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 Table of Contents  
PAPERS PRESENTED AT THE XVII ANNUAL CONFERENCE OF HOSPITAL INFECTION
Year : 2021  |  Volume : 9  |  Issue : 3  |  Page : 83-86

Prevalence of Hepatitis A in and around the Aligarh region


Department of Microbiology, Jawaharlal Nehru Medical College and Hospital, Aligarh Muslim University, Aligarh, Uttar Pradesh, India

Date of Submission16-Apr-2022
Date of Acceptance01-May-2022
Date of Web Publication22-Jul-2022

Correspondence Address:
Dr. Arti Kumari
Department of Microbiology, Jawaharlal Nehru Medical College and Hospital, Aligarh Muslim University, Aligarh, Uttar Pradesh
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/jpsic.jpsic_21_22

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  Abstract 


Background: Hepatitis A virus (HAV) most commonly affects children, is transmitted by faecal–oral route and is prevalent worldwide. It is usually present in the highest concentration in the stool of the infected individuals, with the greatest viral load occurring near the end of the incubation period.
Aim: The aim of the present study was to study the prevalence of hepatitis A in and around the Aligarh region.
Methodology: A total of 524 samples were collected from all age groups, who were suspected of having viral hepatitis. The serum was separated and processed for performing the enzyme-linked immunosorbent assay (DIA. PRO, Italy).
Results: Out of 524 samples tested, 229 (43.7%) were positive for anti-HAV immunoglobulin M, most of which (82.53%) were from the 10 years' age group.
Conclusions: The predominance of hepatitis A was found in under 10-year-old children, with mast case occurrences between June and September.

Keywords: Hepatitis A virus, hepatitis A, prevalence


How to cite this article:
Kumari A, Raza A, Khan HM, Sami H. Prevalence of Hepatitis A in and around the Aligarh region. J Patient Saf Infect Control 2021;9:83-6

How to cite this URL:
Kumari A, Raza A, Khan HM, Sami H. Prevalence of Hepatitis A in and around the Aligarh region. J Patient Saf Infect Control [serial online] 2021 [cited 2022 Aug 18];9:83-6. Available from: https://www.jpsiconline.com/text.asp?2021/9/3/83/351740


  Introduction Top


Hepatitis viruses are a taxonomically diverse group of viruses, belonging to different families. Amongst all hepatitis viruses, hepatitis A virus (HAV) causes liver disease. HAV is an RNA virus belonging to Picornaviridae family.[1] The incubation period of hepatitis A infection averages 28 days (range, 15–50 days).[2] Symptomatic illness due to HAV occurs in more than 70% of adults. Symptoms are uncommon in children <6 years of age. Common symptoms are sudden onset of nausea, vomiting, anorexia, fever, malaise and abdominal pain.[3] The HAV transmitted by faecal–oral route sometimes causes abrupt explosion or may result in epidemics.[4] According to the WHO data (2019), 7134 deaths occur due to hepatitis A and 0.5% mortality occurs due to hepatitis A worldwide.[1]

Geographically distributed areas can be categorised as having high, intermediate or low levels of HAV infection. In areas with high levels of infection, hepatitis A is endemic, and up to 90% of children in the age group of <10 years have been infected with HAV, most often without symptoms.[5] In areas with low levels of infection, adolescents and adults are high-risk groups. Areas with intermediate levels of infection are regions where sanitary conditions are poor and where immunocompromised individuals make up the high-risk groups. The WHO data 2019 show that approximately 1.5 million people are infected with HAV each year.[1] In India, during the period of 2011–13, 7.4% of cases were positive for hepatitis A.[6] Routine hepatitis reporting to the Central Bureau of Health Intelligence is highly underreported, as it includes cases reaching facilities in the public sector only. Due to a paucity of data, the exact burden of disease for the country is not established. However, available literature indicates a wide range and suggests that HAV is responsible for 10%–30% of acute hepatitis and 5%–15% of acute liver failure cases in India.[7] In the Western Pacific region, 19% of deaths occurred due to acute hepatitis A in 2019.[8] In a recent study in Kerala, an HAV outbreak was identified, in which 4.6% of cases were reported in the age group of 15–24 years and 3.1% of cases were reported in the age group of 5–14 years.[9] Consistently from 2016-2018, cases of HAV reported from Uttar Pradesh (Most populous state in India) have been more than 20,000 per year.[10] This is a pioneer study regarding the prevalence of hepatitis A; no such study has been done in this region previously, which is why this study was dedicated to observe the prevalence of hepatitis A in this region.


  Methodology Top


A prospective study was carried out on individuals who were clinically suspected to have jaundice and/or liver disease, in Jawaharlal Nehru Medical College and Hospital, A. M. U., Aligarh, during January 2020 to December 2020. Age wise distribution of Hepatitis A virus cases in shown in [Table 1].
Table 1: Age-wise distribution of hepatitis A virus ELISA-positive cases (n=229)

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Inclusion and exclusion criteria

Patients of all age groups from various OPDs and wards were included in the study. Whole-blood specimens in red-topped Vacutainer (obtained from BD) were received by the virology section at the Department of Microbiology, JNMC, Aligarh. Informed consent was taken from each patient or their guardian, if the patient was <18 years. Patients, with non-infectious aetiologies (i.e. obstructive jaundice, haemolytic jaundice, non-alcoholic fatty liver disease, autoimmune hepatitis, drugs (e.g. antitubercular agents) or hepatotoxin-induced liver insults were excluded from the study.

Serum was separated from the whole blood by centrifugation for 10 min at 1000 g. Aliquoted serum in the labelled cryovials was stored at −20°C till tested. HAV antibodies were detected using 'capture' enzyme-linked immunosorbent assay (DIA. PRO, Italy), according to the manufacturer's instructions. The reading was taken at 450 nm on an Infinite N200 Pro NanoQuant Spectrophotometer (Tecan, Switzerland). The OD value > 0.500 at 450 nm should be considered positive and the OD value < 0.150 at 450 nm should be considered negative.


  Results Top


A total of 524 patients (n = 312 males and n = 212 females) were enrolled in the study and 229 (43.70%) patients were found to be positive for anti-HAV immunoglobulin M (IgM). Out of 229 (43.70%) samples found positive for anti-HAV IgM antibody, 135 (58.95%) were male patients and 94 (41.05%) were female. Laboratory findings of HAV-positive patients is shown in [Figure 1].
Figure 1: Laboratory findings of HAV-positive patients. HAV: Hepatitis A virus

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Less than 5 mg/dl serum bilirubin was found in 137 (59.82%) patients, 5–10 mg/dl in 60 (26.20%) patients and >10 mg/dl in 32 (16.59%) patients. The levels of aspartate aminotransferase (AST) and alanine aminotransferase (ALT) was found to be raised with a mean AST level of 1167.86 ± 669 IU/L in HAV-positive samples, versus 1041.22 ± 885 IU/L in HAV-negative samples. The mean ALT in HAV-positive samples was 1263.852 ± 669.05 IU/L versus 1159.01 ± 568.05 IU/L in HAV-negative samples. Seasonal trends of HAV from January 2020 to December 2020 is shown in [Figure 2].
Figure 2: Seasonal trends of HAV from January 2020 to December 2020. HAV: Hepatitis A virus

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Out of 229 positive samples, 189 (82.53%) were under 10 years (40.17% were < 6-year-old and 42.35% were 6–10-year-old), while 38 (13.10%) belonged to 11–30 years, and <1% positive cases were of above 30 year age group. HAV positivity rates were highest (50%–86.6%) during June to September, and the lowest positivity (25%–38%) was seen during December to February.


  Discussion Top


Acute viral hepatitis due to HAV occurs worldwide and is endemic in Asia, Africa, Latin America and the Middle East.[11] In India, it remains a major public health problem despite improving sanitation, health awareness and socioeconomic conditions. The present study was done on 524 suspected cases of AVH in all age groups, and 43.70% of samples were found positive for anti-HAV IgM antibody. Wide variation in positivity (27.2%–74.5%) has been reported from hospitalised patients in India: Lucknow (27.2%),[10] Chennai (38.6%)[12] and Hyderabad (74.5%).[13] In the present study, higher HAV IgM positivity of 82.53% was observed in children of age group between 0–10 years; however, other authors have reported a positivity of 80.95% and 60% in the similar age group from Shimla[11] and from Chennai respectively.[14]

Males are more affected (58.95%) than females (41.05%). The exact reason is not known, but it may be due to poor maintenance of personal hygiene and lifestyle and consumption of unhygienic food from street vendors.

Most of the positive patients (82.53%) are under 10 years of age, and the positivity rate in 6–10 years of age group was slightly higher than the 0–5 years' age group. The pattern of HAV infection in children is shifting of older children than younger children, because parts of Indian populations have recently become more aware about health and hygiene practices. People have become more health conscious and have begun to incorporate mindful health practices by adopting hygienic habits.[15]

Typical presenting symptoms in patients include fever, malaise, nausea, vomiting, abdominal discomfort, dark urine, and jaundice. These symptoms are very mild or negligible in children <6 years, whereas more pronounced symptoms occur in older children and adolescents. Laboratory abnormalities include elevations of serum aminotransferases (often >1000 international units/L), as in our study, mean AST values were 1167.86 ± 669 IU/L and mean ALT values were 1263.852 ± 669.054 U/L. In our study, serum bilirubin level (Normal ≤10 mg/L) in 86.02% of patients were ≤10 mg/L.[16] The serum aminotransferase elevation precedes the bilirubin elevation. Serum ALT is usually higher than the serum AST. Serum aminotransferases peak around 1 month after exposure to the virus and then decline to 75% per week.[17] The serum bilirubin concentration usually declines within 2 weeks of peak levels.[18] There is a diversity of seasons in India, which leads to changing trends of HAV infection, with maximum occurrences of hepatitis A viral infections during June to September and minimum during December to February.

Our study has some limitations. One major limitation was that all our specimens were from inpatient and outpatient department patients having clinical symptoms. Moreover, in COVID-19 era, there was a drastic drop in patient visitations.


  Conclusions Top


In our study, 43.7% of individuals were found to be HAV positive in Aligarh region, and the most affected age group was of children <10 years. Most of the cases were reported between June and September.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Hepatitis A [Internet]. Available from: https://www.who.int/news-room/fact-sheets/detail/hepatitis-a [Last accessed on 2022 May 28].  Back to cited text no. 1
    
2.
Tan EM, Marcelin JR, Virk A. Pre-travel counseling for immunocompromised travelers: A 12-year single-center retrospective review. Infect Dis Health 2019;24:13-22.  Back to cited text no. 2
    
3.
Lednar WM, Lemon SM, Kirkpatrick JW, Redfield RR, Fields ML, Kelley PW. Frequency of illness associated with epidemic hepatitis A virus infections in adults. Am J Epidemiol 1985;122:226-33.  Back to cited text no. 3
    
4.
Halliday ML, Kang LY, Zhou TK, Hu MD, Pan QC, Fu TY, et al. An epidemic of hepatitis A attributable to the ingestion of raw clams in Shanghai, China. J Infect Dis 1991;164:852-9.  Back to cited text no. 4
    
5.
Jacobsen KH, Wiersma ST. Hepatitis A virus seroprevalence by age and world region, 1990 and 2005. Vaccine 2010;28:6653-7.  Back to cited text no. 5
    
6.
Kumar T, Shrivastava A, Kumar A, Laserson KF, Narain JP, Venkatesh S, et al. Viral hepatitis surveillance-India, 2011-2013. MMWR Morb Mortal Wkly Rep 2015;64:758-62.  Back to cited text no. 6
    
7.
MoHFW-WHO-ILBS. Third GoI-WHO-ILBS National Technical Consultation on Viral Hepatitis towards a National Action Plan for Viral Hepatitis (NAP-VH). New Delhi; 2016.  Back to cited text no. 7
    
8.
Regional hepatitis data [Internet]. Available from: https://www.who.int/westernpacific/health-topics/hepatitis/regional-hepatitis-data [Last accessed on 2022 May 28].  Back to cited text no. 8
    
9.
Rakesh PS, Carmel Regeela Mainu TT, Raj A, Babu D, Rajiv M, Mohandas KS, et al. Investigating a community wide outbreak of hepatitis A in Kerala, India. Journal of Family Medicine and Primary Care 2018;7:1537-41.  Back to cited text no. 9
    
10.
Jain P, Prakash S, Gupta S, Singh KP, Shrivastava S, Singh DD, et al. Prevalence of hepatitis A virus, hepatitis B virus, hepatitis C virus, hepatitis D virus and hepatitis E virus as causes of acute viral hepatitis in North India: A hospital based study. Indian J Med Microbiol 2013;31:261-5.  Back to cited text no. 10
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11.
Chobe LP, Arankalle VA. Investigation of a hepatitis A outbreak from Shimla Himachal Pradesh. Indian J Med Res 2009;130:179-84.  Back to cited text no. 11
[PUBMED]  [Full text]  
12.
Lemon SM. Type A viral hepatitis. New developments in an old disease. N Engl J Med 1985;313:1059-67.  Back to cited text no. 12
    
13.
Syed R, Mohammed AH, Sindiri PK, Nathani AA, Rao VV, Satti VP. Sero-epidemiology of hepatitis A virus in Hyderabad, South India. J Med Allied Sci 2012;2:58-61.  Back to cited text no. 13
    
14.
Malathi S, Mohanavalli B, Menon T, Srilatha P, Sankaranarayanan VS, Raju BB, et al. Clinical and viral marker pattern of acute sporadic hepatitis in children in Madras, South India. J Trop Pediatr 1998;44:275-8.  Back to cited text no. 14
    
15.
Franco E, Meleleo C, Serino L, Sorbara D, Zaratti L. Hepatitis A: Epidemiology and prevention in developing countries. World J Hepatol 2012;4:68-73.  Back to cited text no. 15
    
16.
Tong MJ, el-Farra NS, Grew MI. Clinical manifestations of hepatitis A: recent experience in a community teaching hospital. J Infect Dis 1995;171 Suppl 1:S15-8.  Back to cited text no. 16
    
17.
Koff RS. Clinical manifestations and diagnosis of hepatitis A virus infection. Vaccine 1992;10 Suppl 1:S15-7.  Back to cited text no. 17
    
18.
Cuthbert JA. Hepatitis A: old and new. Clin Microbiol Rev 2001;14:38-58.  Back to cited text no. 18
    


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