Acute generalized exanthematous pustulosis: Pathogenesis, genetic background, clinical variants and therapy
International Journal of Molecular Sciences, ISSN: 1422-0067, Vol: 17, Issue: 8, Page: 1214
2016
- 144Citations
- 194Captures
- 8Mentions
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
Citation Benchmarking is provided by Scopus and SciVal and is different from the metrics context provided by PlumX Metrics.
Metrics Details
- Citations144
- Citation Indexes143
- 143
- CrossRef127
- Policy Citations1
- Policy Citation1
- Captures194
- Readers194
- 194
- Mentions8
- References6
- Wikipedia6
- News Mentions2
- News2
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AGEP Following a New Weight Loss Regimen
A 55-Year-Old Man with Erythematous Papules Following a New Weight Loss Regimen A 55-year-old obese African American male presented with a two-month history of erythematous
Review Description
Acute generalized exanthematous pustulosis (AGEP) is a severe, usually drug-related reaction, characterized by an acute onset of mainly small non-follicular pustules on an erythematous base and spontaneous resolution usually within two weeks. Systemic involvement occurs in about 20% of cases. The course is mostly benign, and only in rare cases complications lead to life-threatening situations. Recent studies highlight the importance of genetic variations in interleukin-36 receptor antagonist gene (IL-36RN) in the pathogenesis of this disease. The physiopathology of AGEP remains unclear, but an involvement of innate and acquired immune cells together with resident cells (keratinocytes), which recruit and activate neutrophils via production of cytokines/chemokines such as IL-17, IL-36, granulocyte-macrophage colony-stimulating factor (GM-CSF), tumor necrosis factor alpha (TNFα) and chemokine (C-X-C motif) ligand 8 (CXCL8)/IL-8, has been postulated. Treatment is based on the removal of the causative drug, supportive care, infection prevention and use of potent topical or systemic steroids.
Bibliographic Details
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