Pub Date : 2014-09-08DOI: 10.4172/2167-0889.1000164
Lianyu Chen, Kun Wang, Zhen Chen
Background: Sorafenib is the current standard treatment for advanced and unresectable hepatocellular carcinoma (HCC). Although the efficacy of sorafenib on the overall survival and time to progression has been repeatedly proven, clinically evident and sustainable response especially Complete Response (CR) is rarely observed after its treatment. Case Report: We report a case of a 64-year old female patient with unresectable HCC who received sorafenib treatment of more than 8 months following a Transarterial Chemoembolization (TACE) treatment. The patient had a rapid and complete response within 1 month of sorafenib treatment, which sustained for more than 7 months after the initiation of the therapy. Conclusions: This result suggests that sorafenib alone or its use with TACE may be useful in the treatment of unresectable HCC. Translational clinical trials are needed to identify and exploit the underlying mechanism for this superb but rare observation.
{"title":"Complete Response of Hepatocellular Carcinoma to Sorafenib: A Case Report and Review of Literatures","authors":"Lianyu Chen, Kun Wang, Zhen Chen","doi":"10.4172/2167-0889.1000164","DOIUrl":"https://doi.org/10.4172/2167-0889.1000164","url":null,"abstract":"Background: Sorafenib is the current standard treatment for advanced and unresectable hepatocellular carcinoma (HCC). Although the efficacy of sorafenib on the overall survival and time to progression has been repeatedly proven, clinically evident and sustainable response especially Complete Response (CR) is rarely observed after its treatment. Case Report: We report a case of a 64-year old female patient with unresectable HCC who received sorafenib treatment of more than 8 months following a Transarterial Chemoembolization (TACE) treatment. The patient had a rapid and complete response within 1 month of sorafenib treatment, which sustained for more than 7 months after the initiation of the therapy. Conclusions: This result suggests that sorafenib alone or its use with TACE may be useful in the treatment of unresectable HCC. Translational clinical trials are needed to identify and exploit the underlying mechanism for this superb but rare observation.","PeriodicalId":16145,"journal":{"name":"Journal of Liver","volume":"24 1","pages":"1-4"},"PeriodicalIF":0.0,"publicationDate":"2014-09-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"77889544","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2014-08-07DOI: 10.4172/2167-0889.1000162
R. Ennaifer, N. Elleuch, H. Romdhane, R. Hefaiedh, M. Cheikh, Sonda Chaabouni, H. B. Nejma, N. Hadj
Introduction: Ascitic decompensation is a common major complication of cirrhosis and is associated with a poor outcome. In 5-10% of patients, ascites become resistant to treatment (either do not respond to a high dose of diuretics or because these drugs induce complications), which is called Refractory Ascites (RA). RA is associated with poor survival: 20-50% at 1 year. Different treatments have been proposed, however, only liver transplantation can improve survival. The aims of this study were to determine prevalence and predictors of RA development in patients with cirrhosis. Methods: Retrospective study including consecutive cirrhotic patients admitted for controlling ascites between January 2010 and April 2013. Patients and cirrhosis characteristics were studied. Development of RA during followup was investigated. Predictive factors for RA development were evaluated. Results: We included 124 cirrhotic patients: 59 females (47.6%) and 65 males (52.4%) with a mean age of 58 years. Ascites was grade 3 in 38.5% and was the first episode in 45.1% of patients. Etiology of cirrhosis was mainly viral (57.3%). Child-Pugh score was B in 39.5% and C in 28.2%. Mean MELD score was 16 (6-40). During follow-up, 27 patients developed RA, meaning a prevalence of 21.8%. RA type was diuretic intractable in all cases. Predictive factors of RA development in univariate analysis were: ascites grade 3 (OR=4.17; p=0.004), Child-Pugh score C (OR=3.9; p=0.02), MELD score ≥ 15 (OR=4.99; p= 16 (OR=4.13; p=0.005), spontaneous bacterial peritonitis at the first admission (OR= 8,14; p=0.002), prothrombin time ≤ 64.5% (OR=3.36; p=0.013) and sodium urinary output ≤ 42 mmol/24 h (OR=5.13; p=0.03). In multivariate analysis, only urine sodium output was an independent predictive factor of RA development (OR= 4.74; p=0.015). Conclusion: In this present study, prevalence of RA was 21.8%. Urinary sodium output at the first admission for controlling ascite could allow early identification of patients who will develop RA.
{"title":"Refractory Ascites in Cirrhosis: Prevalence and Predictive Factors","authors":"R. Ennaifer, N. Elleuch, H. Romdhane, R. Hefaiedh, M. Cheikh, Sonda Chaabouni, H. B. Nejma, N. Hadj","doi":"10.4172/2167-0889.1000162","DOIUrl":"https://doi.org/10.4172/2167-0889.1000162","url":null,"abstract":"Introduction: Ascitic decompensation is a common major complication of cirrhosis and is associated with a poor outcome. In 5-10% of patients, ascites become resistant to treatment (either do not respond to a high dose of diuretics or because these drugs induce complications), which is called Refractory Ascites (RA). RA is associated with poor survival: 20-50% at 1 year. Different treatments have been proposed, however, only liver transplantation can improve survival. The aims of this study were to determine prevalence and predictors of RA development in patients with cirrhosis. Methods: Retrospective study including consecutive cirrhotic patients admitted for controlling ascites between January 2010 and April 2013. Patients and cirrhosis characteristics were studied. Development of RA during followup was investigated. Predictive factors for RA development were evaluated. Results: We included 124 cirrhotic patients: 59 females (47.6%) and 65 males (52.4%) with a mean age of 58 years. Ascites was grade 3 in 38.5% and was the first episode in 45.1% of patients. Etiology of cirrhosis was mainly viral (57.3%). Child-Pugh score was B in 39.5% and C in 28.2%. Mean MELD score was 16 (6-40). During follow-up, 27 patients developed RA, meaning a prevalence of 21.8%. RA type was diuretic intractable in all cases. Predictive factors of RA development in univariate analysis were: ascites grade 3 (OR=4.17; p=0.004), Child-Pugh score C (OR=3.9; p=0.02), MELD score ≥ 15 (OR=4.99; p= 16 (OR=4.13; p=0.005), spontaneous bacterial peritonitis at the first admission (OR= 8,14; p=0.002), prothrombin time ≤ 64.5% (OR=3.36; p=0.013) and sodium urinary output ≤ 42 mmol/24 h (OR=5.13; p=0.03). In multivariate analysis, only urine sodium output was an independent predictive factor of RA development (OR= 4.74; p=0.015). Conclusion: In this present study, prevalence of RA was 21.8%. Urinary sodium output at the first admission for controlling ascite could allow early identification of patients who will develop RA.","PeriodicalId":16145,"journal":{"name":"Journal of Liver","volume":"6 1","pages":"1-4"},"PeriodicalIF":0.0,"publicationDate":"2014-08-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"85849969","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2014-08-03DOI: 10.4172/2167-0889.1000161
D. Dukova, I. Kotzev
Background and aims: Primary biliary cirrhosis is a chronic and slowly progressive cholestatic liver disease characterized by destruction of interlobular bile ducts, which if untreated, leads to fibrosis, cirrhosis and liver failure. It is more frequent among female patients and is usually diagnosed in the fifth decade of life. This study aims to determine the demographic, clinical, biochemical and serological characteristics and histological stage of patients with primary biliary cirrhosis. Methods: Retrospective analysis of the adult patients diagnosed with primary biliary cirrhosis at our center from January 2005 to December 2013 was performed. Data collection included demographics, clinical features, biochemical and serological markers, and histological stage. Results: 75 patients were diagnosed with primary biliary cirrhosis (mean age: 55 years, range: 19-83), of whom 92.0% were women. The most common symptoms at presentation were fatigue (40.0%), pruritus (40.0%), jaundice (28.0%) and dark urine (26.7%). 20.0% were asymptomatic at diagnosis. 48.0% of patients had cirrhosis at presentation. Positive antimitochondrial antibodies were found in 96% of cases. 34.8% of the patients were positive for antinuclear antibodies. Overlap syndromes were present in 10.6%. Liver biopsy was performed in 45.3% of the patients. Conclusions: The clinical features of primary biliary cirrhosis were similar to those reported in the international literature but with a high percentage of symptomatic and cirrhotic patients at diagnosis.
{"title":"Clinical Analysis of 75 Patients with Primary Biliary Cirrhosis","authors":"D. Dukova, I. Kotzev","doi":"10.4172/2167-0889.1000161","DOIUrl":"https://doi.org/10.4172/2167-0889.1000161","url":null,"abstract":"Background and aims: Primary biliary cirrhosis is a chronic and slowly progressive cholestatic liver disease characterized by destruction of interlobular bile ducts, which if untreated, leads to fibrosis, cirrhosis and liver failure. It is more frequent among female patients and is usually diagnosed in the fifth decade of life. This study aims to determine the demographic, clinical, biochemical and serological characteristics and histological stage of patients with primary biliary cirrhosis. Methods: Retrospective analysis of the adult patients diagnosed with primary biliary cirrhosis at our center from January 2005 to December 2013 was performed. Data collection included demographics, clinical features, biochemical and serological markers, and histological stage. Results: 75 patients were diagnosed with primary biliary cirrhosis (mean age: 55 years, range: 19-83), of whom 92.0% were women. The most common symptoms at presentation were fatigue (40.0%), pruritus (40.0%), jaundice (28.0%) and dark urine (26.7%). 20.0% were asymptomatic at diagnosis. 48.0% of patients had cirrhosis at presentation. Positive antimitochondrial antibodies were found in 96% of cases. 34.8% of the patients were positive for antinuclear antibodies. Overlap syndromes were present in 10.6%. Liver biopsy was performed in 45.3% of the patients. Conclusions: The clinical features of primary biliary cirrhosis were similar to those reported in the international literature but with a high percentage of symptomatic and cirrhotic patients at diagnosis.","PeriodicalId":16145,"journal":{"name":"Journal of Liver","volume":"214 1","pages":"1-4"},"PeriodicalIF":0.0,"publicationDate":"2014-08-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"75575906","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2014-07-01Epub Date: 2014-06-12DOI: 10.4172/2167-0889.1000158
Hannan A Qureshi, Jeffrey A Pearl, Kristy A Anderson, Richard M Green
Background: Cholangiocytes are injured in many biliary tract diseases that result in cirrhosis, cholangiocarcinoma and need for liver transplantation. Recent studies demonstrate that the hormone Fibroblast Growth Factor 19 (FGF19) is produced in the ileum and regulates hepatic gene expression via the enterohepatic circulation. However, the role of FGF19 on cholangiocytes remains largely unknown. The purpose of this study was to elucidate the effect of FGF19 on cholangiocyte gene and protein expression.
Methods: Cultured human cholangiocyte-derived H69 cells were treated with FGF19 (0-50ng/ml) and expression of genes and proteins involved in the Unfolded Protein Response (UPR) and mitogen-activated protein kinase (MAPK) pathways were studied using RT-PCR and Western blot analysis.
Results: FGF19-induced gene and protein expression of the UPR genes BiP and CHOP increased in a dose-responsive pattern. The UPR protein P-eIF2a displayed a bimodal pattern of protein expression, with 10ng/ml of FGF19 maximally reducing and 50ng/ml maximally increasing expression. MAPK pathway protein expression (P-JNK, P-ERK, P-38) displayed a similar bimodal pattern of expression with 2.5ng/ml of FGF19 decreasing expression and 25ng/ml of FGF19 increasing expression.
Conclusions: FGF19 treatment of H69 cells selectively activates BiP and CHOP in a dose-dependent manner. FGF19 also regulates P-eIF2a and MAPK protein expression with a bimodal response. We speculate that FGF19 has an important role in the pathogenesis of many human cholangiopathies and cholestatic liver disorders.
{"title":"Fibroblast Growth Factor 19 Activates the Unfolded Protein Response and Mitogen-Activated Protein Kinase Phosphorylation in H-69 Cholangiocyte Cells.","authors":"Hannan A Qureshi, Jeffrey A Pearl, Kristy A Anderson, Richard M Green","doi":"10.4172/2167-0889.1000158","DOIUrl":"https://doi.org/10.4172/2167-0889.1000158","url":null,"abstract":"<p><strong>Background: </strong>Cholangiocytes are injured in many biliary tract diseases that result in cirrhosis, cholangiocarcinoma and need for liver transplantation. Recent studies demonstrate that the hormone Fibroblast Growth Factor 19 (FGF19) is produced in the ileum and regulates hepatic gene expression via the enterohepatic circulation. However, the role of FGF19 on cholangiocytes remains largely unknown. The purpose of this study was to elucidate the effect of FGF19 on cholangiocyte gene and protein expression.</p><p><strong>Methods: </strong>Cultured human cholangiocyte-derived H69 cells were treated with FGF19 (0-50ng/ml) and expression of genes and proteins involved in the Unfolded Protein Response (UPR) and mitogen-activated protein kinase (MAPK) pathways were studied using RT-PCR and Western blot analysis.</p><p><strong>Results: </strong>FGF19-induced gene and protein expression of the UPR genes BiP and CHOP increased in a dose-responsive pattern. The UPR protein P-eIF2a displayed a bimodal pattern of protein expression, with 10ng/ml of FGF19 maximally reducing and 50ng/ml maximally increasing expression. MAPK pathway protein expression (P-JNK, P-ERK, P-38) displayed a similar bimodal pattern of expression with 2.5ng/ml of FGF19 decreasing expression and 25ng/ml of FGF19 increasing expression.</p><p><strong>Conclusions: </strong>FGF19 treatment of H69 cells selectively activates BiP and CHOP in a dose-dependent manner. FGF19 also regulates P-eIF2a and MAPK protein expression with a bimodal response. We speculate that FGF19 has an important role in the pathogenesis of many human cholangiopathies and cholestatic liver disorders.</p>","PeriodicalId":16145,"journal":{"name":"Journal of Liver","volume":"3 3","pages":""},"PeriodicalIF":0.0,"publicationDate":"2014-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.4172/2167-0889.1000158","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"35514156","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2014-06-27DOI: 10.4172/2167-0889.1000160
E. Nour, Ennaifer Rym, R. Hayfa, H. Rania, Cheikh Myriam, Bougassas Wassila, Ben Nejma Houda, B. Najet
Primary Biliary Cirrhosis (PBC) and Autoimmune Hepatitis (AIH) may simultaneously coexist in some patients, designated as PBC-AIH overlap syndrome. Acute hepatic failure is an unusual initial form of presentation of PBCAIH overlap syndrome. We report the case of a 31 year-old woman with autoimmune PBC-AIH overlap syndrome who presented with an acute hepatic failure. She revealed a good response to corticosteroid and ursodeoxycholic acid therapy.
{"title":"Overlap Syndrome of Primary Biliary Cirrhosis and Autoimmune Hepatitis with Unusual Initial Presentation as an Acute Hepatic Failure","authors":"E. Nour, Ennaifer Rym, R. Hayfa, H. Rania, Cheikh Myriam, Bougassas Wassila, Ben Nejma Houda, B. Najet","doi":"10.4172/2167-0889.1000160","DOIUrl":"https://doi.org/10.4172/2167-0889.1000160","url":null,"abstract":"Primary Biliary Cirrhosis (PBC) and Autoimmune Hepatitis (AIH) may simultaneously coexist in some patients, designated as PBC-AIH overlap syndrome. Acute hepatic failure is an unusual initial form of presentation of PBCAIH overlap syndrome. We report the case of a 31 year-old woman with autoimmune PBC-AIH overlap syndrome who presented with an acute hepatic failure. She revealed a good response to corticosteroid and ursodeoxycholic acid therapy.","PeriodicalId":16145,"journal":{"name":"Journal of Liver","volume":"54 1","pages":"1-2"},"PeriodicalIF":0.0,"publicationDate":"2014-06-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"74620959","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2014-06-27DOI: 10.4172/2167-0889.1000159
Le, R. Fern, es, ro Lungato, Tassiane Zaros, Rodolfo Marinho, Vanessa Cavalcante-Silva, M. R. Nagaoka, V. D’Almeida
Many studies have evaluated the effects of physical training on several metabolic parameters, but few studies have been conducted to evaluate the effects of detraining on these variables. Female mice were distributed into three experimental groups: sedentary controls (C-SED, not trained), trained controls (TR, trained for 10 weeks) and a detraining group (DT, animals detrained for 2 weeks after 8 weeks of training). The exercise protocol was performed by swimming applied for 60 min/day on 5 days/week. The DT group showed an increase of body weight in the 10th week when compared to the 8th week (after training cessation) and the TR group. The groups did not show differences in the plasma levels of corticosterone, glucose, total cholesterol or triglycerides. The DT group showed decreased glycogen content when compared to the TR group. No significant differences were found in the gene expression of glycogen synthase or glycogen phosphorylase or in hepatic glycogen content between CT and TR or DT group. We verified that after a training period of 8 weeks, the animals had an increase in body weight after two weeks of detraining. After two weeks of detraining, animals showed a decrease in liver glycogen content, without an altered fasting glucose concentration in their plasma.
{"title":"Detraining Leads to Weight Gain and a Decrease in Hepatic Glycogen after 8 Weeks of Training","authors":"Le, R. Fern, es, ro Lungato, Tassiane Zaros, Rodolfo Marinho, Vanessa Cavalcante-Silva, M. R. Nagaoka, V. D’Almeida","doi":"10.4172/2167-0889.1000159","DOIUrl":"https://doi.org/10.4172/2167-0889.1000159","url":null,"abstract":"Many studies have evaluated the effects of physical training on several metabolic parameters, but few studies have been conducted to evaluate the effects of detraining on these variables. Female mice were distributed into three experimental groups: sedentary controls (C-SED, not trained), trained controls (TR, trained for 10 weeks) and a detraining group (DT, animals detrained for 2 weeks after 8 weeks of training). The exercise protocol was performed by swimming applied for 60 min/day on 5 days/week. The DT group showed an increase of body weight in the 10th week when compared to the 8th week (after training cessation) and the TR group. The groups did not show differences in the plasma levels of corticosterone, glucose, total cholesterol or triglycerides. The DT group showed decreased glycogen content when compared to the TR group. No significant differences were found in the gene expression of glycogen synthase or glycogen phosphorylase or in hepatic glycogen content between CT and TR or DT group. We verified that after a training period of 8 weeks, the animals had an increase in body weight after two weeks of detraining. After two weeks of detraining, animals showed a decrease in liver glycogen content, without an altered fasting glucose concentration in their plasma.","PeriodicalId":16145,"journal":{"name":"Journal of Liver","volume":"48 1","pages":"1-7"},"PeriodicalIF":0.0,"publicationDate":"2014-06-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"89160271","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2014-06-03DOI: 10.4172/2167-0889.1000156
L. Schwartz, D. Coldwell
Background: Inflammation has been noted to occur due to increased interstitial pressure. This same interstitial pressure in the liver is likely the cause of tumors receiving their blood supply primarily from the hepatic artery. Aim: The aim of the present study was to explore whether the same interstitial pressure in the liver is likely the cause of liver tumors receiving their blood supply primarily from the hepatic artery. Methods: Interstitial pressures were measured in normal and tumor parenchyma during the performance of liver biopsies. Results: The interstitial pressures in the tumors were significantly higher than the interstitial pressure in normal tissues and these pressures were high enough that only arterial blood flow could supply them. Conclusion: The interstitial pressure is the cause of the blood supply difference between normal and tumor parenchyma. This increased interstitial pressure may represent a carcinogenic agent.
{"title":"Is Liver Disease Caused by Increased Pressure? Interstitial Pressure as a Causative Mechanism in Carcinogenesis and in the Differential Blood Supply in Liver Tumors from the Hepatic Artery","authors":"L. Schwartz, D. Coldwell","doi":"10.4172/2167-0889.1000156","DOIUrl":"https://doi.org/10.4172/2167-0889.1000156","url":null,"abstract":"Background: Inflammation has been noted to occur due to increased interstitial pressure. This same interstitial pressure in the liver is likely the cause of tumors receiving their blood supply primarily from the hepatic artery. Aim: The aim of the present study was to explore whether the same interstitial pressure in the liver is likely the cause of liver tumors receiving their blood supply primarily from the hepatic artery. Methods: Interstitial pressures were measured in normal and tumor parenchyma during the performance of liver biopsies. Results: The interstitial pressures in the tumors were significantly higher than the interstitial pressure in normal tissues and these pressures were high enough that only arterial blood flow could supply them. Conclusion: The interstitial pressure is the cause of the blood supply difference between normal and tumor parenchyma. This increased interstitial pressure may represent a carcinogenic agent.","PeriodicalId":16145,"journal":{"name":"Journal of Liver","volume":"2012 1","pages":"1-3"},"PeriodicalIF":0.0,"publicationDate":"2014-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"87868159","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2014-05-05DOI: 10.4172/2167-0889.1000155
H. Ikezaki, N. Furusyo, E. Ogawa, Motohiro Shimizu, Satoshi Hiramine, K. Ura, F. Mitsumoto, Kouji Takayama, K. Toyoda, M. Murata, J. Hayashi
Objective: Limited data has been reported comparing natural human interferon β (nIFNβ) and pegylated IFN-α (PEG-IFNα) when Ribavirin (RBV) is combined. This case-control study was done to compare the efficacy and adverse effects of a combination treatment of nIFNβ or PEG-IFNα plus RBV for chronic hepatitis C patients. Methods: Sixty patients with chronic hepatitis C, 42 infected with hepatitis C virus (HCV) genotype 1 and 18 infected with genotype 2, were treated with nIFNβ plus RBV. Of them, 23 (38.3%) suffered pre-treatment severe depression. Their data was compared with 60 undepressed patients treated with a combination of PEG-IFNα plus RBV. nIFNβ was given intravenously and PEG-IFNα was injected subcutaneously. Results: Sustained virological response (undetectable HCV RNA at 24 weeks after the end of treatment) did not significantly differ between the nIFNβ and PEG-IFNα treated patients (genotype 1, 21.4% vs. 33.3%, P=0.328; genotype 2, 72.2% vs. 88.9%, respectively, P=0.402). None of the nIFNβ treated patients showed exacerbation of depression, while 7 (11.7%) of 60 PEG-IFNα treated patients developed severe depression or malaise. The platelet count of nIFNβ treated patients increased to higher than baseline after week 8, but the platelet count of PEG-IFNα treated patients decreased throughout the treatment. There were significant differences of the changes of platelet counts between the both groups throughout the treatment (all P<0.001). Conclusion: nIFNβ plus RBV treatment was well tolerated by chronic hepatitis C patients with depression or thrombpcytopenia.
{"title":"Efficacy and Tolerance of Interferon β Plus Ribavirin Treatment for Chronic Hepatitis C Patients with Depression or ThrombocytopeniaComparison with Pegylated Interferon α Plus Ribavirin Treatment","authors":"H. Ikezaki, N. Furusyo, E. Ogawa, Motohiro Shimizu, Satoshi Hiramine, K. Ura, F. Mitsumoto, Kouji Takayama, K. Toyoda, M. Murata, J. Hayashi","doi":"10.4172/2167-0889.1000155","DOIUrl":"https://doi.org/10.4172/2167-0889.1000155","url":null,"abstract":"Objective: Limited data has been reported comparing natural human interferon β (nIFNβ) and pegylated IFN-α (PEG-IFNα) when Ribavirin (RBV) is combined. This case-control study was done to compare the efficacy and adverse effects of a combination treatment of nIFNβ or PEG-IFNα plus RBV for chronic hepatitis C patients. \u0000Methods: Sixty patients with chronic hepatitis C, 42 infected with hepatitis C virus (HCV) genotype 1 and 18 infected with genotype 2, were treated with nIFNβ plus RBV. Of them, 23 (38.3%) suffered pre-treatment severe depression. Their data was compared with 60 undepressed patients treated with a combination of PEG-IFNα plus RBV. nIFNβ was given intravenously and PEG-IFNα was injected subcutaneously. \u0000 Results: Sustained virological response (undetectable HCV RNA at 24 weeks after the end of treatment) did not significantly differ between the nIFNβ and PEG-IFNα treated patients (genotype 1, 21.4% vs. 33.3%, P=0.328; genotype 2, 72.2% vs. 88.9%, respectively, P=0.402). None of the nIFNβ treated patients showed exacerbation of depression, while 7 (11.7%) of 60 PEG-IFNα treated patients developed severe depression or malaise. The platelet count of nIFNβ treated patients increased to higher than baseline after week 8, but the platelet count of PEG-IFNα treated patients decreased throughout the treatment. There were significant differences of the changes of platelet counts between the both groups throughout the treatment (all P<0.001). \u0000Conclusion: nIFNβ plus RBV treatment was well tolerated by chronic hepatitis C patients with depression or thrombpcytopenia.","PeriodicalId":16145,"journal":{"name":"Journal of Liver","volume":"25 1","pages":"1-7"},"PeriodicalIF":0.0,"publicationDate":"2014-05-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"74242242","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2014-04-25DOI: 10.4172/2167-0889.1000154
T. Shizuma
The coexistence of Primary Biliary Cirrhosis (PBC) and Inflammatory Bowel Disease (IBD) is uncommon, although hepatobiliary complications in IBD patients are not rare. This report reviews the English and Japanese literature and covers reported cases of concomitant PBC and IBD. We identified 2 cases of concomitant PBC and Crohn’s Disease (CD) and 18 cases of concomitant PBC and Ulcerative Colitis (UC). In most instances (15/18), IBD (CD or UC) developed before PBC, with the exception of 2 cases that were almost simultaneously diagnosed with both conditions. There is no evidence that UC cases with concomitant PBC are more severe than those without; however, the clinical features of concomitant PBC and CD are unclear due to few reports.
{"title":"Coexistence of Primary Biliary Cirrhosis and Inflammatory Bowel Disease","authors":"T. Shizuma","doi":"10.4172/2167-0889.1000154","DOIUrl":"https://doi.org/10.4172/2167-0889.1000154","url":null,"abstract":"The coexistence of Primary Biliary Cirrhosis (PBC) and Inflammatory Bowel Disease (IBD) is uncommon, although hepatobiliary complications in IBD patients are not rare. This report reviews the English and Japanese literature and covers reported cases of concomitant PBC and IBD. We identified 2 cases of concomitant PBC and Crohn’s Disease (CD) and 18 cases of concomitant PBC and Ulcerative Colitis (UC). In most instances (15/18), IBD (CD or UC) developed before PBC, with the exception of 2 cases that were almost simultaneously diagnosed with both conditions. There is no evidence that UC cases with concomitant PBC are more severe than those without; however, the clinical features of concomitant PBC and CD are unclear due to few reports.","PeriodicalId":16145,"journal":{"name":"Journal of Liver","volume":"30 1","pages":"1-3"},"PeriodicalIF":0.0,"publicationDate":"2014-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"89555233","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2014-04-23DOI: 10.4172/2167-0889.1000152
K. Kanayama, K. Ishii
Introduction: Previously, we reported that Hepatitis C Virus (HCV) infection had effects for lipid metabolism in patients with Chronic Hepatitis C (CHC). Recently, HCV with substitutions in amino acids (aa) 70 and/or 91 in the core region of HCV (HCV-C) has been reported to be more difficult to treat than HCV without aa 70 and 91 substitutions. The aim of this study was to clarify whether aa 70 or 91 substitution in the HCV-C influenced serum cholesterol fractions in patients with CHC genotype 1b and high viral load. Patients and Methods: Twenty-two patients infected with genotype 1b and high viral loads, whose serum samples taken before the start of therapy had been stored at -80°centigrade, and in whom aa 70 and 91 substitutions in the HCV-C could be detected, were selected. Patients without aa 70 and 91 substitutions in the HCV-C were assigned to wild (n=12), those with aa 70 substitution in the HCV-C assigned to mutant-70 (n=6), and those with aa 91 substitution in the HCV-C were assigned to mutant-91 (n=4). All patients received interferon (IFN)- based therapy. Fasting serum total cholesterol (C) and its fractions were compared before starting IFN therapy and at 24 weeks after the End of Therapy (EOT). When serum HCV-RNA was negative at 24 weeks after EOT, the patient was defined as having SVR. RESULTS: The SVR rates were 42% (5/12) in the wild, and 17i¼Â… (1/6) in the mutant-70, and 0% (0/4) in the mutant-91. Serum levels of LDL-C were significantly lower and those of HDL-C were significantly higher in the mutant-70 patients than in the wild patients before starting therapy. Only serum level of VLDL-C increased significantly at 24 weeks after EOT than before starting therapy in the wild patients. Conclusions: It was clarified that the mutant-70 influenced serum cholesterol fractions before starting therapy.
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