for Journals by Title or ISSN
for Articles by Keywords
Followed Journals
Journal you Follow: 0
Sign Up to follow journals, search in your chosen journals and, optionally, receive Email Alerts when new issues of your Followed Jurnals are published.
Already have an account? Sign In to see the journals you follow.
Journal Cover Journal of Clinical and Experimental Hepatology
   [3 followers]  Follow    
   Full-text available via subscription Subscription journal
     ISSN (Print) 0973-6883
     Published by Elsevier Homepage  [2563 journals]
  • Future of therapy for Hepatitis C in India: A Matter of Accessibility and
    • Authors: Radha K. Dhiman
      Pages: 85 - 86
      Abstract: An estimated 170–185 million people (about 3% of the world's population) are chronically infected with hepatitis C virus (HCV). Untreated chronic hepatitis C increases the risk of cirrhosis of liver, liver failure and hepatocellular carcinoma. Chronic hepatitis C is also the most common cause for liver transplantation and liver related death in USA, which has recently eclipsed human immunodeficiency virus (HIV) infection as a cause of death. Globally, HCV is implicated in 28% of cases of liver cirrhosis and 26% of cases of hepatocellular carcinoma, which accounts for almost 500,000 deaths per year. The burden of HCV is enormous in low- and middle-income countries from South Asia including India, East Asia, North Africa, the Middle East, and Southeast Asia, which accounts for more than 80% of the global HCV burden. Despite a low to moderate (1–1.5%) prevalence of HCV, India accounts for a significant share of global HCV infections due to the large population; approximately 12–18 million population is infected with HCV. A previously validated HCV disease burden model with historical inputs from India projected that under the current standard of care, advanced liver disease and liver-related mortality will increase despite decreasing prevalence. In the absence of therapies with higher sustained virologic response (SVR), prevention of HCV will decrease overall prevalence, but will not impact short-term liver related mortality or development of hepatocellular carcinoma. Hence, in India a dual approach reducing incidence and increasing treatment is appropriate in showing short-term improvements in advanced stage outcomes with reductions in prevalence.
      Citation: Journal of Clinical & Experimental Hepatology 4, 2 (2014)
      PubDate: 2014-06-01
      DOI: 10.1016/j.jceh.2014.06.011
      Issue No: Vol. 4, No. 2 (2014)
  • The New INASL President: Brilliant and Effective
    • Authors: A.K. Jain
      Pages: 87 - 88
      Abstract: Vinod K. Dixit MD (Medicine) DM (Gastroenterology) Department of Gastroenterology, Institute of Medical Sciences, Banaras Hindu University, Varanasi, Uttar Pradesh 221005, India
      Citation: Journal of Clinical & Experimental Hepatology 4, 2 (2014)
      PubDate: 2014-06-01
      DOI: 10.1016/j.jceh.2014.05.008
      Issue No: Vol. 4, No. 2 (2014)
  • Covert Hepatic Encephalopathy: Does the Mini-Mental State Examination
    • Authors: Michela Corrias; Matteo Turco, Michele D. Rui, Angelo Gatta, Paolo Angeli, Carlo Merkel, Piero Amodio, Sami Schiff, Sara Montagnese
      Pages: 89 - 93
      Abstract: Background/objectives: The Mini-Mental State Examination (MMSE) has been utilized for the diagnosis of hepatic encephalopathy (HE). However, its threshold of abnormality has not been formally tested in patients with cirrhosis and its diagnostic/prognostic validity remains unknown. The aim of this study was to assess it in a large group of well-characterized outpatients with cirrhosis and no overt HE.Methods: One-hundred-and-ninety-one patients underwent clinical assessment, MMSE, electroencephalography (EEG) and paper-and-pencil psychometry (PHES); 117 were followed up for 8 ± 5 months in relation to the occurrence of HE-related hospitalizations.Results: On the day of study, 81 patients (42%) had abnormal EEG and 67 (35%) abnormal PHES; 103 (60%) had a history of HE. Average MMSE was 26.6 ± 3.5; 22 (19%) patients had abnormal MMSE based on the standard threshold of 24. Patients with abnormal EEG/PHES/history of HE had worse MMSE performance than their counterparts with normal tests/negative history (25.7 ± 4.2 vs. 27.3 ± 2.7; P 
      Citation: Journal of Clinical & Experimental Hepatology 4, 2 (2014)
      PubDate: 2014-01-06
      DOI: 10.1016/j.jceh.2013.12.005
      Issue No: Vol. 4, No. 2 (2014)
  • Metadoxine Versus Placebo for the Treatment of Non-alcoholic
           Steatohepatitis: A Randomized Controlled Trial
    • Authors: Kotacherry T. Shenoy; Leena K. Balakumaran, Philip Mathew, Mohan Prasad, Boddu Prabhakar, Ajit Sood, Shivaram P. Singh, Nagaraj P. Rao, Shoukat A. Zargar, Angelo A. Bignamini
      Pages: 94 - 100
      Abstract: Objective and design: The study aimed at assessing the therapeutic efficacy and safety of metadoxine versus placebo on the ultrasonographic and histological features of non-alcoholic steatohepatitis (NASH).Subjects: 134 subjects with biopsy-confirmed NASH were randomized to receive metadoxine 500 mg two times daily (n = 75) or placebo (n = 59) added to the standard of care, over 16 weeks.Efficacy endpoints: Originally, the primary efficacy endpoint was the composite of: reduction in the steatosis by ≥1 grade, reduction in hepatic necro-inflammation by ≥1 grade and ALT normalization. Since >50% of patients refused the second biopsy, it was decided to analyze only the individual parameters.Results: There was no significant difference between the treatment and the placebo groups in either liver histology or ALT or AST. Overall, as expected both groups showed reduction in serum ALT and AST compared to baseline. Compared to placebo (9 out 54), patients on metadoxine (34 out of 75) had significantly higher rates of improvement in 1-point in steatosis grade on ultrasound (P-value
      Citation: Journal of Clinical & Experimental Hepatology 4, 2 (2014)
      PubDate: 2014-03-31
      DOI: 10.1016/j.jceh.2014.03.041
      Issue No: Vol. 4, No. 2 (2014)
  • Clinical Profile and Response to Treatment with Pegylated Interferon
           α 2b and Ribavirin in Chronic Hepatitis C—A Reappraisal
           from a Tertiary Care Center in Northern India
    • Authors: Vinod K. Dixit; Jayanta K. Ghosh, Sangey C. Lamtha, Pankaj Kaushik, Sundeep K. Goyal, Manas K. Behera, Neha Singh, Ashok K. Jain
      Pages: 101 - 105
      Abstract: Aim: To assess the clinical profile of 80 chronic hepatitis C patients in a tertiary health care center in Northern India and also to study the efficacy and tolerability of pegylated interferon (Peg-IFN) α 2b and ribavirin therapy in a cohort of chronic hepatitis C patients.Methods: Thirty subjects with chronic hepatitis C (CH–C) with genotypes 2 and 3 received Peg-IFN α 2b 1.5 μg/kg subcutaneously weekly plus daily ribavirin 800 mg for 24 weeks .Subjects with genotype 1 infection received therapy for 48 weeks with ribavirin 1000 mg/day and Peg-IFN α 2b dose remained the same. The primary end point was the sustained viral response (SVR). Drug dosage was modified or temporarily discontinued if anemia or bone marrow suppression developed.Results: The clinical profile of chronic hepatitis C infected patients showed decompensated cirrhosis in the more elderly patients. Genotype 3 was the commonest genotype and was seen in 21 (70%) patients. The mean baseline HCV RNA was high. SVR was achieved less commonly with genotype 1 than with genotype 2/3. Patients who became negative for HCV RNA at 4-weeks (rapid virological response or RVR) and 12 weeks (early virological response or EVR) of treatment showed significantly higher sustained virological response (SVR) rates. Similarly, patients who showed normalization of ALT level at 4-weeks and 12-weeks of treatment showed significant high rate of SVR. Overall treatment was well tolerated.Conclusion: In our region, CHC subjects have high viral load and genotype 3 being the most common. Treatment with Peg-IFN α 2b and ribavirin is effective and well tolerated. Genotype 1 was more resistant to the treatment. Patients who achieved RVR and EVR are more likely to achieve SVR. Although the numbers of patients in this study was small, considering the paucity of data of treatment from India, the data is relevant.
      Citation: Journal of Clinical & Experimental Hepatology 4, 2 (2014)
      PubDate: 2014-06-20
      DOI: 10.1016/j.jceh.2014.05.012
      Issue No: Vol. 4, No. 2 (2014)
  • Consensus Statement of HCV Task Force of the Indian National Association
           for Study of the Liver (INASL). Part I: Status Report of HCV Infection in
    • Authors: Pankaj Puri; Anil C. Anand, Vivek A. Saraswat, Subrat K. Acharya, Radha K. Dhiman, Rakesh Aggarwal, Shivram P. Singh, Deepak Amarapurkar, Anil Arora, Mohinish Chhabra, Kamal Chetri, Gourdas Choudhuri, Vinod K. Dixit, Ajay Duseja, Ajay K. Jain, Dharmesh Kapoorz, Premashis Kar, Abraham Koshy, Ashish Kumar, Kaushal Madan, Sri P. Misra, Mohan V.G. Prasad, Aabha Nagral, Amarendra S. Puri, R. Jeyamani, Sanjiv Saigal, Shiv K. Sarin, Samir Shah, P.K. Sharma, Ajit Sood, Sandeep Thareja, Manav Wadhawan
      Pages: 106 - 116
      Abstract: Globally, around 150 million people are infected with hepatitis C virus (HCV). India contributes a large proportion of this HCV burden. The prevalence of HCV infection in India is estimated at between 0.5% and 1.5%. It is higher in the northeastern part, tribal populations and Punjab, areas which may represent HCV hotspots, and is lower in western and eastern parts of the country. The predominant modes of HCV transmission in India are blood transfusion and unsafe therapeutic injections. There is a need for large field studies to better understand HCV epidemiology and identify high-prevalence areas, and to identify and spread awareness about the modes of transmission of this infection in an attempt to prevent disease transmission.
      Citation: Journal of Clinical & Experimental Hepatology 4, 2 (2014)
      PubDate: 2014-06-11
      DOI: 10.1016/j.jceh.2014.05.006
      Issue No: Vol. 4, No. 2 (2014)
  • Consensus Statement of HCV Task Force of the Indian National
           Association for Study of the Liver (INASL). Part II: INASL
           Recommendations for Management of HCV in India
    • Authors: Pankaj Puri; Anil C. Anand, Vivek A. Saraswat, Subrat K. Acharya, Shiv K. Sarin, Radha K. Dhiman, Rakesh Aggarwal, Shivaram P. Singh, Deepak Amarapurkar, Anil Arora, Mohinish Chhabra, Kamal Chetri, Gourdas Choudhuri, Vinod K. Dixit, Ajay Duseja, Ajay K. Jain, Dharmesh Kapoor, Premashis Kar, Abraham Koshy, Ashish Kumar, Kaushal Madan, Sri P. Misra, Mohan V.G. Prasad, Aabha Nagral, Amarendra S. Puri, R. Jeyamani, Sanjiv Saigal, Samir Shah, Praveen K. Sharma, Ajit Sood, Sandeep Thareja, Manav Wadhawan
      Pages: 117 - 140
      Abstract: The estimated prevalence of hepatitis C virus (HCV) infection in India is between 0.5 and 1.5% with hotspots showing much higher prevalence in some areas of northeast India, in some tribal populations and in certain parts of Punjab. Genotype 3 is the most prevalent type of infection. Recent years have seen development of a large number of new molecules that are revolutionizing the treatment of hepatitis C. Some of the new directly acting agents (DAAs) like sofosbuvir have been called game-changers because they offer the prospect of interferon-free regimens for the treatment of HCV infection. These new drugs have not yet been approved in India and their cost and availability is uncertain at present. Till these drugs become available at an affordable cost, the treatment that was standard of care for the whole world before these newer drugs were approved should continue to be recommended. For India, cheaper options, which are as effective as the standard-of-care (SOC) in carefully selected patients, are also explored to bring treatment within reach of poorer patients. It may be prudent to withhold treatment at present for selected patients with genotype 1 or 4 infection and low levels of fibrosis (F1 or F2), and for patients who are non-responders to initial therapy, interferon intolerant, those with decompensated liver disease, and patients in special populations such as stable patients after liver and kidney transplantation, HIV co-infected patients and those with cirrhosis of liver.
      Citation: Journal of Clinical & Experimental Hepatology 4, 2 (2014)
      PubDate: 2014-06-26
      DOI: 10.1016/j.jceh.2014.06.001
      Issue No: Vol. 4, No. 2 (2014)
  • Pregnancy with Portal Hypertension
    • Authors: Neelam Aggarwal; Neha Negi, Aakash Aggarwal, Vijay Bodh, Radha K. Dhiman
      Pages: 163 - 171
      Abstract: Even though pregnancy is rare with cirrhosis and advanced liver disease, but it may co-exist in the setting of non-cirrhotic portal hypertension as liver function is preserved but whenever encountered together is a complex clinical dilemma. Pregnancy in a patient with portal hypertension presents a special challenge to the obstetrician as so-called physiological hemodynamic changes associated with pregnancy, needed for meeting demands of the growing fetus, worsen the portal hypertension thereby putting mother at risk of potentially life-threatening complications like variceal hemorrhage. Risks of variceal bleed and hepatic decompensation increase many fold during pregnancy. Optimal management revolves round managing the portal hypertension and its complications. Thus management of such cases requires multi-speciality approach involving obstetricians experienced in dealing with high risk cases, hepatologists, anesthetists and neonatologists. With advancement in medical field, pregnancy is not contra-indicated in these women, as was previously believed. This article focuses on the different aspects of pregnancy with portal hypertension with special emphasis on specific cause wise treatment options to decrease the variceal bleed and hepatic decompensation. Based on extensive review of literature, management from pre-conceptional period to postpartum is outlined in order to have optimal maternal and perinatal outcomes.
      Citation: Journal of Clinical & Experimental Hepatology 4, 2 (2014)
      PubDate: 2014-06-25
      DOI: 10.1016/j.jceh.2014.05.014
      Issue No: Vol. 4, No. 2 (2014)
  • Patient with Liver Cirrhosis and Hemorrhagic Ascites
    • Authors: Mukesh Rathor; Anupam Lal, Radha K. Dhiman
      Pages: 178 - 178
      Abstract: A 54-year-old male presented with progressive abdominal distension and loss of appetite for 2 months. Prior to being admitted at this institute, patient got evaluated for abdominal distension at a local hospital. Diagnostic ascites aspiration was done, which was hemorrhagic. Ultrasound abdomen showed features suggestive of chronic liver disease. The patient had mild pallor. Abdomen was distended with no visible veins. Liver and spleen were not palpable. Moderate ascites was present. His hemoglobin was 8.6 g/dL, total leukocyte count was 8800/mm3, and platelet count was 313 × 103/mm3. Liver function tests showed normal serum bilirubin level but elevated aspartate (150 IU/L) and alanine (70 IU/L) aminotransferase levels. His prothrombin time was four seconds prolonged with an INR of 1.2. His ultrasound abdomen had features suggestive of liver cirrhosis with a large heterogeneous hypoechoic lesion in right lobe of liver with multiple tiny hypoechoic liver nodules. Ascitic fluid aspiration was repeated, which showed hemorrhagic fluid. Ascitic fluid cytology showed red blood cells in full field but no malignant cells. Further, patient was found to be hepatitis B surface antigen (HBsAg) positive, and had a high HBV DNA viral load of 3.4 × 106 IU/mL. Serum alpha feto protein was 1210 ng/mL. Patient was started on antiviral therapy with Tab Tenofovir 300 mg daily. Triple phase contrast enhanced CT abdomen was done. Shown below are (A) contrast enhanced CT axial image taken at the level of upper abdomen and (A) sagittal reconstructed contrast enhanced CT Image showing the right lobe of liver.
      Citation: Journal of Clinical & Experimental Hepatology 4, 2 (2014)
      PubDate: 2014-06-23
      DOI: 10.1016/j.jceh.2014.06.002
      Issue No: Vol. 4, No. 2 (2014)
  • Hepatitis C Virus Genotype 3: Hope for Nonresponders and Patients With
    • Authors: Shalimar
      Pages: 179 - 181
      Abstract: Zeuzem S, Dusheiko GM, Salupere R, Mangia A, Flisiak R, Hyland RH, Illeperuma A, Svarovskaia E, Brainard DM, Symonds WT, Subramanian GM, McHutchison JG, Weiland O, Reesink HW, Ferenci P, Hézode C, Esteban R; the VALENCE Investigators. Sofosbuvir and Ribavirin in HCV Genotypes 2 and 3. N Engl J Med. 2014 May 4 [Epub ahead of print].
      Citation: Journal of Clinical & Experimental Hepatology 4, 2 (2014)
      PubDate: 2014-06-12
      DOI: 10.1016/j.jceh.2014.05.009
      Issue No: Vol. 4, No. 2 (2014)
  • Hepatobiliary Quiz—10 (2014)
    • Authors: Swastik Agrawal; Radha K. Dhiman
      Pages: 182 - 183
      Citation: Journal of Clinical & Experimental Hepatology 4, 2 (2014)
      PubDate: 2014-06-17
      DOI: 10.1016/j.jceh.2014.05.010
      Issue No: Vol. 4, No. 2 (2014)
  • Hepatobiliary Quiz—10 (2014)
    • Authors: Swastik Agrawal; Radha K. Dhiman
      Pages: 184 - 187
      Abstract: Progressive familial intrahepatic cholestasis (PIC), benign recurrent intrahepatic cholestasis (BRIC), intrahepatic cholestasis of pregnancy (ICP) and certain drug induced cholestasis are genetically determined disease due to mutations of genes encoding proteins responsible for bile transport from hepatocyte to canaliculi. PFIC is the most severe disease in this spectrum, and results from complete or almost complete absence of functional transporter proteins while the other conditions are associated with milder reduction in functional transporter activity. PFIC is inherited in an autosomal recessive manner and is divided in to PFIC 1 caused by defects in ATP8B1 gene which encodes for familial intrahepatic cholestasis 1 (FIC1) protein; PFIC 2 caused by mutation in the ABCB11 gene encoding bile salt excretory protein (BSEP); and PFIC 3 caused by defects in ABCB4 gene encoding multidrug resistance class III (MDR3) protein. BSEP is a transporter protein, expressed at the canalicular membrane of hepatocyte and functions as the main exporter of bile acids from hepatocyte to canaliculi against a concentration gradient. Defects in BSEP synthesis and/or function lead to reduced bile salt secretion followed by decreased bile flow, accumulation of bile salts in hepatocytes and hepatocellular damage.
      Citation: Journal of Clinical & Experimental Hepatology 4, 2 (2014)
      PubDate: 2014-06-18
      DOI: 10.1016/j.jceh.2014.05.011
      Issue No: Vol. 4, No. 2 (2014)
  • Spontaneous Rupture of Hepatocellular Carcinoma
    • Authors: Mukesh Rathor; Anupam Lal, Radha K. Dhiman
      Pages: 188 - 189
      Abstract: A contrast enhanced computer tomography (CECT) abdomen of the patient showed hepatomegaly with nodular irregular liver margins. A 15.5 × 10.5 cm large exophytic heterogeneously attenuating mass seen arising from segment VI/VII with extension into the subphrenic space. Multiple right hepatic artery branches were supplying it. There was a breech in the lateral margin of the superior part of this mass lesion suggestive of rupture (B).
      Citation: Journal of Clinical & Experimental Hepatology 4, 2 (2014)
      PubDate: 2014-06-23
      DOI: 10.1016/j.jceh.2014.06.003
      Issue No: Vol. 4, No. 2 (2014)
  • Nutrition in the Management of Cirrhosis and its Neurological
    • Authors: Chantal Bémeur; Roger F. Butterworth
      Pages: 141 - 150
      Abstract: Malnutrition is a common feature of chronic liver diseases that is often associated with a poor prognosis including worsening of clinical outcome, neuropsychiatric complications as well as outcome following liver transplantation. Nutritional assessment in patients with cirrhosis is challenging owing to confounding factors related to liver failure. The objectives of nutritional intervention in cirrhotic patients are the support of liver regeneration, the prevention or correction of specific nutritional deficiencies and the prevention and/or treatment of the complications of liver disease per se and of liver transplantation. Nutritional recommendations target the optimal supply of adequate substrates related to requirements linked to energy, protein, carbohydrates, lipids, vitamins and minerals. Some issues relating to malnutrition in chronic liver disease remain to be addressed including the development of an appropriate well-validated nutritional assessment tool, the identification of mechanistic targets or therapy for sarcopenia, the development of nutritional recommendations for obese cirrhotic patients and liver-transplant recipients and the elucidation of the roles of vitamin A hepatotoxicity, as well as the impact of deficiencies in riboflavin and zinc on clinical outcomes. Early identification and treatment of malnutrition in chronic liver disease has the potential to lead to better disease outcome as well as prevention of the complications of chronic liver disease and improved transplant outcomes.
      Citation: Journal of Clinical & Experimental Hepatology 4, 2 (2014)
      PubDate: 2013-05-29
      DOI: 10.1016/j.jceh.2013.05.008
      Issue No: Vol. 4, No. 2 (2013)
  • Pregnancy-Related Liver Disorders
    • Authors: Ashish Goel; Kapil D. Jamwal, Anup Ramachandran, Kunissery A. Balasubramanian, Chundamannil E. Eapen
      Pages: 151 - 162
      Abstract: Pregnancy-related liver disorders accounted for 8% of all maternal deaths at our center from 1999 to 2011. Of the three pregnancy-related liver disorders (acute fatty liver of pregnancy (AFLP), HELLP (Hemolysis, elevated liver enzymes, low platelets) syndrome and pre-eclamptic liver dysfunction, which can lead to adverse maternal and fetal outcome, AFLP is most typically under - diagnosed. Risk of maternal death can be minimised by timely recognition and early/aggressive multi-specialty management of these conditions. Urgent termination of pregnancy remains the cornerstone of therapy for some of these life threatening disorders, but recent advancements in our understanding help us in better overall management of these patients. This review focuses on various aspects of pregnancy-related liver disorders.
      Citation: Journal of Clinical & Experimental Hepatology 4, 2 (2014)
      PubDate: 2013-03-18
      DOI: 10.1016/j.jceh.2013.03.220
      Issue No: Vol. 4, No. 2 (2013)
  • Melioidosis Presenting as Fever and Jaundice: A Rare Presentation
    • Authors: Pankaj Tyagi; Vinit Shah, Praveen Sharma, Naresh Bansal, Vikas Singla, Ashish Kumar, Anil Arora
      Pages: 172 - 174
      Abstract: Melioidosis caused by the environmental Gram-negative bacillus Burkholderia pseudomallei is endemic in northern Australia and Southeast Asia and is being described increasingly from south and west coastal regions of India. Melioidosis is known to have high mortality (14–50%) and the risk factors associated with it are diabetes mellitus and heavy alcohol abuse. Melioidosis primarily presents as pneumonia, genitourinary infection and bacteremia. We present a case of Melioidosis from North India, a 56-year-old diabetic male, presenting with fever and jaundice. His blood culture was positive for the B. pseudomallei. The hepatic involvement was in the form of jaundice with serum bilirubin value of more than 12 mg/dL, hepatic enzymes more than ten times high and without hepatic abscess. He improved with intravenous antibiotics with complete normalization of liver function tests.
      Citation: Journal of Clinical & Experimental Hepatology 4, 2 (2014)
      PubDate: 2013-08-05
      DOI: 10.1016/j.jceh.2013.07.003
      Issue No: Vol. 4, No. 2 (2013)
  • Hemophagocytic Lymphohistiocytosis (HLH) in Children Presenting as Liver
    • Authors: Nomisha Amin; Ira Shah, Sushmita Bhatnagar
      Pages: 175 - 177
      Abstract: Hemophagocytic lymphohistiocytosis (HLH) is a rare acute hyperinflammatory condition presenting with high fever, pancytopenia, splenomegaly with the pathologic finding of hemophagocytic lymphohistiocytosis in bone marrow and other tissues. Predominant hepatic manifestations at presentation are rare. We report a series of three cases which showcase the spectrum of liver disease as presentation in hemophagocytic lymphohistiocytosis.
      Citation: Journal of Clinical & Experimental Hepatology 4, 2 (2014)
      PubDate: 2013-06-24
      DOI: 10.1016/j.jceh.2013.06.003
      Issue No: Vol. 4, No. 2 (2013)
School of Mathematical and Computer Sciences
Heriot-Watt University
Edinburgh, EH14 4AS, UK
Tel: +00 44 (0)131 4513762
Fax: +00 44 (0)131 4513327
About JournalTOCs
News (blog, publications)
JournalTOCs on Twitter   JournalTOCs on Facebook

JournalTOCs © 2009-2014