Psoriasis is not optimally controlled in spite of newly developed treatments, possibly due to the difficulty of objectively quantifying the disease’s severity, considering the limitations of the clinical scores used in clinical practice. A major challenge addresses difficult-to-treat areas, especially in the absence of significant body surface involvement. It is controversial whether the severity evaluation of patients with several affected areas (having at least one difficult-to-treat area) should be done differently from current methods. Scores used for special areas (PSSI, NAPSI and ESIF) allow an accurate assessment of disease severity in difficult-to-treat areas, but the issue of whether to integrate these scores into PASI, BSA or DLQI remains. The review’s purpose resides in providing an overview of the main current issues in determining psoriasis severity in patients with psoriasis in difficult-to-treat areas and suggesting possible solutions for the optimal integration of the area assessment in current scores: severity can be either established according to the highest calculated score (PASI or PSSI or NAPSI or ESIF) or by adding a correction factor in the calculation of PASI for special areas.

Background: Several skin manifestations have been reported since the start of the COVID‐19 pandemic: chilblains‐like, livedoid lesions, urticaria‐like, pseudo‐Kawasaki disease, and others. Histopathologic images of these lesions most often show aspects of endothelitis, images similar to autoimmune vasculitis. Cutaneous lesions are often negative at RT‐PCR for SARS‐CoV‐2 virus.Method and Results: We reviewed recent articles on the mechanisms of COVID‐19 and we synthesized main pathways of inflammatory cascade. After the penetration into the cells of the respiratory epithelium, SARS‐CoV‐2 virus initiates a “cytokine storm” well described in previous publications: the expression of interferon type I (IFN‐I) is one of the key elements of the antiviral response in COVID‐19 patients, IFN‐I expression seems to play an important role in the induction of interleukin 6 (IL‐6), chemotactic factors such as Granulocyte‐Macrophage Colony‐Stimulating Factor (GM‐CSF) and the consequent activation of monocyte‐macrophage system followed by the expression of TNF‐alpha, and finally by the induction of coagulation factors by both extrinsic and intrinsic pathways.Conclusions: The simplified synthesis of the main pathophysiological mechanisms of COVID‐19 could help us to understand at least partially the importance of macrophage activation and its vascular involvement in many skin lesions that remain often negative at in situ tests for SARS‐CoV‐2.

Drug reaction with eosinophilia and systemic symptoms (DRESS) syndrome is a drug reaction commonly related to eosinophilia, from uncertain epidemiology, and without consensus for diagnosis and treatment globally. It presents a great challenge in its management and is characterized by fever, lymphadenopathy, skin rash, and multisystemic involvement. An aggressive and difficult-to-manage clinical case is presented in a 50-year-old man with chronic kidney disease due to diabetes mellitus type 2 and systemic arterial hypertension, who developed an unusual variant similar to DRESS and Stevens–Johnson syndrome (SJS) overlap secondary to allopurinol, with skin manifestations without eosinophilia, but fulfilling clinical and laboratory criteria for DRESS and SJS syndrome.

Stevens–Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) are examples of severe cutaneous adverse reactions to drugs (SCARs) with several international recommendations for global medical management, ranging from pharmacological systemic therapy to skin wound care. There is no defined best management of the skin wounds in SJS/TEN. The care of wounds is essential to initiate re-epithelialization. Our objective is to improve the cicatrization process, avoiding scarring due to deepening of the wounds, as well as prevent infections, achieve pain control, and avoid loss of serum proteins, fluids, and electrolytes. In this retrospective case series, we highlight the value of systemic therapy and the use of silver nitrate for wound management in four patients with TEN.

Skin barrier must be seen as a complex structure with complex functions involving hydrolipidic film, stratum corneum, the intercellular cement and also immunologic barrier as innate adaptive immune system (as Toll Like Receptors - TLR), complement, dendritic cells and antigen-related responses. Skin barrier changes are seen in different skin diseases as atopic dermatitis, rosacea , contact dermatitis and others. In the first part of this article we describe skin physical barrier and its key elements roles (ceramides, filaggrin, tight junctions and claudins), the clinical consequences of barrier damages in different common skin diseases (atopic dermatitis, xeroses of different origins). Immune skin barrier is complex and in this first part of the article we focus only on innate immune system skin represented by Toll Like Receptors and their role in the synthesis of antimicrobial peptides (AMP). In the second part we present ex vivo and in vivo studies on skin physical barrier repair and improvement of AMP expression in human skin by modulating TLR2. The management of human skin barrier damages and their repair by active topicals must by a holistic approach, taking in account the complexity of physical and of immune barriers of the skin.