ReviewActa paediatrica (Oslo, Norway : 1992)2025
Understanding host's response to staphylococcal scalded skin syndrome.
Review in Acta paediatrica (Oslo, Norway : 1992), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
6 citing papers in PubMed.
- Staphylococcal Scalded Skin Syndrome in a Tertiary Pediatric Hospital over an 11-Year Period.Children (Basel, Switzerland) · 2026Article
- Host genetic variation in desmoglein-1 is associated with susceptibility to staphylococcal scalded skin syndrome.European journal of pediatrics · 2026Article
- Hospitalizations for staphylococcal scalded skin syndrome in Spain (2016-2023): unequal disease burden concentrated in infants.Frontiers in pediatrics · 2026Article
- Severe staphylococcal scalded skin syndrome.IDCases · 2026Article
- Staphylococcical scalded skin syndrome: a case series description of a rare and critical disease in a tertiary pediatric center.Italian journal of pediatrics · 2025Article
- Understanding host's response to staphylococcal scalded skin syndrome.Acta paediatrica (Oslo, Norway : 1992) · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
Abstract
aimThe aim of this review was to summarise the current knowledge on host-related factors that contribute to the development and severity of staphylococcal scalded skin syndrome (SSSS) in children.
methodsA comprehensive assessment and analysis of the existing literature on SSSS clinical features, pathogenesis and susceptibility factors.
resultsSSSS is a blistering skin disease caused by circulating exfoliative toxins (ETs) of Staphylococcus aureus (S. aureus), almost exclusively affecting infants, young children and immunocompromised individuals. ETs possess serine protease activity and target desmoglein-1 (Dsg-1) in the superficial epidermis. While the role of S. aureus ETs and site of action are well-described, other host factors such as impaired immune responses to ETs, poor renal clearance and genetic factors are crucial for the onset of and/or the severity of SSSS in children.
conclusionThe fate of desmosomal fractions after cleavage by ETs, as well as the role of dermal inflammatory cell infiltrates remain to be elucidated.
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Registered trials
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