Serum hepatocyte growth factor and clinical outcome in biliary atresia

Vejchapipat, Paisarn; Theamboonlers, Apiradee; Chaokhonchai, Rapeepan; Chongsrisawat, Voranush; Chittmittrapap, Soottiporn; Poovorawan, Yong

doi:10.1016/j.jpedsurg.2004.03.052

Cited by 21 publications

(23 citation statements)

References 26 publications

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“…Hepatotoxins and partial hepatectomy induce the production of HGF (Hasuike et al, 2005). These results in animal models correlate well with elevated levels of serum HGF in liver diseased patients (Vejchapipat et al, 2004). Salazar-Montes et al (2006) found that there was an early activation of NF-κB, STAT-3 and AP-1 along with the expression of iNOS, HGF and c-met after acute CCl 4 intoxication.…”

Section: Nf-kb Promotes Liver Regenerationmentioning

confidence: 83%

NF‐κB in liver diseases: a target for drug therapy

Muriel

2008

J of Applied Toxicology

147

106

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There are five nuclear factor-kB (NF-kB) transcription factors with important roles in innate immunity, liver inflammation, fibrosis and apoptosis prevention. Several inhibitors of NF-kB, like caffeic acid, captopril, curcumin, pyrrolidine dithiocarbamate, resveratrol, silymarin and thalidomide, have demonstrated antinecrotic, anticholestatic, antifibrotic and anticancer activities in the liver. A link between inflammation and hepatocellular carcinoma through the NF-kB pathway has been observed, providing ample experimental support for the tumor-promoting function of NF-kB in various models of cancer. NF-kB has been associated with the induction of proinflammatory gene expression and has attracted interest as a target for the treatment of inflammatory disease. However, despite much attention being focused on the deleterious effects of NF-kB, activation of this factor during the resolution of inflammation is associated with the production of antiinflammatory molecules like interleukin (IL)-10 and the onset of apoptosis. This suggests that NF-kB has an antiinflammatory role in vivo involving the regulation of the resolution of inflammation. Also, NF-kB promotes liver regeneration by upregulating IL-6 and other molecules like hepatocyte growth factor. It has been postulated that the beneficial properties of NF-kB are due to p50 homodimers, whose activation prevents cholestatic and chronic liver injury. More basic understanding on the function of the diverse NF-kB factors is urgently needed in different physiological and pathological conditions, because depending on the subunit composition of the dimmer, the disease and the stage of the illness, inhibition of the factor may result in a beneficial or in a deleterious response. Copyright © 2008 John Wiley & Sons, Ltd.There are five nuclear factor-kB (NF-kB) transcription factors with important roles in innate immunity, liver inflammation, fibrosis, and apoptosis prevention. Several inhibitors of NF-kB have demonstrated antinecrotic, anticholestatic, antifibrotic and anticancer activities in the

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Section: Nf-kb Promotes Liver Regenerationmentioning

confidence: 83%

NF‐κB in liver diseases: a target for drug therapy

Muriel

2008

J of Applied Toxicology

147

106

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“…Persistent intrahepatic bile duct destruction and periportal fibrosis that lead to chronic liver damage are the main pathologic changes in BA. Although there have been several studies concentrating on the pathophysiology of progressive liver fibrosis in post-Kasai BA patients [4,7,12], its mechanism is still unclear [1]. In recent years, one of the molecules being extensively studied regarding liver injury of various conditions, but BA, is NO.…”

Section: Discussionmentioning

confidence: 99%

Elevated serum nitric oxide metabolites in biliary atresia

et al. 2005

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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 mumol/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> or =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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“…Serum VEGF per platelet count in patients with BA was not significantly different from that in healthy controls (1.72±1.21 vs 1.57±0.97x10 6 , p=0.66). In patients with BA, the serum VEGF per platelet count was higher in the group with esophageal varice than in those without esophageal varice (1.98±1.39x10 6 vs. 1.29±0.77x10 6 , p=0.03) (Fig.…”

Section: Figmentioning

confidence: 62%

“…In patients with BA, the serum VEGF per platelet count was higher in the group with esophageal varice than in those without esophageal varice (1.98±1.39x10 6 vs. 1.29±0.77x10 6 , p=0.03) (Fig. 2).…”

Section: Figmentioning

confidence: 92%

Serum vascular endothelial growth factor per platelet count in patients with biliary atresia

2010

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Background: Biliary atresia (BA) is a progressive, sclerosing, inflammatory process resulting in complete obliteration of the extrahepatic bile ducts. The obstruction of bile flow engenders worsening cholestasis, hepatic fibrosis, and cirrhosis, which lead to portal hypertension and a decline in hepatic synthetic function. Hepatic stellate cells, which play roles in hepatic fibrogenesis, are an important source of various inflammatory mediators including vascular endothelial growth factor (VEGF) in the injured liver. Objectives: Investigate the level of serum VEGF and serum VEGF per platelet count in patients with BA and its relation to clinical characteristics. Methods: Peripheral blood samples were taken from 70 BA patients and 15 healthy control children. Serum VEGF was measured by enzyme-linked immunosorbent assay. We compared serum VEGF and serum VEGF per platelet count in BA patients with the respective results obtained in healthy control children. The relation of serum VEGF per platelet count with clinical variables of BA patients was investigated. Results: Serum VEGF levels and serum VEGF per platelet count in BA patients were not significantly different from those in normal controls (289.64±230.01 pg/mL vs. 312.36±189.05 pg/mL; p=0.72 and 1.72±1.21x106 vs. 1.57±0.97x106; p=0.66). Significant differences were observed among BA patients when VEGF per platelet count was categorized by the presence of esophageal varice (p=0.03). Only in BA patients was the serum level of VEGF correlated with the number of platelets (r=0.53, p<0.001). Conclusion: A high serum VEGF per platelet count is a useful marker for the development of portal hypertension in BA patients, especially for esophageal varice. Serum VEGF per platelet count may be useful for monitoring disease course in BA after hepatic portoenterostomy.

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Serum hepatocyte growth factor and clinical outcome in biliary atresia

Cited by 21 publications

References 26 publications

NF‐κB in liver diseases: a target for drug therapy

NF‐κB in liver diseases: a target for drug therapy

Elevated serum nitric oxide metabolites in biliary atresia

Serum vascular endothelial growth factor per platelet count in patients with biliary atresia

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