Adverse drug reactions involving the skin are commonly known as drug eruptions. Severe drug eruption may cause severe cutaneous adverse drug reactions (SCARs), which are considered to be fatal and life-threatening, including Stevens-Johnson syndrome (SJS), toxic epidermal necrolysis (TEN), acute generalized exanthematous pustulosis (AGEP), and drug reaction with eosinophilia and systemic symptoms (DRESS). Although cases are relatively rare, approximately 2% of hospitalized patients are affected by SCARs. There is an incidence of 2 to 7 cases/million per year of SJS/TEN and 1/1000 to 1/10,000 exposures to offending agents result in DRESS. However, the mortality rate of severe drug eruptions can reach up to 50%. SCARs represent a real medical emergency, and early identification and proper management are critical to survival. The common pathogenesis of severe drug eruptions includes genetic linkage with HLA-and non-HLA-genes, drug-specific T cell-mediated cytotoxicity, T cell receptor restriction, and cytotoxicity mechanisms. A multidisciplinary approach is required for acute management. Immediate withdrawal of potentially causative drugs and specific supportive treatment is of great importance. Immunoglobulins, systemic corticosteroids, and cyclosporine A are the most frequently used treatments for SCARs; additionally, new biologics and plasma exchange are reasonable strategies to reduce mortality. Although there are many treatment methods for severe drug eruption, controversies remain regarding the timing and dosage of drug eruption. Types, dosages, and indications of new biological agents, such as tumor necrosis factor antagonists, mepolizumab, and omalizumab, are still under exploration. This review summarizes the clinical characteristics, risk factors, pathogenesis, and treatment strategies of severe drug eruption to guide clinical management. Keywords Severe drug eruption • Stevens-Johnson syndrome • Toxic epidermal necrolysis • Acute generalized exanthematous pustulosis • Drug reaction with eosinophilia and systemic symptoms Abbreviations AGEP Acute generalized exanthematous pustulosis ALT Alanine aminotransferase APCs Antigen-presenting cells AST Aspartate aminotransferase CBZ Carbamazepine CCR CC-chemokine receptor COVID-19 Coronavirus disease 2019 CTL Cytotoxic T cells CXCR CXC chemokine receptor DiHS
Vitiligo is a common acquired depigmenting disease characterized by the loss of functional melanocytes and epidermal melanin. Vitiligo has a long treatment cycle and slow results, which is one of the most difficult challenges for skin diseases. Oxidative stress plays an important role as an initiating and driving factor in the pathogenesis of vitiligo. Antioxidant therapy has recently become a research hotspot in vitiligo treatment. A series of antioxidants has been discovered and applied to the treatment of vitiligo, which has returned satisfactory results. This article briefly reviews the relationship between oxidative stress and vitiligo. We also describe the progress of targeted antioxidant therapy in vitiligo, with the aim of providing a reference for new drug development and treatment options for this condition.
Isorhamnetin (ISO) is a methylated flavonol present in the leaves, flowers, and fruits of many plants with antitumour, anti-inflammatory, antioxidant, and anti-apoptotic properties. ISO has been suggested as the active substance in Vernonia anthelmintica (L.) to treat vitiligo. However, the mechanisms underlying its effects remain unclear. In this study, human keratinocytes (HaCaT cells) were pre-treated with or without ISO and then stimulated with hydrogen peroxide (H2O2) to generate oxidative damage. Pre-treatment with ISO increased HaCaT cell viability, reduced malondialdehyde content, and enhanced superoxide dismutase activity, resulting in a reduction in the loss of mitochondrial membrane potential, improved cell morphological damage, and apoptosis inhibition. Furthermore, we identified 51 significantly dysregulated differentially expressed genes (DEGs) of HaCaT cells treated with ISO using RNA-sequencing. Enrichment analysis using Gene Ontology and Kyoto Encyclopedia of Genes and Genomes databases indicated that the protective effect of ISO could be related to its effects on the Wnt signalling pathway. Our study provides novel insights into key gene regulation in the progression of oxidative damage and the mechanisms of action of ISO.
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