INTRODUCTION

Chronic actinic dermatitis (CAD) is a skin condition of an unknown cause that predominantly affects men with lighter skin and women with darker skin, typically over the age of 50. However, individuals with darker skin may experience the onset of the disease at a younger age [1]. The condition is marked by intensely dry, itchy, red, swollen, and thickened skin, usually affecting areas exposed to the sun [2]. In addition to chronic photosensitivity dermatitis, this condition is referred to as actinic reticuloid, which is derived from the histological appearance of skin biopsies that are reminiscent of reticulosis or cutaneous T-cell lymphoma [3]. Patients with this condition may have a history of various types of dermatitis, such as atopic dermatitis, allergic contact dermatitis (to fragrances and plants like chrysanthemum), and photocontact dermatitis, which can occur for many years before the onset of photosensitivity [4]. This condition is sometimes known as a persistent light reaction [2]. Individuals with CAD have skin hypersensitive to sunlight and, occasionally, artificial light, which can trigger eczema-like reactions. These reactions may manifest within minutes of sun exposure but typically develop between 7 and 24 hours afterward [5]. Skin that is exposed to light, including the face, the V of the neck, the upper chest, and the backs of the hands and forearms, is most susceptible to developing this condition [1]. During the summer, the effects of the sun are often more severe due to its increased strength [3]. Due to the delayed nature of skin reactions, which can take several days to manifest, individuals with CAD may not realize the connection to sun exposure [2]. CAD is thought to result from an allergic reaction to sunlight or artificial light, although the exact reasons for this are not well understood [4]. A diagnosis can be confirmed through photo testing [3]. This test involves applying specific light wavelengths to targeted skin areas to assess skin sensitivity [1]. Patch testing and photo patch testing are utilized to confirm an abnormal reaction to light. These tests show positive reactions to one or more allergens in 75% of patients with chronic actinic dermatitis, commonly to substances such as fragrances, sunscreens, colophony, and sesquiterpene lactones (present in the daisy family) [3]. CAD histopathology indicated acanthosis of the epidermis, spongiosis, and lymphocytic infiltration in the upper dermis, with the possible presence of eosinophils, macrophages, and plasma cells [2]. Sun protection is crucial for individuals with chronic actinic dermatitis [4]. Furthermore, if a contact allergy is diagnosed, it is advisable for the patient to steer clear of the irritant substance [5]. In severe instances, it may be required to administer oral immunosuppressive medications [2]. Included in these treatments are systemic corticosteroids, azathioprine, and cyclosporin. Some patients have been successfully desensitized using photochemotherapy (PUVA) or narrowband UVB therapy, accompanied by systemic steroid coverage [5]. Sometimes, a disease may resolve on its own, many years after its onset [3,5]. Typically, the condition is lifelong and necessitates substantial lifestyle adjustments to minimize sun exposure and contact with allergens [4].

IMMUNOLOGICAL ASPECT IN PATIENTS WITH CHRONIC ACTINIC DERMATITIS

In chronic actinic dermatitis, the presence of elevated T lymphocytes and a lower CD4+/CD8+ ratio serves as a crucial indicator of an overactive immune response in the skin. The severity of CAD is often marked by higher numbers of IFN-γ+, CD4+, CD8+, common-γ-chain receptor, and CD69+ tissue-resident memory cells, along with a further decreased CD4+/CD8+ ratio, which points to a more pronounced immune dysregulation [6,7]. Severe CAD is also associated with elevated total Ig-E levels and eosinophils, along with a shift from Th1/Th2 to Th2 dominance due to increased suppressor T cells, contributing to disease severity. Additionally, CD8-dominant T cell infiltrates and a reduced CD4+/CD8+ ratio are found in CAD eruptions in response to photosensitivity [8,9].

Additionally, the immunological markers of CAD resemble those of conditions such as cutaneous T-cell lymphoma, indicating a need for further research to identify specific immunological responses in CAD. A genome-wide analysis reported that certain mRNAs regulate T-cell-mediated inflammation via TNFAIP3 expression. Immunohistochemical studies have conflicting findings on the role of filaggrin gene mutations in CAD, indicating that the genetic basis for immunological changes in CAD remains poorly understood [10–13].

As a result of our studies of black hair dye dermatitis, we found that many patients had features of chronic photosensitive dermatitis that could not be distinguished clinically, histopathologically, or immunologically from CAD [14,15].

Hence, the purpose of the present report is to gather all cases of chronic actinic dermatitis that have been thoroughly evaluated clinically.

PATIENTS AND METHODS

Fifty-two patients complaining of chronic actinic dermatitis gathered during the period from June 2014 to 2024 were involved in this case-series, descriptive, observational, clinical-histopathological study. The study was conducted following the Declaration of Helsinki. After discussing the nature of the study with all of the patients, informed consent forms were obtained from all. The close-up picture of the object was taken at the same place from a fixed distance and with lighting in the same direction. Also, all of the patients who were included in this study accepted the idea of sharing their photos in this study. A full epidemiological and demographic profile was recorded during the study. In order to establish the right clinical diagnosis, a detailed history of the patient was taken along with a thorough physical examination. The following were recorded: name, age, sex, residence, occupation, atopy history (nasobronchial allergy, asthma, childhood eczema) of the individual, history of photosensitivity, history of applying black hair dye, the duration of the lesions, the chief complaints, the associated symptoms including redness, sores, itching, burning sensation, discomfort, the recurrence, aggravating and relieving factors, the site, type, geographical distribution, family background, past medical, and drug usage. To confirm the results of the biopsy, punch or incisional biopsies were taken for histopathological assessment.

RESULTS

Fifty-two patients complaining of chronic actinic dermatitis were considered in the present work; their ages ranged from 10 to 70 years, with a mean of 50 years, with 33 (63.46%) males and 19 (36.53%) females. There were 4 (7.69%) children, their age ranging from 4 to 8 years, with a mean of 6 years, with 3 females and 1 male. The adult group consisted of 48 (92.3%) patients, with 16 (33.33%) females and 32 (66.66%) males. On careful questioning, no triggering factors were identified apart from sunlight exposure, but on examination, 6 (12.5%) adult patients were discovered to have applied black hair dye for years to the scalp hair, 4 (66.7%) females and 2 (33.33%) males. The duration of illness ranged from 2 months to 4 years. The clinical picture consisted of an acute and chronic rash, while the acute rash presented with itching and erythematous maculopapular rash affecting sun-exposed sites, mainly the face and upper arms. In contrast, the chronic rash consisted of pigmented scaly lichenified and lichenoid rash affecting mainly the face but sparing areas around the eyes. The rash could be associated with erythematous nodules and lumps that might mimic a picture of the leonine face (Fig. 6). Some patients had the rash on the scalp and covered parts of the body that were associated with severe itching. There were no obvious triggering factors that were incriminated in the pathogenesis of the disease, apart from using hair dye in 12.5% of the cases. The histopathological assessment revealed acanthosis of the epidermis with or without parakeratosis, with an intact dermo-epidermal junction. Meanwhile, the dermis showed a dermal superficial perivascular lymphocytic infiltrate with some melanophages (Table 1) (Figs. 1 – 7).

Table 1: Sociodemographic characteristics of the study sample (n=52).

Figure 1: Sex distributi.

	Figure 2: a) A 10-year-old child showing chronic actinic dermatitis of the face. b) The same 10-year-old child showing chronic actinic dermatitis of the face and hands. c) The same 10-year-old child showing chronic actinic dermatitis of the face and neck.
	Figure 3: a) A 60-year-old male with chronic actinic dermatitis of the face. b) The same 60-year-old male with chronic actinic dermatitis involving the scalp. c) The same 60-year-old male with chronic actinic dermatitis affecting the chest. d) The same 60-year-old male with chronic actinic dermatitis of the dorsal aspect of both hands. e) The same 60-year-old male with chronic actinic dermatitis affecting both dorsal aspects of both feet.
	Figure 4: a) A 62-year-old male patient showing chronic actinic dermatitis of the face after the application of black hair dye. b) The same 62-year-old male patient showing chronic actinic dermatitis of the scalp after the application of black hair dye.
	Figure 5: a) A 42-year-old female patient showing chronic actinic dermatitis of the face. b) The same 42-year-old female patient showing chronic actinic dermatitis of the face.
	Figure 6: a) A 45-year-old male patient with chronic actinic dermatitis of the face showing nodular lumps. b) The same 45-year-old male patient showing chronic actinic dermatitis of the side of the face.
	Figure 7: a) Histopathology of chronic actinic dermatitis showing acanthosis of the epidermis with parakeratosis and the dermis showing a perivascular lymphocytic infiltrate (H&E; 10x). b) The same section also showing melanophages in the dermal infiltrate (H&E; 40x).

DISCUSSION

CAD, a rare, idiopathic, photosensitive, immune-mediated disorder, is characterized by pruritic eczematous lesions on sun-exposed areas, which may extend to other body parts. It affects middle-aged males more than females [1]. Evidence suggests that type-IV hypersensitivity to UV-induced neoantigens may contribute to the pathogenesis of the condition [4]. Chronic actinic dermatitis typically affects the exposed areas of the body, but it can also extend to cover other areas [3]. Idiopathic allergic reactions to certain triggers, such as fragrances, sunscreens, and colophony, can exacerbate chronic actinic dermatitis. It is more commonly observed in middle-aged and younger males with fair skin. Histopathologically, CAD initially presents with features of acute dermatitis, which progresses to chronic dermatitis over time [2,4,15].

In the current study, 52 patients were included, with their age ranging from 10 to 70 years and with an average age of 50 years. The sex distribution was 63.46% males and 36.54% females. Two age groups were affected: 1) Children, who comprised 7.69% of the study population, with their age ranging from 4 to 8 years, with an average of 6 years, including 3 females and 1 male. According to our knowledge, no study has reported the presentation of a child with CAD prior to this study. 1) Adults, who constituted 92.31% of the patients, with 33.33% females and 66.67% males. Upon detailed inquiry, no precipitating factors were found except for exposure to sunlight. However, upon examination, it was revealed that 12.5% of the adult patients had been using black hair dye on their scalp for years, with 66.7% being female and 33.3% male. The duration of the illness varied from 2 months to 4 years. The clinical presentations included both acute and chronic rashes, with the acute rash characterized by itching and an erythematous maculopapular rash, primarily affecting sun-exposed areas such as the face and upper arms. In contrast, the chronic rash was characterized by pigmented, scaly, lichenified, and lichenoid lesions primarily affecting the face, yet sparing the areas around the eyes. Some patients experienced the rash on the covered body parts, accompanied by severe itching. No clear triggering factors have been implicated in the pathogenesis of the disease, except for the use of hair dye in 12.5% of the cases. Histopathological evaluation indicated acanthosis of the epidermis, which may or may not be accompanied by parakeratosis while maintaining an intact dermo-epidermal junction. Additionally, the dermis exhibited a superficial perivascular lymphocytic infiltrate along with the presence of some melanophages.

A recent study by Sharquie et al. has revealed that chronic black hair dye dermatitis is sharply on the rise and is now considered a commonly overlooked cause of chronic actinic dermatitis. The study revealed that chronic actinic dermatitis and black hair dye dermatitis have similar characteristics in terms of clinical presentation, histopathological findings, and immunological profiles. Both are caused by the black hair dye paraphenylenediamine (PPD) and preservatives. Both usually affect middle-aged and older men with dark complexions, and both are characterized by erythematous dermatitis, pigmented lichenoid dermatitis, and lichenified photodermatitis, mostly affecting the face, neck, chest, scalp, legs, and trunk. Histopathological evidence indicates that acute dermatitis can progress into chronic dermatitis in early cases. This transition shares features with those observed in chronic actinic dermatitis.

Additionally, chronic black hair dye dermatitis and chronic actinic dermatitis exhibit similar immunological features. In chronic actinic dermatitis, an increase in T lymphocytes and a reduced CD4+/CD8+ cell ratio suggests an overactive immune response in the skin, leading to persistent inflammation [8]. In severe cases, there is an increase in IFN-γ+, CD4+, CD8+, common-γ-chain receptor, and CD69+ tissue-resident memory cells, accompanied by a further reduction in the CD4+/CD8+ cell ratio, which signifies a more marked immune dysregulation [9–10].

In cases of chronic black hair dye dermatitis, delayed-type hypersensitivity reactions occur due to direct contact with PPD and other preservative antigens. When the antigen touches the skin, Langerhans dendritic cells move to a nearby lymph node, prompting CD4+T lymphocytes to proliferate and transform into Th1 cells in reaction to antigen peptide fragments [16–18].

Iraqi patients with CAD predominantly exhibit symptoms of chronic dermatitis associated with black hair dye, whereas other common triggers related to CAD are not typically observed in these patients [14–15,19–21]. Men frequently use black hair dye, while women tend to use blonde hair dye. This usage pattern contributes to the prevalence of chronic black hair dye dermatitis among men.

As a result, chronic black hair dye dermatitis and CAD share similar clinical, histopathological, and immunological features. Hence, for any patients with CAD, black hair dye application should be excluded.

CONCLUSION

Chronic actinic dermatitis is not an uncommon variant of photodermatosis, affecting children and mostly adult males. There are no obvious triggering factors, apart from 12.5% of adult patients applying black hair dye. Hence, in every case of CAD, hair dying should be excluded. The clinical pictures consisted of a course of acute and chronic rash. The acute rash presented with itching and erythematous maculopapular rash affecting sun-exposed sites, mainly the face and upper arms, while the chronic rash consisted of pigmented scaly lichenified and lichenoid rash affecting mainly the face and hands. A histopathological assessment revealed acanthosis of the epidermis with an intact dermo-epidermal junction. The dermis showed a dermal superficial perivascular lymphocytic infiltrate with some melanophages.

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17.  Gupta M, Mahajan VK, Mehta KS, Chauhan PS. Hair dye dermatitis and p-phenylenediamine contact sensitivity:A preliminary report. Indian Dermatol Online J. 2015;6:241-6.

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