Helicobacter pylori link to pernicious anaemia.

An immunological classification of chronic gastritis based on the detection of Helicobacter pylori (H. pylori) antibody, parietal cell antibody, intrinsic factor antibody, is reported. H. pylori chronic gastritis, slowly progresses to atrophic gastritis, in the majority of patients; in a few patients, with genetic susceptibility to form intrinsic factor antibody, it progresses to pernicious anaemia. In majority of patients of pernicious anaemia, H. pylori gradually disappears from the gastric mucosa, on development of intestinal metaplasia in them. Atrophic gastritis results from H. pylori or non H. pylori. H. pylori infection is diagnosed in the presence of H. pylori in the gastric mucosal biopsy and/or H. pylori antibody (IgG) in the serum. The presence of the genetic factor (intrinsic factor antibody) is essential for the diagnosis of pernicious aneamia. Pernicious anaemia patients without intrinsic factor antibody, should be correctly diagnosed as atrophic gastritis, in view of the absence of the genetic factor (intrinsic factor antibody) in them.

Factors responsible for the increasing incidence of oesophageal adenocarcinoma.

Amongst white population of developed countries, the prevalence of oesophageal adenocarcinoma has dramatically increased during the last four decades. During this period, the increased damage to the oesophageal mucosa with gastroesophageal reflux could result from increased acid output (due to absence of Helicobacter pylori in the gastric mucosa with excellent sanitation) and/or increased frequency of reflux due to an "epidemic" of overweight (65% of the population). The most important environmental factors, responsible for the fastest increasing cancer in humans, are discussed.

Investigations proposed to accurately classify chronic gastritis.

Patients of chronic gastritis should be investigated with gastric mucosal biopsy, parietal cell antibody, intrinsic factor antibody, Helicobacter pylori antibody, urea breath test or faecal antigen test for Helicobacter pylori, to accurately classify them. The results of these tests will indicate Helicobacter pylori infection (present or past), the role of hereditary factor (intrinsic factor antibody present or absent) and the success or failure of Helicobacter pylori eradication treatment.

Acquired apolipoprotein B deficiency with chronic hepatitis C virus infection.

Chronic hepatitis C virus (HCV) infection is often associated with fatty liver. Apolipoprotein B (ApoB) deficiency is one of the known causes of fatty liver and acquired ApoB deficiency has recently been reported with HCV infection. We report two patients (47-year-old lady and 48-year-old man) who had asymptomatic transaminase elevation, fatty liver, anti-HCV positive with high viral load (genotype 3). Their lipid profile showed low total cholesterol, low-density lipoprotein, triglycerides and ApoB. One of the patients who received treatment for HCV infection showed improvement in lipid profile and ApoB levels.

Is the presence or absence of Helicobacter pylori in gastric mucosa a greater risk?

Helicobacter pylori is a unique organism which is pathogenic for stomach-duodenum (chronic gastritis, duodenal ulcer, gastric ulcer, gastric malignancy, mucosa-associated lymphoid tissue (MALT) lymphoma) and protective for oesophagus (Barrett's oesophagus, oesophageal adenocarcinoma) at the same time in an individual. For prevention of diseases, the necessity of presence of some bacteria throughout the gastrointestinal lumen needs to be emphasized. The concept--only good Helicobacter pylori is a dead Helicobacter pylori, is dangerous and humans should learn to live in harmony with a few bacteria throughout the gastrointestinal tract.

Acute viral E hepatitis with chronic liver disease (autoimmune hepatitis).

A 36 years old male presented with anorexia, jaundice and ascites. He was suffering from acute viral E hepatitis. In view of ascites, he was investigated for associated asymptomatic chronic liver disease (CLD). The CLD was diagnosed as cirrhosis with autoimmune hepatitis and was treated with steroid with good response. He is maintaining good health with low dose steroid, on follow up for 1 year.

Hepatic failure with flutamide.

A 41-year-old woman, who was on flutamide for hair loss for 3 months, presented with deep jaundice. She developed hepatic encephalopathy but gradually recovered after discontinuing flutamide. Flutamide can cause fatal toxic liver injury and hence should be used with close monitoring of liver profile.

Fatty liver with elevated transaminase levels due to heterozygous apolipoprotein B deficiency.

Elevation of transaminase levels in asymptomatic subjects could be due to a common benign condition such as fatty liver or a more serious disease such as chronic hepatitis due to various causes; in some subjects a liver biopsy is indicated. Heterozygous apolipoprotein B deficiency is an uncommon cause of transaminase elevation, as indicated by low levels of cholesterol and low density lipoprotein-cholesterol. This should be noted to avoid unnecessary investigations (including liver biopsy) in asymptomatic subjects with persistent elevation of transminase levels in the serum.

Primary prophylaxis of variceal bleeding in liver cirrhosis: failure to learn from past experience.

In patients with cirrhosis of liver, variceal bleeding is the most serious complication, with a mortality of up to 50%. Primary prophylaxis of variceal bleeding with shunt surgery or endoscopic variceal sclerotherapy was attempted and then abandoned, as higher rates of complications and mortality were observed. Endoscopic variceal ligation is now being recommended for primary prophylaxis in some centers, as it has fewer complications than sclerotherapy. But this has been done with inadequate evaluation of the cost-effectiveness of variceal ligation. Propranolol therapy is also being widely used for a selected group of patients (large varices with cherry red spots), despite its several limitations and side effects, to reduce frequency of bleeding but without improving survival. Is primary prophylaxis of variceal bleeding cost-effective? The cost involved needs to be accurately assessed in different countries.