Anticonvulsant hypersensitivity syndrome or drug rash with eosinophilia and systemic symptoms (DRESS) induced by anticonvulsants

Alergologia ◽  
2017 ◽  
Vol 1 (1) ◽  
Author(s):  
Cristina Vlaicu
Keyword(s):  
Hypersensitivity Syndrome ◽  
Anticonvulsant Hypersensitivity Syndrome ◽  
Drug Rash ◽  
Systemic Symptoms

scholarly journals Lamotrigine Associated DRESS Syndrome – a Case Report

2015 ◽  
Vol 7 (1) ◽  
pp. 23-33 ◽  
Author(s):  
Jagoda Balaban ◽  
Đuka Ninković-Baroš
Keyword(s):  
Case Report ◽  
Female Patient ◽  
Skin Rash ◽  
Respiratory Symptoms ◽  
Hypersensitivity Syndrome ◽  
Organ Involvement ◽  
Dress Syndrome ◽  
Drug Induced ◽  
Drug Rash ◽  
Systemic Symptoms

AbstractDrug-induced delayed multiorgan hypersensitivity syndrome, also known as drug rash (reaction) with eosinophilia and systemic symptoms (DRESS) syndrome, represents a drug-induced cluster of skin, hematologic and systemic symptoms. More than forty drugs have been associated with this syndrome. We present a case of DRESS syndrome suspecting that lamotrigine was directly responsible for the patient’s rash and other symptoms. A female patient presented with extensive skin rash, fever, hematologic abnormalities, organ involvement such as hepatitis, pancreatitis and respiratory symptoms. The symptoms developed four weeks after the initiation of the offending drug, and disappeared eight weeks after its discontinuation.

Gene expression profiling in allopurinol-induced severe cutaneous adverse reactions in Vietnamese

2020 ◽  
Vol 21 (14) ◽  
pp. 985-994
Author(s):  
Dinh van Nguyen ◽  
Hieu Chi Chu ◽  
Christopher Vidal ◽  
Janet Anderson ◽  
Nguyet Nhu Nguyen ◽  
...  
Keyword(s):  
Gene Expression ◽  
Expression Profiling ◽  
Adverse Reactions ◽  
Hypersensitivity Syndrome ◽  
Stevens Johnson Syndrome ◽  
Johnson Syndrome ◽  
Severe Cutaneous Adverse Reactions ◽  
Drug Rash ◽  
Systemic Symptoms ◽  
Cutaneous Adverse Reactions

Aim: To examine gene expression in different clinical phenotypes of allopurinol-induced severe cutaneous adverse reactions (SCARs). Materials & methods: Gene expression profiling was performed using microarray on 11 RNA samples (four controls, three hypersensitivity syndrome/drug rash with eosinophilia and systemic symptoms, four Stevens–Johnson syndrome/toxic epidermal necrolysis) followed by quantitative real-time PCR in a total of 11 SCARs patients and 11 controls. Results: The biological pathways which were significantly enriched in differentially expressed genes in Stevens–Johnson syndrome/toxic epidermal necrolysis compared with hypersensitivity syndrome/drug rash with eosinophilia and systemic symptoms patients included; cell surface interactions at the vascular wall, immunoregulatory interactions at the immunological synapse and MyD88 signaling pathways. Overexpression of miR146a occurred in allopurinol-tolerant HLA-B*58:01 carriers. Conclusion: Biological pathways are identified which appear to be implicated in determining clinical phenotypes in allopurinol-induced SCARs. Overexpression of miR146a is potentially important for allopurinol tolerance in HLA-B*58:01 carriers.

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