Seroprevalence of hepatitis A virus in patients with chronic liver disease from Kerala: impact on vaccination policy.

Hepatitis A virus (HAV) vaccination is recommended worldwide for patients with chronic liver disease to prevent decompensation due to superinfection with HAV. There are recent reports of decline in HAV seroprevalence in developing countries, where hepatitis A was considered hyperendemic. This phenomenon would have implication on policy of hepatitis A vaccination in chronic liver disease in our region. The aim of the study was to evaluate the seroprevalence of HAV antibodies in patients with chronic liver disease and to assess the relevance of hepatitis A vaccination in these patients. Three hundred patients (268 males and 32 females) with chronic liver disease, seen at the department of gastroenterology at Amrita institute of Medical Sciences and Research Centre, Cochin, were tested for the presence of IgG anti-HAV antibodies in their sera using a commercially available ELISA kit. The mean age of the patients was 53.7 years. Of these 280 patients (93.33%) tested positive for IgG anti-HAV. Routine vaccination without testing for HAV antibodies is not recommended in chronic liver disease, as there is a high prevalence of pre-existing antibodies in these patients in our region.

Acute pancreatitis in viral infections, with possible progression to chronic pancreatitis.

Isolated cases and small series of acute pancreatitis complicating viral infections have been reported. However, data on the natural history of such patients are sparse. We report a series of five patients of acute pancreatitis complicating diverse viral infections. During follow-up ranging from 6 to 36 months, two of these five patients developed evidence of chronic pancreatitis.

Fulminant hepatic failure for herpes simplex virus.

Although exceedingly rare, fulminant hepatic failure in immunocompetent patients can develop with primary or recurrent infection due to herpes simplex virus. The diagnosis is frequently obscured by the absence of mucocutaneous involvement. Elevated transaminases with leucopenia and a relatively low bilirubin level may provide clues to the diagnosis. Here a female patient, 43 years, presented with the complaints of increasing jaundice, anorexia, nausea, vomiting for one week duration. She had hepatomegaly. Investigations revealed markedly raised transaminases and coagulopathy. Herpes simplex virus IGM (by ELISA) was positive. The immunocompetent woman was treated with acyclovir but the result was fatal.

Tropical pancreatitis and fibrocalculous pancreatic diabetes--two sides of the same coin?

Tropical pancreatitis and fibrocalculous pancreatitic diabetes are usually considered two ends of the same disease although some studies suggest the likelihood of distinct entities. We report the occurrence of these two diseases in two siblings. The literature comparing the similarities and differences between them is briefly reviewed.

Tropical pancreatitis - a distinct entity, or merely a type of chronic pancreatitis?

Tropical pancreatitis was described 50 years ago as a disease of the tropical regions, particularly southern India, with young age at onset, malnutrition, rapid progression, severe pancreatic damage with multiple large ductal calculi, and absence of history of alcoholism or biliary tract disease as its hallmarks. Over the years, chronic pancreatitis in southern India has shown a change, with increase in older patients, occurrence of milder disease including milder diabetes, increasing longevity, and increasing association with alcoholism and smoking. This article looks at changes in the disease and in dietetic, environmental and socioeconomic factors over the years, in an attempt to understand the environment-gene interactions in its causation. This analysis shows that tropical pancreatitis may represent one end of the wide spectrum of chronic pancreatitis in the tropics, with alcoholic pancreatitis representing the other extreme.

Oxidative stress in alcoholic liver disease.

We report on the prooxidant (lipid peroxides) and antioxidant levels (ascorbic acid, reduced glutathione, superoxide dismutate activity) in healthy individuals (30) and patients with cirrhosis (37; 22 alcoholic cirrhosis and 15 non alcoholic cirrhosis). A significant increase in plasma lipid peroxide (P < 0.05) and ascorbic acid (P < 0.01) and a significant decrease in reduced glutathione (P < 0.001) and superoxide dismutase activity (P < 0.05) in haemolysate was observed in cirrhosis patients compared to the control group. A significant decrease in reduced glutathione (P < 0.01) and superoxide dismutase (P < 0.05) activity was also observed when the alcoholic cirrhosis group was compared to non alcoholic group. A significant increase in aspartate transaminase (P < 0.05), gamma glutamyl transaminase (P < 0.01) and aspartate transaminase/alanine transaminase (P < 0.05) ratio was seen in alcoholic cirrhosis group. A significant positive correlation between gamma glutamyl transferase and lipid peroxides (r = 0.48, P < 0.05) was observed in alcoholic cirrhosis.

Ranitidine for the prevention of complications following endoscopic sclerotherapy for esophageal varices.

Thirty one patients with significant esophageal variceal bleed were allocated alternately to receive endoscopic sclerotherapy along with ranitidine 300 mg daily or endoscopic sclerotherapy alone till eradication of varices. The mean sclerotherapy sessions, time and volume of sclerosant required for obliteration of varices were similar for the two groups. The esophageal varices were eradicated in all the patients except three in sclerotherapy alone group. There was statistically significant reduction in frequency of post sclerotherapy mucosal ulcers (P < 0.05) after addition of ranitidine to sclerotherapy. Rebleeding was not only significantly reduced (P < 0.05) in the sclerotherapy with ranitidine group but was minor and did not even require blood transfusion. In sclerotherapy alone group rebleeding was controlled by surgery in two patients and one died due to massive bleeding. The results of this study suggest a beneficial role of ranitidine in reducing post sclerotherapy mucosal ulcers and rebleeding. This effect of ranitidine emphasises the role of acid-pepsin in pathogenesis of these ulcers and its associated morbidity.

Exocrine pancreatic function (serum immunoreactive trypsin, fecal chymotrypsin, and pancreatic isoamylase) in Indian diabetics.

Forty-nine patients with tropical calcific pancreatitis (TCP), 51 insulin-dependent diabetics (IDDMs), 87 non-insulin-dependent diabetics (NID-DMs), and 66 nondiabetic controls were studied to evaluate their exocrine pancreatic function by measurement of serum immunoreactive trypsin (IRT, normal for white caucasians from the U.K. of 140-414 micrograms/L), pancreatic isoamylase (PIA, normal of 35-125 U/L), and fecal chymotrypsin (FCT, normal of greater than 6.6 u/g). The majority of patients were studied within 1 year of diagnosis. TCP subjects included 7 nondiabetics, 6 with impaired glucose tolerance (IGT-TCP), and 36 diabetics [fibrocalculous pancreatic diabetes (FCPD)]. There was evidence of active pancreatitis (IRT greater than 800 micrograms/L) and partial preservation of function in nondiabetic TCP subjects [median IRT of 220 micrograms/L (range of 102-1,360 micrograms/L), FCT of 2.2 u/g (range 0.7-12.8 u/g)] and also in IGT-TCP subjects [IRT of 370 micrograms/L (range of 30-1,360 micrograms/L), FCT of 4.2 u/g (range of 1-38 u/g)]. FCPDs showed severely diminished exocrine function [IRT of 50 micrograms/L (range of 0-184 micrograms/L), FCT of 0.23 u/g (range of 0-10.4 u/g)]; none showed IRT greater than 800 micrograms/L. IDDMs and NIDDMs also showed diminished exocrine pancreatic function in approximately 30 and approximately 10%, respectively. Controls showed a wide range of IRT and FCT concentrations; IRT concentrations tended to be higher than those reported in white Caucasians from the U.K. Three controls, one IDDM, and two NIDDMs showed "pancreatic" IRT concentrations in the absence of symptoms. PIA concentrations were diminished in FCPD but were similar in IDDM and NIDDM subjects compared to controls.(ABSTRACT TRUNCATED AT 250 WORDS)

Bilateral recurrent haemorrhagic pleural effusion in asymptomatic chronic pancreatitis.

In a case of bilateral recurrent haemorrhagic pleural effusion due to asymptomatic pancreatitis the diagnosis was suggested by the presence of amylase in the pleural fluid when other possible causes had been excluded. Abdominal computed tomography and laparotomy confirmed the diagnosis. No communications could be seen between the peritoneal and pleural space at laparotomy.