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Biomedical subjects

Y K Joshi

Publications and source records attributed to Y K Joshi.

At least 19 recordsLinked to original sources
PubMed1992

Prospective controlled study of post-transfusion hepatitis after cardiac surgery in a large referral hospital in India.

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.

Adolescent↗
PubMed1991

Hepatitis C virus infection is the major cause of severe liver disease 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.

Hepatitis B↗
PubMed1990

Hepatitis B virus replication in patients with chronic liver diseases.

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.

Adolescent↗
PubMed1990

Significance of anti-pre-S antibodies in patients with fulminant hepatic failure.

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.

Hepatic Encephalopathy↗
PubMed1990

Animal transmission of enteric non-A, non-B hepatitis infection to Macaca mulatta by faeco-oral route.

M. mulatta monkeys were inoculated faeco-orally by enteric non-A, non-B virus to study the development of clinical, biochemical, histopathological and serological changes in the blood and liver. Pooled stool samples positive for putative non-A, non-B viral antigen by micro-ELISA and aggregated viral particles by immune electron microscopy, were administered in two M. mulatta monkeys. Biochemical, histopathological and serological changes were seen in the blood and liver and excretion of 27 nm virus like particles around 27 days of inoculation in the experimental monkey but not in the control animal.

Animals↗
PubMed1989

Ultrasonography in portal hypertension: a sensitive noninvasive test to demonstrate portal-vascular anatomy.

The accuracy of ultrasonography (US) in delineating the portal vascular anatomy was assessed clinically by the clinician in 30 cases of portal hypertension due to noncirrhotic portal fibrosis and extra hepatic portal venous obstruction. Ultrasonography detected portal vein block in 19 and in 11 patients it was found to be patent. These ultrasonic diagnoses were confirmed by spleno-portovenography (SPV) in all, except in 2 cases due to technical failure. Ultrasononic assessment of the splenic vein was found to be accurate in 93.3% (28/30) of cases. SPV also had similar accuracy of splenic vein assessment when compared with the surgical findings. In one patient, intraperitoneal haemorrhage was encounted following SPV, necessitating emergency surgery. Thus, US was found to be as accurate as splenoportovenography in the assessment of portal vascular anatomy. The imaging technique is cheap, easy, safe, and can be repeated as often as necessary. It should be the procedure of choice in assessing the anatomy of portal vascular system.

Adult↗
PubMed1989

Fibronectin in acute and subacute hepatic failure.

The mean plasma fibronectin (FN) concentrations in 30 patients with fulminant hepatic failure (FHF) and in 10 patients with subacute hepatic failure (SAHF) were 111.2 +/- 70 and 123.5 +/- 46.5 micrograms/ml, respectively, significantly lower than that of normal controls (362.0 +/- 69.2 micrograms/ml) and patients with uncomplicated viral hepatitis (320 +/- 58.5 micrograms/ml) (p less than 0.001). Plasma FN levels showed significant negative correlation with serum glutamic pyruvate transaminase values in the FHF group (p less than 0.02) and with prothrombin time in the SAHF group (p less than 0.02). Serial estimation of plasma FN showed that failure of FN levels to rise despite fresh plasma infusions indicates poor prognosis in these patients. The reduced availability of FN may be responsible for the impaired Kupffer cell function and consequent increased susceptibility to endotoxemia and the bacterial infections seen in these patients.

Adult↗
PubMed1989

Role of immune serum globulin in post transfusion virus B infection.

Fifty four blood recipients were administered prophylactic immune serum globulin (31) or hepatitis B immune globulin (23) and followed up for six months. None of the patients developed either acute hepatitis B or HBsAg carrier state. However, 7 (14%) had anicteric self limiting non-B post-transfusion hepatitis. Twenty (40%) of the blood recipients developed anti-HBs during the follow up period suggesting either HBV exposure by subdetectable levels of HBsAg present either in blood or immunoglobulin preparation or due to passive transfer by administration of immunoglobulins.

Adult↗
PubMed1988

An enzyme-linked immunoassay for the possible detection of non-A, non-B viral antigen in patients with epidemic viral hepatitis.

An enzyme-linked immunosorbent assay has been developed by using IgM antibodies from the acute stage as a source to capture the antigen in stools of patients with epidemic non-A, non-B (NANB) viral hepatitis. 29/69 (42.3%) of the patients and 3/9 (33.3%) contacts were positive for a suspected NANB viral antigen. However, only 1/27 (3.7%) of the negative controls drawn from amongst the patients with amoebiasis, giardiasis, hepatitis due to virus A and healthy individuals was positive for NANB antigen in the stool. The suspected NANB viral antigen was more frequently detected in stools collected between the 14th and 18th day of icteric hepatitis. The study suggests that IgM antibodies from patients with acute viral NANB hepatitis react with an antigen present in the stools of a high proportion of patients with epidemic NANB viral hepatitis. This serological test may be useful to establish the etiological diagnosis of non-A, non-B (fecal-oral) viral hepatitis. ELISA-positive stools contained 27 nm viral particles.

Antigens, Viral↗
PubMed1987

An enzyme-linked immunosorbent assay (ELISA) for the detection of IgG and IgM anti-idiotypes directed against anti-HBs molecules.

A simple and specific enzyme-linked immunosorbent assay (ELISA) has been developed to detect circulating IgG and IgM anti-idiotypic antibodies directed against anti-HBs molecules using 96-well polyvinyl microtitre plates as the solid phase and HRPO-labelled goat anti-HBs as conjugate. Anti-idiotype reactions were observed in the supernatant portion after precipitation of immune complexes from sera with polyethylene glycol 6000 (PEG). Both IgG and IgM with anti-idiotype activity were detected concurrently in HBsAg-positive sera from HBV-infected patients and asymptomatic HBV carriers. Anti-idiotype activity was absent in HBsAg-negative sera from healthy persons, and in patients with non-A, non-B hepatitis and viral hepatitis A. However, such antibodies could be demonstrated in the sera of two out of eight HBsAg vaccine recipients negative for anti-HBs but in none of 11 recipients positive for anti-HBs after receiving a booster immunising dose of HBsAg vaccine. Those sera showing positive anti-idiotype reactions were free from rheumatoid factor and HBsAg/IgM or HBsAg/IgG complex activity. An analysis of anti-idiotype positive sera for anti-HBs, HBeAg and HBV-specific DNA-polymerase activity demonstrated these markers in 20%, 30% and 60% of cases, respectively. The presence of anti-idiotypic antibodies was presumed to permit a more active multiplication of hepatitis B virus.

Antibodies, Anti-Idiotypic↗
PubMed1987

Studies on HBsAg binding with polymerised human serum albumin by ELISA.

A simple and sensitive ELISA was developed to characterize the interaction between polymerised human serum albumin (pHSA) and HBsAg, using pHSA-coated polyvinylmicrotitre plates as solid phase and anti-HBs-coupled HRPO as the conjugate. The interaction was found to be specific and dependent on the size of albumin polymer. pHSA-binding activity (pHSA-BA) was studied in both HBsAg-negative and HBsAg-positive sera from various liver diseases including acute viral hepatitis, fulminant hepatitis, cirrhosis of liver, chronic active hepatitis, and healthy HBsAg carriers. pHSA-BA was detected only in HBsAg-positive sera. Analysis of HBsAg-positive sera indicated pHSA-BA in high proportions of patients sera as compared to sera from healthy HBsAg carriers. pHSA-BA was detected both in the presence and absence of HBe markers, though the mean BA was relatively high in presence of HBeAg. The effect of human serum immunoglobulins (IgG, IgA, and IgM) on the BA was investigated and a correlation between pHSA-BA and HBsAg-IgM complex positivity in sera was established. Finally, the probable role of human serum IgM in facilitating the binding process was discussed.

Enzyme-Linked Immunosorbent Assay↗
PubMed1986

Acute liver failure. Experience with 145 patients.

Acute liver failure (ALF) is an uncommon but serious disease still carrying a high mortality. This report describes one of the largest series of cases of acute failure, managed on a simple intensive supportive therapeutic regimen. One hundred fifty-eight patients with ALF were admitted to the Rajgarhia Liver Unit of the All-India Institute of Medical Sciences (AIIMS) during the period July 1976 to December 1981. Data from 145 were completed and analyzed for this report. Of the patients, 85.4% were below the age of 40 years. The female-to-male ratio was 1.3:1. Of the 77 women in the reproductive age group, 59.7% were pregnant. All cases of ALF were secondary to viral hepatitis. Cerebral edema, bleeding, infection, and renal failure were seen in 57.2, 57.2, 39.3, and 16.5% of patients, respectively. Overall survival was 28.9% of patients. It was 33% below the age of 40 years and only 4.8% above this age. Pregnancy did not adversely affect the prognosis. Survival was related to grade of coma, being 22.8% for patients in Grade IV coma and 62% for patients in Grade I coma. In fatal cases the immediate complications resulting in death were cerebral edema (63%), bleeding (30%), renal failure (10.6%), and infection (8.7%). Presence of HBsAg, a serum bilirubin of over 20 mg%, and serum sodium less that 119 mEq/liter were indicators of poor prognosis. A simple, intensive, support therapy yielded results comparable to those reported by centers using a variety of complex therapeutic regimens.

Acute Disease↗
PubMed1986

Acute hepatic failure due to Plasmodium falciparum liver injury.

Nine patients with acute liver failure due to Plasmodium falciparum liver injury admitted to the Rajgarhia Liver Unit of the All-India Institute of Medical Sciences during 1982-84 are presented. The liver was palpable in all the patients, and eight had splenomegaly. Investigations revealed mild to moderate abnormality in liver function tests. All were negative for the markers of acute infection due to hepatitis A and B viruses. Blood film examination showed P. falciparum alone in seven and along with P. vivax in the remaining two patients. Liver histology, which was identical in all eight patients where liver biopsy was done, showed centrizonal necrosis and hyperplastic Kupffer cells loaded with malarial pigment. All the patients recovered with specific anti-malarial and supportive treatment. Our observations suggest that malaria due to P. falciparum may present as jaundice and encephalopathy which stimulates acute hepatic failure due to fulminant hepatitis.

Acute Disease↗