![Dr. Sandra Pérez-León](/image/photo_user/no_image.jpg)
Contributions
Abstract: EP1149
Type: E-Poster Presentation
Session title: Platelet disorders
Background
The complement system activation is one of the mechanisms behind platelet destruction in immune thrombocytopenia, but its role in the clinical setting is still limited.
Aims
Characterized C3, C4, and CH50 levels from ITP patients and its relation with the clinical presentation and treatment response.
Methods
A retrospective observational study in a teaching hospital with specific ITP outpatient consults. Complement levels were measured in any moment of the disease course through turbidimetric immunoassays. The relations between complements levels and characteristics of the disease and the response to treatments were evaluated with regression analysis
Results
Forty-three ITP patients with complement C3, C4, CH50 were included. Medium age was 44 years (16.99). In the moment when complement levels were measured 70% of patients were not receiving any treatment. There were 16% of previously splenectomized patients. Medium C3: 103,5 (34-28), medium C4: 14,5 (4- 171), with 75% of the patients with levels of C4 below the normal range. Medium CH50 49 (12-95). Not responders to first line treatment had lower C3 levels (p: 0,018). Patients receiving treatment had lower mean C4 (p: 0,039) and lower C3 (p: 0,065). In multivariable analyses patients receiving TPO agonist had lower levels of C3, C4, and CH50 (p: 0,024; 0,019 y 0,054). There were no relation between complement level and severity of bleeding, refractory disease or splenectomy status.
Conclusion
ITP patients had lower levels of C4, especially those on active treatment. Patients not responders to first line treatments had lower levels of C3. Those on treatment with thrombopoietin receptor agonists had lower levels of C3,C4, y CH50. Further prospective studies are needed to evaluate the role of complement in the current clinical practice and with the emergent complement- directed therapies.
Keyword(s): Complement, Immune thrombocytopenia (ITP), Platelet
Abstract: EP1149
Type: E-Poster Presentation
Session title: Platelet disorders
Background
The complement system activation is one of the mechanisms behind platelet destruction in immune thrombocytopenia, but its role in the clinical setting is still limited.
Aims
Characterized C3, C4, and CH50 levels from ITP patients and its relation with the clinical presentation and treatment response.
Methods
A retrospective observational study in a teaching hospital with specific ITP outpatient consults. Complement levels were measured in any moment of the disease course through turbidimetric immunoassays. The relations between complements levels and characteristics of the disease and the response to treatments were evaluated with regression analysis
Results
Forty-three ITP patients with complement C3, C4, CH50 were included. Medium age was 44 years (16.99). In the moment when complement levels were measured 70% of patients were not receiving any treatment. There were 16% of previously splenectomized patients. Medium C3: 103,5 (34-28), medium C4: 14,5 (4- 171), with 75% of the patients with levels of C4 below the normal range. Medium CH50 49 (12-95). Not responders to first line treatment had lower C3 levels (p: 0,018). Patients receiving treatment had lower mean C4 (p: 0,039) and lower C3 (p: 0,065). In multivariable analyses patients receiving TPO agonist had lower levels of C3, C4, and CH50 (p: 0,024; 0,019 y 0,054). There were no relation between complement level and severity of bleeding, refractory disease or splenectomy status.
Conclusion
ITP patients had lower levels of C4, especially those on active treatment. Patients not responders to first line treatments had lower levels of C3. Those on treatment with thrombopoietin receptor agonists had lower levels of C3,C4, y CH50. Further prospective studies are needed to evaluate the role of complement in the current clinical practice and with the emergent complement- directed therapies.
Keyword(s): Complement, Immune thrombocytopenia (ITP), Platelet