SUMMARY Lymphocytes from 39 patients with HBsAg positive chronic liver disease were incubated with their own hepatocytes to investigate mechanisms of lymphocyte-mediated liver damage. Cytotoxicity was significantly increased in 46% overall, and in 73% of those with chronic active hepatitis. Unlike HBsAg negative chronic active hepatitis where only non-T cells were cytotoxic, HBsAg positive patients had both cytotoxic T and non-T cells. A purified liver membrane complex (LSP) and aggregated IgG both blocked non-T cytotoxicity without affecting T cell cytotoxicity; this suggests that the former is probably an antibody-dependent cell-mediated reaction against normal membrane components. This was confirmed in preliminary studies which demonstrated that preincubation of hepatocytes with the F(ab)' fragment of an anti-human IgG reduced non-T lymphocyte cytotoxicity. T-cell cytotoxicity was restricted to HBeAg-positive

Abnormalities of platelet aggregation in response to adenosine diphosphate in 56 patients with chronic liver disease correlated with impairment of hepatocellular function but not with the etiology of the liver disease. Platelet-poor plasma from some patients appeared to contain an inhibitor since, in cross-over studies, it reduced the degree of aggregation of control subjects. However, platelet-poor plasma from some other patients enhanced aggregation in controls, and this was thought to be due to the presence of fibrin monomer. In the majority of patients with severe liver disease, platelet function still appeared defective, even after exclusion of the effects of plasma, and was independent of the platelet count in peripheral venous blood. Since patient platelet volumes were smaller than those of controls, these findings might be explained by deficiency of the larger hemostatically active type of platelet as a consequence of either bone marrow failure or splenic sequestration.

SUMMARY In 73 patients with fulminant viral hepatitis, non-A non-B hepatitis (NANB) was most common (43.8%), with hepatitis type A (HAV) diagnosed in 31.5% and hepatitis type B (HBV) in 24.7%. The non-A non-B group had a significantly longer duration from the onset of symptoms to the appearance of encephalopathy (median 21 days) compared with the HAV and HBV groups (medians 10 and seven days, p

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To determine the importance of the presence of serological markers of hepatitis B virus infection in patients with alcohol related liver disease we compared cumulative alcohol intake and clinical and histological features in patients with markers of hepatitis B virus infection and in those without. Hepatitis B surface antigen (HBsAg) was detected in five (

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SUMMARY The haematological variables, haematinic state, and placental function of more than 2000 pregnant women, heterozygous for either a-or f3-thalassaemia genes, were examined during pregnancy. Four features emerged. Firstly, it was possible by discriminant function analysis of haematological variables to distinguish in pregnant patients between the anaemia caused by thalassaemia trait and that caused by iron deficiency. Secondly, patients with thalassaemia become significantly more anaemic in pregnancy, ,8 more than a, but this was mainly due to plasma dilution. From the data percentile curves were drawn for each type of thalassaemia which predicted the patients' expected "normal" haemoglobin throughout gestation. Thirdly, patients with a-thalassaemia had the same incidence of iron deficiency as normal pregnant patients, whereas in those with f8-thalassaemia it was four times less common. The incidence of folic acid and vitamin B12 deficiency was the same in all groups. Finally, as assessed by serum oestriol concentration, there did not appear to be any abnormality of placental function or fetal development associated with maternal thalassaemia, and, also, there seemed to be no increase in maternal or fetal morbidity in pregnancy.Adult male or female carriers of either a-or ,B-thalassaemia trait are not usually seriously anaemic, although there is some variation between ethnic groups, sexes, and individual patients.' The anaemia usually worsens at times of clinical stress, notably infection and commonly (or always) pregnancy. Indeed, female patients may present or be diagnosed for the first time in pregnancy as cases of refractory hypochromic anaemia.Despite thalassaemia trait being the most common maternal genetic abnormality associated with pregnancy, there is still uncertainty regarding the clinical course, complications, and management, probably because there are few well reported studies.2 For example, it is uncertain, because of plasma dilution, whether or not thalassaemia trait can be suspected in pregnancy from an examination of the haematological variables. Also there are few data regarding the pathogenesis of the increased anaemia or the need for iron and folate supplementation. Finally, and most importantly, there is no evidence as to whether or not maternal thalassaemia is associated with an increase in fetal or maternal morbidity.To investigate these problems we studied 2326 pregnant patients heterozygous for either a-thalassaemia (90%) or for ,/-thalassaemia (10%) Accepted for publication 25 March 1985 and compared our findings with those of 7000 pregnant normal subjects. Patients and methods PATIENTS

and conclusions Five patients with cirrhosis proved by biopsy had clinical, biochemical, and serological evidence of an acute hepatitis B infection. In two the illness was 'fulminant and led to death. Only one patient completely recovered. Serological markers for the hepatitis B virus were absent before the onset of the acute illness in four patients, which suggested that a de novo infection had been acquired as a result of recent transfusions of blood or blood products. The fifth patient, who had Goodpasture's syndrome, had antibody to the core of hepatitis B virus, indicating previous exposure to the virus; his acute hepatitis may have been related to immunosuppressive drug treatment, which may have reactivated a dormant virus infection. Thus an acute type B viral hepatitis due to either a de novo or a reactivated infection may be superimposed on cirrhosis.