Exacerbation of Psoriasis Following COVID-19 Vaccination: Report From a Single Center

The temporal association had been reported between vaccination and exacerbation of psoriasis, and episodes of psoriasis flare-up have recently been attributed to COVID-19 vaccines. We recruited 32 unimmunized controls and 51 vaccinated psoriasis patients, 49 of whom were under biological therapy, with regular clinic visits receiving a total of 63 shots of vaccines, including 30 doses of Moderna mRNA-1273 and 33 doses of AstraZeneca-Oxford AZD1222. Fifteen episodes of exacerbation attacked within 9.3 ± 4.3 days, which is higher than two episodes in the control group (p = 0.047). The mean post-vaccination severity of the worsening episodes increased from PASI 3.1 to 8.0 (p < 0.001). Three patients showed morphologic change from chronic plaque-type to guttate psoriasis. Deterioration of psoriasis following COVID-19 vaccination was not associated with age, sex, disease duration, psoriatic arthritis, family history of psoriasis, history of erythroderma, current biologics use, comorbidities, vaccine types, human leukocyte antigen (HLA)-C genotypes, baseline PASI nor pre-vaccination PASI. For those who received two doses of vaccination, all but one patient aggravated after the first shot but not the second. The mechanism of psoriasis exacerbation in immunized individuals is unclear, but Th17 cells induced by COVID-19 vaccines may play a role. In the pandemic era, psoriasis patients and physicians should acknowledge the possibility of fluctuation of disease activity when vaccinated against COVID-19. Nevertheless, compared to a treatable dermatologic disease with rapid resolution of exacerbation, psoriasis patients who do not have contraindications to vaccination should benefit from COVID-19 vaccines in the prevention of severe COVID-19 infection and fatality.

Clinicoprognostic and Histopathological Features of Guttate and Plaque Psoriasis Based on PD-1 Expression

Several studies have determined the correlation between programmed cell death protein-1 (PD-1) and chronic plaque psoriasis (CPP). However, limited studies have assessed the association between PD-1 expression and the clinicoprognostic and distinct clinicopathological characteristics of CPP and guttate psoriasis (GP). Twenty-nine patients with skin biopsy-confirmed CPP were recruited at the Asan Medical Center between January 2018 and June 2020, and 33 patients with biopsy-confirmed GP were enrolled between January 2002 and June 2020. The clinicoprognostic and histopathological characteristics were analyzed according to immunohistochemical PD-1 expression in the epidermal or dermal inflammatory infiltrates. The CPP and GP lesions were divided into PD-1-low and PD-1-high groups. The CPP epidermal PD-1-high group had typical histopathological changes and significantly higher psoriasis area and severity index scores (p = 0.014) and disease duration (p = 0.009) than the epidermal PD-1-low group. In patients with GP, compared with the dermal PD-1-high group, the dermal PD-1-low group exhibited significantly higher disease duration (p = 0.002) and relapse rate of plaque psoriasis (p = 0.005) and significantly lower relapse-free survival (p = 0.016). Upregulated epidermal PD-1 expression was correlated with the chronicity and severity of CPP, while downregulated dermal PD-1 expression was correlated with poor prognosis of GP.

A Novel Light Weight Approach For Identification of Psoriasis Affected Skin Lesion Using Deep Learning.

Psoriasis is a skin disorder which affects the people physically, mentally and emotionally. It is characterized as rough elevated scaly skin which is evident from surrounding skin area. There are various types of psoriasis which include plaque psoriasis, nail psoriasis, guttate psoriasis, inverse psoriasis, pustular psoriasis, erythrodermic psoriasis and psoriatic arthritis. The common trend observed is that the people tend to face difficulties in differentiating and tracking the disorder which will worsen the situation of the affected skin. It is essential to keep track of the affected skin for the prognosis of the disorder. In this work, an attempt is made to identify the psoriasis affected area automatically using MobileNet machine learning model which will become an objective tool in accurate identification of the disorder which in turn helps in effective treatment of the disorder.

Human CLA+ Memory T Cell and Cytokines in Psoriasis

Psoriasis is a common inflammatory skin condition resulting from the interplay between epidermal keratinocytes and immunological cellular components. This sustained inflammation is essentially driven by pro-inflammatory cytokines with the IL-23/IL-17 axis playing a critical central role, as proved by the clinical efficacy of their blockade in patients. Among all the CD45R0+ memory T cell subsets, those with special tropism for cutaneous tissues are identified by the expression of the Cutaneous Lymphocyte-associated Antigen (CLA) carbohydrate on their surface, that is induced during T cell maturation particularly in the skin-draining lymph nodes. Because of their ability to recirculate between the skin and blood, circulating CLA+ memory T cells reflect the immune abnormalities found in different human cutaneous conditions, such as psoriasis. Based on this premise, studying the effect of different environmental microbial triggers and psoriatic lesional cytokines on CLA+ memory T cells, in the presence of autologous epidermal cells from patients, revealed important IL-17 cytokines responses that are likely to enhance the pro-inflammatory loop underlying the development of psoriatic lesions. The goal of this mini-review is to present latest data regarding cytokines implicated in plaque and guttate psoriasis immunopathogenesis from the prism of CLA+ memory T cells, that are specifically related to the cutaneous immune system.

A Guttate Psoriasis That Tends to Spare Three Tattoos: A Macrophage Liaison

Induction of new psoriasis sites was reported in only a small amount of psoriasis patients undergoing tattooing, despite the intuitive belief that tattoo trauma might awaken the disease due to the isomorphic phenomenon of Koebner. In this case report, we discuss a patient who presented with a remarkable sparing of his three tattoo sites during a guttate psoriasis flare-up that was unrelated to tattooing. The spatial concordance of tattoo and psoriasis lesions was analyzed on clinical pictures of tattoo sites taken during the psoriasis episode. For the quantification of the spatial distribution of the psoriasis lesions, Voronoi diagrams were generated, and coefficients of variation and the two-sample t-test were employed to compare the distributions of Voronoi patch sizes in different settings. Compared to skin areas without tattoos, a tattoo introduced a higher variation in the sizes of the Voronoi patches centered around psoriasis lesions. Based on our findings, we would like to discuss the possible role of macrophages as the key cellular link in the complex pathophysiologic relationship between tattooing/tattoo and psoriasis. Taking into account the relationship of autophagy and psoriasis lesions, we propose the hypothesis that tattoos represent a “psoriasis-hostile” tissue environment pertained by a population of LAP active M2-polarized macrophages. Further clinical studies of the relationship of psoriasis lesions to the tattooed skin are needed and may provide important insights into the role of macrophages in the pathogenesis of psoriasis.