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Chinese Journal of General Surgery ; (12): 425-428, 2017.
Article in Chinese | WPRIM | ID: wpr-618752


Objective To evaluate GGT in combination with B ultrasound for the diagnosis of biliary atresia (BA) infants suffering from obstructive jaundice.Methods A retrospective analysis was made on 69 sick infants including 55 BAs and 14 non-BAs as identified by intraoperative cholangiography.The preoperative laboratory GGT and ultrasound data were collected and analyzed.The sensitivity,specificity,positive predictive value,negative predictive value and accuracy were compared.Results BA patients had significantly higher GGT than Non-BA patients (t =-4.164,P < 0.05).The sensitivity,specificity,positive predictive value,negative predictive value and accuracy of GGT > 306 U/L were 69.1%,92.9%,97.4%,43.3%,73.9%,respectively.In BA group,abnormal gallbladder was significantly associated with proadening portal vein,broadening hepatic artery compared with Non-BA patients (x2 =9.995,P <0.05).The accuracy of abnormal gallbladder on ultrasound was 78.3%.When two method combined for the diagnosis of BA,the sensitivity,specificity,positive predictive value,negative predictive value were 92.7%,92.9%,98.1% and 76.5% and accuracy can reach 92.8%.Conclusions For obstructive jaundice infants with GGT > 306 U/L and abdominal gallbladder ultrasound finding intraoperative cholangiography should be carried out to make definite diagnosis of BA.

Tianjin Medical Journal ; (12): 810-813, 2016.
Article in Chinese | WPRIM | ID: wpr-496490


Objective To investigate the expression and function of transforming growth factor (TGF)-β1 and Smad2 in liver fibrosis of biliary atresia (BA). Methods Liver biopsy specimens were collected from autopsy (normal group, n=5), congenital biliary dilatation (CBD group, n=10), BA patients underwent Kasai procedure (early hepatic fibrosis group, n=19) and liver transplantation (transplantation group, n=11). The first three groups were collected from January 2010 to July 2014 in Tianjin Children’s Hospital, and the last group was collected from January 2013 to January 2014 in Tianjin First Central Hospital. The hematoxylin and eosin (HE) stain were used to observe the degree of liver fibrosis of four groups. Immunohistochemistry (IHC) was used to observe expressions of TGF-β1 and Smad2 in liver tissues of these samples. Quantitative real-time polymerase chain reaction (qRT-PCR) was used to test the quantitative mRNA of TGF-β1 and Smad2 in these samples. Results Results of HE showed that no fibrosis in autopsy group, mild fiber cell hyperplasia in CBD group, severe fibrosis in Kasai group and significant pseudolobule in transplantation group. Results of IHC showed that TGF-β1 was expressed in the cytoplasm of hepatocytes, bile duct cells, lymphocytes and neutrophils. The average optical density of TGF-β1 was the highest in Kasai group compared with that of other three groups (P 0.05). Results of qRT-PCR showed that both TGF-β1 mRNA and Smad2 mRNA were the highest in early hepatic fibrosis group than those of CBD group and transplantation group (P<0.017). Conclusion In early stage of BA, TGF-β1 and Smad2 promote liver fibrosis until the formation of P-P,P-C desmosome structure. However, with BA fibrosis becomes more serious, the pro-fibrogenic function of TGF-β1 and Smad2 becomes less.

Tianjin Medical Journal ; (12): 821-823,824, 2016.
Article in Chinese | WPRIM | ID: wpr-604577


Objective To investigate the expression and significance of integrin αvβ8, p38 and extracellular signal-regulated protein kinase 1/2 (ERK1/2) proteins, which are TGF-β1 pathway related regulatory protein, in liver fibrosis of children with biliary atresia (BA). Methods Fifteen cases of BA (Kasai group) and 10 cases of congenital biliary dilatation (CBD group) were collected in Tianjin Children’s Hospital. And liver biopsy specimens were collected in Tianjin first central hospital, including 10 cases of BA children who underwent liver transplantation due to liver failure after Kasai operation (liver transplantation group). The specimens of front part of the right lobe of the liver were taken for HE and immunohistochemistry (IHC) staining. The expressions ofαvβ8, p38 and ERK1/2 in liver were observed by IHC staining in three groups of liver tissues. Results HE staining showed fibroblast hyperplasia occasionally in CBD group, portal area expansion, fibrous tissue proliferation and wide spread bridging fibrosis with few pseudo lobules in Kasai group. In transplantation group, portal area was widened, the degree of fibrosis was severe and bridging fibrosis generally formed resulted in pseudo lobules widely. Imunohistochemistry showed that the expressions of αvβ8 and ERK1/2 were weakly positive, and the expression of p38 was negative in CBD group. In Kasai group, the expressions of αvβ8, p38 and ERK1/2 proteins were all strongly positive in liver cytoplasm, biliary epithelial cells and vascular endothelial cell cytoplasm. In liver transplantation group the expressions of αvβ8, p38 and ERK1/2 proteins were all strongly positive. The semi-quantitative analysis showed that the expressions levels of αvβ8, p38 and ERK1/2 were significantly higher in Kasai and liver transplantation groups than those of CBD group (P0.05). Conclusion The expressions ofαvβ8, p38 and ERK1/2 are gradually increased in liver of BA with the process of fibrosis, which indicate that they may be involved in the process of BA liver fibrosis.

Tianjin Medical Journal ; (12): 4-7, 2015.
Article in Chinese | WPRIM | ID: wpr-473541


Biliary atresia (BA) is one of the most serious digestive system diseases, which threatens the health of infants. Liver fibrosis is a major cause of death in children with BA. In the process of the pathogenesis of BA, virus infection can in?duce a series of immune and inflammatory reaction, result in a decrease of regulatory T cells (Treg cells) and high expression of CD14, activating a variety of inflammatory pathways and TGF-β/Smad2/3 pro-fibrogenic pathway, which produces a large number of medium damage of liver cells and bile duct cells, releases proinflammatory factor, oxygen metabolism matter and cytokines. These changes further aggravate damage of hepatobiliary system and cause the internal environment imbalance of liver parenchyma cells. The imbalance of internal environment with adaptive degeneration and necrosis in liver parenchyma cells, hepatic macrophages and gathered inflammatory cells leads to the activation of hepatic stellate cells (HSCs). HSCs can be converted into fibroblast cells, and promote the process of liver fibrosis. Immune and inflammatory lesions, pro-fibrogenic pathway are the important factors in contributing to liver fibrosis and cirrhosis of biliary atresia.