Tofacitinib in Hypertrophic Lichen Planus

Seiringer, Peter; Lauffer, Felix; Pilz, Anna Caroline; Boehmer, Danielle Franziska; Biedermann, Tilo; Eyerich, Kilian

doi:10.2340/00015555-3585

Cited by 25 publications

(21 citation statements)

References 6 publications

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“…The JAK/STAT pathway, a pathway used by several inflammatory cytokines to downstream their inflammatory signal, gained attention as a potential therapeutic target [136]. First results coming from small case series and case reports showed efficacy in LPP [135, 137] and hypertrophic CLP [138]. In these first three reports, LP has been treated with tofacitinib, a JAK1/2 inhibitor already approved in the treatment of psoriatic arthritis and rheumatoid arthritis [139, 140].…”

Section: Management Of Lichen Planusmentioning

confidence: 99%

Lichen planus – a clinical guide

Solimani

Forchhammer

Schloegl

et al. 2021

J Deutsche Derma Gesell

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Summary Lichen planus (LP) is a chronic lichenoid inflammatory disorder of the skin, mucosa and of the appendages. LP is classically characterized by the presence of a rich infiltration of inflammatory T cells, which migrate in the upper part of the dermis, arranged in a band‐like pattern. Different sub types of the disease have been so far described. Albeit LP is clinically well defined, the disease still represents a therapeutic enigma. Especially with regard to mucosal or scalp affecting LP types, which often present a recalcitrant and treatment unresponsive course, efficacious therapeutic options are still lacking. Thus, LP represents a disease with a high psychosocial burden. Yet, development in the deciphering of LP pathogenesis reveals possible new druggable targets, thus paving the way for future therapeutic options. In this clinical guide, we summarize the current clinical knowledge and therapeutic standards and discuss the future perspective for the management of LP.

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Section: Management Of Lichen Planusmentioning

confidence: 99%

Lichen planus – a clinical guide

Solimani

Forchhammer

Schloegl

et al. 2021

J Deutsche Derma Gesell

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“…In addition, an increased expression IFN-γ and IL-17 in the skin of LP lesions has been described (81,90)-albeit some other studies refuted these observations (91). Case reports indicated that off-label treatment of LP with Janus kinase (JAK) inhibitors (JAKi), such as tofacitinib, led to marked improvement of the disease (92)(93)(94). As IFN-γ-induced signaling centers on the activation of JAK (95), IFN-γ and JAK are likely to be central to the pathogenesis of LP.…”

Section: Cellular and Molecular Pathogenesismentioning

confidence: 99%

Lichen Planus

et al. 2021

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Lichen planus (LP) is a T cell-mediated disease affecting the stratified squamous epithelia of the skin and/or mucus membrane. Histologically, the disease is characterized by a lichenoid inflammatory infiltrate and vacuolar degeneration of the basal layer of the epidermis. LP has three major subtypes: Cutaneous, mucosal and appendageal LP. Rarely, it may affect the nails in the absence of skin and/or mucosal changes. LP may also be induced by several drugs, typically anti-hypertensive medication or be associated with infections, particularly viral hepatitis. The diagnosis is based on the clinical presentation and characteristic histological findings. Although the disease is often self-limiting, the intractable pruritus and painful mucosal erosions result in significant morbidity. The current first-line treatment are topical and/or systemic corticosteroids. In addition, immunosuppressants may be used as corticosteroid-sparing agents. These, however are often not sufficient to control disease. Janus kinase inhibitors and biologics (anti-IL-12/23, anti-IL17) have emerged as novel future treatment options. Thus, one may expect a dramatic change of the treatment landscape of LP in the near future.

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“…To date, three patients with ELP and one patient with hypertrophic LP showed excellent responses to tofacitinib, a JAK1 and JAK3 inhibitor [4,5], which also showed good results in a series of ten patients with lichen planopilaris [6]. However, it is unclear which JAK subtypes contributed to this therapeutic effect.…”

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confidence: 99%