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Chinglung Lai - One of the best experts on this subject based on the ideXlab platform.
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quantification of hepatitis b virus covalently closed circular dna in patients with hepatocellular carcinoma
Journal of Hepatology, 2006Co-Authors: Danny Kaho Wong, Manfung Yuen, Ronnie T P Poon, John Chihang Yuen, James Fung, Chinglung LaiAbstract:Background/Aims This study aimed to measure the Intrahepatic total hepatitis B virus (HBV) DNA and covalently closed circular DNA (cccDNA) levels in tumor and non-tumor tissues in hepatocellular carcinoma (HCC) patients. Methods Intrahepatic total HBV DNA and cccDNA were measured in 25 HCC patients (21 hepatitis B surface antigen [HBsAg]-positive and 4 HBsAg-negative) by the Invader ® assay. Results A low level of Intrahepatic HBV DNA was detectable in all HBsAg-negative patients. For HBsAg-positive patients, the Intrahepatic total HBV DNA levels in the tumor and non-tumor tissues were comparable ( P =0.903). However, the tumor tissues had significantly higher levels of cccDNA (0.35 vs. 0.16copies/cell, P =0.030) and higher proportion of Intrahepatic HBV DNA in the form of cccDNA (100% vs. 84%, P =0.004) than the non-tumor tissues. Seventeen out of 21 (81%) tumor tissues had Intrahepatic HBV DNA solely in cccDNA form. Analysis of HBV mRNA expression indicated that HBV replication appeared to be lower in the tumor tissues than the non-tumor tissues. Conclusions Compared to the non-tumor tissues, the levels of HBV replication in the tumor tissues appeared to be lower, and cccDNA was the predominant form of HBV DNA in the tumor tissues.
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one year entecavir or lamivudine therapy results in reduction of hepatitis b virus Intrahepatic covalently closed circular dna levels
Antiviral Therapy, 2006Co-Authors: Danny Kaho Wong, Manfung Yuen, James Fung, Vincent Wingshun Ngai, Chinglung LaiAbstract:Entecavir and lamivudine are potent nucleoside analogues that can suppress hepatitis B virus (HBV) replication. However, the effects of these two antiviral agents on Intrahepatic total HBV DNA and covalently closed circular DNA (cccDNA) are not known. In this study, we aimed to assess the effect of 48 weeks of entecavir/lamivudine therapy on Intrahepatic total HBV DNA and cccDNA levels. Forty chronic hepatitis B patients, participating in two Phase III entecavir trials at our centre, were randomized to receive 48 weeks of either 0.5 mg once daily of entecavir (n = 21) or 100 mg once daily of lamivudine (n = 19). Their serological, virological and biochemical responses, as well as Intrahepatic HBV DNA levels were monitored. There was no significant difference between entecavir and lamivudine therapy in terms of post-treatment serological, virological and biochemical responses. Both nucleoside analogues reduced serum viral load, Intrahepatic total HBV DNA, and cccDNA by about 4.8 logs, 2 logs, and 1 log respectively. An increase in the proportion of Intrahepatic HBV DNA in the form of cccDNA was seen after 48 weeks of therapy. In conclusion, both entecavir and lamivudine can successfully reduce Intrahepatic HBV DNA and cccDNA. CccDNA becomes the dominant form of HBV DNA during viral suppression and is possibly responsible for viral rebound after short-term antiviral therapy.
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quantitation of covalently closed circular hepatitis b virus dna in chronic hepatitis b patients
Hepatology, 2004Co-Authors: Danny Kaho Wong, Manfung Yuen, Hejun Yuan, Simon Siuman Sum, Cheekin Hui, Jeff Hall, Chinglung LaiAbstract:This study examined a signal amplification assay, the Invader assay, for the quantitation of hepatitis B virus (HBV) covalently closed circular DNA (cccDNA) in liver biopsies and sera. DNA was extracted from liver biopsy and serum samples were collected from 16 hepatitis B e antigen (HBeAg)-positive and 36 antibody-to-HBeAg-positive (anti-HBe-positive) chronic hepatitis B patients. The amount of total HBV DNA and cccDNA was measured using the Invader assay. Anti-HBe-positive patients had lower median total Intrahepatic HBV DNA (P < .001) and Intrahepatic cccDNA levels (P = .001) than HBeAg-positive patients. Intrahepatic cccDNA correlated positively with the total Intrahepatic HBV DNA (r = 0.950, P < .001). However, the proportion of Intrahepatic HBV DNA in the form of cccDNA was inversely related to the amount of total Intrahepatic HBV DNA (r = -0.822, P < .001). A small amount of cccDNA was detected in 39 of 52 (75%) serum samples. Anti-HBe-positive patients had lower median serum cccDNA levels than HBeAg-positive patients (P = .002). Serum HBV DNA correlated positively with Intrahepatic total HBV DNA (r = 0.778, P < .001) and Intrahepatic cccDNA (r = 0.481, P = .002). In conclusion, the Invader assay is a reliable assay for the quantitation of cccDNA. Serum and Intrahepatic total HBV DNA and cccDNA levels become lower as the disease progresses from HBeAg-positive to anti-HBe-positive phase, with cccDNA becoming the predominant form of Intrahepatic HBV DNA.
Hisami Ando - One of the best experts on this subject based on the ideXlab platform.
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Operative treatment of congenital stenoses of the Intrahepatic bile ducts in patients with choledochal cysts.
American journal of surgery, 1997Co-Authors: Hisami Ando, Kenitiro Kaneko, Fujio Ito, Takahiko Seo, Takahiro ItoAbstract:Background Postoperative complications including Intrahepatic calculi may develop after the complete excision of a choledochal cyst. Since congenital stenoses of the Intrahepatic bile ducts are more likely the cause of Intrahepatic calculi, operative procedures for Intrahepatic stenoses are reported. Methods There were 16 patients with choledochal cysts who underwent surgery for stenoses of Intrahepatic bile ducts. The stenoses were excised at the opening of the common hepatic duct. Results In the 16 patients, 25 of the 26 stenoses that involved an intraluminal membrane or septum could be excised from the divided end of the common hepatic duct at the hepatic hilum. In 1 patient, the stenosis could not be accessed from the hepatic hilum, and a left hepatic lobectomy was required. In postoperative follow-up, all 16 patients were in good health. Conclusions Stenoses of the Intrahepatic bile ducts should be treated from the divided end of the common hepatic duct at the initial operation for choledochal cysts. The need for a second operation or hepatic lobectomy may thus be avoided.
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Intrahepatic bile duct stenosis causing Intrahepatic calculi formation following excision of a choledochal cyst
Journal of The American College of Surgeons, 1996Co-Authors: Hisami Ando, Kenitiro Kaneko, T Ito, T Seo, F ItoAbstract:BACKGROUND: Formation of Intrahepatic calculi is one of the major late complications after excision of a choledochal cyst. There are few studies, however, that have examined this complication. Generally, an anastomotic stricture is believed to be the main cause of Intrahepatic calculi. We report our experience with eight patients who had Intrahepatic calculi after excision of a choledochal cyst. STUDY DESIGN: To determine what caused the Intrahepatic calculi to form, seven patients underwent cholangioscopy and direct visual inspection during the operation, and one patient underwent percutaneous transhepatic cholangioscopy. Intrahepatic bile was cultured, and calculi were analyzed. RESULTS: Two types of stenoses (membranous and septal) were demonstrated near the hepatic hilum in all patients. Calculi were always located on the hepatic side of the stenoses. No anastomotic strictures were found in the region of the hepaticojejunostomy. The calculi contained mainly calcium bilirubinate. Escherichia coli and Klebsiella pneumoniae were cultured from the bile in all patients. CONCLUSIONS: Stenoses of the Intrahepatic bile ducts were demonstrated in all eight patients. The stenoses were considered to be the primary cause of Intrahepatic calculi formation after excision of the choledochal cysts.
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Congenital stenosis of the Intrahepatic bile duct associated with choledochal cysts
Journal of the American College of Surgeons, 1995Co-Authors: Hisami Ando, Kenitiro Kaneko, Ito T, Seo TAbstract:BACKGROUND There are few studies that report on stenosis of the Intrahepatic bile ducts associated with choledochal cysts. We investigated the presence and clinical significance of stenosis of the Intrahepatic bile ducts associated with choledochal cysts. STUDY DESIGN We examined Intrahepatic bile ducts in patients with choledochal cysts using cholangiography (93 patients), endoscopy and direct observation during surgery (19 patients), and histologic examination (12 patients). RESULTS Stenosis of the Intrahepatic bile duct was present in 75 (80.6 percent) of 93 patients with choledochal cysts. Endoscopic and direct observation detected membranous stenosis, which consisted of a diaphragm, in 11 of 19 patients. Septal stenosis, which consisted of a bridge-like septum, was present in eight of 19 patients. Stenoses consisted of mucosal and fibromuscular layers. Intrahepatic calculi developed in eight patients with stenosis following resection of the choledochal cysts. CONCLUSIONS Membranous or septal stenosis of the Intrahepatic bile duct is a characteristic feature of choledochal cysts. Our findings suggest that these stenoses should be treated surgically because of the risk of Intrahepatic calculi.
Ronald E Gordon - One of the best experts on this subject based on the ideXlab platform.
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progressive familial Intrahepatic cholestasis type 1 is associated with decreased farnesoid x receptor activity
Gastroenterology, 2004Co-Authors: Frank Chen, A S Knisely, Laura N. Bull, Meenakshisundaram Ananthanarayanan, Sukru Emre, Ezequiel Neimark, Sandra Strautnieks, Richard Thompson, Margret S Magid, Ronald E GordonAbstract:Abstract Background & Aims: The mechanisms by which mutations in the familial Intrahepatic cholestasis-1 gene cause Byler's disease (progressive familial Intrahepatic cholestasis type 1) are unknown. Methods: Interactions among the apical sodium-dependent bile acid transporter, the farnesoid X receptor (FXR), and familial Intrahepatic cholestasis-1 were studied in the ileum of children with progressive familial Intrahepatic cholestasis type 1 and in Caco-2 cells. Results: Increased ileal apical sodium-dependent bile acid transporter messenger RNA (mRNA) expression was detected in 3 patients with progressive familial Intrahepatic cholestasis type 1. Paradoxically, ileal lipid-binding protein mRNA expression was repressed, suggesting a central defect in bile acid response. Ileal FXR and short heterodimer partner mRNA levels were reduced in the same 3 patients. In Caco-2 cells, antisense-mediated knock-down of endogenous familial Intrahepatic cholestasis-1 led to up-regulation of apical sodium-dependent bile acid transporter and down-regulation of FXR, ileal lipid-binding protein, and short heterodimer partner mRNA. In familial Intrahepatic cholestasis-1-negative Caco-2 cells, the activity of the human apical sodium-dependent bile acid transporter promoter was enhanced, whereas the human FXR and bile salt excretory pump promoters' activities were reduced. Overexpression of short heterodimer partner but not of the FXR abrogated the effect of familial Intrahepatic cholestasis-1 antisense oligonucleotides. FXR cis -element binding and FXR protein were reduced primarily in nuclear but not cytoplasmic extracts from familial Intrahepatic cholestasis-1-negative Caco-2 cells. Conclusions: Loss of familial Intrahepatic cholestasis-1 leads to diminished nuclear translocation of the FXR, with the subsequent potential for pathologic alterations in intestinal and hepatic bile acid transporter expression. Marked hypercholanemia and cholestasis are predicted to develop, presumably because of both enhanced ileal uptake of bile salts via up-regulation of the apical sodium-dependent bile acid transporter and diminished canalicular secretion of bile salts secondary to down-regulation of the bile salt excretory pump.
Emmanuel Jacquemin - One of the best experts on this subject based on the ideXlab platform.
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progressive familial Intrahepatic cholestasis type 1 and extrahepatic features no catch up of stature growth exacerbation of diarrhea and appearance of liver steatosis after liver transplantation
Journal of Hepatology, 2003Co-Authors: Panayotis Lykavieris, Saskia W C Van Mil, Daniele Cresteil, Monique Fabre, Michelle Hadchouel, Leo W J Klomp, Olivier Bernard, Emmanuel JacqueminAbstract:Abstract Background/Aims : Progressive familial Intrahepatic cholestasis characterized by normal serum gamma-glutamyltransferase activity can be due to mutations in familial Intrahepatic cholestasis type 1 ( FIC1 ) ( ATP8B1 ), a gene expressed in several organs. In some cases, it is associated with extrahepatic features. We searched for FIC1 mutations and analyzed the outcome of extrahepatic features after liver transplantation in two children with this form of progressive familial Intrahepatic cholestasis associated with chronic unexplained diarrhea and short stature. Methods : FIC1 sequence was determined after polymerase chain reaction (PCR) of genomic lymphocyte DNA and/or reverse transcription-PCR of liver or lymphocyte RNA. Results : A homozygous amino acid change deletion was found in one child. The second child harboured compound heterozygous missense and nonsense mutations. In both children, despite successful liver transplantation, evolution (follow-up: 9.5–11 years) was characterized by exacerbation of diarrhea and no catch-up of stature growth, and appearance of liver steatosis. Conclusions : Progressive familial Intrahepatic cholestasis characterized by normal serum gamma-glutamyltransferase activity and extrahepatic features corresponds to progressive familial Intrahepatic cholestasis type 1. Extrahepatic symptomatology is not corrected or may be aggravated by liver transplantation, impairing life quality.
Kechun Yao - One of the best experts on this subject based on the ideXlab platform.
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targeted puncture of left branch of Intrahepatic portal vein in transjugular Intrahepatic portosystemic shunt to reduce hepatic encephalopathy
World Journal of Gastroenterology, 2019Co-Authors: Shihua Luo, Jianguo Chu, He Huang, Guorui Zhao, Kechun YaoAbstract:Targeted puncture of left branch of Intrahepatic portal vein in transjugular Intrahepatic portosystemic shunt to reduce hepatic encephalopathy
