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Published on: February 21, 2018
Granulocyte-macrophage colony-stimulating factor (GM-CSF) in children with acute immune thrombocytopenic purpura
Elham A Rizk1, Wessam M El-Gendy, Hoda Hassab
1Department of Clinical Pathology, Faculty of Medicine, Alexandria University, Egypt.
Insights
Serum GM-CSF levels are elevated in children with acute ITP and correlate inversely with platelet count and directly with platelet-associated immunoglobulins, suggesting a role in disease pathogenesis.
Area of Science:
- Hematology
- Immunology
Background:
- Immune thrombocytopenia (ITP) is characterized by low platelet counts due to immune-mediated destruction.
- Understanding the factors contributing to platelet destruction in ITP is crucial for developing effective treatments.
Purpose of the Study:
- To evaluate serum levels of granulocyte-macrophage colony-stimulating factor (GM-CSF) in children with acute ITP.
- To investigate the correlation between GM-CSF levels and clinical parameters, including platelet count and platelet-associated immunoglobulins (PAIgG).
Main Methods:
- Serum GM-CSF was measured using ELISA in 30 children with acute ITP and 10 healthy controls.
- Platelet-associated immunoglobulin G (PAIgG) was quantified via flow cytometry.
- Total IgG levels were assessed using radial immunodiffusion.
Main Results:
- Serum GM-CSF levels were significantly higher in ITP patients compared to controls.
- A significant inverse correlation was observed between serum GM-CSF and platelet count (r=-0.4643, P=0.010).
- Serum GM-CSF showed a positive correlation with PAIgG levels (r=0.4224, P=0.020).
Conclusions:
- Elevated serum GM-CSF may contribute to the pathogenesis of ITP.
- GM-CSF might enhance the destruction of antibody-coated platelets via the mononuclear phagocyte system.
- These findings suggest GM-CSF as a potential therapeutic target in ITP.
Background:
The purpose of our study was to assess the serum level of GM-CSF in children with acute ITP and its correlation with clinical parameters and with the level of platelet-associated immunoglobulins.
Material/Methods:
Thirty children with acute ITP were selected from the inpatient department at Alexandria University Children's Hospital at El Shatby. Ten apparently healthy children served as controls. ITP Patients were divided according to platelet count into those with platelet count >20,000/ul and cases with platelet counts <20,000/ul. Serum GM-CSF was measured by the ELISA technique. Total IgG was measured by radial immunodiffusion plates, and PAIgG was detected directly by flow cytometry.
Results:
Total IgG showed significant elevation in ITP patients as compared to controls (t=2.748, P<0.05), but no correlation was detected between platelet antibodies and total IgG (r=-0.140, P=0.460). 86% of the patients had elevated platelet-associated immunoglobulin (PAIgG). No correlation between PAIgG and platelet count was detected (r=-0.072, P=0.72). Serum GM-CSF was significantly higher in ITP patients than controls (t=3.757, P<0.05). An inverse correlation was found between serum GM-CSF and platelet count (r=-0.4643, P=0.010). There was positive correlation between serum GM-CSF and PAIgG (r=0.4224, P=0.020).
Conclusions:
Our results suggest that GM-CSF may have a role in the pathogenesis of ITP through activation of the mononuclear phagocyte system, resulting in accelerated destruction and phagocytosis of antibody-coated platelets and decreased platelet count.
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