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. 2022;10(1):10.13188/2373-1044.1000077.
doi: 10.13188/2373-1044.1000077. Epub 2022 Apr 5.

Insights into Lichen Planus Pigmentosus Inversus using Minimally Invasive Dermal Patch and Whole Transcriptome Analysis

Jacob Dickman  1 , Michael Howell  1 , Robert Hoopes  1 , Yipeng Wang  2 , Tobin J Dickerson  2 , Michael Bottomley  3 , H Nicholas Shamma  4   5 , Christine M Rapp  1 , Matthew J Turner  6   7 , Craig A Rohan  1   4 , Jeffrey B Travers  1   4   8
Affiliations

Insights into Lichen Planus Pigmentosus Inversus using Minimally Invasive Dermal Patch and Whole Transcriptome Analysis

Jacob Dickman et al. J Clin Investig Dermatol. 2022.

Abstract

Lichen Planus Pigmentosus inversus (LPPi) is a rare interface and lichenoid dermatitis (ILD) and supposed variant of lichen planus (LP) that presents as well-demarcated brown to grey macules in flexural and intertriginous areas. LPPi is deemed 'inversus' because its anatomical distribution in skin folds is opposite that seen in lichen planus pigmentosus (LPP) whose pigmented lesions arise on sun-exposed skin. Biopsy is required for the clinical diagnosis of all ILDs. Though multiple clinically-oriented studies have reported differences between LPP, LPPi, and LP, few molecular studies have been performed. In this case study, 3 patients, 2 with LPPi and one with LP, provided samples using minimally invasive whole transcriptome analysis using a dermal biomarker patch. This study confirms the involvement of interferon signaling and T-cell activation in LPPi and suggests an expression profile distinct from LP. Specific genes significantly upregulated in LPPi vs LP include an intergenic splice variant of the primary pigmentation determining receptor in humans and dysregulation of genes essential for ceramide synthesis and construction of the cornified envelope. This work expands upon our knowledge of the pathogenesis of LPPi vs LP, and supports the potential use of this technology in the diagnostic clinical setting to mitigate the need for invasive procedures.

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Conflict of interest statement

Conflicts: None of the authors have a conflict of interest with the exceptions of Y.W. and T.D., who are employed by Mindera Corporation.

Figures

Figure 1.
Figure 1.. Clinical and histopathological studies of the LPPi and LP subjects
A. LPPi axilla lesions in Subject #1. B. LPPi groin lesions in Subject #2. C. LPPi lesional biopsy from Subject #2. Note the vacuolar degeneration of the epidermal basal cell layer, band-like lichenoid or perivascular lymphocytic infiltrates in the papillary dermis as well as superficial pigmentary incontinence and melanophages. (20X magnification). D. LP lesions on the right lower extremity. E. LP lesional biopsy. Note the hyperkeratosis, acanthosis, the sawtooth epidermal appearance, and the band-like dermal lymphohistiocytic infiltrate (10X magnification).
Figure 2.
Figure 2.. Heat map of differentially expressed genes with markers grouped by unsupervised hierarchical clustering.
Unit variance is by row; blue color indicates lower mean expression and red color indicates higher mean expression. Columns are non-lesional skin (NLS), Lichen Planus Pigmentosus lesional skin (LPPi), and Lichen Planus lesional skin (LP). Fold changes for lesional (LS) vs NLS as well as LPPi vs LP. *P < 0.05; **P<0.01; *** P<0.001.
Figure 3.
Figure 3.. Volcano plot of differentially expressed genes in LP and LPPi.
Red dots indicate the 543 genes that have a p<0.05, only 15 of these were preferentially expressed in LPPi. Grey dots indicate genes with a less than 1-fold change.
See this image and copyright information in PMC

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