Hepatitis: India

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A digest of articles written 1999 and later, on the topic "Hepatitis," originating from Planet Earth —» India.  Display:  All Citations ·  All Abstracts
26 Review Production of hepatitis B surface antigen in recombinant plant systems: an update. free! 2007

Kumar GB, Ganapathi TR, Bapat VA. · Plant Cell Culture Technology Section, Nuclear Agriculture and Biotechnology Division, Bhabha Atomic Research Center, Trombay, Mumbai 400 085, India. · Biotechnol Prog. · Pubmed #17348684 links to  free full text

Abstract: There is a growing interest to develop oral vaccines for infectious diseases, as it is the most convenient and effective way to attain mucosal immunity. Hepatitis B continues to be a major infectious disease in many developing countries despite the availability of recombinant vaccine. On a global scenario, Hepatitis B Virus infection is probably the single most prevalent cause of persistent viraemia in humans. There are about 350 million chronic carriers of HBV, which is about 5% of the total world population. It is estimated that 75-100 million of them will die of liver cirrhosis and/or hepatocellular carcinoma. Progress in plant genetic engineering has enabled the transfer of useful genes for desirable traits. The recent trend is to use this technique to exploit plants as biofactories for the production of therapeutic proteins including vaccines. Rapid progress has been made in this area to develop plant-based vaccines for hepatitis B. This review describes the expression, characterization, and immunogenicity studies of hepatitis B vaccines produced in recombinant plant systems and their implications for developing a plant-based vaccine.

27 Review Management of hepatitis C in HIV infected and other immunocompromised individuals. 2006

Seth AK. · Dept of Gastroenterology Army Hospital Research & Referral, New Delhi. · Trop Gastroenterol. · Pubmed #17310553 No free full text.

Abstract: Host immunity is important in determining the natural history of HCV infection. Patients with ineffective polyclonal HCV specific CD4+ response are persistently infected and loss of HCV-specific CD4+ T cells is associated with relapse of viraemia. Weak HCV-specific CD4+ response early in the course of chronic hepatitis C correlates with higher rates of fibrosis during subsequent course of the disease. In HIV co-infected patients, the HCV load is higher by an average of 0.5-1 log than the mono-infected patients. Based on the evidence from randomized control trials, the therapy for chronic hepatitis C in HIV co-infected patients is pegylated interferon and ribavirin for 48 weeks irrespective of genotype. In patients with CD4 counts < 200 cells/l and/or plasma HIV RNA above 100,000 copies/ml, it is recommended to administer HAART before HCV therapy. The sustained viral response rate achieved in the HCV/HIV co-infected patients is lower than that for mono-infected patients. Pre-treatment HCV RNA level and the genotype are the best predictors of sustained viral response. Treatment may be discontinued at 12 weeks if there is no early viral response as the likelihood of sustained viral response in this sub-group is only 2%. Biochemical response may not be relevant in HIV/HCV co-infected patients as a third of them have normal pretreatment ALT and normalization of ALT does not correlate with virological clearance. Histological response may not also correlate with virological response as up to 43% of subjects without sustained viral response may show histological improvement at the end of 48 weeks treatment. Liver disease due to HCV in patients with end stage renal disease on maintenance dialysis, is a significant cause of morbidity. The value of aminotransferases in patients on haemodialysis is lower than in the non-uraemic population and the level may not rise above the 'normal' range despite active liver disease. HCV RNA may be required to diagnose HCV infection, as anti-HCV may not be detectable, in such patients. Weekly pegylated interferon may be effective in them. In renal allograft recipients, paired biopsies may show rapid progression of liver disease in the absence of fibrosing cholestatic hepatitis. Interferon is contraindicated in this population due to increased risk of graft rejection. Following liver transplantation, recurrence of HCV is universal and histological evidence of recurrent infection may occur as early as 1 to 8 weeks after transplantation. Combination therapy with pegylated interferon and ribavirin may be effective in them.

28 Review HCV: the Indian scenario. 2006

Mukhopadhya A. · Department of Gastrointestinal Sciences, Christian Medical College, Vellore, TN 632004, India. · Trop Gastroenterol. · Pubmed #17310552 No free full text.

Abstract: Hepatitis C is a global health problem with an estimated 170 million people infected with this virus worldwide. It is an emerging infection in India and is a major public health concern. The exact magnitude of this infection in India has not been defined and the relative contribution of various risk factors has not been clearly elucidated. This review outlines the prevalence of hepatitis C in various population subsets in India, the association of hepatitis C and liver disease in India and the existing genotypes in India.

29 Review Management of patients with HBeAg-negative chronic hepatitis B. 2007

Saikia N, Talukdar R, Mazumder S, Khanna S, Tandon R. · Department of Gastroenterology, Pushpawati Singhania Research Institute, New Delhi, India. · Postgrad Med J. · Pubmed #17267676 No free full text.

Abstract: Chronic hepatitis B (CHB) is one of the leading causes of morbidity and mortality worldwide. Although various drugs are available for the treatment of CHB, emergence of the hepatitis B e antigen (HBeAg)-negative mutant variant, specifically in Asia, the Middle East and southern Europe, is creating a new challenge as this variant is less responsive to available treatments. HBeAg-negative CHB rapidly progresses to cirrhosis and its related complications. This review discusses the available literature on the approved and under-trial treatment options and their respective efficacies for HBeAg-negative CHB.

30 Review Hepatoprotective herbal drug, silymarin from experimental pharmacology to clinical medicine. free! 2006

Pradhan SC, Girish C. · Department of Pharmacology, Jawaharlal Institute of Postgraduate Medical Education & Research, Pondicherry, India. · Indian J Med Res. · Pubmed #17213517 links to  free full text

Abstract: Silymarin, a flavonolignan from 'milk thistle' (Silybum marianum) plant is used almost exclusively for hepatoprotection and amounts to 180 million US dollars business in Germany alone. In this review we discuss about its safety, efficacy and future uses in liver diseases. The use of silymarin may replace the polyherbal formulations and will avoid the major problems of standardization, quality control and contamination with heavy metals or bacterial toxins. Silymarin consists of four flavonolignan isomers namely--silybin, isosilybin, silydianin and silychristin. Among them, silybin being the most active and commonly used. Silymarin is orally absorbed and is excreted mainly through bile as sulphates and conjugates. Silymarin offers good protection in various toxic models of experimental liver diseases in laboratory animals. It acts by antioxidative, anti-lipid peroxidative, antifibrotic, anti-inflammatory, membrane stabilizing, immunomodulatory and liver regenerating mechanisms. Silymarin has clinical applications in alcoholic liver diseases, liver cirrhosis, Amanita mushroom poisoning, viral hepatitis, toxic and drug induced liver diseases and in diabetic patients. Though silymarin does not have antiviral properties against hepatitis virus, it promotes protein synthesis, helps in regenerating liver tissue, controls inflammation, enhances glucuronidation and protects against glutathione depletion. Silymarin may prove to be a useful drug for hepatoprotection in hepatobiliary diseases and in hepatotoxicity due to drugs. The non traditional use of silymarin may make a breakthrough as a new approach to protect other organs in addition to liver. As it is having a good safety profile, better patient tolerability and an effective drug at an affordable price, in near future new derivatives or new combinations of this drug may prove to be useful.

31 Review Is the anti-sarcoma and anti-viral cytokine "plasma factor" a novel chicken Y-box protein? 2006

Shirodkar MV, Sehgal PB. · Shirodkar Memorial Research Foundation, Mumbai, Pune, India. · Indian J Exp Biol. · Pubmed #17131907 No free full text.

Abstract: A line of research beginning in the early 1960s with the observation that West Nile virus and, later, several strains of rabies virus could inhibit the development of the Rous sarcoma virus-induced tumor in the wing-web of chicken (a "sarcoma-blockade") eventually culminated in the characterization of a 14-kDa circulating anti-sarcoma and anti-viral activity christened "plasma factor" (PF) which, unlike the interferons, inhibited the replication of diverse RNA-containing viruses, but not of any DNA-containing viruses. The possibility that this 14 kDa protein represented a novel antiviral cytokine has been strengthened by analysis of partial amino acid sequencing data which suggest that this 14-kDa cytokine may correspond to the 127-amino acid-long chicken YB2-like protein (Locus: XP_423576) deduced very recently from the genomic sequencing of chicken. Biologically, proteins of the Y-box family (such as chicken YB1 and YB2) not only bind DNA and thus regulate transcription but also bind single-stranded RNA in a sequence-specific and reversible manner, repress viral RNA translation, inhibit retroviral transformation of chicken fibroblasts, and are known to regulate transcription of human immunodeficiency virus and hepatitis B virus. Taken together, the available data point to a novel anti-viral cytokine with a novel mechanism of action.

32 Review Malarial hepatopathy. free! 2006

Bhalla A, Suri V, Singh V. · Department of Internal Medicine, Post Graduate Institute of Medical Education and Research, Chandigarh - 160012, India. · J Postgrad Med. · Pubmed #17102560 links to  free full text

Abstract: Jaundice is a common clinical presentation in severe malaria, seen in approximately 2.5% patients with falciparum infection but hepatitis is unusual. Although hepatic dysfunction is unusual and hepatic encephalopathy is almost never seen in malaria, yet, cases of hepatic dysfunction are being increasingly reported in patients with P.falciparum infection, from different parts of world. The extent of hepatocellular dysfunction varies from mild abnormalities in liver function tests to hepatic failure. Patients with hepatocellular dysfunction in malaria are more prone to develop complications, but have a favorable outcome if hepatic involvement is recognized early and managed properly. It is important to meticulously look for hepatic dysfunction in patients with severe malaria, distinguish it from fulminant hepatic failure and manage it aggressively.

33 Review Viral hepatitis in India. 2006

Acharya SK, Madan K, Dattagupta S, Panda SK. · Department of Gastroenterology, All India Institute of Medical Sciences, Ansari Nagar, New Delhi 110029, India. · Natl Med J India. · Pubmed #17100109 No free full text.

Abstract: Viral hepatitis is a major public health problem in India, which is hyperendemic for HAV and HEV. Seroprevalence studies reveal that 90%-100% of the population acquires anti-HAV antibody and becomes immune by adolescence. Many epidemics of HEV have been reported from India. HAV related liver disease is uncommon in India and occurs mainly in children. HEV is also the major cause of sporadic adult acute viral hepatitis and ALF. Pregnant women and patients with CLD constitute the high risk groups to contract HEV infection, and HEV-induced mortality among them is substantial, which underlines the need for preventive measures for such groups. Children with HAV and HEV coinfection are prone to develop ALF. India has intermediate HBV endemicity, with a carrier frequency of 2%-4%. HBV is the major cause of CLD and HCC. Chronic HBV infection in India is acquired in childhood, presumably before 5 years of age, through horizontal transmission. Vertical transmission of HBV in India is considered to be infrequent. Inclusion of HBV vaccination in the expanded programme of immunization is essential to reduce the HBV carrier frequency and disease burden. HBV genotypes A and D are prevalent in India, which are similar to the HBV genotypes in the West. HCV infection in India has a population prevalence of around 1%, and occurs predominantly through transfusion and the use of unsterile glass syringes. HCV genotypes 3 and 2 are prevalent in 60%-80% of the population and they respond well to a combination of interferon and ribavirin. About 10%-15% of CLD and HCC are associated with HCV infection in India. HCV infection is also a major cause of post-transfusion hepatitis. HDV infection is infrequent in India and is present about 5%-10% of patients with HBV-related liver disease. HCC appears to be less common in India than would be expected from the prevalence rates of HBV and HCV. The high disease burden of viral hepatitis and related CLD in India, calls for the setting up of a hepatitis registry and formulation of government-supported prevention and control strategies.

34 Review Hepatitis E virus: epidemiology, diagnosis, pathology and prevention. 2006

Acharya SK, Panda SK. · Department of Gastroenterology, All India Institute of Medical Sciences, New Delhi. · Trop Gastroenterol. · Pubmed #17089614 No free full text.

Abstract: HEV, a positive stranded RNA virus, is responsible for most of the epidemics of hepatitis in the developing world and is transmitted through contaminated water. It is the major aetiological agent for acute hepatitis and acute liver failure in endemic regions. It causes severe liver disease among pregnant females and patients with chronic liver disease. Serodiagnosis of HEV is now available and should be used routinely for diagnosis. The available evidence suggests that HEV may also be transmitted parenterally as well as vertically particularly in endemic areas. Experimental studies suggest that an HEV vaccine is a distinct possibility in the near future. In the absence of an effective vaccine, public health measures such as clean water supply, improved sanitation and public education are the major tools to prevent HEV epidemics in developing nations.

35 Review Hepatitis E virus. 2007

Panda SK, Thakral D, Rehman S. · Department of Pathology, All India Institute of Medical Sciences, Ansari Nagar, New Delhi, India. · Rev Med Virol. · Pubmed #17051624 No free full text.

Abstract: Hepatitis E virus (HEV) is the aetiological agent of non-HAV enterically transmitted hepatitis. It is the major cause of sporadic as well as epidemic hepatitis, which is no longer confined to Asia and developing countries but has also become a concern of the developed nations. In the Indian subcontinent, it accounts for 30-60% of sporadic hepatitis. It is generally accepted that hepatitis E is mostly self-limited and never progresses to chronicity. It has a higher mortality in pregnant women where the disease condition is accentuated with the development of fulminant liver disease. Currently, no antiviral drug or vaccine is licensed for HEV, although a vaccine candidate is in clinical trials. HEV genome is 7.2kb in size with three open reading frames (ORFs) and 5' and 3' cis acting elements, which have important roles to play in HEV replication and transcription. ORF1 codes for methyl transferase, protease, helicase and replicase; ORF2 codes for the capsid protein and ORF3 for a protein of undefined function. HEV has recently been classified in the genus Hepevirus of the family Hepeviridae. There are four major recognised genotypes with a single known serotype. The absence of a reliable in vitro propagation system is an obstacle to deciphering HEV biology. The genome of HEV has been cloned, sequenced and the infectious nature of these replicons has been established. However, questions related to replication, transcription, virus-host interactions and pathogenesis remain to be answered. This comprehensive review summarises the progress made so far in HEV research, and addresses some of the unanswered questions.

36 Review Hepatitis C virus core protein: an update on its molecular biology, cellular functions and clinical implications. 2006

Irshad M, Dhar I. · Clinical Biochemistry Division, Department of Laboratory Medicine, All India Institute of Medical Sciences, New Delhi, India. · Med Princ Pract. · Pubmed #17047346 No free full text.

Abstract: The present review article is an update on various features of hepatitis C virus (HCV) core protein including its molecular biology, role in HCV replication, involvement in HCV pathogenesis, etiological role in hepatocellular carcinogenesis, significance in diagnosis and vaccination against HCV infection. Core protein is a structural protein of HCV virus and has only recently been characterized. It was found to play a major role in HCV-induced viral hepatitis. Although published information shows a lot about the clinical significance of HCV core protein, several studies are still needed to demonstrate its exact significance in viral biology and underlying HCV pathogenesis.

37 Review Tropical infections in the ICU. 2006

Kothari VM, Karnad DR, Bichile LS. · Medical Intensive Care Unit, Department of Medicine, Seth GS Medical College and KEM College, Mumbai. · J Assoc Physicians India. · Pubmed #16944613 No free full text.

Abstract: Certain arthropod-borne infections are common in tropical regions because of favorable climatic conditions. Water-borne infections like leptospirosis are common due to contamination of water especially during the monsoon floods. Infections like malaria, leptospirosis, dengue fever and typhus sometimes cause life threatening organ dysfunction and have several overlapping features. Most patients present with classicial clinical syndromes: fever and thrombocytopenia are common in dengue, malaria and leptospirosis; coagulopathy is frequent in leptospirosis and viral hepatitis. Hepatorenal syndrome is seen in leptospirosis, falciparum malaria and scrub typhus. The pulmonary renal syndrome is caused by falciparium malaria, leptospirosis, Hantavirus infection and scrub typhus. Fever with altered mental status is produced by bacterial meningitis, Japanese B encephalitis, cerebral malarial, typhoid encephalopathy and fulminant hepatic failure due to viral hepatitis. Subtle differences in features of the organ failure exist among these infections. The diagnosis in some of these diseases is made by demonstration of antibodies in serum, and these may be negative in the first week of the illness. Hence empiric therapy for more than one disorder may be justified in a small proportion of cases. In addition to specific anti-infective therapy, management of organ dysfunction includes use of mechanical ventilation, vasopressor drugs, continuous renal replacement therapy and blood products. Timely transfer of these patients to well-equipped ICUs with experience in managing these cases can considerably decrease mortality and morbidity.

38 Review The metabolism, pharmacokinetics and mechanisms of antiviral activity of ribavirin against hepatitis C virus. 2006

Dixit NM, Perelson AS. · Department of Chemical Engineering, Indian Institute of Science, Bangalore. · Cell Mol Life Sci. · Pubmed #16501888 No free full text.

Abstract: Ribavirin, a broad spectrum antiviral agent, in conjunction with interferon forms the current standard of treatment for hepatitis C virus (HCV) infection in humans. While ribavirin alone fails to induce a significant antiviral response, in combination with interferon, ribavirin dramatically improves the long-term outcome of therapy. The predominant mechanism(s) of ribavirin action against HCV, are yet to be established. In this review, we examine the current status of our understanding of the metabolism, pharmacokinetics and mechanisms of the antiviral activity of ribavirin against HCV, all of which are central to the rational identification of improved treatment protocols.

39 Review Neurologic disorders in pregnancy. 2005

Karnad DR, Guntupalli KK. · Medical-Neuro-Intensive Care Unit, Department of Medicine, Seth G. S. Medical College and King Edward Memorial Hospital (DRK), Mumbai, India. · Crit Care Med. · Pubmed #16215360 No free full text.

Abstract: BACKGROUND: Neurologic dysfunction, coma, and seizures are common in obstetric patients in the intensive care unit. OBJECTIVE: To review common neurologic disorders resulting in critical illness in pregnancy. REVIEW: Obstetric disorders causing coma and seizures include eclampsia, acute fatty liver of pregnancy, and amniotic fluid embolism. Preexisting disorders such as epilepsy may worsen in one-third of pregnant patients, and seizures are common during labor. Changes in hemodynamics, blood volume, and hormonal effects on the vessel wall increase risk of bleeding from berry aneurysms and arteriovenous malformations during pregnancy and the postpartum period. Acute intermittent porphyria produces seizures and hypertension, closely mimicking eclampsia. Cerebral venous sinus thrombosis is common in postpartum patients, especially in developing countries. Brain tumors invariably enlarge during pregnancy because of fluid retention and the presence of estrogen and progesterone receptors on tumor cells. Infections such as cerebral malaria and acute viral hepatitis with fulminant hepatic failure are common causes of coma and seizures during pregnancy in tropical regions of Asia, Africa, and Latin America. Patients may be admitted to the intensive care unit with type II respiratory failure due to myasthenic crisis, Guillain-Barre syndrome and spinal cord disease. Relapses of multiple sclerosis are infrequent during pregnancy but increase in the postpartum period. CONCLUSIONS: In all instances, the effects of the disorders, diagnostic tests, and treatment on the fetus must be carefully weighed. Prompt delivery may be lifesaving for mother and fetus in conditions such as eclampsia and acute fatty liver of pregnancy; expectant treatment may be more appropriate in others.

40 Review Hepatitis B virus: inactive carriers. free! 2005

Sharma SK, Saini N, Chwla Y. · Department of Hepatology, PGIMER, Chandigarh, 160012, India. · Virol J. · Pubmed #16191199 links to  free full text

Abstract: Inactive carriers forms the largest group in chronic HBV infected patients. Around 300 million people are inactive carriers The inactive HBsAg carrier state is diagnosed by absence of HBeAg and presence of anti-HBe, undetectable or low levels of HBV DNA in PCR-based assays, repeatedly normal ALT levels, and minimal or no necroinflammation, slight fibrosis, or even normal histology on biopsy. Inactive cirrhosis may be present in patients who had active liver disease during the replicative phase of infection. The prognosis of the inactive HBsAg carrier state is usually benign. Long-term follow- up (up to 18 years) of these carriers has indicated that the vast majority show sustained biochemical remission and very low risk of cirrhosis or hepatocellular carcinoma (HCC). Rarely, patients, even noncirrhotics, may develop liver cancer during the inactive HBsAg carrier state. In addition, approximately 20 to 30% of persons in the inactive HBsAg carrier state may undergo spontaneous reactivation of hepatitis B during follow-up. Multiple episodes of reactivation or sustained reactivation can cause progressive hepatic damage and even hepatic decompensation.

41 Review Herbal medicines for liver diseases. 2005

Dhiman RK, Chawla YK. · Department of Hepatology, Postgraduate Institute of Medical Education and Research, Chandigarh, 160012, India. · Dig Dis Sci. · Pubmed #16187178 No free full text.

Abstract: Herbal medicines have been used in the treatment of liver diseases for a long time. A number of herbal preparations are available in the market. This article reviews four commonly used herbal preparations: (1) Phyllanthus, (2) Silybum marianum (milk thistle), (3) glycyrrhizin (licorice root extract), and (4) Liv 52 (mixture of herbs). Phyllanthus has a positive effect on clearance of HBV markers and there are no major adverse effects; there are no data from randomized controlled trials on clinically relevant outcomes, such as progression of chronic hepatitis to cirrhosis and/or liver cancer, and on survival. Silymarin does not reduce mortality and does not improve biochemistry and histology among patients with chronic liver disease; however, it appears to be safe and well tolerated. Stronger neominophagen C (SNMC) is a Japanese preparation that contains 0.2% glycyrrhizin, 0.1% cysteine, and 2% glyceine. SNMC does not have antiviral properties; it primarily acts as an anti-inflammatory or cytoprotective drug. It improves mortality in patients with subacute liver failure and improves liver functions in patients with subacute hepatic failure, chronic hepatitis, and cirrhosis with activity. SNMC does not reduce mortality among patients with cirrhosis with activity. SNMC may prevent the development of hepatocellular carcinoma in patients with chronic hepatitis C, however, prospective data are lacking. Liv 52, an Ayurvedic hepatoprotective agent, is not useful in the management of alcohol-induced liver disease. Standardization of herbal medicines has been a problem and prospective, randomized, placebo-controlled clinical trials are lacking to support their efficacy. The methodological qualities of clinical trials of treatment with herbal preparations are poor. The efficacy of these herbal preparations need to be evaluated in rigorously designed, larger randomized, double-blind, placebo-controlled multicenter trials.

42 Review TT viruses: how much do we know? free! 2005

Abraham P. · Department of Clinical Virology Christian Medical College Ida Scudder Road Vellore 632004, India. · Indian J Med Res. · Pubmed #16106084 links to  free full text

This publication has no abstract.

43 Review Jaundice in malaria. 2005

Anand AC, Puri P. · Department of Medicine, Armed Forces Medical College, Pune, India. · J Gastroenterol Hepatol. · Pubmed #16105116 No free full text.

Abstract: Jaundice is not an unusual accompaniment of malaria. It can occur due to intravascular hemolysis, disseminated intravascular coagulation, and, rarely, 'malarial hepatitis'. Although the primary schizogony of the malarial parasite always leads to the rupture of the infected hepatocyte, alteration of the hepatic functions is uncommonly recorded due to this event. Histologically, the hepatitis or the actual inflammation in the liver has never been demonstrated. Nonetheless, the term 'malarial hepatitis' (MH) has been used in the literature to describe the occurrence of hepatocellular jaundice in patients with Plasmodium falciparum infection. The authors' own data and review of the literature indicate that it is not an uncommon entity. In endemic areas, jaundice is seen in approximately 2.5% of patients with falciparum malaria. It also appears to be a heterogeneous syndrome and one can recognize two clinical subsets. In one group there was an acute, virulent presentation with coma, renal failure and in some cases even hemorrhagic manifestations. It is only in this setting that jaundice signified a 'severe' disease as noted by the World Health Organization action program. This presentation is often confused with acute viral hepatitis and acute hepatic failure in non-endemic areas, but can be clinically differentiated.

44 Review Non-alcoholic steatohepatitis. 2005

Das K, Kar P. · Department of Medicine, Maulana Azad Medical College and Associated LN Hospital, New Delhi - 2. · J Assoc Physicians India. · Pubmed #15926603 No free full text.

Abstract: Non-alcoholic steatohepatitis (NASH) represents only a part of a wide spectrum of non-alcoholic fatty liver disease (NAFLD) and its prevalence is only 2 - 3% in the general population. Obesity, diabetes, hyperlipidemia and female sex are important risk factors for NASH. Two hit theory describes very well the pathogenesis of NASH wherein hepatic steatosis, the first hit is followed up by the second hit, one of which may be reactive oxygen species. Mitochondria is the main source of reactive oxygen species which may trigger steatohepatitis by lipid peroxidation, cytokine induction or induction of fas-ligand. Insulin resistance syndrome is the only metabolic syndrome that has been consistently associated with NASH. The diagnosis rests on the hallmark histological features and rigorous exclusion of significant alcohol consumption. Most patients are asymptomatic, have mild-to-moderate elevations of serum aminotransferase levels, clinical hepatomegaly and features of fatty liver on imaging. Liver biopsy is essential for positive diagnosis and prognostication of NASH. Histologically, fat deposition is typically macrovesicular and inflammation of steatohepatitis is predominantly lobular. Neutrophilic cells in lobular inflammatory infilterate are a distinguishing feature of steatohepatitis and differentiate it from other chronic hepatitis. The pattern of collagen deposition is perivenular & peri-sinusoidal spaces in zone 3. NASH is a progressive disease in more than one in four and has spontaneous regression in less than one in six. Therapy options include weight reduction in obese, good control in diabetics and exercise. Ursodeoxycholic acid has membrane stabilizing, cytoprotective and immunological effect and normalizes raised transaminases. Liver transplantation has been done in NASH but transplanted liver shows re-development in more than two thirds. Many more therapies are in the pipeline and show promise for the future.

45 Review Kawasaki disease. 2005

Singh S, Kansra S. · Department of Paediatrics, Postgraduate Institute of Medical Education and Research, Chandigarh 160012, India. · Natl Med J India. · Pubmed #15835487 No free full text.

Abstract: Kawasaki disease (KD) is a common vasculitic disorder usually seen in children below 5 years of age. The disease can present with protean clinical manifestations which include high grade fever (for at least 5 days), rash, redness of the lips and a typical strawberry tongue, cervical lymph node enlargement (often unilateral), swelling over the hands/feet and, later a characteristic peripheral desquamation over the fingers and toes. These clinical features appear sequentially and the findings may change from day-to-day. Thus, all these features may not be seen together at any one point of time. The diagnosis rests on the recognition of this characteristic temporal sequence of clinical events, none of which are, by themselves, pathognomonic. Establishing a diagnosis of KD may be further complicated by the occurrence of several other, seemingly unrelated, clinical features. These include irritability, neck stiffness, sterile pyuria, pneumonitis, hydrops of the gallbladder and hepatitis among many others. There is no laboratory test that can help in confirming a diagnosis of KD. Left untreated, up to 20% of children with KD can develop coronary aneurysms with catastrophic long term sequelae. It is important to diagnose KD in the first 10 days of the illness so that appropriate therapy with intravenous immunoglobulin and aspirin can be Initiated. All paediatricians, and physicians looking after children, need to be aware of this condition which is now being increasingly recognized in India.

46 Review Fibrosing cholestatic hepatitis in renal transplant recipient with CMV infection: a case report. 2004

Agarwal SK, Kalra V, Dinda A, Gupta S, Dash SC, Bhowmik D, Tiwari SC. · Department of Nephrology, All India Institute of Medical Sciences, New Delhi 110029, India. · Int Urol Nephrol. · Pubmed #15783120 No free full text.

Abstract: Fibrosing cholestatic hepatitis (FCH) is an uncommon complication of renal transplantation. It is usually associated with hepatitis B and C viral infection. It is further rare in renal transplantation in absence of HBV and HCV infection. To the best of our knowledge, only three cases of FCH in renal transplantation, which were both HBV and HCV negative, have been reported to date. Out of these, two cases were diagnosed to have CMV infection and the third was attributed to azathioprin. We are presenting another case of FCH in a renal transplant recipient with CMV infection.

47 Review Prospects for hepatitis C vaccine. 2004

Bhopale GM, Nanda RK. · Research and Development Division, Hindustan Antibiotics Ltd., Pimpri, Pune 411018, India. · Acta Virol. · Pubmed #15745044 No free full text.

Abstract: Hepatitis C virus (HCV) is a major cause of chronic liver disease, cirrhosis and hepatocellular carcinoma worldwide. Unfortunately, neither a vaccine nor any effective therapy is available. Efforts are now directed towards the development of an effective vaccine besides chemotherapy. This review briefly summarizes the properties of an effective vaccine for the control of HCV infection. The mechanisms of protective immune response induced by HCV are not well understood. It is presumed that humoral and cellular immune responses play an important role. Even though there are various obstacles in the development of HCV vaccine, we describe a few promising approaches such as DNA vaccine, recombinant virus vaccine, HCV-like particles (HCV-LPs), peptide-based vaccine and plant-derived recombinant subunit vaccine.

48 Review Hepatitis B vaccine boosters: is there a clinical need in high endemicity populations? 2005

John TJ, Cooksley G, Anonymous00064. · Kerala State Institute of Virology and Infectious Diseases, Kerala, India. · J Gastroenterol Hepatol. · Pubmed #15610440 No free full text.

Abstract: The Steering Committee for the Prevention and Control of Infectious Diseases in Asia recently conducted a survey of primary-care physicians in Asia, which revealed that many physicians administer boosters in their clinical practice and that there is considerable variation and uncertainty among physicians regarding this practice. This paper serves as a response to physicians' uncertainties by reviewing the literature regarding the administration of hepatitis B vaccine boosters in high endemicity areas and presenting the Steering Committee's guidelines for booster administration. While there are few data to support a need for routine hepatitis B vaccine boosters as a public health measure, they help to provide reassurance of immunity against breakthrough infection in certain risk groups. In clinical practice, primary-care physicians must exercise their judgment regarding the need for booster vaccination on an individual basis. This paper examines the available literature on the administration and value of hepatitis B vaccine boosters, explores the differences between the public health approach and clinical practice, and provides guidelines for those who use boosters in high endemicity Asian populations. Relevant articles were identified through searches of MEDLINE (1975-2003) and the Cochrane Library, using 'hepatitis B' and 'booster' as primary search terms. Guidelines for those who decide to administer hepatitis B vaccine boosters include: boosting approximately 10-15 years after primary vaccination; boosting rather than not when monitoring of antibody levels is not feasible; boosting immunocompromised patients when the antibody to hepatitis B surface antigen titer falls below 10 mIU/mL; and boosting healthcare workers based on the endemicity of the particular country.

49 Review Preventing and treating hepatitis B infection. free! 2004

Aggarwal R, Ranjan P. · Department of Gastroenterology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow 226 014, India. · BMJ. · Pubmed #15528620 links to  free full text

This publication has no abstract.

50 Review Antituberculosis drug-induced hepatitis: risk factors, prevention and management. 2003

Hussain Z, Kar P, Husain SA. · Department of Medicine, Maulana Azad Medical College, New Delhi 110 002, India. · Indian J Exp Biol. · Pubmed #15332488 No free full text.

Abstract: Apart from infectious or viral hepatitis, other most common non-infectious causes of hepatitis are alcohol, cholestatic, drugs and toxic materials. The most common mode that leads to liver injuries is antituberculosis drug-induced hepatitis. The severity of drug-induced liver injury varies from minor nonspecific changes in hepatic structure to fulminant hepatic failure, cirrhosis and liver cancer. Patients receiving antitubercular drug frequently develop acute or chronic hepatitis. The time required for the metabolites to reach hepatotoxic levels is much earlier with isoniazid plus rifampicin treatment than isoniazid alone and this has been shown to be synergistic rather than additive. Antituberculosis drug (ATT)-inducible cytochrome P-4502E1 (CYP2E1) is constitutively expressed in the liver. Recent studies show that polymorphism of the N-acetyltransferase 2 (NAT2) genes and glutathione-S-transferase (GST) are the major susceptibility risk factors for ATT-induced hepatitis. The hepatic NAT and GST are involved in the metabolism of several carcinogenic arylamines and drugs. The NAT2 enzyme has a genetic polymorphism in human. N-acetyltransferase 2 genes (NAT2) have been identified to be responsible for genetic polymorphism of slow and rapid acetylation in humans. Slow acetylators of NAT2 prove to develop more severe hepatotoxicity than rapid acetylators making it a significant risk factor. Deficiency of GST activity, because of homozygous null mutations at GSTM1 and GSTT1 loci, may modulate susceptibility to drug and xenobiotic-induced hepatotoxicity. Polymorphisms at GSTM1, GSTT1 and NAT2 loci had been linked to various forms of liver injury, including hepatocellular carcinoma.


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