Diverse clinical manifestations of lichen planus actinicus annulare v. lichen planus actinicus diffusum as new subtyping in a series of 152 patients

Khalifa E. Sharquie1, Waqas S. Abdulwahhab2, Inas K. Sharquie3

1Department of Dermatology, College of Medicine, University of Baghdad, Center of Dermatology, Medical City Teaching Hospital, Iraq, 2Department of Dermatology & Venereology, Al-Qassimi Hospital, Sharjah. UAE, College of Medicine, University of Sharjah. Sharjah, UAE, 3Department of Microbiology and Immunology, College of Medicine, University of Baghdad, Iraq

Corresponding author: Prof. Khalifa E. Sharquie, MD PhD, E-mail: ksharquieprof@yahoo.com

How to cite this article: Sharquie KE, Abdulwahhab WS, Sharquie IK. Diverse clinical manifestations of lichen planus actinicus annulare v. lichen planus actinicus diffusum as new subtyping in a series of 152 patients. Our Dermatol Online. 2026;17(1):61-68.
Submission: 03.05.2025; Acceptance: 15.08.2025
DOI: 10.7241/ourd.20261.11

Citation tools: 

Related Content

Copyright information

© Our Dermatology Online 2026. No commercial re-use. See rights and permissions. Published by Our Dermatology Online.


ABSTRACT

Background: Lichen planus is a common skin problem with different clinical manifestations, and this diversity is also observed in lichen planus actinicus.

Objective: Lichen planus actinicus might have different clinical manifestations, commonly the lichen planus actinicus annulare and diffusum variants. The aim of the present study is to do a comparative evaluation including all aspects of these types.

Patients and Methods: This is a cross-sectional, descriptive, comparative study conducted during the period from 2014 to 2023 where 152 patients with lichen planus actinicus were collected and all demographic features were recorded. Full clinical examination was done, including sites, types of rash, seasonal variation, and any symptomatic complaints. These different demographic and clinical manifestations were compared with each other in these two different variants. Biopsy and histopathological assessment were carried out as a confirmation.

Results: Lichen planus actinicus annulare: A total of 44 patients were included, with ages ranging from 6 to 40 years with a median of 15 years, mostly young children and adolescents with 41 (93.2%) males and 3 (6.8%) females, giving a female-to-male ratio of 13.6:1. All patients had outdoor activities, either being school students or workers. The location of rash was on the exposed parts, mostly the face and upper limbs. The severity of rash varied according to the sites of affection; it could be severe on the face while sparse on the extensor surfaces of hands and arms, and vice versa. The type of rash was usually pigmented with annular configuration, with slight atrophy at the centers and with slightly erythematous peripheral active borders. The same rash was commonly noticed on both lips. All patients complained of its cosmetic appearance with mild itching or burning. There was marked and obvious seasonal variation of rash, and it was the most prominent in summertime. Lichen planus actinicus diffusum: A total of 108 patients were included during the period from 2014 to 2023 years, with ages ranging from 25 to 60 years, with a mean of 50 years, with 66 (61.1%) females and 42 (38.9%) males, giving a female-to-male ratio 1.7:1. All patients with outdoor activities either as housewives or workers. The sites of rash were mostly the face and some patients had hands and forearm involvement. The rash severity could vary from mild to severe affection of the whole face. The morphology of the rash was pigmented diffuse, affecting all sites of the face and with some erythematous elements in many patients, but could be severe in one area of the face. The butterfly configuration was a common feature mimicking the rash of lupus erythematosus while mask-like pigmentation of the whole face was frequently observed. Lip involvement was a common complaint but it more commonly and more severely involved the lower lip. On healing, and in many cases, the rash gave the picture of dermal melasma. The ugly cosmetic appearance was the common complaints. The seasonal accentuation was not very prominent during winter and summer.

Conclusion: There are diverse clinical manifestations between the two groups regarding age, sex, sites of rash, type and configuration of rash, seasonal aggravation, and resolution of rash. Accordingly, we can conclude that annulare and diffusum are well distinctive and demarcated variants but still could be two different diseases.

Key words: Lichen planus, Lichen planus actinicus, Annular lichen planus actinicus, Lichen planus pigmentosus, Riehl melanosis


INTRODUCTION

Lichen planus is an idiopathic, inflammatory disorder of the skin and mucous membranes that causes pruritic, violaceous papules and plaques. It has been noted that lichen planus can present in various clinical variations, including annular LP, linear LP, hypertrophic LP, atrophic LP, vesiculobullous LP, erosive LP, lichen planopilaris, lichen planus pigmentosus, and lichen planus actinicus [1]. Typically found in sun-exposed areas, lichen planus actinicus (LPA) is a photosensitive variety of lichen planus. The condition is also known as LP subtropicus, LP tropicus, lichenoid melanodermatitis, and summertime actinic lichenoid eruption. Dark-skinned young adults of Middle Eastern descent are more likely to suffer from this condition [2]. LPA is the most common photo-distributed variant of lichen planus [35]. Despite the fact that its etiology is unknown, sunlight appears to be the most common trigger [6,7]. Usually, lesions of lichen planus actinicus are found on the forehead, face, and neck, as well as the extensor surface of their hands and arms, affecting children and young adults [8]. A variety of morphologic patterns have been reported, including butterfly lichen planus actinicus, annular hyperpigmented plaques, melasma-like patches (gray, brown, or black patches on the face and neck; size ranges from 5 mm to 5 cm), dyschromic papules (Pinhead-sized, white, angular papules coalescing into patches; small, horny plugs present in the center of the papule), and classic lichenoid papules/plaques [3,4,6]. It has been noted that lesions are often aggravated by sun exposure and sometimes improve spontaneously during the winter months [4]. LPA, unlike classical lichen planus, occurs earlier in life, lasts longer, tends to affect darker-complexed women, and often occurs at a particular time of year; it also does not typically involve pruritus, scaling, nail involvement, or the Koebner reaction [3,4,6]. Its histologic features are similar to those of classic lichen planus (hyperkeratosis of the stratum corneum, hypergranulosis, basal cell vacuolization, Civatte bodies are usually present, as are numerous melanophages, pigmentary incontinence, and bandlike lymphocytic inflammatory infiltrates in the papillary dermis) [9]. Sun avoidance, sunscreen, topical corticosteroids, hydroxychloroquine, intralesional corticosteroids, and acitretin have been reported to have variable effects on lichen planus actinicus [1012].

A very common manifestation of LPA is annular actinic LP, which manifests as erythematous brown plaques that are annular in shape, with a dark core at the center of the plaque in the late stages of the disease. Atrophy may or may not accompany these lesions. The diagnosis is confirmed by distribution over photo-exposed areas and by histological examination revealing classic LP findings [13].

LP Pigmentosus (LPP), an atypical condition occurring more commonly in India and the Middle East, usually develops in the third and fourth decades of life. It occurs more frequently in women than men. Lesions usually involve the face, neck, and less commonly, flexor areas such as the axilla, groin, and infra-mammary folds; they are largely distributed symmetrically. Like LPA, this type of LP is more common in sun-exposed areas [14,15]. It is described as a disease characterized by brown to gray-brown macules and patches on areas exposed to the sun and, in the rare inversus variants, on the flexural areas and intertriginous areas of the body [16]. The pigmentation pattern is generally diffuse, although there are follicular, reticular, and unilateral linear variants [17]. The annular form of LPP has been documented in a limited number of published photographs and is common both in inversus and actinic forms [18]. Lesions of LPP differ from classic LP in that they are flat, never hyperkeratotic, and rarely symptomatic. It has been found that LPP may occur concurrently with other forms of lichen planus, but there have been few studies examining their co-occurrence. Unlike the classic lesions of lichen planus, LPP is generally asymptomatic, although some lesions may cause pruritus or burning [14]. An individual with this disease will experience exacerbations and remissions throughout the course of the disease. In addition to epidermal atrophy and vacuolar degeneration of the epidermis, perivascular lymphohistiocytic infiltrates are seen in histopathology in the upper dermis, as well as dermal melanophages [19]. There is no clear etiology for this condition, although ultraviolet light has been suggested to play a role in the photo-distributed eruption. Several retrospective studies have reported an association between LPP and mustard and amla oil topical applications [14,20]. The allyl thiocyanate in mustard oil can act as a photosensitizer as well as a pathogen in LPP [14]. Since the clinical course of LPP is inherently variable, treatment can be challenging. There are few effective therapies available. It is possible for some cases to resolve spontaneously within several weeks; however, other cases can persist for years [21,22]. Sunscreen use and sun avoidance should always be part of treatment strategies [21]. Few studies have shown significant improvements with topical steroids, topical calcineurin inhibitors, and systemic acitretin [2123]. It is important to distinguish LPP from Riehl melanosis (RM) and ashy dermatoses as other causes of facial melanosis.

Riehl’s melanosis (RM) as a pigmented contact dermatitis (PCD), typically presents as abnormal hyperpigmentation on the face and neck resulting from an allergic reaction to fragrances and cosmetic products. Patients of Asian descent are more likely to suffer from the disorder [24]. In most cases, it is caused by direct contact with several allergens. A few cases have also been reported secondary to contact with airborne allergens. In some PCD, UV exposure may play a role since hyperpigmentation is often photo-localized, and some of the causative chemicals are known photosensitizers [25]. Aniline dyes and red and yellow pigments are common cosmetics allergens; perfume allergens include geraniol oil and lemon oil (photosensitizer allergen); textile allergens include Tinopal CH3566: optical whitener in washing powder and Naphthol AS: coupling agent for azo dyes; coal tar and chromium are common occupational allergens [26,27]. The incidence of RM is unknown. Darkly pigmented races are more likely to suffer from Riehl melanosis. Most concerned are young to middle-aged women. PCD can also affect men and children [25]. Satellite-pigmented follicular-based macules and patchy to diffuse pigmentation are common features of Riehl melanosis. There is often a reticular pattern at the center of pigmented areas [28]. The sites of involvement vary depending on the allergen. A pigmented cosmetic dermatitis is usually found on the face (forehead, zygomatic, and temple regions), while a textile contact dermatitis is usually found on axillary borders, sparing the vault [27]. Interface dermatitis has been found in most biopsy results. The first signs of Riehl melanosis are vacuolar basal layer degeneration, perivascular or band-like lymphohistiocytic infiltrates, and pigmentary deficiency of the dermis. A later histological examination shows upper dermal melanophages infiltrating. Direct immunofluorescence results are negative [29]. The treatment options for RM include removing causal agents, protecting the skin from the sun, and using topical agents such as hydroquinone, topical corticosteroids, retinoids, vitamin C, and azelaic acid, along with or without light to medium chemical peels (trichloroacetic acid, glycolic acid), using intense pulsed light therapy or Q-switched Nd: YAG lasers [30]. We are not convinced that RM is a special entity or a disease; rather, it may be part of other causes of facial melanosis, like melasma (dermal type), LPP actinicus diffusum, black hair dye dermatitis, and early-stage frictional melanosis [31].

In spite of the fact that LPP is considered a variant of lichen planus, the main differential diagnosis is erythema dyschromium perstans (EDP) or ashy dermatosis. It has been widely acknowledged that LPP and EDP share many clinical similarities; both conditions are characterized by gray-to-brown macules and patches, and both were first described in 1992 as distinct clinical and histopathologic entities [19]. Early EDP lesions often have an inflammatory phase, where hyperpigmented macules and patches are surrounded by a thin ring of erythema. LPP does not typically undergo such an inflammatory phase [32]. Melanin deposition is a histopathological feature that distinguishes LPP from EDP. Melanin deposits occur in the deeper dermis of EDP, which produces blue-grey colored lesions due to the Tyndall effect; in LPP, melanin deposits are found in the superficial dermis [18].

Immunological changes in Lichen planus actinicus

Lichen planus (LP) involves a cell-mediated immune response and is categorized as an autoimmune disease and similarly, lichen planus actinicus is also characterized by an autoimmune reaction but triggered by sunlight exposure as a Koebner phenomenon. The lesions exhibit a substantial presence of lymphocytic infiltrates, predominantly T cells. Localized lesions trigger the activation of numerous lymphocytes, leading to increased secretion of adhesion molecules and cellular kinases. While B lymphocytes and natural killer (NK) cells are infrequent, T lymphocytes play a pivotal role, particularly CD4+ and CD8+ T cells [3335]. In a normal immune state, CD4+ and CD8+ T cells are in dynamic equilibrium, but with LP progression, there is a notable increase in both. This suggests that the invasion of the epidermis by CD4+ and CD8+ T cells contributes to LP by accelerating the injury progression through the destruction of epidermal and basal cells. Treatment was found to decrease the expression of CD4+ and CD8+ T cells, with a more significant reduction in CD8+ T cells. This shift positively affects symptoms and regulates the distribution of these T cell subsets [3638]. Further investigation reveals the involvement of Th cell subsets, including Th1, Th2, and Th17. Th2 cytokines IL-4 and IL-6 are elevated during LP development, causing damage to normal cells [3941]. A study indicates that Th differentiation is altered post-treatment, with increased Th1 cytokines (IL-2 and IFN-g), decreased Th2 cytokines (IL-4 and IL-6), and reduced secretion of Th17 cytokines (IL-17 and IL-22). This alteration helps inhibit tissue damage caused by cytokines [42].

The lichen planus actinicus annulare variant was the commonest type seen among children and young adults but is now decreasing in its frequency, while lichen planus actinicus diffusum was a rare variant but, now, it is commonly observed in clinical practice among adults while rare in children [8,12].

The present study compares two variants of LPA, the annulare variant and the new LP actinicus diffusum type, assessing the sites, forms of rash, seasonal variation, and any symptoms such as itching and burning.

PATIENTS AND METHODS

One hundred fifty-two patients with lichen planus actinicus were involved in this cross-sectional clinical-histopathological work that was carried out during the period from 2014 to 2023 years. There was adherence to the Helsinki Declaration in this study. Photos with close-up views were taken at the same location with a fixed illumination and distance. Additionally, all patients included in this study accepted the idea of sharing their photos. Full epidemiological and demographic features were recorded. A thorough history was taken to have the right diagnosis, along with a thorough assessment: name, age, sex, age at onset, duration of the disease, sites and types of rashes, seasonal variation, pruritus, and any other symptomatic complaints. These different demographic and clinical manifestations were compared with each other in these two different variants. Exposure to external topical allergic agents like fragrances and cosmetic products was excluded. Biopsy and histopathological assessment were carried out as a confirmation.

RESULTS

This study consisted of the following two parts.

Part One, Lichen Planus Actinicus Annulare

A total of 44 patients complaining of lichen planus actinicus annulare were analyzed and considered in the present work. Their ages ranged from 6 to 40 years with a median of 15 years, mostly young children and adolescents, with 41 (93.2%) males and 3 (6.8%) females, giving a ratio of 13.6:1. All patients had outdoor activities, being either school students or workers. The location of rash was on the exposed parts, mostly the face and upper limbs. The severity of rash varied according to the sites of affection; it could be severe on the face while sparse on the extensor surfaces of the hands and arms, and vice versa. The type of rash was usually pigmented with an annular configuration, with slight atrophy at the centers and with slightly erythematous peripheral active borders. The same rash was commonly noticed on both lips. All patients complained of its cosmetic appearance with mild itching or burning. There was marked and obvious seasonal variation of the rash, and it was most prominent in summertime (Figs 1a1d).

Figure 1: (a) 10-year-old patient showing a typical case of lichen planus actinicus annulare affecting the face and hands. (b) 20-year-old patient showing features of lichen planus actinicus annulare. (c) 40-year-old female showing features of lichen planus actinicus annulare. (d) Penile involvement in a patient with lichen planus actinicus annulare.

Part Two, Lichen Planus Actinicus Diffusum

A total of 108 patients with lichen planus actinicus diffusum were included. Their ages ranged from 25 to 60 years, with a mean of 50 years, with 66 (61.1%) females and 42 (38.9%) males, giving a female-to-male ratio of 1.7:1. All patients engaged in outdoor activities either as housewives or workers. The sites of rash were mostly the face, and some patients had hands and forear involvement. The rash severity could vary from mild to severe affection of the whole face. The morphology of rash was pigmented diffuse, affecting all sites of face and with some erythematous elements in many patients, but could be severe in one area of the face. The butterfly configuration was a common feature mimicking the rash of lupus erythematosus while mask-like pigmentation of the whole face was frequently observed. Lip involvement was a common complaint but more commonly and severely involved the lower lip. On healing and in many cases, the rash gave a picture of melasma resembling a road paved with asphalt both in the clinical and histopathological pictures. The ugly cosmetic appearance was the common complaint. The seasonal accentuation was not very prominent during winter and summer (Tables 1 and 2); (Figs 25). When the frequency of these two types compared with each other, the diffusum type was much more common than annulare, with a ratio 2.45:1.

Table 1: Sociodemographic characteristics of the present study (n=152).

Table 2: Clinical characteristic differences in disease presentation between lichen planus actinicus annulare and diffusum.

Figure 2: (a) 45-year-old female showing lichen planus actinicus diffusum. (b) 36-year-old female showing features of lichen planus actinicus diffusum. (c) 51-year-old patient showing features of planus actinicus diffusum. (d) 45-year-old patient showing lichen planus actinicus diffusum. (e) 60-year-old patient showing lichen planus actinicus diffusum. (f) 59-year-old patient showing lichen planus actinicus diffusum.
Figure 3: (a) 50-year-old patient showing lichen planus actinicus diffusum. (b) 50-year-old patient showing lichen planus actinicus diffusum.
Figure 4: (a) Lichen planus actinicus diffusum. The facial and dermal melanosis resembling a road paved with asphalt. (b) The facial and dermal melanosis resembling a road paved with asphalt. (c) The facial and dermal melanosis resembling a road paved with asphalt.
Figure 5: (a) Histopathology of lichen planus actinicus diffusum showing mainly a dermal inflammatory reaction with numerous melanophages arranged in one line and resembling a road paved with asphalt. (H&E; 40x). (b) Histopathology of lichen planus actinicus diffusum (H&E; 40x).

DISCUSSION

The frequency of lichen planus has been increasing over years as a recent study by Sharquie et al., in 2015, reported an upsurge in cases of lichen planus in the Iraqi population, with a change in the clinical pictures of the illness as it is more complex, pigmented in color, widely distributed, and more severe with flexural involvement in the large joints. Among them, 22.6% of LP patients are subtypes with lichen planus actinicus, including both annulare and diffusum variants [7,3,43]. Sun-exposed areas such as the face, neck, and dorsal arms are commonly affected by LPA lesions. LP actinicus presents as melasma-like LP actinicus, and butterfly LP actinicus, patients reported the pigmentation as facial melanosis, dark brown to gray-brown., and mostly pruritic in nature [3,43].

Actinic LP affects dark-skinned individuals living in tropical or subtropical regions, especially those with areas exposed to the sun on the forehead or upper extremities. During the summer months, the disorder is often more prevalent. Contrary to classical LP, features such as pruritus, the Koebner phenomenon, and the involvement of the mucosal surfaces are not often observed in this disorder. The nails are almost never involved [44]. Actinic lichen planus is estimated to affect one case per million people each year [45]. A variety of types of actinic lichen planus can be found: annular, pigmented, dyschromic, butterfly Lichen Planus actinicus, melasma-like patches, classic lichenoid papules/plaques, and LP actinicus diffusum pattern [3,4,6]. The most commonly presenting form is annular actinic LP, which accounts for more than 80% of cases, and manifests as erythematous brown plaques that are arranged in an annular pattern. Atrophy may or may not accompany these lesions. The diagnosis is confirmed by the distribution over photo-exposed areas, followed by a histological examination, which reveals findings similar to those present in classic LP [13]. This variant of lichen planus actinicus was the commonest type seen but now it is decreasing in its frequency [3]. Meanwhile, cases of lichen planus actinicus diffusum are increasing as a cause of facial melanosis [3,31]. This is similarly documented in the present work.

Our present study compares LPA annulare versus LPA diffusum, including the types of rashes, seasonal variations, and symptomatic complaints. A total of 44 patients with lichen planus actinicus annulare were included, ranging from 6 to 40 years, with a median of 15 years, mostly young children and adolescents, with 93.2% males and 6.8% females, giving a ratio of 13.6:1. In all cases, the patients had outdoor activities, either as school students or as workers. Mostly the face and upper limbs were affected by the rash. As the sites of affection varied, rash severity could vary from severe on the face to sparse on the hands and arms, and vice versa. It usually presented as a pigmented annular rash with slight atrophy at the centers and an erythematous peripheral border. Both lips were commonly affected by the same rash. A mild itch or burning sensation was reported by all patients. Summertime was the time of year when rash occurred most frequently and was markedly seasonal.

A total of 108 patients with lichen planus actinicus diffusum in the present study were aged 25–60 years, with a mean of 50 years, 61.1% females and 38.9% males, giving a female-to-male ratio of 1.7:1. All patients engaged in outdoor activities either as housewives or workers. Many patients experienced a rash on their faces, but some also had it on their hands and forearms. A mild to severe rash could affect the entire face. In many patients, the rash was diffusely pigmented, affecting all sites of the face, with some erythematous elements, but could be severe in one area. Often, the configuration of the face looked like a butterfly, mimicking the rash associated with lupus erythematosus, while mask-like pigmentation was seen frequently on the whole face. Lip involvement was a common complaint, but was more severe in the lower lip. In many cases, after healing, the rash looked like melasma. A common complaint was the ugly cosmetic appearance. As for the seasonal accentuation, it was less prominent during the winter and summer months. Comparatively to classical LP pigmentosus, which involves both the face and body, LP actinicus diffusum is favorable for the face only [14,15]. In addition, LP actinicus diffusum might mimic melasma, black hair dye dermatitis, and facial frictional melanosis in terms of clinical and histopathological features, and sometimes, it is difficult to differentiate between them. LP actinicus diffusum can appear as a severe form in older age groups, with a road-paved appearance, which may resemble asphalt. The LP actinicus diffusum might resemble Riehl’s melanosis (RM), but our patients had no history of contact dermatitis. We believe that RM is neither a special entity nor a disease, but rather a combination of miscellaneous diseases that share a facial melanosis, such as dermal melasma, lichen planus pigmentosum, lichen planus actinicus diffusum, black hair dye dermatitis, and early-onset frictional melanosis [31].

CONCLUSION

There are diverse clinical manifestations between the two groups regarding frequency, age, sex, sites of rash, type and configuration of rash, seasonal aggravation, and resolution of rash. Accordingly, we can conclude that annulare and diffusum are well distinctive and demarcated variants but still could be two different diseases. Both types are aggravated by sunlight exposure and the diffusum type was increasing much more common than annulare, with a ratio of 2.45:1.

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.

REFERENCES

1.Ghoreschi K, Balato A, Enerbäck C, Sabat R. Therapeutics targeting the IL-23 and IL-17 pathway in psoriasis. Lancet. 2021;397:754-66.

2.Rendon A, Schäkel K. Psoriasis pathogenesis and treatment. Int J Mol Sci. 2019;20:1475.

3.Michalek IM, Loring B, John SM. A systematic review of worldwide epidemiology of psoriasis. J Eur Acad Dermatol Venereol. 2017;31:205-12.

4.Boehncke WH, Schön MP. Psoriasis. Lancet. 2015;386:983-94.

5.Griffiths CE, Armstrong AW, Gudjonsson JE, Barker JN. Psoriasis. Lancet. 2021;397:1301-15.

6.Parisi R, Iskandar IY, Kontopantelis E, Augustin M, Griffiths CE, Ashcroft DM. National, regional, and worldwide epidemiology of psoriasis:Systematic analysis and modelling study. BMJ. 2020;369:m1590.

7.Blauvelt A, Chiricozzi A. The immunologic role of IL-17 in psoriasis and psoriatic arthritis pathogenesis. Clin Rev Allergy Immunol. 2018;55:379-90.

8.Armstrong AW, Read C. Pathophysiology, clinical presentation, and treatment of psoriasis:A review. JAMA. 2020;323:1945-60.

9.Shalom G, Cohen AD, Babaev M, Freud T, Tzur Bitan D, Vardy DA, et al. Biologic drug survival in Israeli patients with psoriasis:A real-world evidence study. J Dermatolog Treat. 2021;32:372-6.

10.Gisondi P, Del Giglio M, Girolomoni G. Treatment approaches to moderate to severe psoriasis. Int J Mol Sci. 2017;18:2427.

11.Puig L. Treatment of moderate-to-severe plaque psoriasis with biologics:An evidence-based review. Actas Dermosifiliogr. 2014;105:424-32.

12.Chiricozzi A, De Simone C, Fossati B, Peris K. Immunopathogenesis of psoriasis and mechanisms of action of systemic treatments. G Ital Dermatol Venereol. 2020;155:1-11.

13.Nestle FO, Kaplan DH, Barker J. Psoriasis. N Engl J Med. 2009;361:496-509.

14.Damiani G, Radaeli A, Olivini A, Calzavara-Pinton P, Colombo D. Increased burden of psoriasis in women. Int J Womens Dermatol. 2019;5:130-5.

15.Carrascosa JM, Notario J, Suarez C. Economic impact of biological therapies for moderate to severe psoriasis. Expert Rev Pharmacoecon Outcomes Res. 2019;19:23-31.

16.Iskandar IY, Parisi R, Griffiths CE, Ashcroft DM. Demographics and disease characteristics of patients with psoriasis in the British Association of Dermatologists Biologic Interventions Register. Br J Dermatol. 2015;173:510-8.

17.Damiani G, Pimpinelli N, Agostinelli L, Iorizzo M, Iacovelli P, Di Lernia V, et al. Biologic therapies and infections in psoriasis:Analysis of the Italian pharmacovigilance database. J Eur Acad Dermatol Venereol. 2021;35:573-7.

18.Samarasekera EJ, Sawyer L, Wonderling D, Tucker R, Smith CH. Topical therapies for psoriasis:A network meta-analysis. Cochrane Database Syst Rev. 2013;10:CD008587.

19.Cline A, Cardwell LA, Feldman SR. Methotrexate in psoriasis:An updated review. Am J Clin Dermatol. 2019;20:503-16.

20.Atzeni F, Defendenti C, Ditto MC, Batticciotto A, Pacini G, Sarzi-Puttini P. Immunogenicity and autoimmunity during anti-TNF therapy. Autoimmun Rev. 2013;12:703-8.

21.Papp KA, Reich K, Paul C, Blauvelt A, Baran W, Bolduc C, et al. A prospective phase III, randomized, double-blind, placebo-controlled study of risankizumab in patients with moderate-to-severe plaque psoriasis. Lancet. 2018;392:650-61.

22.Chiu HY, Huang HL, Chen WL, Chen CY, Tsai TF. Risk of major cardiovascular events and all-cause mortality in patients with psoriasis receiving biologic therapies:A nationwide population-based cohort study. J Am Acad Dermatol. 2020;82:1237-45.

23.Oliveira Mde F, Rocha BO, Duarte GV. Psoriasis:classical and emerging comorbidities. An Bras Dermatol. 2015;90:9-20.

24.Gisondi P, Fostini AC, FossàI, Girolomoni G, Targher G. Psoriasis and the metabolic syndrome. Clin Dermatol. 2018;36:21-8.

25.Takeshita J, Grewal S, Langan SM, Mehta NN, Ogdie A, Van Voorhees AS, et al. Psoriasis and comorbid diseases:Epidemiology. J Am Acad Dermatol. 2017;76:377-90.

26.Armstrong AW, Harskamp CT, Armstrong EJ. Psoriasis and the risk of diabetes mellitus:A systematic review and meta-analysis. JAMA Dermatol. 2013;149:84-91.

27.Hugh J, Van Voorhees AS, Nijhawan RI, Bagel J, Lebwohl MG, Blauvelt A, et al. The risk of cardiovascular disease in patients with psoriasis. J Am Acad Dermatol. 2014;70:168-77.

28.Zafiriou E, Fotis L, Arida A, Sfikakis PP, Liossis SN. Comorbidities in psoriasis. Reumatologia. 2021;59:369-73.

29.Cohen AD, Dreiher J, Birkenfeld S. Psoriasis associated with ulcerative colitis and Crohn’s disease. J Eur Acad Dermatol Venereol. 2009;23:561-5.

30.Pérez-Bernal A, Muñoz-Pérez MA, Camacho F. Management of facial hyperpigmentation. Am J Clin Dermatol. 2000;1:261-8.

31.Sharquie KE, Abdulwahhab WS, Sharquie IK. Black hair dye dermatitis is a major cause of concealed facial melanosis in patients with dark complexion. J Pak Assoc Dermatol. 2024;34:474-9.

32.Chang M. Disorders of hyperpigmentation. In:Bolognia JL, Schaffer JV, Cerroni L, Heymann WR, Callen JP, Horn TD, et al., editors. Dermatology. 2nd ed. Elsevier;2012. 1052.

33.Ke Y, Dang E, Shen S, Zhang T, Qiao H, Chang Y, et al. Semaphorin4D drives CD8(+) T-cell lesional trafficking in oral lichen planus via CXCL9/CXCL10 upregulations in oral keratinocytes. J Invest Dermatol. 2017;137:2396-406.

34.Yamauchi M, Moriyama M, Hayashida JN, Maehara T, Ishiguro N, Kubota K, et al. Myeloid dendritic cells stimulated by thymic stromal lymphopoietin promote Th2 immune responses and the pathogenesis of oral lichen planus. PLoS One. 2017;12:e0173017.

35.Farid C, Sheikh WE, Swelem R, El-Ghitany E. Frequency of FOXP3+regulatory T-cells in the blood of chronic hepatitis C patients with immune-mediated skin manifestations;relationship to hepatic condition and viral load. Clin Lab. 2016;62:2339-48.

36.Zhang J, Tan YQ, Wei MH, Ye XJ, Chen GY, Lu R, et al. TLR4-induced B7-H1 on keratinocytes negatively regulates CD4(+) T cells and CD8(+) T cells responses in oral lichen planus. Exp Dermatol. 2017;26:409-15.

37.Javvadi LR, Parachuru VP, Milne TJ, Seymour GJ, Rich AM. Regulatory T-cells and IL17A (+) cells infiltrate oral lichen planus lesions. Pathology. 2016;48:564-73.

38.Tan YQ, Zhang J, Du GF, Lu R, Chen GY, Zhou G. Altered autophagy-associated genes expression in T cells of oral lichen planus correlated with clinical features. Mediators Inflamm. 2016;2016:1-5.

39.Yang JG, Sun YR, Chen GY, Liang XY, Zhang J, Zhou G. Different expression of MicroRNA-146a in peripheral blood CD4(+) T cells and lesions of oral lichen planus. Inflammation. 2016;39:860-6.

40.Wang H, Zhang D, Han Q, Zhao X, Zeng X, Xu Y, et al. Role of distinct CD4(+) T helper subset in the pathogenesis of oral lichen planus. J Oral Pathol Med. 2016;45:385-93.

41.Wang H, Bai J, Luo Z, Fu J, Wang H, Sun Z. Overexpression and varied clinical significance of Th9 versus Th17 cells in distinct subtypes of oral lichen planus. Arch Oral Biol. 2017;80:110-6.

42.Qian H, Jiao L, Fan Z, Wang L, Liu B, Miao G. Analysis of immunologic function changes in lichen planus after clinical treatment. Med Sci Monit. 2018;24:8716-21.

43.Sharquie KE, Noaimi AA. Upsurge of cases of lichen planus in Iraqi population in Baghdad city with frequency of hepatitis viruses. J Dermatol Case Rep. 2015.

44.BachaspatiMayum R, Adavi V, Guite Z, Bipin T. Eruptive actinic lichen planus:A case report. Int J Adv Res. 2015;3:445-7.

45.Bouassida S, Ben Romdhane F, El Goulli A. Actinic lichen planus:32 cases. Ann Dermatol Venereol. 1998;125:408-13.

Notes

Source of Support: This article has no funding source.

Conflict of Interest: The authors have no conflict of interest to declare.

Copyright by authors of this article. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Request permissions
If you wish to reuse any or all of this article please use the e-mail (contact@odermatol.com) to contact with publisher.

Related Content:

Related Articles Search Authors in

http://orcid.org/0000-0002-0265-2040
http://orcid.org/0000-0002-1234-704X
http://orcid.org/0000-0002-4953-7365

Rights and permissions

This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License.

Comments are closed.