Vitiligo at a keloid scar: A possible case of Koebner phenomenon

Eun, Sung Hye; Lee, Ji Hae; Kim, Gyong Moon; Kim, Ki Ho; Bae, Jung Min

doi:10.1111/1346-8138.14514

Cited by 4 publications

(9 citation statements)

References 6 publications

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“…The common friction or pressure derives from activities in daily life such as wearing watches, necklaces, or belts; brushing hair; and shaving. Interestingly, keloid scar and striae formation due to pregnancy may represent distinctive forms of trauma that cause vitiligo, as they are not sharp or penetrating [39,40]. Additionally, history of sun exposure or virus infection could impose a higher risk of developing the disease, particularly in vitiligo patients with sunburn blistering or hepatitis C virus (HCV) infection [41][42][43][44].…”

Section: Precipitating Factorsmentioning

confidence: 99%

Clinical Features, Immunopathogenesis, and Therapeutic Strategies in Vitiligo

Wang

2021

Clinic Rev Allerg Immunol

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Vitiligo is an autoimmune disease of the skin characterized by epidermal melanocyte loss resulting in white patches, with an approximate prevalence of 0.5-2% worldwide. Several precipitating factors by chemical exposure and skin injury present commonly in patients with vitiligo. Although the diagnosis appears to be straightforward for the distinct clinical phenotype and specific histological features, vitiligo provides many challenges including chronicity, treatment resistance, frequent relapse, associated profound psychosocial effect, and negative impact on quality of life. Multiple mechanisms are involved in melanocyte disappearance, including genetics, environmental factors, and immune-mediated inflammation. Compelling evidence supports the melanocyte intrinsic abnormalities with poor adaptation to stressors leading to instability and release of danger signals, which will activate dendritic cells, natural killer cells, and innate lymphoid cells to initiate innate immunity, ultimately resulting in T-cell mediated adaptive immune response and melanocyte destruction. Importantly, the cross-talk between keratinocytes, melanocytes, and immune cells, such as interferon (IFN)-γ signaling pathway, builds inflammatory loops that give rise to the disease deterioration. Improved understanding of the immune pathogenesis of vitiligo has led to the development of new therapeutic options including Janus kinase (JAK) inhibitors targeting IFN-γ signaling pathways, which can effectively reverse depigmentation. Furthermore, definition of treatment goals and integration of comorbid diseases into vitiligo management have revolutionized the way vitiligo is treated. In this review, we highlight recent developments in vitiligo clinical aspects and immune pathogenesis. Our key objective is to raise awareness of the complexity of this disease, the potential of prospective therapy strategies, and the need for early and comprehensive management.

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Section: Precipitating Factorsmentioning

confidence: 99%

Clinical Features, Immunopathogenesis, and Therapeutic Strategies in Vitiligo

Wang

2021

Clinic Rev Allerg Immunol

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“…The continuous stretching tension in a keloid scar can cause a new vitiliginous patch by weakening the adhesion between melanocytes and keratinocytes. 3 Additionally,…”

Section: Triggering Factorsmentioning

confidence: 99%

“…Physical trauma Trauma [109] Concis [113] Burns [114,115] Freezing [165] Tattoo [116][117][118] UV radiation [102] Facial hair plucking [119] Mechanical stress [57,120] Stretch [15,80,81] Repeated friction or pressure [22] Surgical mask [121,122] Hearing aid [123] Use of computer mouses [124] Keloid/ Hypertrophic scar [3,125,126] Striae distensae [127] Chemical stimulation…”

Section: Triggering Factors Refsmentioning

confidence: 99%

“…It has been known that the true KP occurs in vitiligo, psoriasis and lichen planus, and can be induced by trauma, repeated friction or pressure, scars and tattoos. 2,3 In addition, KP is also instrumental in the occurrence, progression, persistence and relapse of the primary disease. Therefore, it is essential to consider the possibility of KP in patients with skin disorders in order to evaluate disease progression and treatment options and prevent recurrence.…”

Section: Introductionmentioning

confidence: 99%

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Characteristics and pathogenesis of Koebner phenomenon

Zhang

Jiang

et al. 2022

Experimental Dermatology

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The Koebner phenomenon, also known as isomorphic reaction, refers to the development of secondary lesions with the same clinical manifestations and histopathological characteristics as the primary lesions in normal skin after trauma or other stimuli. The triggering factors of Koebner phenomenon include physical trauma, chemical stimulation, mechanical stress, iatrogenic stimulation and pathogenic infection. Vitiligo, psoriasis and lichen planus are considered true Koebner phenomenon. Recent studies have shown that immunological disorders, oxidative stress, defective melanocyte adhesion and growth factor deficiency are the main pathological mechanisms of vitiligo Koebner phenomenon. In psoriasis, triggers may drive skin inflammation to induce a psoriatic phenotype through multiple signalling pathways and thereby cause Koebner phenomenon in susceptible individuals. Significantly, keratinocytes mediate the occurrence of Koebner phenomenon in psoriasis through mechano‐induced signalling pathways after sensing mechanical signals and explains the high frequency of psoriasis lesions on the extensor side of the elbow and knee joints. On the contrary, TRPA1‐driven mechano‐transduction, autoimmunity and actinic damage are the underlying mechanisms of Koebner phenomenon in lichen planus. In this review, we have summarized the current understanding of the characteristics and pathogenesis of Koebner phenomenon.

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“…2 KP following surgical procedures has been reported in vesicular-bullous disorders, Kaposi's sarcoma, psoriasis, necrobiosis lipoidica, lichen sclerosus and atrophicus, angiosarcoma, granuloma anulare, Darier's disease, condyloma acuminatum, sarcoidosis, pyoderma gangrenosum, and vitiligo. [2][3][4] KP in HS has not been described on surgical scars but has been observed in 14 obese patients in whom HS lesions developed on the abdomen as a result of mechanical stress. 5 Other cases of HS that followed mechanical stress, friction, pressure, and radiotherapy have been reported but have not specifically defined as KP.…”

Section: Dear Editorsmentioning

confidence: 99%