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Chronic black hair dye dermatitis is a common cause of chronic actinic dermatitis in patients with a dark complexion
Khalifa E. Sharquie
1, Waqas S. Abdulwahhab2,3, Inas K. Sharquie3
1Department of Dermatology, College of Medicine, University of Baghdad, Center of Dermatology, Medical City Teaching Hospital, Iraq, 2Department of Dermatology, Al-Qassimi Hospital, Sharjah, UAE. College of Medicine, University of Sharjah, Sharjah, UAE, 3Department of Microbiology and Immunology, College of Medicine, University of Baghdad, Baghdad, Iraq
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ABSTRACT
Background: Chronic black hair dye dermatitis is now a major dermatological health problem presenting as chronic dermatitis with different clinical patterns such as chronic photosensitivity impossible to be distinguished from chronic actinic dermatitis.
Objective: The aim of the present study was to do a full clinical assessment of all patients with chronic black hair dermatitis that have clinical features mimicking chronic actinic dermatitis (CAD).
Materials and Methods: This was a case-series, descriptive study in which all patients with chronic black hair dermatitis during the period from June 2020 to 2023 were recorded. Full demographic features were registered. In addition, clinical history taking and examination were conducted. Biopsies for histopathological evaluation were taken.
Results: A total of 51 patients with chronic black hair dye dermatitis were analyzed and assessed, their ages ranging from 35 to 65 years, with a mean of 52 years, with 45 (88.2%) males and 6 (11.76%) females, giving a ratio of 7.5:1. The Fitzpatrick skin types were 111 and 1V. All patients applied black hair dye for 1–5 years. The sites of rash were the face in 51 (100%), the neck and V area of the chest in 40 (78.43%), the scalp in 22 (43.13%), and the limbs and trunk in 21 (41.17%) patients. The patterns of rash were erythematous dermatitis in 5 (9.8%) and pigmented lichenoid and lichenified photodermatitis in 46 (90.19%) patients. Histopathological assessment showed features of dermatitis.
Conclusion: Chronic black hair dye dermatitis is a major skin problem now considered a common cause of chronic actinic dermatitis based on clinical, histopathological, and immunological aspects. Hence, in any patient with chronic actinic dermatitis, black hair dye application should be excluded.
Key words: Black hair dye dermatitis, PPD, Chronic actinic dermatitis, Facial melanosis
INTRODUCTION
A hair dye is primarily composed of paraphenylenediamine (PPD), resorcinol, propylene glycol, sodium ethylene diamine tetra acetic acid (EDTA), and all sorts of preservatives, along with fragrances and other cosmetic ingredients that impart a special fragrance to the hair [1]. Hair dyeing products may cause a variety of adverse side effects [2]. Allergies, irritant contact dermatitis, photo contact dermatitis, urticaria, leukoderma, anaphylaxis, lichenoid eruptions, actinic dermatitis, facial melanosis, and erythema multiforme-like eruptions are some of the most common adverse effects [2–8]. These reactions are characterized by redness, sores, itching, burning sensations, and discomfort [2]. These features may not become apparent immediately after the tint is applied and processed, yet they may become apparent hours or days later [3]. Currently, PPD is one of the most commonly used hair dyes on the market today, as well as the most common allergen [8]. The prevalence of sensitization to paraphenylenediamine (PPD) in Asia ranges from 2% to 12%, with Asian men having a higher prevalence than Asian women [9]. European prevalence is 4%, while North American prevalence is 6.2% [10]. Sharquie et al. found that black hair dye dermatitis is on the rise in Iraq, forming an outbreak with a male-to-female ratio of 5.2:1 and an average age of 52.3 years [4]. In general, black hair dye dermatitis is a disease associated with males of a dark complexion who are of skin types III and IV [4–7].
Immunopathogenesis of Black Hair Dye Dermatitis
A number of ingredients in hair dyes may irritate the skin, leading to irritant contact dermatitis that develops through non-immunological mechanisms [11]. The mechanism behind allergic contact dermatitis is more complex [12]. As a result of direct contact with chemical allergens, delayed-type hypersensitivity develops in the skin [10]. Prior sensitization is required for ACD development, which is termed the induction phase [13]. Langerhans dendritic cells migrate to a lymph node near the place where the antigen contacts the skin [12]. In response to the peptide fragments of the antigen, the CD4+T lymphocytes proliferate and differentiate into Th1 cells [10]. Hypersensitivity to a chemical allergen in the composition of hair dyes is determined by numerous factors, primarily the state of the immune system, since allergic contact dermatitis is a delayed-type allergy [12]. People with hereditary predispositions to allergic diseases and those living in environments conducive to chronic infections are more likely to develop the disease [14]. Depending on the phase of the disease, histopathological examination demonstrates acute and chronic dermatitis characteristics [5]. The epidermis of the patient with acute dermatitis develops acanthosis along with spongiosis and intraepidermal blisters, whereas the dermis shows superficial perivascular lymphocytic infiltrates [4]. Chronic dermatitis cases show epidermal acanthosis with or without parakeratosis and mild spongiosis [5]. A superficial perivascular lymphocytic infiltrate dominates the dermal changes [5, 7]. In general, hair dye allergies are treated mainly by withdrawal of the causative dye, topical steroids, and antihistamines at the systemic level [14].
Chronic actinic dermatitis (CAD) is an idiopathic skin disease that affects primarily men of lighter skin types and women of darker skin types over the age of fifty. People with darker skin may develop the disease earlier [15]. It is characterized by severely dry, itchy, red, inflamed, and thickened skin, typically on sun-exposed areas [16]. Besides chronic photosensitivity dermatitis, the condition is also known as actinic reticuloid (from histological findings of skin biopsies that resemble reticulosis or cutaneous T-cell lymphoma) [17]. There may be a history of other types of dermatitis in patients with the condition, such as atopic dermatitis, allergic contact dermatitis to fragrances and plants such as chrysanthemum, and photo contact dermatitis occurring many years prior to the development of photosensitivity [18]. This is sometimes referred to as a persistent light reaction [16]. The skin of people with CAD is over-sensitive to sunlight or artificial light, leading to eczema reactions that often occur within minutes of exposure to the sun, although they usually appear between 7 and 24 hours later [19]. Light-exposed skin, such as the face, V of the neck, upper chest, and back of the hands/forearms, is most likely to develop this condition [15]. During the summer, when the sun is strongest, it usually worsens [17]. Since skin reactions may occur several days after sun exposure, people with CAD may not be aware or their relation [16]. CAD is believed to be caused by an allergic reaction to sunlight or artificial light. However, it is unclear why this occurs [18]. The diagnosis may be confirmed with photo testing [17]. In this type of test, specific wavelengths of light are applied to specific parts of the skin in order to determine if the skin is sensitive [15]. Patch testing and photo patch testing are also used to confirm the presence of an abnormal reaction to light. Patch tests reveal positive reactions to one or more allergens in 75% of patients with chronic actinic dermatitis, most often fragrances, sunscreens, colophony, and sesquiterpene lactones (found in the daisy family) [17]. CAD histopathology reveals epidermis acanthosis, spongiosis, lymphocytic infiltration in the upper dermis, and eosinophils, macrophages, and plasma cells may be present [16]. Sun protection is essential for patients with chronic actinic dermatitis [18]. Moreover, if a contact allergy is present, the patient should avoid the offending substance [19]. It may be necessary to take oral immune suppressive treatments in severe cases [16]. Among them are systemic corticosteroids, azathioprine, and cyclosporin. Some patients were successfully desensitized with photochemotherapy (PUVA) or narrowband UVB with a systemic steroid cover [19]. Occasionally, the disease resolves spontaneously many years after the onset [17,19]. In most cases, the condition lasts a lifetime and requires significant lifestyle changes to avoid sun exposure and contact allergens [18].
Immunopathogenesis of Chronic Actinic Dermatitis
In CAD, a spectrum of immunological abnormalities is evident, including elevated T lymphocytes and a lower CD4+/CD8+ cell ratio, suggesting an overactive immune response in the skin and contributing to chronic inflammation [20]. Severe CAD cases exhibit higher amounts of IFN-g+, CD4+, CD8+, common-g-chain receptor, and CD69+ tissue-resident memory cells, with a further decrease in the CD4+/CD8+ cell ratio, indicating more pronounced immune dysregulation [21].
The role of T-cells in CAD eruptions is crucial [22]. Elevated total Ig-E levels and eosinophils in severe CAD, along with a shift from Th1/Th2 to Th2 dominance due to increased suppressor T cells, suggest a deviation from the normal immune response and contribute to disease severity [23]. In CAD eruptions triggered by photosensitivity, infiltrating T cells are CD8-dominant, and the reduced CD4+/CD8+ ratio of circulating T cells appears to contribute to these eruptions [24].
The immunological markers of CAD and the findings from negative T-cell clonality studies are similar to those in conditions such as eczematous variants of cutaneous T-cell lymphoma or Sezary syndrome, highlighting the need for further research to identify specific immunological responses leading to CAD and its characteristic eruptions [25].
Genome-wide analyses of mRNA and long non-coding RNA profiles in CAD patients reveal that 198 annotated and 45 novel mRNAs may regulate T-cell mediated inflammation via differential expression of genes influencing TNFAIP3 expression [26]. Studies indicate that loss-of-function mutations in filaggrin-coding genes do not explain the altered immunology in CAD eruptions [25]. However, other research suggests these mutations affect the CD4+/CD8+ ratio in circulating T cells [27]. The genetic basis for immunological changes in CAD eruptions remains poorly understood [26].
Based on our studies of black hair dye dermatitis, we noted many patients had features of chronic photosensitive dermatitis that cannot be differentiated clinically, histopathologically, or immunologically from CAD [4–5]. Accordingly, the objective of the present work was to do a full evaluation of chronic black hair dye dermatitis that shares features of CAD.
Patients and Methods
Fifty-one patients complaining of chronic hair dye dermatitis gathered during the period from June 2020 to 2023 were involved in this cross-sectional descriptive, observational, case-series clinical–histopathological study. The study was conducted following the Declaration of Helsinki. After discussing the nature of the study with all patients, informed consent forms were obtained from all. The close-up picture of the object was taken at the same place with a fixed distance and lighting in the same direction. Also, all of the patients included in this study accepted the idea of sharing their photos in the study. A full epidemiological and demographic profile was recorded during the study. The scientific name of all dyes used by the patients was paraphenylenediamine (PPD) dye, which was found to be the same name as all dyes used by patients. In order to establish the right clinical diagnosis, a detailed history of the patient was taken along with performing a thorough physical examination. This encompassed the name, age, sex, residence, occupation, and atopy history (nasobronchial allergy, asthma, childhood eczema) of the individual, the duration of the lesions, the chief complaints, the associated symptoms including redness, sores, itching, burning sensation, and discomfort, the recurrence, aggravating and relieving factors, the site, type, geographical distribution, the type and duration of hair dye, the work environment, 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-one patients complaining of chronic black hair dye dermatitis were considered in the present work, their ages ranging from 35 to 65 years, with a mean of 52 years, with 45 (88.2%) males and 6 (11.76%) females, giving a ratio of 7.5:1. Fitzpatrick skin types for all patients were 111 and 1V. All patients applied black hair dye for 1–5 years. The sites of rash were the face in 51 (100%), neck and V area of the chest in 40 (78.43%), scalp in 22 (43.13%), and limbs and trunk in 21 (41.17%) patients. The patterns of rash were erythematous dermatitis in 5 (9.8%) and pigmented lichenoid and lichenified photodermatitis in 46 (90.19%) patients. The histopathological findings of the cases with acute black hair dye dermatitis showed acanthosis along with spongiosis and intraepidermal blisters, whereas the dermis showed superficial perivascular lymphocytic infiltrates. Meanwhile, chronic dermatitis cases showed epidermal acanthosis with or without parakeratosis and mild spongiosis. Superficial perivascular lymphocytic infiltrate dominated the dermal changes (Tables 1 and 2) (Figs. 1 – 5, 6a, 6b).
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Table 1: Sociodemographic characteristics of the patients with chronic black hair dye dermatitis (n=51). |
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Table 2: Clinical characteristics of the patients with chronic black hair dye dermatitis (n=51). |
DISCUSSION
Although CAD is a rare skin problem, during our studies regarding chronic black hair dye dermatitis, we noticed that many cases had features of CAD, and this clinical finding encouraged us to conduct the present work [4,5].
CAD is a rare idiopathic photosensitive immune-mediated disorder, characterized by pruritic eczematous lesions on sun-exposed areas that might extend to other parts of the body. It is most commonly seen in middle-aged males and less commonly in females [15]. There is some evidence that type-IV hypersensitivity to UV-induced neoantigens plays a role in the pathogenesis of the condition [18]. CAD usually affects the exposed areas of the body, although it has been known to extend to the covered areas as well [17]. Idiopathic allergic reactions to some triggering factors such as fragrance, sunscreen, and colophony are aggravating factors in CAD. Males of middle and younger ages with a white complexion are more likely to develop this disorder. The histopathological features of CAD show in early cases acute dermatitis changes to chronic dermatitis [5,16,18]. Chronic black hair dye dermatitis is now considered a major dermatological problem that also affects middle-aged people and older men in particular [4–5].
51 patients who complained of chronic black hair dye dermatitis were included in our study, with the mean age being 52 years, with 88.2% males and 11.76% females, resulting in a 7.5:1 male-to-female ratio. The patients’ Fitzpatrick skin types were 111 and 1V. A black hair dye was applied to all patients for a period of one to five years. In 100% of the patients, the rash was on the face; in 78.43%, on the neck and V area of the chest; in 43.13%, on the scalp; and in 41.17%, on the limbs and trunk. In 90.19% of the patients, there was pigmented lichenoid and lichenified photodermatitis, and 9.8% of the cases had erythematous dermatitis. Depending on the stage of the disease, the histopathological findings exhibited features of both acute and chronic dermatitis similar to CAD. There was acanthosis of the epidermis with spongiosis and intraepidermal blistering and a superficial perivascular lymphocytic infiltration of the dermis in acute dermatitis. Meanwhile, there was acanthosis of the epidermis with or without parakeratosis and mild spongiosis in chronic dermatitis. Infiltrates of superficial perivascular lymphocytes dominated the dermal changes.
The present study showed that all features of chronic black hair dye dermatitis were similar to those reported in the literature [1–7]. All caused by black hair dye PPD and preservatives usually affected middle-aged and older men with dark complexions, and almost all cases of the dermatitis were characterized by erythematous dermatitis, pigmented lichenoid dermatitis, and lichenified photodermatitis, mostly affecting the face, neck, chest, scalp, legs, and trunk of the affected individual. On the basis of histopathology, it was shown that, in early cases, acute dermatitis changes into chronic dermatitis. These features are similar to those found in CAD (Table 3).
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Table 3: Comparison between chronic black hair dye dermatitis with features of CAD and chronic actinic dermatitis. |
In addition, both chronic black hair dye dermatitis and chronic actinic dermatitis share common immunological characteristics. In CAD, there is an elevation of T lymphocytes and a lower CD4+/CD8+ cell ratio, indicating an overactive immune response in the skin and contributing to chronic inflammation. Severe cases exhibit higher amounts of IFN-g+, CD4+, CD8+, common-g-chain receptor, and CD69+ tissue-resident memory cells, with a further decrease in the CD4+/CD8+ cell ratio, indicating more pronounced immune dysregulation [22–24]. While in chronic black hair dye dermatitis, as a result of direct contact with PPD and other preservative antigens, delayed-type hypersensitivity reactions develop. As the antigen contacts the skin, Langerhans dendritic cells migrate to a lymph node nearby, and this leads to CD4+T lymphocytes proliferating and differentiating into Th1 cells in response to antigen peptide fragments [10–12]. Iraqi patients with CAD mainly present with features of chronic black hair dye dermatitis while other triggering factors in relation to CAD were not observed in our patients [4–5,16–18]. Men often use black hair dye but women use blonde hair dye, which is the cause of chronic black hair dye dermatitis being more common among men.
As a consequence, chronic black hair dye dermatitis and CAD share similar clinical, histopathological, and immunological characteristics. Hence, for any patients with CAD, black hair dye application should be excluded.
CONCLUSION
Chronic black hair dye dermatitis is becoming increasingly common and is now considered a frequently overlooked cause of chronic actinic dermatitis based on clinical, histopathological, and immunological aspects. Accordingly, in any patient with chronic actinic dermatitis, black hair dye application should be excluded.
Statement of Human and Animal Rights
All the procedures followed were in accordance with the ethical standards of the responsible committee on human experimentation (institutional and national) and with the 2008 revision of the Declaration of Helsinki of 1975.
Statement of Informed Consent
Informed consent for participation in this study was obtained from all patients.
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