Psoriasis, Pityriasis Alba, and Vitiligo
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Our Dermatology Online Review Article PPsoriasis,soriasis, ppityriasisityriasis aalba,lba, aandnd vvitiligoitiligo ((PPV)PPV) aarere a ttriadriad ooff oonene ddisease:isease: NNewew oobservationbservation Khalifa E. Sharquie1,2, Inas K. Sharquie3, Ali N. Al Hamza2,4 1Department of Dermatology, College of Medicine, University of Baghdad, Iraq, 2Deprtment of Dermatology, Medical City Teaching Hospital, Baghdad, Iraq, 3Department of Microbiology & Immunology, College of Medicine, University of Baghdad, Baghdad, Iraq, 4College of Medicine/ University of Basrah, Iraq Corresponding author: Ali N. Al Hamza, MBChB, MS, E-mail: [email protected] ABSTRACT Keratinocytes and melanocytes live in the epidermis, which is considered to be a very good environment for both. Therefore, any change in this regard will affect the function of both of them. Keratinocytes form the main bulk of the epidermis and are the only melanin storage as the dendrites of the basal melanocytes run between keratinocytes and gift melanin granules to surrounding keratinocytes. Consequently, any immunoinflammatory reaction in the epidermis will influence the function of both of them. Recent evidence has shown that psoriasis, pityriasis alba, and vitiligo are closely related diseases and might reflect one etiopathogenesis initially targeting the hair follicles and then extending into the epidermis proper. Hence, the three diseases form one condition: the so-called PPV triad. Consequently, the objective of the following work is to show how these three skin problems are closely related clinically, immunologically, and pathologically, thus constituting the PPV triad. Key words: Psoriasis; Pityriasis alba; Vitiligo; PPV Sharquie triad; Follicular leukoderma EPIDEMIOLOGY AND itself with hyperplasia, rapid turnover, and intensified PATHOPHYSIOLOGY OF PSORIASIS mitosis [4]. Psoriatic skin turnover occurs every 3–4 days [5] leading to keratinocyte hyperproliferation, Psoriasis is a common chronic inflammatory skin which is a characteristic feature of psoriasis. Several disease affecting 1–3% of the population [1]. Psoriasis cell types and cell–cell interactions have been involved vulgaris, the most common variant, characterized in the disease process, including keratinocytes, by scaly erythematous plaques, mainly affects the antigen-presenting cells, Langerhans cells, T cells, epidermis and involves the extensor surfaces, although macrophages, and natural killer cells. In addition, any cutaneous site may be affected. Follicular psoriasis, various Th1 cytokines, keratinocyte growth factor although common, is not well recognized in the (KGF), vascular endothelial growth factor (VEGF), dermatological literature [2]. This could be explained and interleukins are suggested to play a role in by the fact that the initial event in the clinical psoriasis pathogenesis [6]. picture of psoriasis is minute or even microscopic, a transient lesion affecting the upper stable segment of On the other hand, the genetic role is considered hair follicles and progressing into ordinary psoriasis from the observation of a high concordance rate in (Figs. 1 and 2). Psoriasis is a multifactorial disease monozygotic twins (63–73%) compared to a lower with a complex pathogenesis. Normally, the skin rate in dizygotic twins (17–20%). There is considerable epidermis shows regular and constant turnover, heterogeneity in psoriasis, and different genetic loci occurring every 26–28 days [3]. In comparison to a have been identified (PSORS1–10) [7,8], although normal skin epidermis, a psoriatic epidermis manifests psoriasis susceptibility locus 1 (PSORS1) remains the How to cite this article: Sharquie KE, Sharquie IK, Al Hamza AN. Psoriasis, pityriasis alba, and vitiligo (PPV) are a triad of one disease: New observation. Our Dermatol Online. 2021;12(3):314-323. Submission: 02.08.2020; Acceptance: 01.11.2020 DOI: 10.7241/ourd.20213.21 © Our Dermatol Online 3.2021 314 www.odermatol.com most determinant genetic factor, accounting for 50% and IL-17 blockade [15]. Lande et al. identified the role of genetic variance in psoriasis [9,10]. of LL-37 in breaking innate tolerance to self-DNA as a fundamental player in the autoimmunological process THE ROLE OF KERATINOCYTES IN of psoriasis. They found that LL-37 converts self-DNA PSORIASIS ETIOPATHOGENESIS into a potent trigger for INF production by forming aggregates and condensed structures that stimulate The exact sequence of events in the initiation of psoriasis plasmacytoid dendritic cells (pDCs) through toll-like remains unknown. Although activated T lymphocytes receptor 9 TLR9 [16,17]. Also, LL-37 binds to self-RNA and IL-17 are crucial to the development and persistence and activates myeloid dendritic cells (mDC) through of psoriatic lesions. The pathophysiology of psoriasis TLR7 and TLR8 in psoriatic lesions, leading to IL-6 cannot be explained merely by T lymphocytes as other and TNF production and differentiation of mDCs into skin-resident cells, such as keratinocytes and dendritic mature DCs [18]. cells, are also involved [11]. The epidermal skin plays a significant role in early skin lesions by activation and Furthermore, as keratinocyte autocrine stimulation recruitment of immune and inflammatory cells. The by IL-1 exists in the epidermis, an experimental psoriatic auto-antigen loop concept is considered in the aberration of this highly controlled autocrine function pathogenesis of psoriasis [11]. Antimicrobial peptide has been tested using double transgenic mice, which LL37 (cathelicidin) is overexpressed in psoriatic skin show overexpression of the functional IL-1 receptor and triggers the activation of innate immune cells. and 17 kD IL-1α in basal keratinocytes. It has been It has been found that 2/3 of moderate-to-severe found that IL-1 has the ability to cross the basement psoriatic patients have LL-37–specific CD4 and/or membrane and activate dermal cells in addition CD8 T lymphocytes, which can produce INF-ɣ and to activating nearby cells such as keratinocytes, Th-17 cytokines. The presence of LL-37–specific T Langerhans cells, and melanocytes. Also, it leads to cells in circulation correlates significantly with the disease process [12]. ADAMTSL5 (A disintegrin and a wide variety of secondary responses, including the metalloprotease domain containing thrombospondin induction of secondary cytokines such as IL-6 and type 1 motif-like 5), which is a melanocyte-derived GM-CSF, leading to epidermal hyperplasia and dermal protein, has also been observed to be strongly expressed inflammatory cell infiltrate [19]. in keratinocytes throughout the epidermis along with scattered expression in some dermal blood vessels and The characteristic histopathological findings of other perivascular dermal cells in psoriasis [13]. This psoriasis include uniform elongation of the rete protein has recently been implicated as an activating ridges, thinning of the suprapapillary plate, dilated antigen for IL-17–producing T cells in psoriasis [14]. blood vessels, intermittent parakeratosis, neutrophil Both LL-37 and ADAMTSL5 autoantigens are aggregates in the epidermis, and perivascular infiltration downregulated following treatment with etanercept of lymphocytes [20]. Figure 1: A 25-year-old male patient with follicular psoriasis involving Figure 2: A 23-year-old male patient with follicular plaques of psoriasis the trunk. involving the back. © Our Dermatol Online 3.2021 315 www.odermatol.com VITILIGO: EPIDEMIOLOGY AND significantly higher than the normal skin control and FOLLICULAR LEUKODERMA are markedly higher in stage-one vitiligo specimens. This staging of pigmentation loss may be observed Vitiligo is an acquired depigmenting skin disorder affecting the scalp hair as, in stage one, the hair appears affecting approximately 1% of the population blonde because of the partial melanin loss (Fig. 5). worldwide, and is considered one of the most common dermatoses [21]. Generally, two major Etiology of Vitiligo types of vitiligo are categorized clinically. The more common type is the nonsegmental, or generalized, The etiology of vitiligo is complex and the available data variant, which has a gradual onset of symmetrical and supports the development of autoimmune phenomena nondermatomal distribution. The less common variant in genetically predisposed individuals [25]. Several is the segmental vitiligo, which has a rapid onset and theories have emerged to explain the pathogenesis of unilateral semidermatomal distribution and stabilizes vitiligo, mainly including autoimmune, autodestructive, once fully developed [22]. Follicular vitiligo is not an and neurohormonal theories [26-28]. Other studies uncommon variant, commonly seen in segmental and have suggested a convergence theory, which claims nonsegmental vitiligo [23]. Sharquie et al. observed that, in addition to the aforementioned theories, that all types of vitiligo begin in the upper stable melanocytorrhagy, impaired melanocyte migration, and segment of hair follicles, and the initial lesions, similarly an altered cellular environment each contribute to the to psoriasis, may be minute or even microscopic disease process and none is mutually exclusive [29]. and transient, leading to follicular leukoderma and progressing into ordinary vitiligo (Fig. 3). In the case of graying of hair, the loss of melanocytes is from the hair matrix, while in ordinary vitiligo, the loss of melanocytes is from the infundibulum and the basal layer of the epidermis. Another uncommon subtype is mucosal vitiligo, with a restricted involvement