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Aim: To evaluate the clinical and biochemical profile of patients with non alcoholic fatty liver disease (NAFLD) and to assess their histological severity at presentation., Methods: Consecutive patients presenting to the liver clinic of All India Institute of Medical Sciences (AIIMS) with raised transaminases to at least 1.5 times upper limit of normal, and histologically confirmed non-alcoholic fatty liver disease were included. Patients who had significant alcohol intake or positive markers of other liver diseases or who were taking drugs known to produce fatty liver were excluded. The clinical, biochemical and histological profile of this group was studied., Results: Fifty-one patients with NAFLD formed the study population. Their median age and BMI were 34(17-58) years and 26.7(21.3-32.5) kg/m(2) respectively and 46 (90.1%) were males. The majority of the patients had mild inflammation, either grade 1 [32 (63%)] or grade 2 [16 (31%)] and only 3 (6%) patients had severe (grade 3) inflammation. Twenty-three (45%), 19 (37%), 8(16%) and 1(2%) patient had stage 0, 1, 2 and 3 fibrosis respectively on index biopsy and none had cirrhosis. On univariate analysis, triglyceride levels more than 150 mg % (OR = 7.1; 95% CI: 1.6-31.5, P = 0.002) and AST/ALT ratio>1 (OR = 14.3; 95% CI: 1.4-678.5, P = 0.008) were associated with high grades of inflammation and none was associated with advanced fibrosis. On multivariate logistic regression analysis, hypertriglyceridemia >150 mg% was the only factor independently associated with presence of high grade of inflammation (OR = 1.6; 95% CI: 1.3-22.7, P = 0.02), while none was associated with advanced fibrosis. Triglyceride levels correlated positively with inflammatory grade (r = 0.412; P = 0.003)., Conclusion: NAFLD in North Indian patients is a disease of young over-weight males, most of whom are insulin resistant and they tend to have a mild histological disease at presentation.

Background: Gallbladder cancer (GBC) is one of the most common gastrointestinal malignancies. The data regarding GBC are, however, limited., Methods: Records of 634 patients with GBC over a 10-year period were examined with regard to the clinical presentation, investigative findings, treatment, operative findings and outcome., Results: The mean age of patients was 51 +/- 11 years and men : women ratio was 0.36:1.00. Pain, jaundice and hepatomegaly were seen in 81.0%, 76.0% and 61.5% patients, respectively. On imaging, a mass replacing the gallbladder was seen in 73% patients. Gallstones were present in 54% patients. Surgery was carried out in 291 (46%) patients and endoscopic treatment in 72 (19%) patients but no intervention was carried out in the remaining patients because of disseminated disease. Among the patients who were operated on, 2.0% had stage I GBC, 3.4% stage II, 17.5% stage III, 47.0% stage IVa and 29.8% stage IVb. Radical resection was possible in 133 (46%) patients. The 30-day mortality was 10% with most (90%) deaths in patients with stage IV disease. The median survival after simple cholecystectomy and radical surgery was 33.5 and 12.0 months, respectively. However, among those who underwent debulking, palliative bypass or exploratory laparotomy alone, the survival ranged between 1 and 3 months. Logistic regression analysis showed that only radical resection improved the long-term survival (P < 0.05)., Conclusions: The majority of patients with GBC in India have advanced unresectable disease. Detection of GBC at an early stage is incidental and rare but is associated with long-term survival. Radical surgery, when feasible, is the only option for achieving long-term survival., ((c) 2004 Blackwell Publishing Asia Pty Ltd.)

Background: Universal vaccination against hepatitis A virus (HAV) has been recommended for children because of the changing epidemiological pattern of HAV. Vaccination has also been advised for patients with chronic liver disease as HAV superinfection in these patients can result in severe or even fatal disease. In India, the indications for HAV vaccination are not clear due to contradictory seroepidemiological data in children and lack of data on HAV seroprevalence in patients with chronic liver disease., Methods: Sera were collected from children studying in two government-run schools and from patients with chronic liver disease attending the Liver Clinic at the All India Institute of Medical Sciences (AIIMS). The sera were tested for anti-HAV antibodies. The incidence of HAV-induced acute hepatitis and acute liver failure at AIIMS over the last 10 years was also assessed., Results: A total of 93.2% (1328/1424) of the school children between 4-18 years of age who were included in the study had anti-HAV antibody in their sera. Eighty percent of the children had antibodies against HAV in their sera by the age of 5 years, whereas all the children above 16 years were positive for anti-HAV antibody. A total of 256 patients with chronic liver disease (94 with cirrhosis of the liver, 160 with chronic hepatitis) were tested for the presence of anti-HAV antibody. Of them, 97.6% (248/254) had anti-HAV antibody in their sera. The annual frequency of HAV-induced acute viral hepatitis and acute liver failure at AIIMS during the last 10 years did not show any change., Conclusion: Mass vaccination against HAV is not required in north India because of the presence of protective antibodies against HAV in the majority of the population., (Copyright 2003 Blackwell Publishing Asia Pty Ltd)

Etiopathogenesis of acute hepatic failure (AHF) in Eastern and Western countries is distinct. In the East hepatitis viruses cause AHF in more than 95% of such cases, while causes of AHF in the West are quite heterogenous. Hepatitis E virus is the major etiological agent of AHF in countries like India where the virus is hyperendemic. Occult HBV infection may also be causing AHF in a sizable proportion of cases in areas where chronic HBV infection frequency is high. Paracetamol causes AHF in about 70% cases in the UK and about 20% cases in USA, whereas in France and Denmark, non-steroidal anti-inflammatory drugs are more frequently associated with AHF. Hepatitis B virus causes AHF in about one-third of cases in the latter two countries., (Copyright 2002 Blackwell Publishing Asia Pty Ltd)

Objectives: To evaluate the current seroprevalence of antibodies against hepatitis A virus (HAV) in a sample of schoolchildren above 10 years of age and to determine the prevalence of HAV-induced hepatitis in adults at a tertiary care hospital in northern India between January 1992 and December 2000., Methods: Sera from 276 male and 224 female schoolchildren aged 10-17 years were tested for anti-HAV antibodies by enzyme-linked immunosorbent assay. Consecutive patients with a diagnosis of acute viral hepatitis who attended a liver clinic were tested for the serological markers of HAV, hepatitis B Virus, hepatitis C virus, hepatitis D virus, and hepatitis E virus., Findings: Of the male and female children, 96.3% and 98.2%, respectively had anti-HAV antibodies in their sera. The prevalence of these antibodies in the age groups 10-12, 13- 14, and 15-17 years were 98.6%, 94.8%, and 98.3% respectively. The frequency of HAV- induced acute viral hepatitis (69/870, 8%) in adults did not show an increasing trend., Conclusion: Mass HAV vaccination may be unnecessary in northern India because the seroprevalence of protective antibodies against HAV in schoolchildren aged over 10 years remains above 95% and there has been no apparent increase in HAV-induced acute viral hepatitis in adults.

Between January 1990 and December 1992, 18 patients with severe organophosphate poisoning (OPP) were admitted to our respiratory intensive care unit (RICU). Suicidal ingestion was the commonest cause of poisoning (15/18). The treatment comprised of atropine in bolus doses. 2-PAM in conventional dose and mechanical ventilation (MV) with positive end expiratory pressure (PEEP) wherever indicated. The mean dose of atropine on day 1 was 178.9 mg (range 60-480 mg) and then gradually reduced. The mean duration of treatment with atropine was 9.6 days (range 1-24 days). We felt that aggressive atropinization and MV with PEEP is adequate and the role of 2-PAM given in 3 gm dose in 12 h is not clear. There is a need for controlled study to assess the efficacy of atropine and MV alone vs. atropine, 2-PAM in suggested doses and MV in severe OPP patients.