Antacids can reduce gastroduodenal acidity for long periods if taken in substantial quantities after food. Their healing effect on gastric ulcer is minimal, if present at all, and easily overwhelmed by the benefit obtained from admission to hospital. Intensive antacid therapy appears effective in healing duodenal ulcer and preventing haemorrhage from stress ulcer, and is comparable in these respects with cimetidine but with a higher incidence of side-effects. Clinical impression strongly suggests that antacids relieve pain in peptic ulcer but objective confirmation is lacking.

This paper reviews the experience gained over the past few years in two techniques of liver support, charcoal haemoperfusion and polyacrylonitrile membrane haemodialysis. Problems with charcoal haemoperfusion have centred around platelet aggregation and hypertension, and new carbon preparations with a variety of different coatings to overcome these problems are described. Haemodialysis using the PAN membrane has caused fewer side-effects and current results show that 33% of patients so treated recover consciousness. The new techniques for liver support currently being developed, including combined dialysis/perfusion systems and those based on plasma separation, are also described.

Schistosomiasis mansoni and japonica, helminth infections involving the livers of 100 million people, are among the 'great neglected diseases of mankind' on the basis both of their prevalence and the relative lack of interest shown in them by clinicians and biomedical investigators. Schistosomiasis is not only an interesting disease in itself but has the added advantage of providing unique human and animal models of hepatic pathophysiology, immunopathogenesis, and collagen metabolism.

The classification of chronic hepatitis introduced in 1968 is still current, but has been modified. The concept of bridging hepatic necrosis has been incorporated, and is recognised as an important feature of both acute and chronic aggressive (active) hepatitis (CAH). In the pathogenesis of the latter, piecemeal necrosis is, however, thought to be the more important factor. The histological picture of CAH varies widely. Several causes of CAH have been identified, including hepatitis B virus. Recognition of surface and core components of the virus in tissue sections has facilitated study of the relationship between host response and pathological lesion in chronic hepatitis. CAH and primary biliary cirrhosis share histological features, and a mixed form has been postulated. Staining for copper sometimes helps to distinguish the two lesions. A third histological category, chronic lobular hepatitis, comprises patients with histological lesions like those of acute hepatitis, but with a chronic or recurrent course.

The mechanisms underlying the cause of the major clinical features of liver cell failure are reviewed. These include jaundice, fluid retention, hepatic encephalopathy, bleeding tendency, etc.

There are many changes in the plasma, lipids, and lipoproteins in patients with liver disease. They have proved difficult to study but our understanding of these changes has increased greatly during recent years. In obstructive jaundice hyperlipidaemia is a fairly constant finding and this appears to be due to the regurgitation of phospholipid from the obstructed biliary tree. The plasma lipids tend to fall with parenchymal liver disease. The composition of the lipoproteins depends on the activity of the plasma enzyme lecithin: cholesterol acyl transferase. When LCAT activity is high the individual lipoprotein fractions are normal. When it is reduced all of the lipoprotein fractions are affected but the pattern found with obstruction is quite different from that found with parenchymal disease. The changes in plasma lipoproteins appear to be associated with change in the lipid composition of cellular membranes and this may have important functional implications.

Disturbance of ammonia metabolism is an important but not the only factor in the genesis of hepatic coma. In this review mechanisms controlling the concentration of ammonia in the blood other than disturbed liver function have been discussed. The key function of ammonia in the pyridine nucleotide cyde has been outlined and it is suggested that the function of this cycle in patients with liver disease would repay further study.

We review the estimation of total and individual serum bile acids to detect the presence and nature of hepatobiliary disease. The different methods for measuring serum bile acids are discussed.

The association of certain forms of liver disease and a deficiency of alpha-1-antitrypsin is an observation which raises the possibility that other forms of liver disease ultimately will be found to have as their proximate cause a defined metabolic aberration, which may in turn be inherited. Although alpha-1-antitrypsin deficiency is a genetically determined error of protein synthesis, environmental factors, unrecognised at present, are required for the disease to become overt. Thus, this interesting association may herald an increasing number of clinical diseases in which the interaction of environmental stimuli and single genetically determined aberrations are crucially important. The diseases to which we succumb may be largely determined by a genetically determined susceptibility, a point of view which was stated so well by Archibalt Garrod in his essay Inborn Factors in Disease published nearly half a century ago.

This review deals with the development of our understanding of the chemistry of bilirubin and its glucuronide derivatives during the years 1952-1977. It examines the relation between haem metabolism and bilirubin formation and our present knowledge of hepatic transport of bilirubin. The heterogeneity of familial hyperbilirubinaemia is discussed.

Gilbert's syndrome is typically associated with a deficiency in hepatic bilirubin UDP-glucuronosyltransferase activity (B-GTA). The overproduction of bilirubin that is often found in this condition could be a fortuitous coincidence that leads to the unmasking of the disease, which otherwise often remains latent. Some cases of chronic unconjugated hyperbilirubinaemia could, however, be related to a defect in hepatic uptake, as reflected by alterations in BSP kinetics. Severe deficiencies of hepatic B-GTA exist in all types of Crigler-Najjar disease. An increased proportion of bilirubin monoglucuronide is always found in bile when a B-GTA deficiency is present. This observation strongly suggests a common biochemical defect in Gilbert's syndrome and in Crigler-Najjar disease, and thus renders the suggestion that the latter condition may be separated into two groups somewhat inappropriate. There is, however, no doubt that further knowledge of the conjugating enzyme, or enzymes, is required: such information may lead to the characterisation of several types of enzymic defects. Whereas little is new as far as the Dubin-Johnson syndrome is concerned, Rotor's syndrome can no longer be considered to be a variant of the former. The transport defect which is involved in most cases of Rotor's syndrome, if not in all, is an impairment of hepatic storage, thus distinguishing it from the impairment of excretion which is involved in the Dubin-Johnson syndrome. The distinct patterns of urinary coproporphyrin excretion, which were recently reported in Dubin-Johnson and Rotor's syndromes, offer additional evidence for a clear differentiation between these two entities.

During the last 25 years, there have been important developments in visualising the portal vein, in examining its contents, and in measuring the pressure of blood flowing within it. Radiologists have set the scene and now is the time of the scanner. These technical advances have been applied to the diagnosis and treatment of patients with portal hypertension, and many ingenious surgical techniques have been proposed. The problem of successful treatment of the patient with bleeding oesophageal varices and cirrhosis of the liver, however, has not yet been solved. This report discusses the portal vein in terms of pressure, flow, and regeneration factors. Portal hypertension is classified and methods of relief are discussed.