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Year : 2013  |  Volume : 138  |  Issue : 1  |  Page : 8-10

This is hepatitis: Know it, confront it

Department of Gastroenterology All India Institute of Medical Sciences New Delhi 110 029, India

Date of Web Publication6-Aug-2013

Correspondence Address:
Subrat Kumar Acharya
Department of Gastroenterology All India Institute of Medical Sciences New Delhi 110 029
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Source of Support: None, Conflict of Interest: None

PMID: 24056549

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How to cite this article:
Acharya SK. This is hepatitis: Know it, confront it. Indian J Med Res 2013;138:8-10

How to cite this URL:
Acharya SK. This is hepatitis: Know it, confront it. Indian J Med Res [serial online] 2013 [cited 2020 Aug 12];138:8-10. Available from:

Liver is the barrier between the environment and the human body and has multiple synthetic, metabolic, detoxifying, homeostatic and immune functions. Therefore, during evolution, liver has acquired substantial reserve as well regenerative capacity. While such reserve and regenerative capacity imparts protective effect, the diseases of liver do not clinically manifest until substantial hepatic reserve or hepatocyte loss ensues. Most liver diseases in their initial stages remain silent. Hepatitis is the most common ailment of liver and is usually caused by various hepatotoxic agents such as hepatitis viruses, alcohol, drugs, toxins, excessive fat, etc.

Hepatitis is a term used to describe inflammation of the liver and its consequences. Viral hepatitis is caused by five hepatitis viruses A through E. While hepatitis A virus (HAV) and hepatitis E virus (HEV) are transmitted by contaminated water and food through the enteric route, hepatitis B, C and D are parenterally transmitted viruses (through unsterile needle, instrumentation, transfusion , sexual route and from pregnant mother to the baby during child birth) . All the hepatitis viruses can cause acute hepatitis, but only HBV and HCV are major cause of chronic hepatitis, cirrhosis and liver cancer globally [1] .

Viral hepatitis is a major public health problem in our country as India is hyperendemic for hepatitis A and E [1],[2],[3],[4],[5],[6] . Hepatitis A and E viruses have been responsible for most of the epidemics of hepatitis in this country [1],[2],[3],[4],[5],[6] . In the sporadic situation, hepatitis E was reported to be the major cause of acute hepatitis in 30-70 per cent of the cases and has been incriminated as the major cause of acute liver failure (ALF) [7] . Hepatitis A is the predominant aetiology of acute hepatitis in the paediatric age group [8],[9] . Dual infection of hepatitis A and E was reported as the major cause of ALF among children [10] .

About 30 million hepatitis B virus (HBV) carriers without any symptomatic liver disease are present in India [11],[12] . Depending on the carrier frequency, the world has been categorized into high endemic zone for HBV (carrier frequency of >8% in population), intermediate endemic zone (carrier frequency of 2-8%) and low endemic zone (carrier frequency of less than 2%) [11] India, with a carrier frequency of about 3 per cent (2 to 4%) has been placed in the intermediate endemic zone. Hepatitis C virus infection frequency, evaluated by anti HCV antibody positivity has been reported to be between 1-2 per cent among voluntary blood donors and 0.87 per cent in the community [11] , which is similar to that seen in the developed and industrialized countries like Japan and USA [13] . HBV and HCV are parenterally transmitted and cause both acute as well as chronic disease. About 15 to 30 per cent of acute hepatitis in India are due to HBV [11] , however, HCV as a cause of acute icteric hepatitis has been infrequent, but remains as the major cause of post-transfusion hepatitis. HBV is the major cause of chronic hepatitis, cirrhosis and primary liver cell cancer in India [11] . About 50 per cent of patients with chronic liver diseases are due to HBV and 20 per cent are due to HCV [1] . Frequency of hepatitis D virus infection among both acute and chronic HBV patients in India has been reported to be infrequent [1] . Approximately 2.5 lakh patients die annually due to viral hepatitis and its sequlae [1] .

These data indicate that the magnitude of viral hepatitis in India is substantial. During the last three decades, substantial information on the viral genomics, diagnostic assays, understanding of pathogenesis, natural course, therapy against the viruses and sequels of liver disease has been generated. These advances have resulted in a situation to prevent and cure viral hepatitis globally. However, in India we have yet to use this information in an organized and structured manner to devise effective control strategy for viral hepatitis. It has become necessary now to increase the awareness about these advances among the health care providers to establish capability with an aim to control viral hepatitis in India.

The most established and effective method to control viral hepatitis is prevention of the infection. The two well known methods to prevent hepatitis viral infection would include: (i) interruption of the route of transmission, and (ii) vaccination against the specific virus.

HAV and HEV infections occur due to their transmission through enteric route by contaminated water and food. In rural India, defecating in the open is common and in many cities like Delhi, the sewerage and water supply pipelines are adjacent leading to contamination of water from the corroded sewage lines [1],[2],[3],[4],[5],[6] . This is the major source of well water contamination in the rural areas and the water supply pipelines in urban areas, especially during the rainy season [1],[2],[3],[4],[5],[6] . An improvement in sanitation, provision of clean drinking water, proper sewage disposal, public education and awareness of defecation habits are the mainstay for the prevention of epidemics of hepatitis A and E. Person to person contamination has been documented in HAV infection but not in HEV, therefore, HAV infected patient may require to take necessary precaution to avoid person to person transmission [1] . However, simple awareness that 'these viruses can be eradicated by boiling water at 100 degree centigrade or by appropriate chlorination' can be very effective [1] . Similarly, interruption processes of transmission of HBV and HCV through parenteral route have been well established [1] . Despite the similarity of transmission route and pattern of HIV and HCV, their transmission dynamics varies in India. The most frequent cause of HCV transmission has been implicated to transfusion of blood and blood products, unsafe injection practices and, haemodyalisis in patients with chronic renal failure [1] . HBV even though is transmitted through all the above mentioned routes, the presumable cause of most of the HBV transmission in India is childhood infection either through horizontal transmission or vertical transmission from mother to baby [1] . Unsafe injection practices have been documented to cause HBV epidemics in India and other parts of the globe [14] . Another route of transmission of these two parenterally transmitted viruses is the nosocomial infections and to high risk individuals comprising various health care workers [15] . Based on the information strategies have been devised to prevent the transfusion related transmission by donor screening of various transfusion transmitted virus infection, use of safe injection practices, protocols for post exposure prophylaxis with which effective reduction of HBV and HCV infection has been documented.

Effective vaccines to prevent HBV and HAV infections are commercially available and many countries have included these in their universal immunization programmes [1] . Inclusion of HBV vaccine in the universal immunization schedule would be the most cost effective strategy to decrease HBV carrier frequency and disease burden in India. Aggarwal et al[16],[17] have reported that if horizontal transmission is the predominant mode of HBV transmission in India, then the universal immunization would be more cost-effective than selective immunization. While adopting universal immunization, programmes to evaluate durability of protection, appearance of vaccine escape mutants, compliance frequency of population may be relevant for a successful HBV control. The countries where HBV vaccination has successfully decreased the carrier frequency and disease burden, at least 80% of target population has been vaccinated [1],[8] . Post needle prick HBV transmission dynamics are not available from this country. Therefore, post needle stick injuries should be dealt with as anywhere else, i.e. with passive active immunization combining hepatitis B immune globulin (HBIG) and HBV vaccine. Preventive steps for household contacts, nosocomial spread must be included in the prevention strategy of HBV control in India. HBV vaccination of all household contacts and medical/paramedical staff should be recommended [1] .

Due to extremely high prevalence of anti HAV protective antibody in general population, (both adult and paediatric population) [8] , mass immunization against HAV would not be cost effective in India. HAV vaccine is expensive while the test to detect presence of anti HAV antibody is cheap. Two candidate vaccines against HEV has been tested in endemic region of HEV with a short term protection in about 95 to 98 per cent of the people , but till date these are not commercially available [19] . With their availability, at risk population (during onset of epidemics, pregnant females who are prone to contract HEV infection and are known to develop severe liver disease, and patient with chronic liver disease who develop rapid decompensation with HEV superinfection) [14] are likely to benefit and avail protection against the HEV infection.

While prevention of these hepatitis virus infections ultimately decreases the disease burden and the disease related morbidity and mortality in long term, it is imperative to identify the infected individuals particularly with chronic HBV and HCV infections. Advances in therapy for chronic HCV and HBV infections have resulted in cure (for HCV) and control (for HBV) of such chronic liver diseases. Chronic HBV and HCV infection may remain silent and, therefore, high risk groups such as individuals with history of transfusion, dental interventions, surgery, unsafe sexual exposures, household contacts of index HBV cases, etc. need screening for such infections. Antivirals and immunomodulators like interferons to eradicate these viruses have been developed and tried successfully in these patients, and have become the mainstay of therapy in such patients. The most dangerous sequel liver cancer at an early stage is curable and patients with end stage liver diseases with overt liver failure can be subjected to liver transplant whose results are excellent (5 year survival reaching up to 75 to 80%) [1] . Today hepatitis and its sequel can be treated with an aim to cure or control these effectively to obtain a normal quality of life. Today all experts dealing with the liver believe that "Hepatitis is preventable and curable".

Hepatitis due to hepatitis viruses detected at any stage of its natural course can be managed efficiently with resultant benefit. Knowledge about the virus, the way it is transmitted, its diagnostic processes, and intervention strategy are clearly defined and can be used widely. Knowing about it will be the way to confront it and control it. Ultimately, we aim to eradicate it. However, such results will be possible only by co-ordinated, persistent, evidence based, cost-effective strategies involving multidisciplinary teams such as epidemiologists, hepatologists, transplant surgeons, virologists, cellular biologists, and pharmaceutical and administrative agencies. The most important of all the control strategies is the people's awareness and participation in controlling these menacing ailments.

   References Top

1.Acharya SK, Madan K, Dattagupta S, Panda SK. Viral hepatitis in India. Natl Med J India 2006; 19 : 203-17.  Back to cited text no. 1
2.Vishwanathan R. Infectious hepatitis in Delhi (1955-1956). A critical study: Epidemiology. Indian J Med Res 1957; 45 (Suppl): 1-29.  Back to cited text no. 2
3.Khuroo MS. Study of an epidemic of non-A, non-B hepatitis. Possibility of another human hepatitis virus distinct from post-transfusion non-A, non-B type. Am J Med 1980; 68 : 818-24.  Back to cited text no. 3
4.Naik SR, Aggarwal R, Salunke PN, Mehrotra NN. A large waterborne viral hepatitis E epidemic in Kanpur, India. Bull World Health Organ 1992; 70 : 597-604.  Back to cited text no. 4
5.Ray R, Aggarwal R, Salunke PN, Mehrotra NN, Talwar GP, Naik SR. Hepatitis E virus genome in stools of hepatitis patients during large epidemic in north India. Lancet 1991; 338 : 783-4.  Back to cited text no. 5
6.Wong DC, Purcell RH, Sreenivasan MA, Prasad SR, Pavri KM. Epidemic and Endemic hepatitis in India: evidence for a non-A, non-B hepatitis virus etiology. Lancet 1980; 2 : 876-9.  Back to cited text no. 6
7.Acharya SK, Panda SK, Saxena A, Gupta SD. Acute hepatic failure in India: a perspective from the East. J Gastroenterol Hepatol 2000; 15 : 473-9.  Back to cited text no. 7
8.Acharya SK, Batra Y, Bhatkal B, Ojha B, Kaur K, Hazari S, et al. Seroepidemiology of hepatitis A virus infection among school children in Delhi and North Indian patients with chronic liver diseases: implications for HAV vaccination. J Gastroenterol Hepatol 2003; 18 : 822-7.   Back to cited text no. 8
9.Tandon BN, Gandhi BM, Joshi YK. Etiological spectrum of viral hepatitis and prevalence of markers of hepatitis A and B virus infection in northern India. Bull World Health Organ 1984; 62 : 67-73.  Back to cited text no. 9
10.Arora NK, Nanda SK, Gulati S, Ansari IH, Chawla MK, Gupta SD, et al. Acute viral hepatitis types E, A and B singly and in combination in acute liver failure in children in north India. J Med Virol 1996; 48 : 215-21.  Back to cited text no. 10
11.Batham A, Narula D, Toteja T, Sreenivas V, Puliyel JM. Systematic review & metaanalysis of prevalence of hepatitis B in India. Indian Paediatr 2007; 44 : 663-74.  Back to cited text no. 11
12.Puliyel JM, Rastogi P, Mathew JL. Hepatitis B in India: systematic review and report of the IMA sub-committee on immunization. Indian J Med Res 2008; 127 : 494-7.  Back to cited text no. 12
13.Ghanny MG, Strader DB, Thomas DL, Seeff LB. American Association for the Study of Liver Diseases. Diagnosis, management and treatment of hepatitis C: an update: Hepatology 2009; 49 : 1335-74  Back to cited text no. 13
14.Arankalle VA, Gandhi S, Lole KS, Chadha MS, Gupte GM, Lokhande MU. An outbreak of hepatitis B with high mortality in India: association with precore, basal core promoter mutants and improperly sterilized syringes. J Viral Hepat 2011; 18 : e20-8.  Back to cited text no. 14
15.Acharya SK. Does the level of hepatitis B virus vaccination in health-care workers need improvement? J Gastroenterol Hepatol 2008; 23 : 1628-31.   Back to cited text no. 15
16.Aggarwal R, Naik SR. Prevention of hepatitis B infection: The appropriate strategy for India. Natl Med J India 1994; 7 : 216-20.  Back to cited text no. 16
17.Aggarwal R, Ghoshal UC, Naik SR. Assessment of cost-effectiveness of universal hepatitis B immunization in a low-income country with intermediate endemicity using a Markov model. J Hepatol 2003; 38 : 215-22.  Back to cited text no. 17
18.Ni YH, Chang MH, Huang LM, Chen HL, Hsu HY, Chiu TY. Hepatitis B virus infection in children and adolescent in a hyperendemic area: 15 years after mass hepatitis B vaccination. Ann Intern Med 2001; 135 : 796-800.  Back to cited text no. 18
19.Sarin SK, Kumar M. A vaccine for hepatitis E: has it finally arrived? Gastroenterology 2011; 140 : 1349-52; discussion 1352-3.  Back to cited text no. 19


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