Pharmacogenomics of Hypersensitivity to Non-steroidal Anti-inflammatory Drugs

Trinh, Hoang Kim Tu; Pham, Duy Le; Le, Kieu Minh; Park, Hae‐Sim

doi:10.3389/fgene.2021.647257

Cited by 8 publications

(6 citation statements)

References 119 publications

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“…Overexpression of COX-2 can lead to increased production of prostaglandins, promoting inflammation and vasodilation. 50,51 In CU, up-regulated PTGS2 contributes to the vasodilation, edema, and itching associated with urticarial reactions.…”

Section: Discussionmentioning

confidence: 99%

“…PTGS2 encodes the COX‐2 enzyme, which is involved in the production of prostaglandins (molecules that mediate inflammation and various physiological processes). Overexpression of COX‐2 can lead to increased production of prostaglandins, promoting inflammation and vasodilation 50,51 . In CU, up‐regulated PTGS2 contributes to the vasodilation, edema, and itching associated with urticarial reactions.…”

Section: Discussionmentioning

confidence: 99%

“…Overexpression of COX‐2 can lead to increased production of prostaglandins, promoting inflammation and vasodilation. 50 , 51 In CU, up‐regulated PTGS2 contributes to the vasodilation, edema, and itching associated with urticarial reactions. ICAM1 (Intercellular Adhesion Molecule 1) is involved in cell adhesion and migration, critical for immune cell interactions and inflammatory responses.…”

Section: Discussionmentioning

confidence: 99%

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Identification of key genes and molecular mechanisms of chronic urticaria based on bioinformatics

Guo,

et al. 2024

Skin Research and Technology

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Chronic urticaria (CU) is characterized by persistent skin hives, redness, and itching, enhanced by immune dysregulation and inflammation. Our main objective is identifying key genes and molecular mechanisms of chronic urticaria based on bioinformatics. We used the Gene Expression Omnibus (GEO) database and retrieved two GEO datasets, GSE57178 and GSE72540. The raw data were extracted, pre‐processed, and analyzed using the GEO2R tool to identify the differentially expressed genes (DEGs). The samples were divided into two groups: healthy samples and CU samples. We defined cut‐off values of log2 fold change ≥1 and p < .05. Analyses were performed in the Kyoto Encyclopaedia of Genes and Genomes (KEGG), the Database for Annotation, Visualization and Integrated Discovery (DAVID), Metascape, Search Tool for the Retrieval of Interacting Genes/Proteins (STRING) and CIBERSOFT databases. We obtained 1613 differentially expressed genes. There were 114 overlapping genes in both datasets, out of which 102 genes were up‐regulated while 12 were down‐regulated. The biological processes included activation of myeloid leukocytes, response to inflammations, and response to organic substances. Moreover, the KEGG pathways of CU were enriched in the Nuclear Factor‐Kappa B (NF‐kB) signaling pathway, Tumor Necrosis Factor (TNF) signaling pathway, and Janus kinase/signal transducers and activators of transcription (JAK‐STAT) signaling pathway. We identified 27 hub genes that were implicated in the pathogenesis of CU, such as interleukin‐6 (IL‐6), Prostaglandin‐endoperoxide synthase 2 (PTGS2), and intercellular adhesion molecule‐1 (ICAM1). The complex interplay between immune responses, inflammatory pathways, cytokine networks, and specific genes enhances CU. Understanding these mechanisms paves the way for potential interventions to mitigate symptoms and improve the quality of life of CU patients.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Identification of key genes and molecular mechanisms of chronic urticaria based on bioinformatics

Guo,

et al. 2024

Skin Research and Technology

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“…NSAIDs also cause hypersensitivity reactions in patients, which can result in anaphylaxis and death [ 37 ]. The indiscriminate use of NSAIDs has stimulated the search for new therapeutic methods and medicinal plants represent a reservoir of chemical compounds that show strong potential in the development and production of new and effective drugs [ 38 ].…”

Section: Discussionmentioning

confidence: 99%

Mass Spectrometric Identification of Licania rigida Benth Leaf Extracts and Evaluation of Their Therapeutic Effects on Lipopolysaccharide-Induced Inflammatory Response

et al. 2022

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Licania rigida Benth has been evaluated as an alternative drug to treat diseases associated with inflammatory processes. This study evaluated the anti-inflammatory effects of aqueous and hydroalcoholic leaf extracts of L. rigida with inflammation induced by lipopolysaccharides in in vitro and in vivo inflammation models. The phytochemical profile of the extracts, analyzed by ultra-fast liquid chromatography coupled with tandem mass spectrometry, revealed the presence of gallic and ellagic acids in both extracts, whereas isovitexin, ferulate, bulky amino acids (e.g., phenylalanine), pheophorbide, lactic acid, and pyridoxine were detected in the hydroalcoholic extract. The extracts displayed the ability to modulate in vitro and in vivo inflammatory responses, reducing approximately 50% of pro-inflammatory cytokine secretion (TNF-α, IL-1β, and IL-6), and inhibiting both NO production and leukocyte migration by approximately 30 and 40% at 100 and 500 µg/mL, respectively. Overall, the results highlight and identify, for the first time, the ability of L. rigida leaf extract to modulate inflammatory processes. These data suggest that the leaf extracts of this plant have potential in the development of herbal formulations for the treatment of inflammation.

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“…Los medicamentos asociados con las reacciones incluyen: metamizol, ibuprofeno, diclofenaco y ácido acetilsalicílico. 25,26…”

Section: Epidemiologíaunclassified

Alergia a medicamentos: aspectos fundamentales en el diagnóstico y tratamiento

et al. 2023

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Antecedentes: Cualquier sustancia prescrita en el tratamiento de algún padecimiento es capaz de producir eventos dañinos o desagradables, y se denominan reacciones adversas a medicamentos. Estas reacciones se originan por mecanismos inmunológicos y no inmunológicos. Objetivos: Describir los mecanismos inmunológicos de las reacciones de hipersensibilidad a medicamentos, epidemiologia, factores de riesgo, clasificación, manifestaciones clínicas, diagnóstico, tratamiento y pronóstico. Métodos: Se revisó la bibliografía actualizada, en inglés y español, asociada con reacciones de hipersensibilidad a medicamentos en las principales bases de datos. Resultados: Se describen los términos para definir las reacciones adversas y de hipersensibilidad a medicamentos, su clasificación y manifestaciones clínicas, métodos diagnósticos actuales y en estudio, algoritmos de tratamiento y pronóstico de los medicamentos más frecuentemente prescritos y con mayor prevalencia de eventos adversos reportados. Conclusión: Las reacciones adversas a medicamentos representan un reto, con una fisiopatología compleja y no del todo comprendida. Su abordaje requiere un enfoque cuidadoso, porque no todos los fármacos cuentan con pruebas validadas para establecer el diagnóstico y tratamiento específico. Antes de indicar cualquier medicamento debe considerarse la gravedad de la enfermedad, disponibilidad de otros tratamientos y riesgos potenciales de sufrir eventos adversos.

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Pharmacogenomics of Hypersensitivity to Non-steroidal Anti-inflammatory Drugs

Cited by 8 publications

References 119 publications

Identification of key genes and molecular mechanisms of chronic urticaria based on bioinformatics

Identification of key genes and molecular mechanisms of chronic urticaria based on bioinformatics

Mass Spectrometric Identification of Licania rigida Benth Leaf Extracts and Evaluation of Their Therapeutic Effects on Lipopolysaccharide-Induced Inflammatory Response

Alergia a medicamentos: aspectos fundamentales en el diagnóstico y tratamiento

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