Elevation of serum stem-cell factor in postoperative biliary atresia
Sittisak Honsawek1, Voranush Chongsrisawat, Paisarn Vejchapipat
1Department of Biochemistry, Faculty of Medicine, Chulalongkorn University, Bangkok, Thailand.
Insights
Biliary atresia patients show elevated stem cell factor (SCF) levels, indicating its role in liver injury and fibrosis. Higher SCF correlates with portal hypertension and hepatic damage post-Kasai operation.
Area of Science:
- Pediatric Gastroenterology
- Hepatology
- Fibrosis Research
Background:
- Biliary atresia (BA) is a leading cause of neonatal cholestasis.
- Stem cell factor (SCF) is linked to fibrosis in various conditions.
- The role of SCF in BA pathogenesis requires investigation.
Purpose of the Study:
- To investigate the role of stem cell factor (SCF) in pediatric patients with biliary atresia (BA).
- To determine if SCF levels correlate with disease severity and complications in BA.
Main Methods:
- Serum SCF levels were measured using ELISA in 57 pediatric BA patients post-Kasai operation and 30 healthy controls.
- Patients were stratified by total bilirubin and alanine aminotransferase (ALT) levels.
- Correlation with portal hypertension (PH) was assessed.
Main Results:
- BA patients exhibited significantly higher serum SCF levels than controls (748.3 vs 582.2 pg/mL).
- Elevated SCF was associated with higher ALT levels (indicating greater hepatic injury) and the presence of portal hypertension (PH).
- SCF levels were significantly higher in BA patients with PH (810.0 pg/mL) compared to those without (634.1 pg/mL).
Conclusions:
- Elevated serum SCF levels are characteristic of biliary atresia (BA) patients.
- SCF elevation is associated with increased hepatic injury and portal hypertension in BA.
- SCF may be a key factor in the development of hepatic fibrosis following the Kasai procedure for BA.
Background:
Biliary atresia (BA) is one of the most common causes of neonatal cholestasis. Stem-cell factor (SCF) has been implicated in the development of fibrosis in various diseases. The objective of the present study was to examine the significant role of SCF in BA.
Methods:
Fifty-seven pediatric patients with BA after Kasai operation and 30 healthy children were recruited. The mean ages of BA patients and controls were 6.1 +/- 0.6 years and 6.1 +/- 0.7 years, respectively. The patients were categorized into two groups according to their serum levels of total bilirubin (TBil < 2 mg/dL, no jaundice vs TBil > or = 2 mg/dL, persistent jaundice) and alanine aminotransferase (ALT < 100 vs ALT > or = 100 U/L). The serum SCF levels were determined on commercially available enzyme-linked immunosorbent assay.
Results:
The mean serum SCF level of the BA children was higher than that of normal controls (748.3 +/- 17.9 pg/mL vs 582.2 +/- 17.3 pg/mL; P < 0.001). Subsequent analysis demonstrated that the BA patients with serum ALT > or = 100 U/L had significantly greater levels of serum SCF compared to those with serum ALT < 100 U/L (796.5 +/- 22.6 pg/mL vs 694.7 +/- 25.0 pg/mL, respectively; P = 0.002). In addition, serum SCF levels were significantly elevated in the patients with portal hypertension (PH) compared with those without PH (810.0 +/- 18.8 pg/mL vs 634.1 +/- 20.1 pg/mL, P < 0.001).
Conclusion:
The current study showed that BA patients had higher serum SCF levels compared with controls. The significant elevation in SCF levels is associated with the presence of PH and the degree of hepatic injury. These findings suggest that SCF may play a part in the pathogenesis of hepatic fibrosis in BA patients after Kasai procedure.
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