ID Design Press, Skopje, Republic of Macedonia Open Access Macedonian Journal of Medical Sciences. 2019 Sep 30; 7(18):2969-2975. https://doi.org/10.3889/oamjms.2019.680 eISSN: 1857-9655 Global Dermatology Immunocompromised Districts of Skin: A Case Series and a Literature Review Aleksandra Vojvodic1, Michael Tirant2,3, Veronica di Nardo2, Torello Lotti2, Uwe Wollina4* 1Department of Dermatology and Venereology, Military Medical Academy of Belgrade, Belgrade, Serbia; 2Department of Dermatology, University of Rome “G. Marconi”, Rome, Italy; 3Hanoi Medical University, Hanoi, Vietnam; 4Department of Dermatology and Allergology, Städtisches Klinikum Dresden, Academic Teaching Hospital, Dresden, Germany Abstract Citation: Vojvodic A, Tirant M, di Nardo V, Lotti T, BACKGROUND: The concept of immunocompromised districts of skin has been developed by Ruocco and helps Wollina U. Immunocompromised Districts of Skin: A Case to explain certain aspects of the macromorphology of skin diseases. This concept unites the isomorphic response Series and a Literature Review. Open Access Maced J Med Sci. 2019 Sep 30; 7(18):2969-2975. of Koebner and the isotopic response of Wolf. https://doi.org/10.3889/oamjms.2019.680 Keywords: Immunocompromised districts of the skin; CASE REPORTS: We present different cutaneous conditions which can lead to immunocompromised districts of Macromorphology of skin diseases; Koebner skin such as scars, radiodermatitis, lymphedema, disturbed innervation or mechanical friction etc. Typical and phenomenon; Wolf’s isotopic response rarer skin disorders associated with them are discussed and illustrated by their observations. *Correspondence: Uwe Wollina. Department of Dermatology and Allergology, Städtisches Klinikum CONCLUSION: At this moment, we wish to inform dermatologists and non-dermatologists about Ruocco’s Dresden, Academic Teaching Hospital, 01067 Dresden, Germany. E-mail: [email protected] concept and its implications. Received: 08-Aug-2019; Revised: 07-Sep-2019; Accepted: 08-Sep-2019; Online first: 10-Sep-2019 Copyright: © 2019 Aleksandra Vojvodic, Michael Tirant, Veronica di Nardo, Torello Lotti, Uwe Wollina. This is an open-access article distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 International License (CC BY-NC 4.0) Funding: This research did not receive any financial support Competing Interests: The authors have declared that no competing interests exist Introduction electrolytes and protein, and failure of the skin barrier function [6]. However, impairment of skin function is quite The skin is one of our main protective tissues often seen in a sectorial area. Different pathways may to support body homeostasis. Protection is generated lead to sectorial skin function impairment such as by the dynamic structure of the outmost part of skin, trauma, infection, or vascular dysfunction. The the stratum corneum, and supported by specific cells sectorial impairment of immune and other functions of such as melanocytes (UV-protection), Langerhans skin has been described by the term Ruocco’s cells (antigen control), Mast cells and macrophages immunocompromised districts (ICD’s) [7]. It unites (innate immunity), lymphocytes (including γδ T cells, different phenomena such as isomorphic (Koebner) innate lymphoid cells - specific immunity), and Merkel and isotopic (Wolf) responses of skin and helps to cells (neuroimmunology). Keratinocytes, sweat glands understand macromorphology of dermatoses. and sebaceous glands are part of the innate immune Although the concept had been developed during the system [1], [2], [3]. last decade, it has yet to gain widespread knowledge Skin failure is one of the most important [8], [9]. causes of mortality in the intensive care units [4], [5]. It In this review article, we will provide a has been defined as loss of temperature control with collection of clinical examples supporting the concept the inability to maintain the core body temperature, ICD from our departments. and failure to prevent percutaneous loss of fluid, _______________________________________________________________________________________________________________________________ Open Access Maced J Med Sci. 2019 Sep 30; 7(18):2969-2975. 2969 Global Dermatology _______________________________________________________________________________________________________________________________ Skin grafts as ICD’s nervous system, innervating peripheral visceral sites. Vagus nerve efferent cholinergic fibres project to visceral organs. Acetylcholine represents the principal Autologous split skin grafts are a mainstay for neuro mediators released from postganglionic fibres. defect closure after trauma and tumour surgery. Split This molecule interacts with G protein-coupled skin is not a primary vascularized graft. Grafts survive muscarinic acetylcholine receptors that mediate initially by the oxygen supply from the wound bed. among others exocrine function of skin glands. The Skin grafts have to establish their blood availability of molecular sensors for detecting vascularisation. Grafts are not passive but can secrete pathogen fragments and inflammatory molecules on soluble mediators involved in wound healing [10]. both neurons and immune cells allows their During the first 48 h after transplantation, the graft is simultaneous involvement in inflammatory responses bulged by plasmatic fluid. Neo-angiogenesis leads to [21]. If neural components are impaired, this will harm improved supply of oxygen and nutrients. Pre- the control of tissue homeostasis vascularization of grafts further enhances therapeutic The infrapatellar branches of the saphenous effects [11]. nerve may be damaged by either trauma or surgery Graft-associated wound healing may show with resultant anterior or anteromedial pain and an some peculiarities compare to “normal” wound associated lateral area of altered sensation. The healing. For instance, there is no involvement of acronym SKINTED (surgery of the knee, injury to the sweat gland progenitors in grafts [12]. Skin grafts are infrapatellar branch of the saphenous nerve, traumatic not primarily vascularized. Both T and B lymphocytes, eczematous dermatitis) describes the eruption of natural killer cells, and last not least antigen- eczematous lesions in the skin after total knee presenting cells will infiltrate the graft only after endoprosthesis [22]. successful neovascularisation. This results in changes Acquired nevoid telangiectasia results from a of local immunity, as demonstrated by case reports on segmental dilatation of papillary plexus vessels. It is localised bullous pemphigoid in sites of grafting [13]. asymptomatic. The disease indicates spinal or Nevertheless, split skin grafts preserve peculiarities of neuromuscular complaints with disturbed autonomic functionality for a long period [14]. vascular nerve function (Figure 1) [23]. The occurrence of eczema restricted donor sites of split skin grafts has rarely been observed [15], [16], [17]. Eczema or atopic dermatitis is a common disease. The basic pathogenetic mechanism is disturbances of skin barrier function, dysregulated immune response, and disturbances of gut and skin associated microbiome. The leading symptom is itch [18], [19], [20]. Split skin grafts are characterised by a barrier function impairment, demonstrated by increased transepidermal water loss (TEWL) [14]. In split skin grafts, cutaneous adnexae such as hair follicles, sebaceous and sweat glands are absent. Sweat and sebaceous glands, however, are involved in innate immunity and regulate skin hydration among other Figure 1: Acquired nevoid telangiectasia functions. This creates a certain vulnerability. In addition to trauma, infections of the nervous system have to be considered as a cause of ICD. Herpes zoster is caused by the varicella-zoster Disturbances of local innervation as a virus (VZV or herpes virus type 3). The primary cause of ICD – SKINTED and acquired infection leads to varicella. During the viraemic period nevus teleangiectaticus of primary infection, VZV infects sensible dorsal spinal nerve ganglia and/or cephalic nerve ganglia. VZV lies dormant in the nervous system – neurons and glia Sympathetic neurons localised in the spinal satellite cells – for years. Endogenous reactivation of cord project to paravertebral or prevertebral ganglia viral infection occurs after impairment of immune and synapse with relatively long postganglionic fibres surveillance. Herpes zoster temporarily alters the innervating blood vessels, lymphoid tissue and function of neurons and ganglia leading to a painful organs. The vagus nerve, with cell bodies residing in inflammatory response [24]. the brainstem medulla oblongata, is the main nerve of Wolf’s isotopic response describes the onset the parasympathetic division of the autonomic of secondary skin disease on the site of healed _______________________________________________________________________________________________________________________________ 2970 https://www.id-press.eu/mjms/index Vojvodic et al. Immunocompromised Districts of Skin: A Case Series and a Literature Review _______________________________________________________________________________________________________________________________ herpetic lesions [25], [26]. We observed the and periods of a rapid increase of body weight or development of hypertrophic scars and keloids four muscle mass. They are characterised by disturbances weeks after herpes zoster infection in a 28-year-old in the connective tissue and increased