Elevation of serum urokinase plasminogen activator receptor and liver stiffness in postoperative biliary atresia
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Wanvisa Udomsinprasert1, Sittisak Honsawek1, Napaphat Jirathanathornnukul1
1Wanvisa Udomsinprasert, Sittisak Honsawek, Napaphat Jirathanathornnukul, Department of Biochemistry, Faculty of Medicine, Chulalongkorn University, King Chulalongkorn Memorial Hospital, Thai Red Cross Society, Bangkok 10330, Thailand.
Insights
Serum urokinase-type plasminogen activator receptor (uPAR) and liver stiffness are elevated in biliary atresia (BA) patients. These markers may serve as noninvasive indicators of liver fibrosis progression in children with BA.
Area of Science:
- Hepatology
- Biochemistry
- Pediatric Gastroenterology
Background:
- Biliary atresia (BA) is a severe neonatal liver disease requiring prompt intervention.
- Assessing liver fibrosis progression in post-Kasai BA patients is crucial for management.
- Noninvasive biomarkers are needed to monitor liver health in pediatric BA.
Purpose of the Study:
- To investigate serum urokinase-type plasminogen activator receptor (uPAR) levels and liver stiffness in BA.
- To examine the correlation between circulating uPAR, liver stiffness, and clinical outcomes in postoperative BA children.
Main Methods:
- Enzyme-linked immunosorbent assay (ELISA) was used to measure serum uPAR.
- Transient elastography was employed to assess liver stiffness.
- Study included 85 post-Kasai BA children and 24 controls.
Main Results:
- BA children exhibited significantly higher serum uPAR and liver stiffness than controls (P < 0.001).
- Elevated uPAR and liver stiffness were observed in jaundiced BA children compared to non-jaundiced.
- Circulating uPAR positively correlated with liver dysfunction markers and liver stiffness (r=0.508, P < 0.001).
Conclusions:
- Serum uPAR and liver stiffness are elevated in BA patients compared to healthy controls.
- Increased circulating uPAR is linked to liver dysfunction in BA.
- Serum uPAR and liver stiffness show potential as noninvasive biomarkers for liver fibrosis in post-Kasai BA.
Aim:
To investigate serum urokinase-type plasminogen activator receptor (uPAR) and liver stiffness in biliary atresia (BA) and examine the correlation of circulating uPAR, liver stiffness, and clinical outcomes in postoperative BA children.
Methods:
Eighty-five postKasai BA children and 24 control subjects were registered. Circulating uPAR was measured using enzyme-linked immunosorbent essay. Liver stiffness was analyzed using transient elastography.
Results:
BA children had significantly greater circulating uPAR and liver stiffness scores than control subjects (P < 0.001). Circulating uPAR and liver stiffness were substantially higher in jaundiced BA children than non-jaundiced BA children (P < 0.001). In addition, circulating uPAR was positively associated with serum aspartate aminotransferase (r = 0.507, P < 0.001), alanine aminotransferase (r = 0.364, P < 0.001), total bilirubin (r = 0.559, P < 0.001), alkaline phosphatase (r = 0.325, P < 0.001), and liver stiffness scores (r = 0.508, P < 0.001).
Conclusion:
Circulating uPAR and liver stiffness values were greater in BA children than healthy controls. The increased circulating uPAR was associated with liver dysfunction in BA. As a consequence, serum uPAR and liver stiffness may be used as noninvasive biomarkers indicating the progression of liver fibrosis in postKasai BA.
