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Elevated serum nitric oxide metabolites in biliary atresia

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Abstract

Biliary atresia (BA) remains one of the most intractable liver diseases in children. The aim of this study was to investigate the possible roles of nitric oxide (NO) in BA. Serum levels of nitrite and nitrate (NO production) were determined using a colorimetric method from 65 post-operative BA patients and 12 healthy children. The patients were categorized into two groups according to their jaundice status, and serum alanine aminotransferase (ALT, a marker for liver injury). Unpaired t tests were used. Data are expressed as mean and SD in terms of μmol/l. Age and gender between BA patients and controls were comparable. Serum NO metabolites of BA patients was higher than the controls (79.77±21.22 vs. 65.75±9.44, P=0.001). Subgroup analysis revealed that there was no difference in serum nitrate/nitrite levels of BA patients without jaundice compared to those with jaundice (78.85±23.23 vs. 80.90±18.76, P=0.70). However, patients with serum ALT≥100 IU/l had higher levels of serum NO metabolites compared to those with serum ALT<100 IU/l. In conclusion, NO production was elevated in BA patients compared to normal controls. Serum NO was associated with serum ALT levels, but not with jaundice status, in BA patients. These suggest that NO plays a role in the pathophysiology of liver injury in post-operative BA.

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Acknowledgments

We are grateful to the Thailand Research Fund and Center of Excellence of Thailand for their generous support. Also, we would like to express our gratitude to the entire staff of the Viral Hepatitis Research Unit, Chulalongkorn University and Hospital for their efforts in the present study. This project was supported by Rachadaphisek Somphot Fund, Faculty of Medicine, Chulalongkorn University, Thailand.

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Correspondence to Paisarn Vejchapipat.

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Vejchapipat, P., Chongsrisawat, V., Theamboonlers, A. et al. Elevated serum nitric oxide metabolites in biliary atresia. Ped Surgery Int 22, 106–109 (2006). https://doi.org/10.1007/s00383-005-1581-8

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