The Experts below are selected from a list of 327 Experts worldwide ranked by ideXlab platform
Hua-rong Li - One of the best experts on this subject based on the ideXlab platform.
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Role of farnesoid X receptor in rats with acute Cholestatic Hepatitis
Chinese Journal of Hepatology, 2016Co-Authors: Yan Ding, Xiong Xl, Lei Zhao, Hua-rong LiAbstract:OBJECTIVE: To investigate the role of farnesoid X receptor (FXR) and its downstream molecules small heterodimer partner (SHP), UDP-glucuronosyltransferase 2B4 (UGT2B4), and bile salt export pump (BSEP) in rats with acute Cholestatic Hepatitis. METHODS: A total of 20 Sprague-Dawley rats were randomly divided into normal control group and model group, with 10 rats in each group. The rats in the model group were given a single dose (50 mg/kg) ofα-naphthyl isothiocyanate by gavage to establish the animal model of acute Cholestatic Hepatitis. Quantitative real-time PCR was used to measure the mRNA expression of FXR, UGT2B4, and BSEP in liver tissue at 48 hours after gavage. An automatic biochemical analyzer was used to measure the serum levels of total bilirubin, direct bilirubin, alanine aminotransferase, total bile acid, aspartate aminotransferase, alkaline phosphatase, andγ-glutamyl transferase. The independent samples t-test was used for comparison of means between groups. RESULTS: The model group had significantly lower mRNA expression of FXR, SHP, UGT2B4, and BSEP in liver tissue than the normal control group (0.152±0.088/0.559±0.194/0.177±0.039/0.561±0.123 vs 1.137±0.215/1.512±0.309/2.394±0.462/1.631±0.376, t = 13.408, 8.260, 15.121, and 8.553, all P < 0.05). The model group had significantly higher liver function parameters than the normal control group (all P < 0.01). CONCLUSION: FXR, SHP, UGT2B4, and BSEP are involved in the development of acute Cholestatic Hepatitis. Reduced expression of FXR may cause reduced expression of downstream SHP, UGT2B4, and BSEP, increase the synthesis of bile acid, weaken detoxicating and transporting functions, and thus mediate the development of Cholestatic Hepatitis.
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role of farnesoid x receptor in rats with acute Cholestatic Hepatitis
Chinese Journal of Hepatology, 2016Co-Authors: Yan Ding, Lei Zhao, Xiaoli Xiong, Hua-rong LiAbstract:Objective To investigate the role of farnesoid X receptor (FXR) and its downstream molecules small heterodimer partner (SHP), UDP-glucuronosyltransferase 2B4 (UGT2B4), and bile salt export pump (BSEP) in rats with acute Cholestatic Hepatitis. Methods A total of 20 Sprague-Dawley rats were randomly divided into normal control group and model group, with 10 rats in each group. The rats in the model group were given a single dose (50 mg/kg) ofα-naphthyl isothiocyanate by gavage to establish the animal model of acute Cholestatic Hepatitis. Quantitative real-time PCR was used to measure the mRNA expression of FXR, UGT2B4, and BSEP in liver tissue at 48 hours after gavage. An automatic biochemical analyzer was used to measure the serum levels of total bilirubin, direct bilirubin, alanine aminotransferase, total bile acid, aspartate aminotransferase, alkaline phosphatase, andγ-glutamyl transferase. The independent samples t-test was used for comparison of means between groups. Results The model group had significantly lower mRNA expression of FXR, SHP, UGT2B4, and BSEP in liver tissue than the normal control group (0.152±0.088/0.559±0.194/0.177±0.039/0.561±0.123 vs 1.137±0.215/1.512±0.309/2.394±0.462/1.631±0.376, t = 13.408, 8.260, 15.121, and 8.553, all P < 0.05). The model group had significantly higher liver function parameters than the normal control group (all P < 0.01). Conclusion FXR, SHP, UGT2B4, and BSEP are involved in the development of acute Cholestatic Hepatitis. Reduced expression of FXR may cause reduced expression of downstream SHP, UGT2B4, and BSEP, increase the synthesis of bile acid, weaken detoxicating and transporting functions, and thus mediate the development of Cholestatic Hepatitis. Key words: Cholestasis; Farnesoid X receptor; Small heterodimer partner; UDP-glucuronosyltransferases; Bile salt export pump
Yan Ding - One of the best experts on this subject based on the ideXlab platform.
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Role of farnesoid X receptor in rats with acute Cholestatic Hepatitis
Chinese Journal of Hepatology, 2016Co-Authors: Yan Ding, Xiong Xl, Lei Zhao, Hua-rong LiAbstract:OBJECTIVE: To investigate the role of farnesoid X receptor (FXR) and its downstream molecules small heterodimer partner (SHP), UDP-glucuronosyltransferase 2B4 (UGT2B4), and bile salt export pump (BSEP) in rats with acute Cholestatic Hepatitis. METHODS: A total of 20 Sprague-Dawley rats were randomly divided into normal control group and model group, with 10 rats in each group. The rats in the model group were given a single dose (50 mg/kg) ofα-naphthyl isothiocyanate by gavage to establish the animal model of acute Cholestatic Hepatitis. Quantitative real-time PCR was used to measure the mRNA expression of FXR, UGT2B4, and BSEP in liver tissue at 48 hours after gavage. An automatic biochemical analyzer was used to measure the serum levels of total bilirubin, direct bilirubin, alanine aminotransferase, total bile acid, aspartate aminotransferase, alkaline phosphatase, andγ-glutamyl transferase. The independent samples t-test was used for comparison of means between groups. RESULTS: The model group had significantly lower mRNA expression of FXR, SHP, UGT2B4, and BSEP in liver tissue than the normal control group (0.152±0.088/0.559±0.194/0.177±0.039/0.561±0.123 vs 1.137±0.215/1.512±0.309/2.394±0.462/1.631±0.376, t = 13.408, 8.260, 15.121, and 8.553, all P < 0.05). The model group had significantly higher liver function parameters than the normal control group (all P < 0.01). CONCLUSION: FXR, SHP, UGT2B4, and BSEP are involved in the development of acute Cholestatic Hepatitis. Reduced expression of FXR may cause reduced expression of downstream SHP, UGT2B4, and BSEP, increase the synthesis of bile acid, weaken detoxicating and transporting functions, and thus mediate the development of Cholestatic Hepatitis.
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role of farnesoid x receptor in rats with acute Cholestatic Hepatitis
Chinese Journal of Hepatology, 2016Co-Authors: Yan Ding, Lei Zhao, Xiaoli Xiong, Hua-rong LiAbstract:Objective To investigate the role of farnesoid X receptor (FXR) and its downstream molecules small heterodimer partner (SHP), UDP-glucuronosyltransferase 2B4 (UGT2B4), and bile salt export pump (BSEP) in rats with acute Cholestatic Hepatitis. Methods A total of 20 Sprague-Dawley rats were randomly divided into normal control group and model group, with 10 rats in each group. The rats in the model group were given a single dose (50 mg/kg) ofα-naphthyl isothiocyanate by gavage to establish the animal model of acute Cholestatic Hepatitis. Quantitative real-time PCR was used to measure the mRNA expression of FXR, UGT2B4, and BSEP in liver tissue at 48 hours after gavage. An automatic biochemical analyzer was used to measure the serum levels of total bilirubin, direct bilirubin, alanine aminotransferase, total bile acid, aspartate aminotransferase, alkaline phosphatase, andγ-glutamyl transferase. The independent samples t-test was used for comparison of means between groups. Results The model group had significantly lower mRNA expression of FXR, SHP, UGT2B4, and BSEP in liver tissue than the normal control group (0.152±0.088/0.559±0.194/0.177±0.039/0.561±0.123 vs 1.137±0.215/1.512±0.309/2.394±0.462/1.631±0.376, t = 13.408, 8.260, 15.121, and 8.553, all P < 0.05). The model group had significantly higher liver function parameters than the normal control group (all P < 0.01). Conclusion FXR, SHP, UGT2B4, and BSEP are involved in the development of acute Cholestatic Hepatitis. Reduced expression of FXR may cause reduced expression of downstream SHP, UGT2B4, and BSEP, increase the synthesis of bile acid, weaken detoxicating and transporting functions, and thus mediate the development of Cholestatic Hepatitis. Key words: Cholestasis; Farnesoid X receptor; Small heterodimer partner; UDP-glucuronosyltransferases; Bile salt export pump
H P Roeser - One of the best experts on this subject based on the ideXlab platform.
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flucloxacillin associated Cholestatic Hepatitis an australian and swedish epidemic
European Journal of Clinical Pharmacology, 1995Co-Authors: B M Devereaux, Darrell H G Crawford, P Purcell, Lawrie W Powell, H P RoeserAbstract:The clinico-pathological entity of flucloxacillin-associated Cholestatic Hepatitis is described and the recognition and documentation of cholestasis associated with flucloxacillin and with related isoxazolyl-penicillins (cloxacillin, dicloxacillin) is examined on an international basis, with particular reference to Australia. Data were obtained from the literature, from the Australian adverse drug reaction monitoring agency and from the Collaborative Centre for International Drug Monitoring (World Health Organisation) in Sweden. Approximately 600 cases of flucloxacillin-associated Cholestatic Hepatitis were collected, as well as 164 cases associated with other isoxazolyl penicillins.
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Flucloxacillin associated Cholestatic Hepatitis. An Australian and Swedish epidemic?
European journal of clinical pharmacology, 1995Co-Authors: B M Devereaux, Darrell H G Crawford, P Purcell, Lawrie W Powell, H P RoeserAbstract:The clinico-pathological entity of flucloxacillin-associated Cholestatic Hepatitis is described and the recognition and documentation of cholestasis associated with flucloxacillin and with related isoxazolyl-penicillins (cloxacillin, dicloxacillin) is examined on an international basis, with particular reference to Australia. Data were obtained from the literature, from the Australian adverse drug reaction monitoring agency and from the Collaborative Centre for International Drug Monitoring (World Health Organisation) in Sweden. Approximately 600 cases of flucloxacillin-associated Cholestatic Hepatitis were collected, as well as 164 cases associated with other isoxazolyl penicillins. Jaundice and pruritus may first appear several weeks after administration of the drug has ceased and typically are severe and protracted. Liver tests may be abnormal for months after symptomatic recovery. Death is uncommon. Liver pathology shows centrizonal bile stasis with portal tract inflammation and variable loss of bile ducts. Approximately 1 in 15,000 users of flucloxacillin will develop the reaction. Increasing age (> 55 years) and prolonged intake (> 14 days) are particular risk factors. Cholestasis associated with cloxacillin/dicloxacillin appears to be similar in nature but is less well defined. Recognition and reporting of the reaction have been uncommon in the United Kingdom inter alia and high in Sweden and Australia, although estimates of risk have been similar. In Australia, the remarkably high rate of reports appears to be the result of sustained publicity for the reaction. There is only a trickle of reports of Cholestatic Hepatitis in association with the use of cloxacillin and dicloxacillin from the USA and Canada. The high level of awareness of the reaction and consequential regulatory action so far have not resulted in a diminution of its occurrence in Australia.
George Chandy - One of the best experts on this subject based on the ideXlab platform.
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generalized lymphadenopathy as a marker of ongoing inflammation in prolonged Cholestatic Hepatitis a
European Journal of Gastroenterology & Hepatology, 2002Co-Authors: Ashis Mukhopadhya, George ChandyAbstract:: Extrahepatic manifestations of Hepatitis A are very unusual. We describe a case of prolonged Cholestatic Hepatitis A in a patient with generalized lymphadenopathy. With normalization of transaminases, there was an accompanying reduction in size of these lymph nodes. Lymphadenopathy reflects ongoing hepatic inflammation in prolonged Cholestatic Hepatitis A.
Toru Ikegami - One of the best experts on this subject based on the ideXlab platform.
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early extensive viremia but not rs8099917 genotype is the only predictor for Cholestatic Hepatitis c after living donor liver transplantation
Hepatology Research, 2013Co-Authors: Toru Ikegami, Ken Shirabe, Takasuke Fukuhara, Norihiro Furusyo, Kazuhiro Kotoh, Masaki Kato, Shinji Shimoda, Shinichi Aishima, Yuji Soejima, Tomoharu YoshizumiAbstract:Aim Cholestatic Hepatitis C is one of the most serious but still unaddressed disorders after liver transplantation. Methods In this study, we analyzed 49 patients who underwent living-donor liver transplantation (LDLT) to treat Hepatitis C virus (HCV) infection. Results Five patients developed Cholestatic Hepatitis C, with total bilirubin of 15.2 ± 3.1 mg/dL at diagnosis 6.2 ± 1.0 weeks after LDLT. Univariate analysis showed that larger graft to standard liver volume ratio, higher HCV RNA titer at 2 weeks, earlier peak HCV RNA titer and cytomegalovirus infection were the significant risk factors. The development of Cholestatic Hepatitis C was not significantly associated with interleukin-28B genotype (rs8099917); four out of five affected patients had the T/T genotype. Multivariate analysis showed that higher HCV RNA titer at 2 weeks was the only significant factor (P = 0.026) for the development of Cholestatic Hepatitis C. Receiver–operator curve analysis showed that that HCV RNA titer of more than 7.2 log10IU/mL was the optimal cut-off for characterizing Cholestatic Hepatitis C. All of the patients were serum HCV RNA negative after treatment with pegylated interferon and ribavirin and all the patients are alive. Conclusion Early extensive viremia, but not the rs8099917 genotype, was the only predictor for Cholestatic Hepatitis C after LDLT.
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early diagnosis and treatment resolved Cholestatic Hepatitis c without fibrosis after living donor liver transplantation report of a case
Surgery Today, 2010Co-Authors: Takasuke Fukuhara, Toru Ikegami, Kazutoyo Morita, Kazuki Takeishi, Takeo Toshima, Kenji Umeda, Shigeyuki Nagata, Keishi Sugimachi, Tomonobu Gion, Yuji SoejimaAbstract:Cholestatic Hepatitis is a life-threatening recurrent pattern of Hepatitis C virus (HCV) in immunosuppressed patients, for which curative treatment has not yet been established. We report the successful treatment of Cholestatic Hepatitis in a 59-year-old man who had undergone right lobe living donor liver transplantation (LDLT) for liver cirrhosis (LC) caused by HCV. Following uneventful surgery and an uncomplicated posttransplant clinical course, there was an abrupt increase in total bilirubin in comparison to aminotransferase on postoperative day (POD) 60 (total bilirubin 16.2 mg/dl, alanine aminotransferase 100 U/l, HCV-RNA 390 kIU/ml). The histological findings of the liver tissue showed lymphocyte infiltration in the periportal zone and severe cholestasis. Considering the clinical course, Cholestatic Hepatitis was strongly suspected and pegylated interferon and ribavirin therapy was started immediately, resulting in not only a viral response, but minimal progression of fibrosis. This case serves to demonstrate that early diagnosis and timely initiation of optimal antiviral therapy is essential for the resolution of Cholestatic Hepatitis C.