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Hepatitis: HELP
Articles by C. E. Eapen
Based on 14 articles published since 2010
(Why 14 articles?)
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Between 2010 and 2020, C. E. Eapen wrote the following 14 articles about Hepatitis.
 
+ Citations + Abstracts
1 Editorial Acute-on-chronic liver failure: consensus recommendations of the Asian Pacific association for the study of the liver (APASL): an update. 2019

Sarin, Shiv Kumar / Choudhury, Ashok / Sharma, Manoj K / Maiwall, Rakhi / Al Mahtab, Mamun / Rahman, Salimur / Saigal, Sanjiv / Saraf, Neeraj / Soin, A S / Devarbhavi, Harshad / Kim, Dong Joon / Dhiman, R K / Duseja, Ajay / Taneja, Sunil / Eapen, C E / Goel, Ashish / Ning, Q / Chen, Tao / Ma, Ke / Duan, Z / Yu, Chen / Treeprasertsuk, Sombat / Hamid, S S / Butt, Amna S / Jafri, Wasim / Shukla, Akash / Saraswat, Vivek / Tan, Soek Siam / Sood, Ajit / Midha, Vandana / Goyal, Omesh / Ghazinyan, Hasmik / Arora, Anil / Hu, Jinhua / Sahu, Manoj / Rao, P N / Lee, Guan H / Lim, Seng G / Lesmana, Laurentius A / Lesmana, Cosmas Rinaldi / Shah, Samir / Prasad, V G Mohan / Payawal, Diana A / Abbas, Zaigham / Dokmeci, A Kadir / Sollano, Jose D / Carpio, Gian / Shresta, Ananta / Lau, G K / Fazal Karim, Md / Shiha, Gamal / Gani, Rino / Kalista, Kemal Fariz / Yuen, Man-Fung / Alam, Seema / Khanna, Rajeev / Sood, Vikrant / Lal, Bikrant Bihari / Pamecha, Viniyendra / Jindal, Ankur / Rajan, V / Arora, Vinod / Yokosuka, Osamu / Niriella, Madunil A / Li, Hai / Qi, Xiaolong / Tanaka, Atsushi / Mochida, Satoshi / Chaudhuri, Dominic Ray / Gane, Ed / Win, Khin Maung / Chen, Wei Ting / Rela, Mohd / Kapoor, Dharmesh / Rastogi, Amit / Kale, Pratibha / Rastogi, Archana / Sharma, Chhagan Bihari / Bajpai, Meenu / Singh, Virender / Premkumar, Madhumita / Maharashi, Sudhir / Olithselvan, A / Philips, Cyriac Abby / Srivastava, Anshu / Yachha, Surender K / Wani, Zeeshan Ahmad / Thapa, B R / Saraya, Anoop / Shalimar, ? / Kumar, Ashish / Wadhawan, Manav / Gupta, Subash / Madan, Kaushal / Sakhuja, Puja / Vij, Vivek / Sharma, Barjesh C / Garg, Hitendra / Garg, Vishal / Kalal, Chetan / Anand, Lovkesh / Vyas, Tanmay / Mathur, Rajan P / Kumar, Guresh / Jain, Priyanka / Pasupuleti, Samba Siva Rao / Chawla, Yogesh K / Chowdhury, Abhijit / Alam, Shahinul / Song, Do Seon / Yang, Jin Mo / Yoon, Eileen L / Anonymous1771066. ·Department of Hepatology, Institute of Liver and Biliary Sciences, New Delhi, 110070, India. sksarin@ilbs.in. · Department of Hepatology, Institute of Liver and Biliary Sciences, New Delhi, 110070, India. · Department of Hepatology, Bangabandhu Sheikh Mujib Medical University, Dhaka, Bangladesh. · Department of Hepatology, Medanta The Medicity, Gurgaon, India. · Department of Hepatology, St John Medical College, Bangalore, India. · Department of Internal Medicine, Hallym University College of Medicine, Seoul, South Korea. · Department of Hepatology, PGIMER, Chandigarh, India. · Department of Hepatology, CMC, Vellore, India. · Institute and Department of Infectious Disease, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China. · Translational Hepatology Institute Capital Medical University, Beijing You'an Hospital, Beijing, China. · Department of Medicine, Chulalongkorn University, Bangkok, Thailand. · Department of Medicine, Aga Khan University Hospital, Karachi, Pakistan. · Department of Gastroenterology, Lokmanya Tilak Municipal General Hospital and Lokmanya Tilak Municipal Medical College, Sion, Mumbai, India. · Department of Gastroenterology, SGPGIMS, Lucknow, India. · Department of Medicine, Hospital Selayang, Bata Caves, Selangor, Malaysia. · Department of Gastroenterology, DMC, Ludhiana, India. · Department of Hepatology, Nork Clinical Hospital of Infectious Disease, Yerevan, Armenia. · Department of Gastroenterology and Hepatology, Sir Ganga Ram Hospital and GRIPMER, New Delhi, Delhi, India. · Department of Medicine, 302 Millitary Hospital, Beijing, China. · Department of Gastroenterology and Hepatology Sciences, IMS & SUM Hospital, Bhubaneswar, Odisha, India. · Asian Institute of Gastroenterology, Hyderabad, India. · Division of Gastroenterology and Hepatology, Department of Medicine, National University Health System, Singapore, Singapore. · Digestive Disease and GI Oncology Centre, Medistra Hospital, Jakarta, Indonesia. · Department of Hepatology, Global Hospitals, Mumbai, India. · Department of Gastroenterology, VGM Hospital, Coimbatore, India. · Fatima University Medical Center Manila, Manila, Philippines. · Department of Medicine, Ziauddin University Hospital, Karachi, Pakistan. · Department of Medicine, Ankara University School of Medicine, Ankara, Turkey. · Department of Medicine, University of Santo Tomas, Manila, Philippines. · Department of Hepatology, Foundation Nepal Sitapaila Height, Kathmandu, Nepal. · Department of Medicine, Humanity and Health Medical Group, New Kowloon, Hong Kong, China. · Department of Hepatology, Sir Salimullah Medical College, Dhaka, Bangladesh. · Egyptian Liver Research Institute And Hospital, Cairo, Egypt. · Division of Hepatobiliary, Department of Internal Medicine, Faculty of Medicine, Cipto Mangunkusumo Hospital, Universitas Indonesia, Jakarta, Indonesia. · Department of Medicine, Queen Mary Hospital Hong Kong, The University of Hong Kong, Hong Kong, China. · Department of Pediatric Hepatology, Institute of Liver and Biliary Sciences, New Delhi, Delhi, India. · Department of Hepatobilliary Pancreatic Surgery and Liver Transplant, Institute of Liver and Biliary Sciences, New Delhi, Delhi, India. · Professor Emeritus, Chiba University, Chiba, Japan. · Department of Medicine, University of Kelaniya, Ragama, Sri Lanka. · Department of Gastroenterology, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China. · CHESS Frontier Center, The First Hospital of Lanzhou University, Lanzhou University, Lanzhou, China. · Department of Medicine, Tokyo University School of Medicine, Tokyo, Japan. · Department of Gastroenterology and Hepatology, Faculty of Medicine, Saitama Medical University, Saitama, Japan. · New Zealand Liver Transplant Unit, Auckland Hospital, Auckland, New Zealand. · Yangon GI and Liver Centre, Pabedan, Yangon, Myanmar. · Division of Hepatology, Department of Gastroenterology and Hepatology, Chang Gung Medical Foundation, Linkou Chang Gung Memorial Hospital, Taoyuan, Taiwan. · Department of Liver Transplant Surgery, Dr. Rela Institute and Medical Centre, Chennai, India. · Department of Microbiology, Institute of Liver and Biliary Sciences, New Delhi, Delhi, India. · Department of Pathology, Institute of Liver and Biliary Sciences, New Delhi, Delhi, India. · Department of Immunohematology and Transfusion Medicine, Institute of Liver and Biliary Sciences, New Delhi, Delhi, India. · Department of Gatroenterology, SMS Med College, Jaipur, India. · Division of Liver Transplantation and Hepatology, Manipal Hospitals, Bangalore, India. · The Liver Unit, Cochin Gastroenterology Group, Ernakulam Medical Centre, Kochi, India. · Department of Pediatric Gastroenterology, SGPGIMS, Lucknow, India. · Noora Hospital in Srinagar, Shrinagar, India. · Department of Gastroenterology and Pediatric Gastroenterology, PGIMER, Chandigarh, India. · Department of Gastroenterology and Human Nutrition, AIIMS, New Delhi, India. · Department of Gastroenterology, Hepatology and Liver Transplant, B L K Hospital, New Delhi, India. · Centre for Liver and Biliary Science, Max Hospital, New Delhi, India. · Department of Gastroenterology, Hepatology and Liver Transplant, Max Hospital, New Delhi, India. · Department of Pathology, GB Pant Hospital, New Delhi, India. · Department of Liver Transplant and Hepatobilliary Surgery, Fortis Hospital, New Delhi, India. · Department of Gastroenterology, GB Pant Hospital, New Delhi, India. · Department of Gastroenterology, Hepatology and Liver Transplant, Apollo Hospital, New Delhi, India. · Department of Hepatology, Sir H N Reliance Hospital and Research Centre, Mumbai, India. · Department of Gastroenterology and Hepatology, Narayana Hospital, Gurugram, India. · Department of Hepatology, Parimal Multi-Speciality Hospital, Ahmedabad, India. · Department of Nephrology, Institute of Liver and Biliary Sciences, New Delhi, India. · Department of Statistics and Clinical Research, Institute of Liver and Biliary Sciences, New Delhi, India. · Department of Hepatology and Gastroenterology, Kalinga Institute of Med Sciences, KIIT University, Bhubaneswar, India. · Department of Hepatology, Institute of Post Graduate Medical Education and Research, Kolkata, India. · Department of Internal Medicine, College of Medicine, The Catholic University of Korea, Seoul, South Korea. · Department Of Internal Medicine, Inje University College of Medicine, Busan, South Korea. ·Hepatol Int · Pubmed #31172417.

ABSTRACT: The first consensus report of the working party of the Asian Pacific Association for the Study of the Liver (APASL) set up in 2004 on acute-on-chronic liver failure (ACLF) was published in 2009. With international groups volunteering to join, the "APASL ACLF Research Consortium (AARC)" was formed in 2012, which continued to collect prospective ACLF patient data. Based on the prospective data analysis of nearly 1400 patients, the AARC consensus was published in 2014. In the past nearly four-and-a-half years, the AARC database has been enriched to about 5200 cases by major hepatology centers across Asia. The data published during the interim period were carefully analyzed and areas of contention and new developments in the field of ACLF were prioritized in a systematic manner. The AARC database was also approached for answering some of the issues where published data were limited, such as liver failure grading, its impact on the 'Golden Therapeutic Window', extrahepatic organ dysfunction and failure, development of sepsis, distinctive features of acute decompensation from ACLF and pediatric ACLF and the issues were analyzed. These initiatives concluded in a two-day meeting in October 2018 at New Delhi with finalization of the new AARC consensus. Only those statements, which were based on evidence using the Grade System and were unanimously recommended, were accepted. Finalized statements were again circulated to all the experts and subsequently presented at the AARC investigators meeting at the AASLD in November 2018. The suggestions from the experts were used to revise and finalize the consensus. After detailed deliberations and data analysis, the original definition of ACLF was found to withstand the test of time and be able to identify a homogenous group of patients presenting with liver failure. New management options including the algorithms for the management of coagulation disorders, renal replacement therapy, sepsis, variceal bleed, antivirals and criteria for liver transplantation for ACLF patients were proposed. The final consensus statements along with the relevant background information and areas requiring future studies are presented here.

2 Editorial Infliximab and occult hepatitis B infection: to treat or not to treat? 2013

Goel, Ashish / Eapen, C E / Danda, Debashish. · ·Int J Rheum Dis · Pubmed #23992254.

ABSTRACT: -- No abstract --

3 Review Indian National Association for Study of the Liver (INASL) Guidance for Antiviral Therapy Against HCV Infection in 2015. 2015

Puri, Pankaj / Anand, Anil C / Saraswat, Vivek A / Acharya, Subrat K / Dhiman, Radha K / Sarin, Shiv K / Singh, Shivaram P / Chawla, Yogesh K / Aggarwal, Rakesh / Amarapurkar, Deepak / Arora, Anil / Dixit, Vinod K / Sood, Ajit / Shah, Samir / Duseja, Ajay / Kapoor, Dharmesh / Shalimar, ? / Madan, Kaushal / Pande, Gaurav / Nagral, Aabha / Kar, Premashis / Koshy, Abraham / Puri, Amarender S / Eapen, C E / Thareja, Sandeep. ·Department of Internal Medicine, Armed Forces Medical College, Pune 411040, India. · Department of Gastroenterology and Hepatology, Indraprastha Apollo Hospital, New Delhi 110076, India. · Department of Gastroenterology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow 226014, India. · Department of Gastroenterology, All India Institute of Medical Sciences, New Delhi 110029, India. · Department of Hepatology, Postgraduate Institute of Medical Education and Research, Chandigarh 160012, India. · Institute of Liver and Biliary Sciences, VasantKunj, New Delhi 110070, India. · Department of Gastroenterology, SCB Medical College, Cuttack 753007, India. · Department of Gastroenterology, Bombay Hospital, Mumbai 400020, India. · Department of Gastroenterology and Hepatology, Sir Ganga Ram Hospital, New Delhi 110060, India. · Department of Gastroenterology, Banaras Hindu University, Varanasi 221005, India. · Department of Gastroenterology, Dayanand Medical College, Ludhiana 141001, India. · Department of Gastroenterology, Global Hospital, Mumbai 400078, India. · Department of Gastroenterology, Global Hospital, Hyderabad 500004, India. · Department of Gastroenterology, Artemis Hospital, Gurgaon 122001, India. · Department of Gastroenterology, Jaslok Hospital, Mumbai 400026, India. · Department of Gastroenterology, LNJP Hospital, and Maulana Azad Medical College, New Delhi 110002, India. · Department of Hepatology, Lakeshore Hospital, Cochin 682304, India. · Department of Gastroenterology, GB Pant Hospital, New Delhi 110002, India. · Department of Gastroenterology, Christian Medical College, Vellore 632004, India. · Department of Gastroenterology, Army Hospital (R & R), New Delhi 110010, India. ·J Clin Exp Hepatol · Pubmed #26628840.

ABSTRACT: Overall prevalence of HCV infection in India has been estimated to be approximately 1.3% in the general population. Recent introduction of sofosbuvir in India at a relatively affordable price has led to great optimism about prospects of cure for these patients. This drug is likely to form the backbone of current and future treatment regimes for HCV infection, displacing pegylated interferon. Availability of directly acting antiviral drugs (DAAs) has necessitated revision of INASL guidelines for the treatment of HCV published in 2014, as has happened across the world. Current considerations for the treatment of HCV in India include the poorer response of genotype 3, nonavailability of many of the DAAs recommended by other guidelines and the cost of therapy. Since only one DAA, sofosbuvir, is available in India, only two sofosbuvir-based regimes are possible: either dual drug therapy in combination with ribavirin alone for 6 months or triple drug therapy in combination with ribavirin and pegylated interferon for 3 months. The utility of these regimes in various situations has been discussed. Availability of a few other newer DAAs, expected in 2016, is expected to lead to more widespread use of these agents. Current guidance will be updated once newer DAAs, newer evidence with DAAs and 'real-life experience' with use of DAAs accumulate in India.

4 Article Risk factors for non-alcoholic fatty liver disease are common in patients with non-B non-C hepatocellular carcinoma in India. 2017

David, Deepu / Raghavendran, Anantharam / Goel, Ashish / Bharath Kumar, C / Kodiatte, Thomas Alex / Burad, Deepak / Abraham, Priya / Ramakrishna, Banumathi / Joseph, Philip / Ramachandran, Jeyamani / Eapen, C E. ·Department of Gastroenterology, Division of Gastrointestinal Sciences, Christian Medical College and Hospital, Vellore, 632 004, India. deepudavid@gmail.com. · Department of Virology, Christian Medical College and Hospital, Vellore, 632 004, India. · Department of Hepatology, Christian Medical College and Hospital, Vellore, 632 004, India. · Department of Gastroenterology, Division of Gastrointestinal Sciences, Christian Medical College and Hospital, Vellore, 632 004, India. · Department of Pathology, Christian Medical College and Hospital, Vellore, 632 004, India. · Department of Surgery, Christian Medical College and Hospital, Vellore, 632 004, India. ·Indian J Gastroenterol · Pubmed #28975595.

ABSTRACT: AIM OF THE STUDY: The aim of the study was to analyze the prevalence of risk factors for non-alcoholic fatty liver disease (NAFLD) in patients with non-B non-C hepatocellular carcinoma (HCC). METHODS: Between June 2012 and November 2014, patients with HCC, negative for hepatitis B surface antigen and hepatitis C virus antibody, were included in this study. All patients were assessed for risk factors for NAFLD such as diabetes mellitus (DM), hypertension, dyslipidemia, metabolic syndrome, and obesity. RESULTS: Forty-seven patients with non-B non-C HCC (males, 37; age, 60±10 years; mean±SD) were studied. Model for end-stage liver disease score was 11±4. Twenty-five patients were in Child's class A. History of significant alcohol intake was noted in 11 (23%) patients. Prevalence of risk factors for NAFLD were obesity 24 (51%), DM 22 (47%), metabolic syndrome 21 (45%), hypertension 16 (34%), and dyslipidemia 13 (28%). Forty (85%) patients had at least one risk factor for NAFLD. The mean duration of at least one NAFLD risk factor was 7.5 years, prior to diagnosis of HCC. Thirteen (28%) patients were positive for anti-HBc; however, none of the study patients had detectable HBV DNA in blood. CONCLUSIONS: Eighty-five percent of the patients with non-B non-C HCC had at least one risk factor for NAFLD. None of the study patients had occult hepatitis B infection. NAFLD is emerging as the major etiological contributing factor for non-B non-C HCC in India.

5 Article Prevalence of non-responsiveness to an indigenous recombinant hepatitis B vaccine: a study among South Indian health care workers in a tertiary hospital. 2015

Thomas, R J / Fletcher, G J / Kirupakaran, H / Chacko, M P / Thenmozhi, S / Eapen, C E / Chandy, G / Abraham, P. ·Department of Clinical Virology, Christian Medical College Hospital, Vellore, Tamil Nadu, India. ·Indian J Med Microbiol · Pubmed #25657153.

ABSTRACT: BACKGROUND AND AIM: Health care workers (HCW) are at higher risk of contracting HBV infection. Non-response to HBV vaccine is one of the major impediments to prevent healthcare associated HBV infection (HAHI). We estimated the prevalence of non-responsiveness to initial 3-dose regimen of an indigenous recombinant HBV vaccine (GeneVac-B) among South Indian HCWs and typed the HLA in non-responders. STUDY DESIGN AND METHOD: Of the 778 subjects screened over 1 year, 454 completed all three doses of the hepatitis B vaccination. Anti-HBs titers were estimated by microparticle enzyme immunoassay AxSYM AUSAB, (Abbott, Germany). HLA typing was done using SSP-PCR assay AllSet+™ Gold SSP (Invitrogen, USA). RESULTS: The overall seroconversion rate (anti-HBs>10 mIU/mL) was 98.89% wherein 90.8% had titers>1000mIU/mL, 7.6% had titers 100-1000mIU/mL, 0.43% had titers<100 mIU/mL and 1.1% were non-responsive (<10 mIU/mL) to the initial 3-dose regimen. Antibody titers<1000 mIU/mL were significantly associated with the highest quartile of body mass index (BMI) (P<0.001). We found no significant difference in seroprotection rate between gender (P=0.088). There was no difference in seroprotection rates among various ethnic groups (P=0.62). Subjects who were non-responsive in our study had at least one HLA allele earlier known to be associated with non-responsiveness to the vaccine. CONCLUSION: Our findings suggest that non-response to HBV vaccine is not a major impediment to prevent HAHI. Robust seroprotection rates can be achieved using this indigenous HBV vaccine. However, gender and BMI might influence the level of anti-HBs titers. We recommend the use of this cost effective HBV vaccine as well as postvaccination anti-HBs testing to prevent HAHI among HCWs.

6 Article Investigation into celiac disease in Indian patients with portal hypertension. 2014

Maiwall, Rakhi / Goel, Ashish / Pulimood, Anna B / Babji, Sudhir / Sophia, J / Prasad, Chaya / Balasubramanian, K A / Ramakrishna, Banumathi / Kurian, Susy / Fletcher, G John / Abraham, Priya / Kang, Gagandeep / Ramakrishna, B S / Elias, Elwyn / Eapen, C E. ·Department of Gastrointestinal Sciences, Christian Medical College, Vellore, 632 004, India. ·Indian J Gastroenterol · Pubmed #25231910.

ABSTRACT: BACKGROUND: There is limited data on celiac disease in patients with cryptogenic cirrhosis or idiopathic noncirrhotic intrahepatic portal hypertension (NCIPH). Our objective was to evaluate for celiac disease in patients with portal hypertension in India. METHODS: Consecutive patients with portal hypertension having cryptogenic chronic liver disease (cases) and hepatitis B- or C-related cirrhosis (controls) were prospectively enrolled. We studied tissue transglutaminase (tTG) antibody and duodenal histology in study patients. RESULT: Sixty-one cases (including 14 NCIPH patients) and 59 controls were enrolled. Celiac disease was noted in six cases (including two NCIPH patients) as compared to none in controls. In a significant proportion of the remaining study subjects, duodenal biopsy showed villous atrophy, crypt hyperplasia, and lamina propria inflammation, not accompanied by raised intraepithelial lymphocytes (IELs); this was seen more commonly in cases as compared to controls. An unexpectedly high rate of tTG antibody positivity was seen in study subjects (66 %) of cases as compared to 29 % in controls (p-value < 0.001), which could indicate false-positive test result. CONCLUSION: In this study, 10 % of patients with unexplained portal hypertension (cryptogenic chronic liver disease) had associated celiac disease. In addition, an unexplained enteropathy was seen in a significant proportion of study patients, more so in patients with cryptogenic chronic liver disease. This finding warrants further investigation.

7 Article Serum HBsAg quantification in treatment-naïve Indian patients with chronic hepatitis B. 2014

Ramachandran, Jeyamani / Ismail, Ashrafali Mohamed / Chawla, Gaurav / Fletcher, Gnanadurai John / Goel, Ashish / Eapen, C E / Abraham, Priya. ·Department of Hepatology, Christian Medical College, Vellore, 632 004, India, jeyamani@cmcvellore.ac.in. ·Indian J Gastroenterol · Pubmed #24052375.

ABSTRACT: BACKGROUND AND AIMS: There is paucity of Indian data regarding serum HBsAg levels (qHBsAg) in treatment-naïve chronic hepatitis B (CHB). This study was done to determine correlation of qHBsAg with hepatitis B e antigen (HBeAg) and hepatitis B virus (HBV) DNA levels and its ability to independently categorize subgroups of CHB. METHODS: We studied 131 treatment-naive CHB patients and initially classified them based on HBeAg status. The HBeAg-positive group was further classified into immune tolerance (IT) and immune clearance (IC) phases based on serum alanine aminotransferase. HBeAg-negative patients were classified into low replicators (LR) and HBeAg-negative chronic hepatitis (ENH) based on DNA levels. HBsAg quantification was performed using the Architect chemiluminescence system. RESULTS: HBeAg-positive patients had higher DNA (7.89 vs. 2.69 log10 IU/mL) and higher qHBsAg (4.60 vs. 3.85 log10 IU/mL) compared to the HBeAg-negative group. Good correlation between qHBsAg and DNA was seen in HBeAg-positive (ρ = 0.6, p < 0.001) but not in HBeAg-negative CHB (ρ = 0.2). A qHBsAg level greater than 4.39 log10 IU/mL predicted HBeAg-positive state with 81 % sensitivity and 85 % specificity. However, among HBeAg-negative CHB, qHBsAg failed to discriminate between LR and ENH. CONCLUSIONS: A single point estimation of qHBsAg in treatment-naïve patients could predict replicative HBeAg-positive CHB, but was not helpful in defining replicative status in the HBeAg-negative CHB.

8 Article A study of aetiology of portal hypertension in adults (including the elderly) at a tertiary centre in southern India. 2013

Goel, Ashish / Madhu, Kadiyala / Zachariah, Uday / Sajith, K G / Ramachandran, Jeyamani / Ramakrishna, Banumathi / Gibikote, Sridhar / Jude, John / Chandy, George M / Elias, Elwyn / Eapen, C E. ·Department of Hepatology, Christian Medical College, Vellore, India. ·Indian J Med Res · Pubmed #23760378.

ABSTRACT: BACKGROUND & OBJECTIVES: There are only a few studies on aetiology of portal hypertension among adults presenting to tertiary care centres in India; hence we conducted this study to assess the aetiological reasons for portal hypertension in adult patients attending a tertiary care centre in southern India. METHODS: Causes of portal hypertension were studied in consecutive new adult patients with portal hypertension attending department of Hepatatology at a tertiary care centre in south India during July 2009 to July 2010. RESULTS: A total of 583 adult patients (>18 yr old) were enrolled in the study. After non-invasive testing, commonest causes of portal hypertension were cryptogenic chronic liver disease (35%), chronic liver disease due to alcohol (29%), hepatitis B (17%) or hepatitis C (9%). Of the 203 patients with cryptogenic chronic liver disease, 39 had liver biopsy - amongst the latter, idiopathic non cirrhotic intrahepatic portal hypertension (NCIPH) was seen in 16 patients (41%), while five patients had cirrhosis due to non alcoholic fatty liver disease. Fifty six (10%) adult patients with portal hypertension had vascular liver disorders. Predominant causes of portal hypertension in elderly (>60 yrs; n=83) were cryptogenic chronic liver disease (54%) and alcohol related chronic liver disease (16%). INTERPRETATION & CONCLUSIONS: Cryptogenic chronic liver disease was the commonest cause of portal hypertension in adults, followed by alcohol or hepatitis B related chronic liver disease. Of patients with cryptogenic chronic liver disease who had liver biopsy, NCIPH was the commonest cause identified. Vascular liver disorders caused portal hypertension in 10 per cent of adult patients. Cryptogenic chronic liver disease was also the commonest cause in elderly patients.

9 Article Use of serum vitamin B12 level as a marker to differentiate idiopathic noncirrhotic intrahepatic portal hypertension from cryptogenic cirrhosis. 2013

Goel, Ashish / Ramakrishna, Banumathi / Muliyil, Jayaprakash / Madhu, Kadiyala / Sajith, K G / Zachariah, Uday / Ramachandran, Jeyamani / Keshava, Shyamkumar N / Selvakumar, R / Chandy, George M / Elias, Elwyn / Eapen, C E. ·Hepatology Department, Christian Medical College, Vellore, Tamil Nadu, 632004, India. drashishgoel@cmcvellore.ac.in ·Dig Dis Sci · Pubmed #22918688.

ABSTRACT: BACKGROUND AND AIMS: Idiopathic non-cirrhotic intrahepatic portal hypertension (NCIPH) is often mis-diagnosed as cryptogenic cirrhosis. Serum vitamin B12 levels can be raised in cirrhosis, probably because of excess release or reduced clearance. Because NCIPH is characterised by long periods of preserved liver function, we examined whether serum B12 level could be used as a marker to differentiate NCIPH from cryptogenic cirrhosis. METHODS: We analysed serum B12 levels in 45 NCIPH and 43 cryptogenic cirrhosis patients from January 2009 to September 2011. RESULTS: Serum B12 levels were significantly lower in NCIPH patients than in cryptogenic cirrhosis patients (p < 0.001) and were useful in differentiating the two disorders (area under ROC: 0.84; 95% C.I: 0.76-0.93). Low serum B12 level (≤250 pg/ml) was noted in 25/72 (35%) healthy controls, 14/42 (33%) NCIPH patients, and 1/38 (3 %) cryptogenic cirrhosis patients. In patients with intrahepatic portal hypertension of unknown cause, serum B12 level ≤ 250 pg/ml was useful for diagnosing NCIPH (positive predictive value: 93 %, positive likelihood ratio 12.7), and serum B12 level >1,000 pg/ml was useful in ruling out NCIPH (negative predictive value: 86 %, negative likelihood ratio: 6.67). Low serum B12 levels (≤250 pg/ml) correlated with diagnosis of NCIPH after adjusting for possible confounders (O.R: 13.6; 95% C.I:1.5-126.2). Among patients in Child's class A, serum B12 level was ≤250 pg/ml in 14/35 NCIPH patients compared with 1/21 cryptogenic cirrhosis patients (O.R: 13.3; 95% C.I: 1.6-111). CONCLUSION: Serum vitamin B12 level seems to be a useful non-invasive marker for differentiation of NCIPH from cryptogenic cirrhosis.

10 Article Antiviral resistance mutations and genotype-associated amino acid substitutions in treatment-naïve hepatitis B virus-infected individuals from the Indian subcontinent. 2012

Ismail, A M / Samuel, P / Eapen, C E / Kannangai, R / Abraham, P. ·Department of Clinical Virology, Christian Medical College, Vellore, India. ·Intervirology · Pubmed #21311172.

ABSTRACT: BACKGROUND/AIMS: Antiviral resistance is a major challenge to the treatment currently available for hepatitis B virus (HBV). In this study, mutations that may affect the antiviral efficacy in treatment-naïve HBV-infected individuals were analyzed. METHODS: Ninety-seven treatment-naïve HBV-infected individuals were included in this study. HBV reverse transcriptase (rt) domains were sequenced and nucleotide differences were compared to GenBank wild-type sequences. Furthermore, HBV genotypes, subgenotypes and subtypes were determined by analyzing surface gene sequences. RESULTS: An adefovir-related rtI233V mutation was identified in 4 subjects. The rtS213T lamivudine and entecavir refractory mutant was presented in 3 individuals. Altogether, drug-related, atypical and novel HBVrt amino acid substitutions were seen in 73 positions. The HBV genotypes A, C, D and G were depicted in 15, 21, 60 and 1 individuals, respectively. There were 17 HBVrt amino acid substitutions that are associated with certain genotypes of HBV. Mutations in HBVrt corresponded to established surface gene mutations in 9 patients. CONCLUSION: This data shows that antiviral-resistant HBV strains do exist in treatment-naïve individuals in this region. Further studies are essential to characterize the role of HBVrt amino acid substitutions in response to anti-HBV therapy.

11 Article Association of HLA and TNF polymorphisms with the outcome of HBV infection in the South Indian population. 2011

Fletcher, G J / Samuel, P / Christdas, J / Gnanamony, M / Ismail, A M / Anantharam, R / Eapen, C E / Chacko, M P / Daniel, D / Kannangai, R / Abraham, P. ·Department of Clinical Virology, Christian Medical College, Vellore, Tamil Nadu, India. ·Genes Immun · Pubmed #21593777.

ABSTRACT: The role of host genetic factors in the pathogenesis and outcome of hepatitis B virus (HBV) infection is not well known. We assessed the association of HLA and TNF (rs361525, rs1800629, rs1799724, rs1800630 and rs1799964) polymorphisms with HBV outcome in the South Indian population. Association of HLA polymorphism was analyzed in 90 individuals from each group, that is, spontaneous recovery (SR) and chronic-HBV (C-HBV) infection. The role of TNF polymorphisms was evaluated in 150 subjects with SR and 137 patients with C-HBV infection. After adjusting for age and sex, HLA-DRB1*07:01 was strongly associated with chronicity (corrected P-value (pc) <0.005, odds ratio (OR) 3.76, 95% confidence interval (CI) 1.84-7.68). The rs1800630 genotype was associated with HBV outcome in codominant (pc<0.01, OR=1.99, 95% CI 1.30-3.05) and dominant (pc<0.01, OR=2.28, 95% CI 1.35-3.84) analyzing models after adjusting for age and sex. Similarly, the rs1799964 genotype was associated with HBV outcome in codominant (pc=0.01, OR=1.57, 95% CI 1.09-2.27) and dominant (pc<0.01, OR=2.21, 95% CI 1.27-3.83) analyzing models. Haplotype analysis (rs1799964/rs1800630/rs1799724/rs1800629/rs361525) revealed that the CACGG haplotype was strongly associated with C-HBV infection (P=0.0004). Our study suggests that inheritance of HLA and TNF polymorphisms might explain the outcome of HBV infection in the South Indian population.

12 Article Investigation of an epidemic of Hepatitis E in Nellore in south India. 2010

Vivek, Rosario / Nihal, Lalit / Illiayaraja, Jeyaram / Reddy, Pawan K / Sarkar, Rajiv / Eapen, C E / Kang, Gagandeep. ·Department of Gastrointestinal Sciences, Christian Medical College, Ida Scudder Road, Vellore, India. ·Trop Med Int Health · Pubmed #20955497.

ABSTRACT: OBJECTIVE: To determine the incidence of acute hepatitis because of hepatitis E virus (HEV) and the source of the epidemic in Nellore in south India in 2008. METHODS: Anti-HEV IgM ELISA and RT-PCR for HEV-RNA were carried out on blood and stool samples from patients with acute hepatitis presenting to different hospitals in the city. The city was divided into 33 clusters, and 20 families from each cluster were systematically interviewed to determine the incidence of hepatitis E in the city. The survey was conducted on 2685 residents of 673 households from 24th November to 4th December 2008. RESULTS: The overall incidence of hepatitis was 5.7% (152/2685), i.e. an estimated 23,915 persons in the city were affected. There were two deaths because of acute hepatitis in the population surveyed translating to an estimated 315 deaths. Men had higher attack rates than women (7.8%vs. 3.5%) and young adults compared to children under 5 years (6.9%vs. 2.9%). Families drinking water from the pumping station at Bujjamarevu had the highest attack rate of 54.5% (39.8-69.2%). HEV IgM antibodies were present in 80/100 plasma samples tested. HEV-RNA was detected in 43/100 individuals tested, and isolates were characterized as genotype 1 by sequencing. CONCLUSION: Sewage draining into the river close to the pumping stations and broken pipelines crossing sewage drains may have triggered this large outbreak.

13 Article Infection with hepatitis C virus genotype 3--experience of a tertiary health care centre in south India. 2010

David, J / Rajasekar, A / Daniel, H D D / Ngui, S L / Ramakrishna, B / Zachariah, U G / Eapen, C E / Abraham, P. ·Department of Clinical Virology, Christian Medical College, Vellore - 632 004, India. ·Indian J Med Microbiol · Pubmed #20404464.

ABSTRACT: To analyse the response rate and the predictive values of virological, biochemical and histological factors on HCV antiviral therapy in HCV genotype 3 infected patients, we retrospectively studied 21 HCV genotype 3 infected patients, who underwent HCV antiviral therapy. Low (57%) sustained viral response (SVR) rate and significant association of SVR with normalization of alanine transaminase (ALT) levels were observed in our study. Absence of early viral response (EVR) showed high (80%) predictive value on SVR. Absence of EVR and normalisation of the ALT levels can predict the outcome of HCV antiviral therapy.

14 Article Association of mannose-binding lectin polymorphisms and HBV outcome in a South Indian population. 2010

Fletcher, G J / Gnanamony, M / Samuel, P / Ismail, A M / Kannangai, R / Daniel, D / Eapen, C E / Abraham, P. ·Department of Gastrointestinal Sciences, Christian Medical College, Vellore, Tamil Nadu, India. ·Int J Immunogenet · Pubmed #20193030.

ABSTRACT: Mannose binding lectin (MBL) is an important innate immune system pattern recognition molecule. The MBL gene polymorphisms are reported to play a crucial role in outcome of hepatitis B virus (HBV) infection. In this study, we ascertained the association of MBL genotypes with HBV outcome in a South Indian population. The MBL gene polymorphisms at codons 52, 54 and 57 of exon I, and promoter polymorphisms at -221 were typed by polymerase chain reaction-sequence specific primer in spontaneously recovered and in chronic HBV group. The allele frequency of codon 52 'C' was significantly higher in chronic HBV group than in the recovered group (98.5% vs. 93.6%; P = 0.003) and codon 52 'T' was significantly higher in recovered group than in the chronic group (6.4% vs. 1.5%; P = 0.003). In multivariate analysis, after adjusting for age, sex and state of origin, codon 52 'CC' and 'CT' genotypes were significantly associated with chronicity and recovery respectively [odds ratio (OR), 0.25; 95% confidence interval (CI), 0.08-0.80, P = 0.02] in co-dominant analyzing models. This was re-affirmed in analysis performed exclusively on Tamil Nadu subjects (OR, 0.23; 95% CI, 0.06-0.93, P = 0.039). The frequency of low/none haplotype (XY/O) was significantly higher in recovered group than in chronic group (15.6% vs 7.5%) and associated with spontaneous recovery (OR, 2.28; 95% CI, 1.04-4.99, P = 0.035). Our results provide preliminary evidence that inheritance of codon 52 genotypes and XY/O haplotype associated with low MBL level substantially determine the outcome of HBV infection in a sympatrically isolated South Indian population.