Biomedical subjects
Publications and source records attributed to M Irshad.
The present overview gives a summary of HEV infection comprising its discovery, a characterisation of the virus, its diagnosis, epidemiology, course of the disease, and finally its prevention.
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The profiles of patients with fulminant hepatic failure (FHF) from developing countries have not been reported earlier. The current study was conducted prospectively, at a single tertiary care center in India, to document the demographic and clinical characteristics, natural course, and causative profile of patients with FHF as well as to define simple prognostic markers in these patients. Four hundred twenty-three consecutive patients with FHF admitted from January 1987 to June 1993 were included in the study. Each patient's serum was tested for various hepatotropic viruses. Univariate Cox's regression for 28 variables, multivariate Cox's proportional hazard regression, stepwise logistic regression, and Kaplan-Meier survival analysis were done to identify independent predictors of outcome at admission. All patients presented with encephalopathy within 4 weeks of onset of symptoms. Hepatotropic viruses were the likely cause in most of these patients. Hepatitis A (HAV), hepatitis B (HBV), hepatitis D (HDV) viruses, and antitubercular drugs could be implicated as the cause of FHF in 1.7% (n= 7), 28% (n= 117), 3.8% (n= 16), and 4.5% (n= 19) patients, respectively. In the remaining 62% (n= 264) of patients the serological evidence of HAV, HBV, or HDV infection was lacking, and none of them had ingested hepatotoxins. FHF was presumed to be caused by non-A, non-B virus(es) infection. Sera of 50 patients from the latter group were tested for hepatitis E virus (HEV) RNA and HCV RNA. In 31 (62%), HEV could be implicated as the causative agent, and isolated HCV RNA could be detected in 7 (19%). Two hundred eighty eight (66%) patients died. Approximately 75% of those who died did so within 72 hours of hospitalisation. One quarter of the female patients with FHF were pregnant. Mortality among pregnant females, nonpregnant females, and male patients with FHF was similar (P > .1). Univariate analysis showed that age, size of the liver assessed by percussion, grade of coma, presence of clinical features of cerebral edema, presence of infection, serum bilirubin, and prothrombin time prolongation over controls at admission were related to survival (P < .01). The rapidity of onset of encephalopathy and cause of FHF did not influence the outcome. Cox's proportional hazard regression showed age > or = 40 years, presence of cerebral edema, serum bilirubin > or = 15 mg/dL, and prothrombin time prolongation of 25 seconds or more over controls were independent predictors of outcome. Ninety-three percent of the patients with three or more of the above prognostic markers died. The sensitivity, specificity, positive predictive value, and the negative predictive value of the presence of three or more of these prognostic factors for mortality was 93%, 80%, 86%, and 89.5%, respectively, with a diagnostic accuracy of 87.3%. We conclude that most of our patients with FHF might have been caused by hepatotropic viral infection, and non-A, non-B virus(es) seems to be the dominant hepatotropic viral infection among these patients. They presented with encephalopathy within 4 weeks of the onset of symptoms. Pregnancy, cause, and rapidity of onset of encephalopathy did not influence survival. The prognostic model developed in the current study is simple and can be performed at admission.
BACKGROUND: Preliminary reports indicate that hepatitis D virus (HDV) infection exists in India. However, its prevalence in patients with different types of liver diseases has not been studied in detail. The aim of this study was to evaluate the status of HDV infection in severe types of liver disease in India. METHODS: Using commercial kits for various hepatitis viral markers, the present study was undertaken to determine the serological status of hepatitis B virus (HBV) and hepatitis D virus (HDV) markers in 208 patients with severe liver diseases. This total included 110 cases with fulminant hepatic failure (FHF), 65 cases with subacute hepatic failure (SHF) and 33 cases with chronic active hepatitis (CAH). RESULTS: The hepatitis B surface antigen (HBsAg) carrier population, indicated by the presence of HBsAg without IgM anti-HBc (hepatitis B core) in serum, was recorded in 23.6%, 24.6% and 60.6% cases of FHF, SHF and CAH groups, respectively. HBV infection, as indicated by serum positivity of IgM anti-HBc in the FHF and SHF groups and HBsAg and/or IgM anti-HBc in the CAH group, was detected in 19.1%, 23.1% and 69.7% of cases from these three groups, respectively. IgM anti-HDV, demonstrating active/recent HDV infection, was found in 8.1% cases of FHF and 9.2% cases of SHF patients. HDV as a superinfection in HBsAg carriers was noted in 4.5% and 4.6% cases, respectively of FHF and SHF groups. Similarly, HDV-HBV coinfection, diagnosed by simultaneous presence of IgM anti-HBc and IgM anti-HDV in the FHF and SHF groups, was recorded in 3.6% and 4.6% of cases from these two groups, respectively. In the CAH group, HDV infection was observed in 9.2% cases. CONCLUSION: HDV infection, recorded in less than 10% of patients with different liver diseases in India, seems to be an unimportant factor in inducing severe liver diseases in this country.
BACKGROUND/AIMS: Plasma fibronectin is an opsonic glycoprotein, normally synthesized by the liver, which decreases subsequent to severe liver damage and low levels of which may contribute to reticuloendothelial system dysfunction by compromising opsonic activity. This may result in an increased frequency of infection and death. The present study was conducted to evaluate the association of plasma fibronectin activity with infection and mortality in patients with fulminant hepatic failure. METHODS: Plasma fibronectin was estimated serially in 69 consecutive patients with fulminant hepatic failure, nine patients with uncomplicated acute viral hepatitis and 32 normal volunteers. RESULTS: Plasma fibronectin levels in patients with fulminant hepatic failure (85.6 +/- 75.8 micrograms/ml) were significantly lower than in patients with uncomplicated acute viral hepatitis (295.5 +/- 88.5 micrograms/ml) and healthy volunteers (362.6 +/- 69.2 micrograms/ml). Forty-nine (72%) patients with fulminant hepatic failure died. The initial values of fibronectin in fulminant hepatic failure did not correlate with mortality. Patients with fulminant hepatic failure who survived showed a progressive rise in the fibronectin levels compared to the absence of an increase in fibronectin levels in the non-survivors. The mortality in patients with fulminant hepatic failure with infection (24/27) was significantly higher (p < 0.05) compared to those without infection (25/42). Initial fibronectin levels in patients with infection (70.3 +/- 54.2 micrograms/ml) were significantly lower (p < 0.05) than in those without infection (92.3 +/- 64.4 micrograms/ml). We conclude that plasma fibronectin levels in patients with fulminant hepatic failure are decreased compared to healthy subjects and the absence of an increase in levels indicates a poor prognosis. Low levels of fibronectin are associated with an increased incidence of infection, which increases the mortality in these patients.
We report on the prevalence of anti-HCV antibodies in healthy individuals and patient groups with different liver diseases. The healthy population comprising 234 voluntary blood donors and 65 pregnant women with no history of liver diseases, had a per cent positivity of 1.5 anti-HCV in each group. The patients groups comprising 32 with acute viral hepatitis, 110 with fulminant hepatic failure, 65 with subacute hepatic failure, 33 with chronic active hepatitis, 45 with cirrhosis and 10 with hepatocellular carcinoma, had anti-HCV per cent positivity of 12.5, 43.6, 41.5, 48.5, 8.8 and 0 respectively. Anti-HCV was also tested in sera from 9 patients who had developed post-transfusion hepatitis and was recorded in 2 (22.2%) within one year of transfusion.
The present study describes the frequency of hepatitis viral markers in patients with uncomplicated acute viral hepatitis (AVH; n = 32) and in patients with severe liver diseases, including those with fulminant hepatic failure (FHF; n = 110), subacute hepatic failure (SAHF; n = 65), and chronic active hepatitis (CAH; n = 33). The results indicate that hepatitis A virus infection is quite rare, whereas hepatitis B virus (HBV) and hepatitis C virus (HCV) infections are the predominant causes of acute and chronic liver failure in India. The incidence of HBV infection in AVH, FHF, SAHF, and CAH groups was recorded in 3.7, 19.1, 23.1, and 69.7% of the cases, respectively. Similarly, HCV infection in these four groups was noted in 12.5, 45, 44.6, and 48.5% of the cases, respectively. Further analysis of HCV infection demonstrated that it was as frequent as single infection in acute cases, but more commonly found in association with HBV infection in chronic liver failure cases. Hepatitis D virus (HDV) infection, as indicated by the presence of IgM anti-HDV antibodies, was recorded in 7.3% of the cases with AVH, in 7.3% of the cases with FHF, in 9.2% of the cases with SAHF, and in 6.1% of the cases with CAH. HDV was associated with HBV both as superinfection as well as coinfection. Interestingly, nearly 2-6% of the cases in each group showed the presence of simultaneous HBV, HCV, and HDV infection. 83.3% of the AVH, 42.1% of the FHF, 37.0% of the SAHF, and 15.1% of the CAH patients had unknown viral markers.(ABSTRACT TRUNCATED AT 250 WORDS)
To define the association of the ingestion of nonsteroidal anti-inflammatory drugs (NSAIDs), including aspirin (ASA), and lower gastrointestinal bleeding (GIB) a retrospective, case-controlled study was undertaken of 188 patients admitted to three community hospitals in three cities with a diagnosis of lower GIB. Information was obtained about NSAID usage among these patients, and the data were compared with an age- and sex-matched control group of 185 patients admitted with a nongastrointestinal diagnosis, derived from a daily admission list. At the time of admission, in the New Jersey group, NSAID consumption was present in 26 of 90 (29%) patients with lower GIB compared with 16 of 90 (18%) of controls (P < 0.05, odds ratio 1.88, 95% CI 1.2-3.1) whereas, in the South Carolina group 34 of 98 (35%) were taking NSAID compared with 18 of 95 (19%) of controls (P < 0.01, odds ratio 2.27, 95% CI 1.2-4.4). These data indicate that there is a significantly increased rate of NSAID ingestion in patients admitted with lower GIB, implying that NSAID may unmask bleeding from a variety of lower gastrointestinal lesions.
By means of simple and specific ELISA techniques, the plasma concentrations of soluble fibronectin and C3d, a breakdown product of C3 complement, were determined in patients with amoebic liver abscesses (ALA) and in healthy controls. The mean plasma fibronectin concentrations in 23 patients with ALA and in 20 controls were found to be 441 +/- 89 mg/l and 442 +/- 66 mg/l, respectively. The difference between these two values was not statistically significant. The mean C3d value in 21 patients with ALA, however, was found to be 84 +/- 14 AU/l which was significantly different from the value of 12 +/- 4.7 AU/l noted in 20 healthy persons. Plasma concentrations of these two proteins are discussed in relation to their possible implications in the immunopathogenesis of amoebic liver abscess.
We studied the risk of post-transfusion hepatitis (PTH) in recipients of blood collected from voluntary donors screened for HBsAg. Two hundred and fifty patients without any previous history of liver disease or transfusion were followed up for 12 months subsequent to cardiac surgery. Thirty-five of them had closed-heart surgery without receiving transfusion and served as controls. The remaining 215 patients received single-point transfusions (mean 4 +/- 2.4 units). None of the controls and 15 (6.9%) blood recipients developed PTH. Three (20%) patients had hepatitis-B-virus-induced hepatitis while the remainder (80%) had non A, non B (NANB) hepatitis. The number of units of blood transfused and surrogate markers for development of PTH (donor alanine aminotransferase, anti-HBc and anti-HBs antibody) were not associated with the occurrence of PTH (p greater than 0.05). Nine (60%) of the 15 patients developing PTH were asymptomatic. All the patients recovered from the PTH, except one who died of fulminant hepatitis. At the end of 1 year of follow-up, none of the patients had evidence of chronic hepatitis. Only three (25%) of the patients with NANB-PTH developed anti-hepatitis C virus (HCV) antibody during the follow-up. We conclude that the incidence of PTH in India is similar to other parts of the world and NANB virus was the major cause of the PTH. The absence of chronicity and lack of seroconversion to anti-HCV antibody in the majority of the patients after 1 year of follow-up may suggest the possibility of a NANB virus other than HCV as the major cause of PTH in India.
The present study describes the status of hepatitis C virus infection in 167 patients with severe forms of liver diseases in India. The anti-HCV positivity rate was recorded as 43%, 47%, and 42% in patients with FHF, SAHF, and CAH respectively. HBV and HCV coinfection was recorded in 28% of FHF, 43% of SAHF and 75% of the CAH cases. Superinfection of HCV in HBsAg carriers was recorded in the 54% cases of FHF, 60% of SAHF and 42% of the CAH. None of these 167 patients was positive of HAV-IgM. Further, 27.7% of FHF, 26.4% of SAHF and 15.2% of CAH cases were neither HBV nor HCV markers positive. These can be labelled as non-A, non-B and non-C infections.
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The prevalence of HBsAg and anti-HBs was studied in sera from 982 children of different age groups below 5 yr. HBsAg was detected in 0.9, 2.3, 4.1, 2.3 and 1.6 per cent children of 0-1, 2-6, 7-12, 13-36 and 37-60 months age groups respectively. Anti-HBs in these five groups was noted in 17.0, 12.9, 18.4, 14.2 and 13.7 per cent children, respectively. The findings suggest that the carrier pool is built up in the preschool age group, particularly, below the age of 6 months. Perinatal transmission and the relative role of transplacental need re-evaluation. Cost analysis does not permit inclusion of HBV in the Expanded Programme of Immunisation.
In the present study, 2.5% of 367 preschool children has HBsAg positivity. Of 11 mothers who were HBsAg positive during the third trimester of pregnancy, 4 had babies (36.4%) who developed HBsAg positivity by 2.5-3 months of age (vertical transmission). Two babies born of HBsAg negative mothers, with history of jaundice during first trimester, were HBsAg negative. All the relatives of HBsAg positive cases screened were negative for HBsAg.
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One hundred and seventy five subjects with chronic liver diseases which included patients with chronic active hepatitis (90), liver cirrhosis (31) and asymptomatic hepatitis B carriers (54), were included in the study. Hepatitis B virus (HBV) specific DNA-polymerase activity and HBe-markers were tested as markers of HBV-multiplication. In HBsAg positive samples, DNA-P activity was positive in 44.4% of the HBV carriers, 52.9% of the patients with chronic active hepatitis and 81.8% of the patients with liver cirrhosis. The corresponding figures for the presence of HBeAg in these groups were 18.5, 26.5 and 45.5% respectively. Virus multiplication was also observed in 41.1 and 44.4% patients with chronic active hepatitis and liver cirrhosis respectively, in the absence of HBsAg. The results of the present study show that hepatitis B virus is the most important etiological factor of chronic liver diseases in India. Most of our patients of chronic liver diseases seems to have contacted HBV infection as young adults and the mode of transmission is likely to be horizontal rather than vertical. The virus replicating markers correlate well with the severity of the liver injury and decreased with the age. DNA-P activity is a more sensitive marker of viral multiplication than HBeAg. Viral multiplication was also found to occur in the absence of the usual HBV markers. Continued viral multiplication in patients with chronic active hepatitis and liver cirrhosis is implicated in continued liver injury and progressive liver disease.
Anti-pre-S antibody was tested in 38 sera from patients with fulminant hepatitis (positive for HBsAg and/or IgM anti-HBc) using a specific solid phase enzyme linked immunosorbent assay (ELISA). Anti-pre-S activity was detected in 50 percent sera samples positive for HBsAg but negative for IgM anti-HBc. There were 12.5% sera positive for both HBsAg as well as IgM anti-HBc and 75% sera negative for HBsAg but positive for IgM anti-HBc. The prevalence of HBV-specific DNA-polymerase activity was high in all the three groups whereas anti-HBs positivity was low. Anti-pre-S activity was observed both in the presence as well as in the absence of DNA-polymerase activity. High-anti-pre-S level in fulminant hepatitis B patients was assumed to be implicated in the fast clearance of HBsAg from circulation.