Biomedical subjects
P Kar
Publications and source records attributed to P Kar.
Serological study of hepatitis A virus infection amongst the students of a medical college in Delhi & evaluation of the need of vaccination.
BACKGROUND & OBJECTIVES: Recent seroepidemiological studies have demonstrated a decrease in the seroprevalence of hepatitis A virus (HAV) infection, thereby increasing the pool of susceptible adult population. Health care workers, especially those working in paediatric wards and nurseries, are at an increased risk of developing HAV infection. The present study was undertaken to determine the prevalence of antibody against HAV (IgG anti-HAV) among a batch of medical students of the Maulana Azad Medical College, New Delhi, so as to identify the proportion of students who would be susceptible to HAV infection and hence would benefit from a vaccination programme against HAV. METHODS: A total of 91 medical students were enrolled and divided into groups on the basis of sex. The serum samples were evaluated for the presence of immunoglobulin (IgG) against HAV (IgG anti-HAV) using a commercially available enzyme linked immunosorbent assay (ELISA) kit. RESULTS: The mean age of all the subjects was 19.9 +/- 1.5 yr and the male: female ratio was 1.2: 1. Fifty seven (62.6 +/- 5.1%) students were positive for IgG anti-HAV while 34 (37.4%) were seronegative and hence susceptible to HAV infection. No statistically significant difference was observed in the seroprevalence of HAV between males and females [64 +/- 6.7% (32/50) versus 60.9 +/- 7.6% (25/41)]. INTERPRETATION & CONCLUSION: our results indicate that more than one-third of the medical students were seronegative for IgG anti-HAV and hence at an increased risk of developing HAV infection as a result of occupational exposure. Therefore, we suggest that students in a health care set up should undergo vaccination against HAV after pre-vaccination immunity screening.
Etiology of endemic viral hepatitis in urban North India.
This study was carried out to determine the presence of markers of hepatitis viruses in patients with acute liver disease. Coinfection of HAV, HBV, HCV, and HEV was studied. Sera from 306 patients with a clinical diagnosis of acute liver disease were tested for the presence of anti-HAV antibody, HBsAg, anti-HBc antibody, anti-HBs antibody, anti-HCV antibody and IgM anti-HEV antibody by ELISA. Liver function tests were correlated with the presence of infection. Of the 306 cases, 7 (2.3%) had IgM anti-HAV, 9 (2.9%) had IgM anti-HBc, 37 (12.1%) had HBsAg, 84 (27.4%) had anti-HBs, 10 (3.3%) were HCV infected and 63 (20.6%) had IgM anti-HEV. There was no significant difference in the clinical and liver function profiles of infected and uninfected patients. Similarly, no difference was observed in cases coinfected with more than one virus compared with those infected with a single pathogen. HEV had the highest prevalence amongst our cases. There was no difference in the clinical profiles of patients with non-A, non-B, non-C, non-E hepatitis by antibody assays and testing for viremia could be helpful in making the correct diagnosis.
Tubercular abscess of the liver.
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Hepatitis G virus (HGV) infection in voluntary and commercial blood donors in India.
The prevalence of hepatitis G virus (HGV) has been determined in commercial as well as voluntary blood donors from India by detecting viral RNA genome using reverse transcription polymerase chain reaction (RT-PCR) assay. 45 professional blood donors from private blood banks and 50 healthy controls who opted for voluntary blood donation were recruited for the study. Both the groups were also screened serologically for HBV and HCV infection. The prevalence of HGV in the general population in India was found to be 4% but significantly a higher frequency (46.6%; p<0.001) of HGV was observed in commercial blood donors.
The changing epidemiological pattern of hepatitis A in an urban population of India: emergence of a trend similar to the European countries.
The present study was undertaken to determine the seroprevalence of the antibody against hepatitis A virus (IgG anti-HAV) in an urban population sample from Delhi (India) and to assess any change in the epidemiological pattern of HAV infection in this part of the world. A total of 500 healthy subjects were enrolled and divided into groups on the basis of age, sex and per capita income and evaluated for the presence of IgG anti HAV antibodies using a commercially available kit. The mean age of all the subjects was 32.6 +/- 13.2 yr. and the male:female ratio was 1.5:1. The overall prevalence of IgG anti-HAV in all subjects was 71.2% (356/500). The prevalence in subjects >35 years (92.1% [186/202]) was significantly higher than that in subjects <35 years (92.1% [186/202]) was significantly higher than in subjects <35 years (57% [170/298]). No statistically significant difference was observed between male and female subjects (71.4% [217/304] vs. 70.9% [139/196]) or between subjects belonging to middle and low socioeconomic groups (68.9% [135/196] vs. 72.7% [221/304]). These findings when compared with the results that were obtained in 1982, showed a decreasing prevalence of IgG anti-HAV, most significantly in younger age groups (16-35 years). Thus, we may conclude that the seroepidemiology of hepatitis A virus infection in urban population of India seems to be changing with seroprevalence in the younger population approaching a figure similar to that of the more developed European countries.
Role of hepatitis E and other hepatotropic virus in aetiology of sporadic acute viral hepatitis: a hospital based study from urban Delhi.
Major hepatotropic virus continues to be an important cause of acute viral hepatitis (AVH) in developing countries like India. While epidemics of AVH have been well studied few serious sporadic cases from developing countries have been reviewed. We studied prospectively 75 cases of sporadic AVH who reported to our hospital and were evaluated for the presence of various hepatotropic viruses. The seroprevalence of IgG anti-HEV antibodies was studied in the general population as a control. We found 53.3% (40/75) of sporadic AVH cases were due to hepatitis E virus while 11% (8/75) were due to hepatitis B virus. Hepatitis C virus was responsible for 8% (6/75) of the sporadic AVH cases and hepatitis A was found in 5% (4/75) of the cases. No causative agent was found in 23% (17/75) of the sporadic AVH cases. The sporadic AVH cases due to HEV were not clinically or biochemically not different from AVH due to other viruses. We found a high prevalence of IgG anti-HEV in 35.6% (178/500) among the general population of urban Delhi. The study suggested that hepatitis E was the most common cause of sporadic AVH in urban Delhi. High seroprevalence of IgG anti-HEV antibodies in the general population and amongst the sporadic AVH cases suggests that it is unlikely to be protective antibody. IgM anti-HEV positive serology is considered diagnostic of acute hepatitis E infection in India, where hepatitis E is endemic.
Clinical implications of hepatitis G virus (HGV) infection in patients of acute viral hepatitis & fulminant hepatic failure.
BACKGROUND & OBJECTIVES: Viral hepatitis is a major public health problem especially in developing countries such as India. Hepatitis viruses A, B, C, D and E are all well characterized and molecularly defined agents with unequivocal association with human liver disease but there is evidence of hepatitis in humans caused by certain transmissible agents which cannot be classified with the above hepatotoric viruses. The role of recently discovered hepatitis G virus (HGV/GBV-C) as an independent heaptitis agent is controversial. Recently, we have shown a relatively high frequency of HGV infection in fulminant hepatic failure but the virus was often detected in co-infection with hepatitis B or E virus. The present study has therefore been carried out to evaluate the clinical significance of HGV infection in acute viral hepatitis (AVH) and fulminant hepatic failure (FHF) through follow up of HGV positive patients till their clinical and biochemical recovery. METHODS: The study included 50 patients comprising 35 of AVH and 15 of FHF. These patients were evaluated on the basis of history, physical examination, liver function profile and serological markers for hepatitis A, B, C and E. Those patients serologically negative for HBV and HCV infection were further screened for HBV DNA and HCV RNA by PCR. All the samples were screened for presence of HGV-RNA by RT-PCR using inner and outer primers sequences selected from NS3 helicase region of the HGV genome. FHF patients who died were subjected to postmortem liver biopsy and these biopsy specimens were also screened for HGV-RNA. Repeat detection of HGV-RNA was done after clinical and biochemical recovery of the patients. RESULTS: Of 35 AVH patients, HGV infection was detected in 5 patients (14.3%) while 4 of 15 patients (26.6%) in the FHF group were positive for HGV-RNA. Five HGV positive AVH patients were followed till clinical and biochemical recovery and all of them tested positive for HGV-RNA at follow up (6 weeks to 6 months). Out of 4 HGV positive FHF patients, only one survived and his repeat sample after clinical and biochemical recovery tested positive for HGV-RNA. INTERPRETATION & CONCLUSIONS: The results suggest that HGV infection does occur in patients of AVH and FHF and HGV viraemia persists for a long time even after clinical and biochemical recovery. These observations point towards a possible non-pathogenic role of hepatitis G virus infection.
Analysis of serological evidence of different hepatitis viruses in acute viral hepatitis in prisoners in relation to risk factors.
BACKGROUND & OBJECTIVES: The present study describes an outbreak of acute viral hepatitis in an institutional population (inmates of a prison) with an aim to delineate the etiological agents of this outbreak and to analyse the clinical, biochemical and serological evidence of different hepatitis viruses in relation to risk factors. METHODS: Fifty patients of acute viral hepatitis identified during the outbreak were evaluated on the basis of history, clinical examination, risk factor distribution, biochemical profile and serological markers for hepatitis A-E infection. Adequate epidemiological data were collected from prison administration including housing of prisoners, food and water supply. RESULTS: Of the 50 patients, 35 (70%) had serological evidence of HEV infection. Evidence of HBV infection was found in 17 patients (34%), HAV infection in 2 (4%) and HCV in 8 (16%) patients. While 16 patients (32%) had evidence of multiple viral infections, none of the viral markers could be detected in 8 patients (16%). One or more risk factor(s) could be identified in more than half of the subjects (26/50; 52%). There were 11 patients who gave history of more than one risk factor while 24 (48%) patients had none of the risk factors. INTERPRETATION & CONCLUSIONS: HEV was found to be the major cause of the outbreak and contamination of drinking water supply could be the possible source of infection. This outbreak was seroepidemiologically similar to other outbreaks of hepatitis occurring in the country with HEV being the most common cause. However, there was evidence of multiple viral infections, particularly HBV and HCV in the high-risk predisposed prison population.
HCV seroreactivity and detection of HCV RNA in cirrhotics.
This study was carried out to determine the presence of HCV infection in cirrhotic patients and to compare their serologic profiles with detection of HCV RNA by RT-PCR. Liver function profiles were assessed and correlated with infection. Coinfection of HCV with HBV was studied in the Indian context Sera from 62 patients of biopsy confirmed cirrhosis and an equal number of asymptomatic controls were tested for HCV by two ELISA (third generation) kits and nested reverse transcription PCR using primers from the 5'NCR. Other tests included HBV serology (ELISA for HBsAg and anti-HBc) and liver function tests. Twenty-four (38.7%) cases were HCV infected, of which 17 (70.8%) had past exposure to HBV or were coinfected with HBV (either being chronically infected or carriers of HBV). There was no significant difference in the clinical and liver function profiles of HCV infected and uninfected cirrhotics. Similarly, no difference was observed in cases coinfected with both HCV and HBV compared with those infected with HCV alone. Although the difference between positivity of HCV RNA and of anti-HCV was not significant, HCV RNA and anti HCV were present together in only 7/62 (11.3%) cases. Thus testing for both antibody and HCV RNA would be more appropriate than either test alone. HBV infection was seen in about one-fourth of HCV infected cirrhotics. About one-fourth (25.8%) patients had non-B, non-C cirrhosis in whom testing for HCV variants and other recently characterized hepatitis viruses could be performed.
Hepatitis C virus infection in sporadic fulminant viral hepatitis in North India: cause or co-factor?
INTRODUCTION: The role of hepatitis C virus (HCV) infection in fulminant hepatitis (FH) is poorly understood and the available data are conflicting. We have examined the aetiological role of HCV in 50 consecutive patients with sporadic FH by employing serology and reverse transcription-polymerase chain reaction (RT-PCR). MATERIALS AND METHODS: A total of 50 consecutive patients with sporadic FH were included. After an initial clinical and biochemical assessment, tests were performed for detection of HBsAg, IgM anti-HBc, IgM anti-HAV, IgM anti-HEV and anti-HCV. RT-PCR was carried out for detection of HCV RNA in sera of all the patients and in post mortem liver biopsy tissue of 20 subjects, using primers selected from the conserved 5' non-coding region of the HCV genome. RESULTS: Hepatitis E virus (HEV) was found to be the most common viral infection (21/50; 42%) followed by HBV (14/50; 28%), HCV (7/50; 14%) and HAV (2/50; 4%). No viral markers could be detected in nine patients (18%) and multiple infections were seen in seven (14%). Of the seven subjects who tested positive for HCV-related markers, two had both anti-HCV and HCV RNA, three had HCV RNA alone and the remaining two had anti-HCV alone. Interestingly, all the HCV-infected subjects were co-infected with other hepatotropic viruses and the most common co-infecting agent was found to be HBV (5/7). Liver tissue was available in 20 cases and HCV RNA was detected in three of them. All of these patients were also positive for the viral genome in their serum samples. Comparison of the biological attributes of HCV-positive and HCV-negative cases revealed that haemorrhagic symptomatology (haematemesis, melaena and purpurae) was significantly more common, prothrombin time more deranged and mortality was much higher in the former group. The overall mortality was 68% and the most common cause of death was cerebral oedema (70.6%). No significant correlation was observed between mortality and the duration of the icterus-encephalopathy interval. The study included a total of 21 pregnant females; HEV infection was found to be significantly greater in this group and was associated with a higher mortality rate. CONCLUSIONS: The results clearly suggest that HCV is not an important aetiological factor for FH in North India. However, it may act as a co-factor in the development of FH leading to a higher mortality. HEV appears to contribute substantially to the causation of sporadic FH in India and advanced stage pregnancy is a potential risk factor for HEV-induced FH and high rate of mortality. Our study also suggests that the length of the icterus-encephalopathy period may not have significant prognostic implications in Indian patients with FH.
Hepatitis G virus (HGV) infection & its pathogenic significance in patients of cirrhosis.
In the present study the hepatitis G virus (HGV) infection and its pathogenic significance in patients of cirrhosis were assessed using reverse transcription plus nested polymerase chain reaction (RT-PCR). Serum samples were collected from a total of 50 patients of histologically proven non-alcoholic cirrhosis and from a control group consisting of 50 healthy voluntary blood donors. HGV RNA was detected by RT-PCR using primer sequences located in the conserved NS3 helicase region of HGV genome. Serological evaluation for markers of chronic infection with HBV (HBsAg, IgG anti-HBc, HBeAg) and HCV (anti-HCV) was carried out using commercially available kits. HBV DNA and HCV RNA were also tested by PCR in those samples that were found to be non-B, non-C by serological assays. Serological evidence of exposure to HBV was found in 31 (62%) and to HCV in 15 (30%) patients. HGV RNA was detected in 6 (12%) cirrhosis patients and in 2 (4%) healthy blood donors but the difference between the two groups was not statistically significant. Of the 6 HGV positive patients, 2 were coinfected with HBV, 1 with HCV, while the remaining 3 belonged to non-B, non-C category. No significant difference was observed in the clinical and biochemical profiles of HGV-positive and HGV-negative patients except that a history of blood transfusion was significantly (P < 0.005) more common in the former. The findings indicate that the HGV infection is commonly observed in both cirrhosis patients as well as healthy blood donors. A significant association of the virus with blood transfusion is indicative of a parenteral route of transmission. The observations of this study also suggest that the pathogenic role of HGV in the causation of liver disease may be insignificant.
Ampullary carcinoma in the elderly.
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Profuse variceal hemorrhage as a presenting feature of pancreatic adenocarcinoma in a young non-icteric patient.
Pancreatic adenocarcinoma can present with a vast spectrum of rare manifestations. It usually occurs after the age of 50 years, the peak incidence being in sixth and seventh decades. We report a previously asymptomatic subject of pancreatic adenocarcinoma who presented for the first time with massive upper gastrointestinal hemorrhage. Endoscopy revealed ruptured esophageal varices which were secondary to tumour-induced thrombosis of the portal vein. Besides the uncommon mode of presentation, the patient was unusual because of his young age. Further, he was non-icteric at the time of presentation and remained so throughout the clinical course despite having a large lesion in the head of the pancreas.
Detection of hepatitis C and E virus genomes in sera of patients with acute viral hepatitis and fulminant hepatitis by their simultaneous amplification in PCR.
A study was undertaken to investigate the role of hepatitis C virus (HCV) and hepatitis E virus (HEV), either alone or together, in the causation of sporadic acute viral hepatitis (AVH) and fulminant hepatitis (FH) by simultaneous detection of their genomes in serum samples using the reverse transcription and nested polymerase chain reaction (RT-PCR). A total of 50 patients were enrolled in the study of which 34 had AVH and 16 had sporadic FH. The serum samples were first tested for hepatitis B surface antigen (HBsAg) and immunoglobulin (Ig)M antibodies against hepatitis A virus (HAV), hepatitis B core antigen (HBcAg) and HEV and also antibodies against HCV using commercially available enzyme-linked immunosorbent assay (ELISA) kits. All samples were then subjected to RT-PCR using primers for both HCV and HEV simultaneously in the same reaction mixture. Hepatitis C or hepatitis E was diagnosed when either the antibodies or PCR or both were positive for the respective viruses. Evidence of hepatitis C was present in six of the 34 (17.6%) cases of AVH and two out of 16 (12.5%) cases of FH. Four patients in the AVH group and one of the fulminant hepatic failure (FHF) group were found to be positive by PCR and the rest by serology. But as a sole aetiological agent, HCV infection was found in only one (2.9%) case of AVH and in none of the FHF cases. Evidence of HEV infection was found in 22/34 (64.7%) and 8/16 (50%) cases of AVH and FHF, respectively. Excluding co-infection with other viruses, HEV was found to be the sole aetiological agent in 15/34 (44.1%) of AVH and 7/16 (43.7%) cases of FHF. In five (10%) (four AVH and one FHF) of the 50 cases, evidence of infection with both HCV and HEV was present. But only in two of these five cases, genomes of both HCV and HEV were co-amplified. In seven (four AVH and three FHF) out of 50 (14%) cases, no known viral agent could be detected. Our results suggest that HEV is the most common aetiological agent for both acute viral hepatitis and fulminant hepatic failure and that HCV is a rare cause of acute liver diseases although along with other viruses, evidence of either present or past HCV infection may be present in a substantial number of cases. Furthermore, advanced-stage pregnancy appears to be a potential risk factor for HEV infection and high rate of mortality in women. The study suggests that the method of simultaneous amplification of both HCV and HEV genomes could reduce the time, labour and cost involved in diagnostic work up of acute liver disease patients.
Association of hepatitis C virus & hepatitis B virus in chronic liver disease.
Hepatitis C virus (HCV) as a cause of chronic liver disease (CLD) was assessed by testing anti-HCV antibodies in the serum samples of 55 patients of chronic hepatitis (17), cirrhosis (32) and hepatocellular carcinoma (6). All the samples were also tested for the presence of HCV RNA by reverse transcription polymerase chain reaction (RT-PCR) using primers from the 5' non-coding region (NCR) and the relationship between the serological parameters and presence of HCV RNA was studied. The association of hepatitis B virus (HBV) with HCV in this group was evaluated by testing for the anti HBc antibodies (IgG and IgM separately) and HBsAg. The biochemical parameters and involvement of other risk factors were also studied. Twenty two (40%) patients were found to be HCV positive and 17 (77.3%) of these had evidence of infection or past exposure to HBV. On comparing the sensitivities of ELISA with that of PCR for the detection of HCV, we observed no significant difference between the two methods (P > 0.05, McNemar's test). Eighteen patients had no evidence of HBV or HCV infection. Our results indicate that HCV is next only to HBV in the causation of CLD. It is suggested that RT-PCR be used with antibody detection by ELISA for reliable detection of HCV infection.
Etiology of sporadic acute and fulminant non-A, non-B viral hepatitis in north India.
BACKGROUND: Viral hepatitis is a major public health problem in India. AIM: To investigate the association of various hepatitis viruses in patients with acute liver diseases in north India. METHODS: One hundred and thirteen patients with acute viral hepatitis (AVH; n = 70) or fulminant hepatic failure (FHF; N = 43) were evaluated for the presence of hepatitis A, B, C and E virus infection. Hepatitis C virus (HCV) testing was done using second-generation anti-HCV ELISA test and reverse transcriptase polymerase chain reaction (PCR) for the detection of HCV RNA in the serum of patients with non-A, non-B (NANB) hepatitis. Detection of IgM anti-HEV antibody was done in patients found negative for the above viruses (n = 53). RESULTS: Hepatitis A and B viruses accounted for 3.5% and 42.5% of the 113 cases, respectively. HCV infection accounted for 12% of the NANB cases with AVH and 15.5% with FHF. PCR was more useful than serological tests for the detection of HCV infection. HEV infection accounted for 49% of the NANB, non-C cases with AVH and 25% with FHF; pregnant women with HEV infection had a fulminant course. No etiological agent could be established in 28.3% of cases. CONCLUSION: HEV is the most important cause of NANB hepatitis; hepatitis B virus is still a major concern, while HCV is not an important cause of acute viral liver disease in India.
Comparative evaluation of serology and polymerase chain reaction for hepatitis C viral infection in liver diseases.
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