Thrombopoietin Receptor Agonist Eltrombopag Alleviates Cognitive Impairment in Minimal Hepatic Encephalopathy via Activating NRG1/ErbB4 Signaling

2021 ◽  
Author(s):  
Saidan Ding ◽  
Jian Wang ◽  
Leping Liu ◽  
He Yu ◽  
Shuya Feng ◽  
...  
Keyword(s):  
Cognitive Impairment ◽  
Hepatic Encephalopathy ◽  
Receptor Agonist ◽  
Minimal Hepatic Encephalopathy ◽  
Thrombopoietin Receptor ◽  
Thrombopoietin Receptor Agonist

Quality of Life Improvements Following Eltrombopag Treatment in Children with Chronic Immune Thrombocytopenia: Case Report

2021 ◽  
Vol 104 (4) ◽  
pp. 672-675
Keyword(s):  
Quality Of Life ◽  
Platelet Count ◽  
Receptor Agonist ◽  
Immune Thrombocytopenia ◽  
Case Series ◽  
Thrombopoietin Receptor ◽  
Thrombopoietin Receptor Agonist ◽  
Low Platelet Count ◽  
Chronic Immune Thrombocytopenia

The present case series described six chronic immune thrombocytopenia patients (cITP), with a median age of 7.7 (7.0 to 13.0) years and low platelet count at 15,500 (7,000 to 20,000)/uL. They were suffering from bleeding symptoms and side effects of treatment. After enrollment, they were treated with thrombopoietin receptor agonist (eltrombopag). Five patients responded positively, showing a median platelet count of 115,000 (39,000 to 433,000)/uL. The median dose of eltrombopag used was 1.3 (0.8 to 2.2) mg/kg/day. The quality of life (QoL) improved for all patients, with their median overall score using a Pediatric QoL questionnaire showing 25.0% improvement. Median scores also showed improvements in each sphere of life functioning as physical (30.8%), emotional (26.4%), social (16.4%), and school (21.4%). The present report demonstrated that a select group of cITP patients, with low platelet count and bleeding symptoms, benefitted from treatment with eltrombopag, as shown by increased platelet counts and improved QoL. Keywords: Chronic ITP, Thrombopoietin receptor agonist, Children

CP-080 Thrombopoietin receptor agonist treatment in idiopathic thrombocytopenic purpura

2015 ◽  
Vol 22 (Suppl 1) ◽  
pp. A32.1-A32
Author(s):  
MH García Lagunar ◽  
I Español Morales ◽  
M Martínez Penella ◽  
I Muñoz García ◽  
M Gutiérrez Cívicos ◽  
...  
Keyword(s):  
Idiopathic Thrombocytopenic Purpura ◽  
Receptor Agonist ◽  
Thrombocytopenic Purpura ◽  
Thrombopoietin Receptor ◽  
Thrombopoietin Receptor Agonist

scholarly journals Thrombopoietin Receptor Agonist Eltrombopag Prevents Insulin Resistance and Synaptic Pathology via HIF1α/COX2/Sirt1 Signaling Pathway 

2021 ◽  
Author(s):  
he yu ◽  
xuebao wang ◽  
leping liu ◽  
baihui chen ◽  
shuya feng ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Learning And Memory ◽  
Receptor Agonist ◽  
Synaptic Activity ◽  
Sirtuin 1 ◽  
High Dose ◽  
Thrombopoietin Receptor ◽  
Thrombopoietin Receptor Agonist ◽  
Synaptic Formation

Abstract Background: Insulin resistance has been reported to be closely correlated with the pathogenesis of MHE. The mechanism underlying the effects of thrombopoietin receptor agonist eltrombopag (ELT) on synaptic activity and formation involved in MHE pathogenesis remains unclear. Methods: The effect of ELT on neurodegeneration and insulin resistance was examined in the primary rat neurons and an MHE rat model. Results: We found that the level of thrombopoietin receptor c-MPL (MPL) expression was decreased in MHE brains, and ELT administration improved insulin resistance, alleviated the destruction of synaptic formation and enhanced learning and memory in the MHE rats, indicating the relationship between dowregulated ELT and insulin resistance. Then in vitro, ELT treatment ameliorated the impairment of glucose uptake, indicating the reduction of insulin resistance. High dose of glucose inhibited insulin-stimulated downregulation of Hypoxia-inducible factor-1α (HIF1α) expression, the inhibition of inflammatory response and upregulation of sirtuin-1 (Sirt1), destruction of synaptic formation and activity, which were all reversed by ELT treatment in insulin resistant neurons.Conclusions: These results indicate that ELT is a promising potential therapeutic agent for insulin resistance and defect in learning and memory.

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