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Sweet syndrome associated with G-CSF treatment in a child with glycogen storage disease type Ib
Insights
Acute febrile neutrophilic dermatosis (Sweet syndrome) is rare in children. A case study suggests granulocyte colony-stimulating factor (G-CSF) therapy may trigger Sweet syndrome in children with glycogen storage disease type Ib.
Area of Science:
- Pediatric Dermatology
- Hematology
- Immunology
Background:
- Acute febrile neutrophilic dermatosis, or Sweet syndrome, is uncommon in pediatric patients.
- It is frequently linked to underlying cancers or inflammatory conditions.
- Glycogen storage disease type Ib is a rare genetic disorder associated with neutropenia and recurrent infections.
Observation:
- A 5-year-old female patient with glycogen storage disease type Ib, neutropenia, and recurrent infections presented with a characteristic Sweet syndrome skin eruption.
- The eruption developed after two years of treatment with granulocyte colony-stimulating factor (G-CSF).
Findings:
- This case highlights a potential association between G-CSF therapy and the development of Sweet syndrome in a pediatric patient with a specific underlying condition.
- The findings suggest that G-CSF-induced granulopoiesis and granulocyte activation may play a role in the pathogenesis of Sweet syndrome.
Implications:
- This observation may inform clinical practice regarding the use of G-CSF in children with glycogen storage disease type Ib or similar conditions.
- Further research is warranted to elucidate the precise mechanisms linking G-CSF therapy to Sweet syndrome in this population.
- Understanding this association could lead to improved management strategies for pediatric patients at risk for both Sweet syndrome and G-CSF-related complications.
Abstract:
Acute febrile neutrophilic dermatosis (Sweet syndrome) is rare in children and is regularly associated with underlying malignancies or inflammtory diseases. A 5-year-old girl with glycogen storage disease type Ib, neutropenia, and recurrent infections developed characteristic skin eruption of Sweet syndrome after 2 years of granulocyte colony-stimulating factor (G-CSF) therapy. This association points to a possible role of G-CSF-induced granulopoiesis and granulodyte activation in the pathogenesis of Sweet syndrome.