the efficacy of tofacitinib in managing sun-induced pruritic plaques and suggests it as a potential therapeutic option in similar cases.

Deficiency of N6-Methyladenosine Demethylase ALKBH5 Alleviates Ultraviolet B Radiation-Induced Chronic Actinic Dermatitis via Regulating Pyroptosis.

Pyroptosis is an inflammatory programmed cell death (PCD) and is reported to be associated with N6-methyladenosine (m6A) modification. This study aimed to investigate the mechanism of m6A demethylase AlkB homolog 5 (ALKBH5) in pyroptosis in the process of chronic actinic dermatitis (CAD). Changes of m6A-related genes were evaluated between CAD and normal samples using quantitative reverse-transcription polymerase chain reaction (qRT-PCR). Human keratinocytes (HaCaT cells) exposed to ultraviolet B (UVB; 10, 20, and 30 mJ/cm2), followed by evaluation of cell proliferation, cell apoptosis, inflammatory cytokines (interleukin (IL)-1ß, IL-18, and tumor necrosis factor (TNF-α)), and pyroptosis-related proteins (gasdermin D (GSDMD), Caspase-1, and Caspase-4). Small interfering RNA (siRNA) targeting ALKBH5 was transfected into HaCaT cells to assess the effect of si-ALKBH5 on CAD. A CAD mice model was induced after exposure to UVB (250 mJ/cm2 per day) to confirm the role of ALKBH5 in CAD. AKKBH5 was highly expressed in CAD patients. UVB also promoted ALKBH5 expression, increased cell apoptosis, and induced the release of inflammatory cytokines (IL-1ß, IL-18, and TNF-α) as well as pyroptosis-related proteins (GSDMD, Caspase-1, and Caspase-4). Silencing ALKBH5 repressed cell apoptosis and suppressed UVB-induced pyroptosis and inflammatory response. Meanwhile, silencing ALKBH5 attenuated UVB-induced skin damage of CAD mice, accompanied with the reduction in expression of inflammatory cytokines and pyroptosis-related proteins. This study helps to further understand the mechanism of ALKBH5 in CAD-induced pyroptosis and provides novel ideas for the research and management of CAD.

The Effectiveness and Safety of Dupilumab for the Treatment of Recalcitrant Chronic Actinic Dermatitis: A Case Series.

Background: Although dupilumab is an effective treatment approach for chronic actinic dermatitis (CAD) in some cases, its effectiveness and safety in CAD have not been sufficiently assessed. Purpose: Evaluation of the effectiveness and safety of dupilumab in patients with recalcitrant CAD was performed. Methods: We retrospectively reviewed the medical records of CAD patients treated with dupilumab. Data regarding demographics were collected, and disease severity scores were assessed using the following: Clinical Severity Score of CAD (CSS-CAD), Atopic Dermatitis Control Tool (ADCT), Dermatology Life Quality Index (DLQI), and Numeric Rating Scale (NRS)-itch scores. Results: After 12 weeks of treatment, there was a significant decrease in disease severity scores of 16 CAD patients. Only one patient achieved a good response and most of the patients (62.5%, 10/16) had no significant symptom improvement after 4 weeks of treatment. However, after 12 weeks of treatment, 43.75% (7/16) of the patients reached excellent response (>75% improvement of CSS-CAD), 31.25% (5/16) good response (50%-75% improvement of CSS-CAD), 6.25% (1/16) partial response (25%-50% improvement of CSS-CAD), and only 18.75% (3/16) no response (<25% improvement of CSS-CAD). One patient complained of injection site reaction at the first injection. Conclusion: This study supports dupilumab as an effective and safe treatment option for patients with recalcitrant CAD. Patients may require at least 4 weeks of treatment before the partial response is noted.

Role of interleukin-36γ induced by ultraviolet radiation in chronic actinic dermatitis.

BACKGROUND: Chronic actinic dermatitis (CAD) is an immune-mediated photodermatosis characterized by a high eosinophil count and total immunoglobulin E (IgE) in the peripheral blood of patients. At present, however, the reasons for their elevation remain unclear. OBJECTIVE: The current study aimed to detect changes in inflammatory cytokines in CAD and explore their role in this disease. METHODS: Enzyme-linked immunosorbent assay and Luminex assay were conducted to measure inflammatory factor levels. Immunohistochemical analysis and quantitative real-time polymerase chain reaction were performed to evaluate the expression levels of interleukin-36γ (IL-36γ), IL-8, chemokine (C-C motif) ligand 17 (CCL17), and CCL18. CCK8 kits were used to assess cell proliferation. Immunofluorescence was used to detect nuclear factor κB (NF-κB) p65 nuclear translocation. Western blot analysis was performed to detect the protein expression level of phosphorylated NF-κB (p-NF-κB) p65. Hematoxylin and eosin and Masson trichrome staining were applied to observe histological changes in a chronic photo-damaged mouse model. RESULTS: Eosinophils, total IgE, IL-36γ, IL-8, tumor necrosis factor α, CCL17, and CCL18 were elevated in CAD. Of note, IL-36γ promoted the proliferation of eosinophilic cells (EOL-1) and the production of IgE in peripheral blood mononuclear cells. IL-36γ also promoted the production of IL-8 and CCL18 in immortalized human keratinocytes (HaCaT cells), while ultraviolet radiation (UVR)-induced IL-36γ via activation of the NF-κB signaling pathway. CONCLUSIONS: IL-36γ was involved in the pathogenesis of CAD and UVR contributed to the production of IL-36γ, which may provide a novel therapeutic target for CAD.

Clinical characteristics of patients with human immunodeficiency virus and immune-mediated photodermatoses: A retrospective study of 39 patients.

BACKGROUND: HIV/AIDS patients are susceptible to various infectious and inflammatory dermatoses. No systemic work has been done on HIV/AIDS patients with immune-mediated photodermatoses in China. Here, we aim to determine the clinical features of immune-mediated photodermatoses in HIV/AIDS patients. METHODS: A retrospective analysis of HIV/AIDS patients with immune-mediated photodermatoses was carried out with demographic data, clinical characteristics, laboratory data, and follow-up data at the First Affiliated Hospital of Kunming Medical University between 2012 and 2019. The data were subjected to statistical analysis. RESULTS: A total of 39 HIV/AIDS patients with immune-mediated photodermatoses were enrolled, including 22 cases of polymorphic light eruption (PLE), 16 cases of chronic actinic dermatitis (CAD), and one actinic reticuloid. The CD4 count at the visit of the HIV-positive CAD group was lower than the PLE group (p = .049). The HIV-positive CAD group was more sensitive toward UVB than the PLE group (p = .020) and had a lower MED-UVB value (p = .044). There was no significant difference in UV tests among different categories of skin types. CONCLUSION: Immune-mediated photodermatoses are a manifestation of the advanced symptom of HIV infection, and sometimes also the presenting feature of HIV infection. Compared with HIV-positive PLE patients, CAD patients showed higher sensitivity to UVB radiation and had a lower MED-UVB value. The primary treatment for immune-mediated photodermatoses in HIV/AIDS patients is HAART and sun avoidance.

A postulated model for photoimmunopathogenesis of chronic actinic dermatitis around adaptive immunity, including Th17 cells, Tregs, TRMs, cytotoxic T cells, and/or common-γ chain receptor+ cells.

BACKGROUND/PURPOSE: The pathogenesis of chronic actinic dermatitis (CAD) is more complicated than other photodermatoses. However, the relationship between the clinical severity of CAD and the offending photocontact or contact allergens or both, and the correlations of CAD immunopathogenesis with the immunoregulatory molecules involved in adaptive immunity are yet to be investigated. METHODS: We performed phototesting with broad-spectrum ultraviolet (UV) B, UVA, and visible light to establish the presence of photosensitivity in 121 patients with CAD, together with photopatch and contact patch testing. Nine patients with CAD were selected according to their clinical severity score for CAD (CSS-CAD), and triple direct immunofluorescence analysis was performed with paraffin-embedded skin biopsy samples. RESULTS: As CSS-CAD was closely correlated with the multiplicity of photo(contact) allergens, particularly photoallergens, three or more photoallergens were detected in the severe CAD group (52.5%); less in the moderate group (32.8%); and only one in the mild group (14.8%; P = .025). In the groups showing greater severity of disease, the absolute numbers of IFN-γ+ , IL-17+ , CD4+, CD8+, common-γ chain receptor (common-γCR)+ , and CD69+ tissue-resident memory cells increased on average; there was also an increase in the CD4+/CD8+ cell ratio, with the more severely affected groups. However, the levels of TNF-α+ and FoxP3+ regulatory T (Treg) cells and the mean IL-17/IFN-γ cell ratio decreased in the more severely affected CSS-CAD subgroups. CONCLUSIONS: Based on the clinical analysis and immunopathogenic results, avoidance of excessive sun exposure, and topical and systemic blocking agents for photo(contact) allergens are recommended. Additionally, conventional immunomodulators and emerging agents including JAK-STAT inhibitors may be administered for CAD treatment in the future.

LncRNA-WAKMAR2 regulates expression of CLDN1 to affect skin barrier through recruiting c-Fos.

BACKGROUND: Chronic actinic dermatitis (CAD) is an immune-mediated photo-allergic skin disease. In the clinic, the treatment of this disease is hampered by the lack of proper understanding of the skin barrier dysfunction mechanism. OBJECTIVE: To illuminate the mechanism of skin barrier dysfunction in CAD. METHODS: Transcriptome sequencing and protein profiling were used to detect skin barrier injury-related genes. RNA pull down, a promoter-reporter gene assay, and chromatin isolation by RNA purification-sequencing were used to elucidate the effect of WAKMAR2 in skin barrier functionality. RESULTS: Transcriptome sequencing from patient's tissues showed a significantly decreased expression of WAKMAR2. Down-regulation of WAKMAR2 destroyed the keratinocyte barrier. Moreover, WAKMAR2 can directly bind to the c-Fos protein. This novel long non-coding RNA (LncRNA)-protein complexes were targeted to the CLDN1 promotor. Overexpression of WAKMAR2 enhanced the promoter activity of CLDN1, while the addition of AP-1 inhibitor could reverse this phenomenon. Furthermore, our in vivo results suggested that expression of WAKMAR2 was required for the repair of skin damage in mice induced by ultraviolet irradiation. CONCLUSIONS: We identified a crucial LncRNA (WAKMAR2) for the protection of the skin barrier in vitro and in vivo. Mechanically, it can specifically interact with c-Fos protein for the regulation of CLDN1, a finding which could be applied for CAD treatment.

Chronic actinic dermatitis: A 5-year clinical analysis of 488 patients in China.

BACKGROUND/PURPOSE: Chronic actinic dermatitis (CAD) is a spectrum of diseases with chronic photosensitivity occurring mostly among middle-aged and older men. We seek to explore the characteristics and pathogenesis of CAD among the Chinese population. METHODS: The medical records of 488 CAD cases diagnosed by phototesting at Huashan Hospital, Fudan University from January 2014 to December 2018 were analyzed retrospectively. RESULTS: Among the 488 patients, 344 were male and 144 were female. 84.8% of the cases were over 40 years old at the age of onset, while the remaining with an early age of onset had a prevalence of atopic history of 21.6%. Up to 45.0% of the patients reported excessive sun exposure and outdoor activities before the initiation of symptoms. The typical skin lesions were erythema, papules and plaques laid predominantly in sun-exposed areas. 42.8% of the cases showed sensitivity to UVB only, 20.7% were both sensitive to UVA and UVB, and 18.2% had UVA sensitivity only. The most predominant photoallergens were chlorpromazine (80.1%), thimerosal (17.2%), potassium dichromate (12.7%), etc. The most prevalent patch test allergens were potassium dichromate (24.4%), thimerosal (20.5%), formaldehyde (16.8%), etc. CONCLUSIONS: CAD was more commonly seen in males over 40 years old. The action spectrum of Chinese patients is primarily in the UVB range. Exposure to excessive sunlight or contact allergens and photoallergens are important risk factors. Photobiology tests are essential in detecting photosensitivity and recognizing potential photosensitizers. Early avoidance of confirmed photoallergens and sun exposure may prevent photosensitive reactions from progressing into persistent photosensitivity.

Allergic contact dermatitis to Compositae: An Australian case series.

BACKGROUND: Allergic contact dermatitis (ACD) to Compositae is caused by sensitisation to sesquiterpene lactones (SQLs) and subsequent exposure can occur from direct handling or from airborne transmission. Plants from the Compositae family are ubiquitous globally and their plant extracts are also used in various products. OBJECTIVES: Investigation of contact allergy (CA) and allergic contact dermatitis (ACD) to Compositae at a single dermatology centre. METHODS: A retrospective case review was performed on patients undergoing patch testing to Compositae between January 2011 and December 2020 in Melbourne, Australia. RESULTS: Of 3679 patients, 44 (1.2%) patch tested positive to Compositae and 19 (43.2%) reactions were deemed relevant. Thirteen cases (68.4%) were from direct contact with Compositae plants, mostly in gardeners. Six cases (31.6%) were from personal products and all these patients were female. Involvement of the face was significant (p = 0.007). Simultaneous allergic reactions included SQL mix in eight (42.1%), fragrance mix in seven (36.8%), potassium dichromate in three (15.8%) and colophonium in two (10.5%) cases. CONCLUSION: Contact with Compositae from gardening contributed most cases of ACD; however, personal products accounted almost one-third of cases. Treatment options remain limited and avoidance is the most important aspect of management.

Clearance of Chronic Actinic Dermatitis With Dupilumab Therapy in Chinese Patients: A Case Series.

Chronic actinic dermatitis (CAD) is a rare chronic immunological photo-dermatosis resulting in pruritic eczematous eruption on sun-exposed skin to ultraviolet (UV) light. The disease mechanism may include a delay-type hypersensitivity reaction to an endogenous photo-induced antigen, postulated to be UVR-altered DNA, but the exact pathophysiology is unknown. Minimum erythema dosing and patch testing are diagnostic tools of CAD. There are limited safe and effective treatment options for CAD. Herein, a case series of three patients with severe recalcitrant CAD is presented after being treated with dupilumab off-label. The patients in this study had persistent severe disease and taken the first-line management plan, which consists of topical calcineurin inhibitors (TCI), topical corticosteroids (TCS), and strict photoprotection. However, the above treatment options were not able to control the symptoms. The patients were treated with dupilumab 600 mg first dose, 300 mg biweekly subcutaneously (SC), and hydroxychloroquine. Dupilumab showed excellent clinical benefits, including safe and well-tolerated in chronic actinic dermatitis. Further studies are required to be carried out before being applied in clinical practice.

The Immunogenetics of Photodermatoses.

Photodermatosis is an abnormal skin inflammatory reaction to light. The major classifications of photodermatoses are idiopathic photodermatoses, photodermatoses due to exogenous or endogenous agents, photo-exacerbated dermatoses, and photosensitive genodermatoses. In this chapter, we focus on idiopathic photodermatoses and drug-related photodermatoses and emphasize on the epidemiology and immunogenetic backgrounds. Idiopathic photodermatoses, a spectrum of diseases with abnormal responses to ultraviolet radiation (UVR), include polymorphous light eruption, actinic prurigo, hydroa vacciniforme, chronic actinic dermatitis, and solar urticaria. Young people are more susceptible to most idiopathic photodermatoses except for chronic actinic dermatitis. Interestingly, idiopathic photodermatoses exhibit different characteristics between Caucasians and Asians. For example, the average age of Asian actinic prurigo patients is older than that of Caucasians in which genetic backgrounds or Fitzpatrick skin type might play a role. Drug-induced photodermatoses can be classified into phototoxic and photoallergic drug reactions. Certain drug-induced photodermatoses may mimic other dermatoses. For instance, drug-induced lupus erythematosus (LE) should be considered if an old man is diagnosed with LE but had a poor response to standard treatments.

Clinical and pathological findings of chronic actinic dermatitis.

BACKGROUND: Chronic actinic dermatitis (CAD) is a recurrent photosensitive disease occurs predominantly in elderly men on sun-exposed areas, which seriously affect the patient's life quality. The etiology of CAD remains unknown. METHODS: Sixty-six CAD patients, 66 atopic dermatitis (AD) patients, and 46 healthy people were enrolled into this study. Patient-level data were obtained from the electronic medical record and laboratory databases. We also obtained 29 tissue samples including 16 lichenoid lesions, 7 minimal erythematous dose (MED) analysis induced lesions, and 6 normal skin samples. Histopathologic and immunohistochemical analysis were performed. RESULTS: In the clinical characteristics, albumin was lower and uric acid was higher significantly in patients diagnosed as CAD. The infection rate of CAD patient after skin biopsy was considerably high (23.3%). The serum allergen test was prone to be negative in CAD patients. Lymphocytes were the dominate infiltrating cells in early and late CAD lesions, while more CD4+, CD8+, CD69+, and CD103 + cells were found in the late lesions. There is no difference in CD4+/CD8 + ratio and CD69+/CD103 + ratio among groups. More mast cells were observed in the early-stage lesions, and more dendritic cell was observed in the late-stage lesions. CONCLUSIONS: CAD patients have certain oxidative stress and are prone to be infected after skin biopsy. Serum allergen detection is of little significance for CAD diagnosis. Mast cells may be involved in the early process of CAD, while dendritic cells and tissue-resident memory T cell (TRM) may be related to the chronic process of the disease.

Up-regulation of hsa-miR-221-3p induced by UVB affects proliferation and apoptosis of keratinocytes via Bcl-xL/Bax pathway.

BACKGROUND: Chronic actinic dermatitis (CAD) is a photoallergic skin disease with abnormal hyperplasia. At present, the mechanism of abnormal proliferation is not clear. OBJECTIVE: To explore possible mechanism of CAD proliferative lesions. METHODS: Immunohistochemistry (IHC) assay and small RNA sequencing were carried out. Quantitative real-time PCR (qRT-PCR) analysis was performed to evaluate expression levels of hsa-miR-221-3p and FOS. The interaction between hsa-miR-221-3p and FOS was identified by dual-luciferase reporter assay. Expression of hsa-miR-221-3p also was detected by qRT-PCR after UVB irradiation. Influences of hsa-miR-221-3p and FOS on cell viability and apoptosis were assessed through a series of functional experiments and rescue experiments. Western blot analysis was used to detect protein expression of fos, Bax, Bcl-xL, and caspase-3. RESULTS: Patients with CAD had marked epidermal hyperplasia. The expression of hsa-miR-221-3p was up-regulated in CAD while FOS was significantly down-regulated. Dual-luciferase reporter assay confirmed that hsa-miR-221-3p targeted FOS 3'UTR. Hsa-miR-221-3p induced by UVB ranged from 0 to 30 mJ. Moreover, hsa-miR-221-3p overexpression or FOS knockdown promoted cell proliferation and reduced cell apoptosis. Western blot showed that hsa-miR-221-3p negatively regulated fos, which regulated Bcl-xL/Bax. Cell proliferation caused by hsa-miR-221-3p overexpression or FOS knockdown could be reversed by Bcl-xL inhibitor. CONCLUSION: Hsa-miR-221-3p induced by UVB targeted FOS 3'UTR, which played an important role in regulating proliferation and apoptosis of keratinocytes via Bcl-xL/Bax pathway; this may provide a new insight for CAD proliferative lesions.

Successful Treatment of Chronic Actinic Dermatitis with Dupilumab: A Case Report and Review of the Literature.

Chronic actinic dermatitis (CAD) is a rather rare photosensitive disease characterized by a persistent eczematous eruption in sun-exposed sites. The pathogenesis of CAD has not been completely elucidated. The clinical treatment of CAD is still challenging and not standardized. Some patients with severe CAD have achieved satisfactory clinical results with dupilumab when conventional therapies have failed. We herein report the case of a 45-year-old male with severe CAD who responded rapidly to combined treatment with dupilumab (600 mg for 1 week, and then 300 mg every 2 weeks) in 2 months. The patient experienced continuous improvement and no side effects from dupilumab (300 mg every month), having ceased other systemic medications. Dupilumab could be considered as an alternative or adjunctive treatment for CAD.

Ultraviolet A rush hardening for chronic actinic dermatitis: Pilot treatment outcomes.

Chronic actinic dermatitis (CAD) is a common debilitating photodermatosis. Patients often have to completely avoid outdoor activities, which severely impacts their quality of life. Phototherapy is effective for CAD and seems to increase patients' tolerance towards sunlight and consequently decrease the extent of disease. Unfortunately, the slower onset and time-consuming nature of phototherapy limits the clinical application. Considering the effectiveness and time-saving nature of ultraviolet (UV)-A rush hardening in solar urticaria, we performed a pilot study to determine whether UV-A rush hardening is effective in CAD. Six patients with CAD were exposed to multiple sessions of UV-A for 4-5 days at 1-h intervals/day. Subsequently, maintenance UV-A exposure was performed at 1-2-week intervals. Phototesting at baseline showed that three patients were sensitive to both UV-A and -B, and the other three patients only showed UV-A sensitivity. All of the patients responded well to UV-A rush hardening and four (67%) maintained a good remission status after 1 year. The results of this pilot study suggest that UV-A rush hardening phototherapy is effective and well tolerated in the treatment of CAD, while future larger prospective studies using objective scores of disease activity and quality of life are needed.

Upregulation of hsa-miR-31-3p induced by ultraviolet affects keratinocytes permeability barrier by targeting CLDN1.

Chronic actinic dermatitis (CAD) is a photoallergic skin disease with complicated pathogenesis. However, skin barrier dysfunction may be involved according to clinical manifestation. To investigate the mechanism of CAD barrier dysfunction, noninvasive detection of skin barrier and small RNA sequencing were carried out. Quantitative real-time PCR (qRT-PCR) was used to evaluate the expression levels of hsa-miR-31-3p and CLDN1. The correlation between hsa-miR-31-3p and CAD severity was explored. Further, dual-luciferase reporter assay was performed to identify the relationship between hsa-miR-31-3p and CLDN1. In addition, expression of hsa-miR-31-3p was detected after ultraviolet (UV) irradiation. Influences of hsa-miR-31-3p on primary human keratinocytes barrier were assessed by FITC-Dextran permeability assay. Moreover, western blot was used to detect the expression of claudin-1, filaggrin, loricrin and involucrin. Our results showed that transepidermal water loss (TEWL) significantly increased in CAD, while stratum corneum hydration (SCH) significantly decreased. The expression of hsa-miR-31-3p was up-regulated in CAD while CLDN1 was down-regulated. Hsa-miR-31-3p was correlated with TEWL, UV-MED (minimal erythema dose) and clinical severity scores of CAD (CSS-CAD). Dual-luciferase reporter assay confirmed that hsa-miR-31-3p targeted the 3'UTR region of CLDN1. Moreover, hsa-miR-31-3p was induced by UVB (0-30 mJ/cm2) and UVA (0-4 J/cm2). Furthermore, overexpression of hsa-miR-31-3p increased FITC-Dextran flux of primary human keratinocytes and reduced the expression of claudin-1, filaggrin, loricrin and involucrin. In conclusion, we demonstrated that hsa-miR-31-3p induced by UV was correlated with CAD severity, which played an important role in regulating keratinocytes permeability barrier through targeting CLDN1.

Dermatitis actínica crónica / Chronic actinic dermatitis

RESUMEN La dermatitis actínica crónica (DAC) - dermatitis por fotosensibilidad, reacción solar persistente o su variante extrema el reticuloide actínico- es una fotodermatosis crónica, propia del adulto más frecuente en el sexo masculino provocada por rayos ultravioletas (UVB), (UVA) y luz visible. El diagnóstico es clínico, caracterizado por placas eccematosas y liquenificadas pruriginosas en aéreas expuestas al sol. Se cree que el DAC se debe a la fotosensibilización secundaria de un antígeno endógeno de la piel.

ABSTRACT Chronic actinic dermatitis (ACD) - photosensitivity dermatitis, persistent solar reaction or its extreme variant actinic reticuloid - is a chronic photodermatosis, typical of the adult male caused by ultraviolet (UVB), (UVA) and visible light. The diagnosis suggested by clinical researchers, characterized by eczematous and lichenified pruritic plaques in areas exposed to the sun. It is believed that DAC is due to the secondary photosensitization of an endogenous skin antigen.