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The frequency of asymptomatic carriage of the hepatitis virus types B and C in an inner city area (South London) was assessed in a survey of 1002 subjects attending their General Practitioner for minor, non-hepatic complaints. Ten subjects were seropositive for hepatitis B surface antigen (HBsAg) (1 per cent), but only one, who declined liver biopsy, had any clinical laboratory evidence of hepatitis B virus-related chronic liver disease. Carriage of, and exposure to, hepatitis B virus was significantly more frequent among people born outside the UK/Eire and those with a history of jaundice. Among people of Caribbean origin the frequency of hepatitis B virus markers fell from 31 per cent among those born in the Caribbean to 11 per cent amongst second generation subjects born in this country. Despite careful counselling, offers of further investigation and treatment of those affected, and vaccination of vulnerable children or partners, were often declined. Four percent of the same population had antibodies to the hepatitis C virus using the Ortho anti-hepatitis C virus enzyme-linked immunosorbent assay but this figure fell to 0.9 per cent when a second test, based on synthetic peptides rather than a recombinant antigen, was used. None had any abnormality of standard liver function tests. Chronic asymptomatic carriage of hepatitis, particularly in inner city areas, may be more common than previously recognized. Effective use of antiviral agents and vaccination will be limited until appropriate health education dispels the widespread misconceptions and fears associated with a diagnosis of chronic viral hepatitis.

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To determine the factors underlying the apparent reduction in binding ability of thyroxine-binding globulin in hepatocellular carcinoma, hormone-binding characteristics were further examined in patients with this disease and in control subjects. No differences in affinity constants with respect to triodothyronine or serum thyroxine-binding globulin from hepatocellular carcinoma, cirrhotic and normal subjects were found. The affinity for thyroxine was significantly reduced in hepatocellular carcinoma (0.41 +/- 0.13 x 10(10) mol-1) and cirrhotic (0.65 +/- 0.1 x 10(10) mol-1) patients compared with normal subjects (0.94 +/- 0.7 x 10(10) mol-1). Investigations carried out on liver tissue obtained from patients with hepatocellular carcinoma and chronic liver disease showed that thyroxine-binding globulin within tumor tissue was elevated and bound less exogenous tracer hormone compared with that obtained from nontumor tissue. Tumor-derived thyroxine-binding globulin with altered binding properties is, at least partly, responsible for the abnormal behavior of the serum protein in patients with hepatocellular carcinoma.

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As part of a larger study designed to investigate the interaction of factors such as cirrhosis and hepatitis B virus infection as aetiological agents in the development of hepatocellular carcinoma, we investigated the status of hepatic HBV-DNA sequences in 156 cirrhotic patients. Forty-one were HBsAg seropositive and 18 (44%) of these had HBV-DNA sequences detectable in their livers. There are also 26 subjects who showed markers of a previous HBV infection (anti-HBs/anti-HBc), only one (4%) of whom had demonstrable hepatic HBV-DNA sequences. No sequences were found in any of the remaining 89 patients who were seronegative for all markers. Thus, liver HBV-DNA was only detected in the presence of a serum marker, usually HBsAg.

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To determine whether previous observations suggesting reduced ability of thyroxine-binding globulin (TBG) to bind exogenous thyroid hormones in hepatocellular carcinoma (HCC) might form the basis of a useful clinical test, we have investigated a larger series involving 49 patients and 10 healthy subjects. The binding ratio (mol hormone bound/mol TBG at a given hormone concentration) for both T4 and T3 was significantly reduced when compared to both cirrhotic and normal subjects. No overlap in T4 binding occurred between HCC patients and the control groups. Serial measurements on serum samples obtained from five cirrhotic patients who ultimately developed HCC revealed significant reductions in binding for both hormones up to 60 months prior to the clinical diagnosis of HCC. A reduced ability to bind thyroid hormones appears to be a specific feature of serum TBG from HCC patients and is one of the earliest alterations seen among cirrhotic subjects who ultimately develop the disease.

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The haematological variables, haematinic state, and placental function of more than 2000 pregnant women, heterozygous for either alpha- or beta-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, beta more than alpha, 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 alpha-thalassaemia had the same incidence of iron deficiency as normal pregnant patients, whereas in those with beta-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.

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The haematological indices of Peninsular Arabs (United Arab Emirate Nationals, Yemeni and Omani) have been examined. The most outstanding feature, seen in 40-50% of all subjects, was one of hypochromia, microcytosis associated with erythrocytosis. In approximately 5% the hypochromia was severe (MCH 19-22 pg) and 20% of these were found to have beta thalassaemia trait. In 10% of subjects the hypochromia was moderate (MCH 23-24 pg) and beta thalassaemia was confirmed in only 10%. The remaining 25% had a mild hypochromia (MCH 25-27 pg) and no beta thalassaemia was detected. The cause of the hypochromia in subjects with a normal Hb A2 (30% of the total population) is probably alpha thalassaemia, firstly because in those patients with an MCH of 19-24 pg the other haematological parameters are statistically the same as those with proven beta thalassaemia and, secondly, in those with an MCH of 25-27 pg iron deficiency is not common (6% of the population). The degree and pattern of the distribution of hypochromia of the three major ethnic groups of the Peninsular Arabs could be explained either by different alpha and beta thalassaemia genes being operative or by different degrees of inbreeding of the same genes.

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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 less than 0.01 and p less than 0.005 respectively). In the HAV group the severity of liver damage, judged by the maximum prolongation of the prothrombin time, was significantly less than in the HBV group (58 and 150 seconds prolonged respectively, p less than 0.005), and cerebral oedema was significantly less frequent (39% and 72% respectively, p less than 0.05). Consistent with this, the survival rate was higher in the HAV group (43.4%) compared with the HBV group (16.6%) and NANB group (9.3%) (p less than 0.005). These variations in presentation and clinical course may be a consequence of differences in the pathogenesis of the hepatic necrosis.

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Serological markers for hepatitis B virus infection have been examined in 34 patients with acute hepatitis B, 17 of whom developed fulminant hepatic failure. Hepatitis B surface antigen concentrations were significantly lower and hepatitis Be antigen was less frequently detectable in patients with fulminant hepatic failure compared with those with acute hepatitis (median 0.64 micrograms, range 16-0 and median 32 micrograms and range 100-4 micrograms respectively, p less than 0.001; HBeAg detected in 12% and 88% respectively, p less than 0.001). The IgM component of hepatitis B core antibody was significantly higher in the patients with fulminant hepatic failure with median values of 500 IU/ml compared with those with uncomplicated hepatitis (median 202 IU/ml, p less than 0.05 Wilcoxon's rank test). Three patients who developed a fulminant course had detectable levels of either anti-HBs or anti-HBe. These results are consistent with enhanced antibody responses to all three hepatitis B virus antigens and more rapid clearance of the latter during fulminant hepatic failure.

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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 (2%) out of 285 patients studied and antibody to HBsAg (anti-HBs) in 41 (14%); one patient had antibody to hepatitis B core antigen alone. The combined prevalence of markers of hepatitis B virus infection was similar in patients with alcoholic cirrhosis (18%) and precirrhotic liver disease (13%). Two patients positive for HBsAg had histological features of both alcoholic liver disease and chronic active hepatitis, with stainable HBsAg. Patients with anti-HBs were, however, histologically indistinguishable from patients without markers, and the mean cumulative alcohol intake of patients with anti-HBs was similar to or even higher than that of patients with liver disease of comparable severity who had no evidence of previous infection. The presence of markers of hepatitis B virus infection was related to former residence in countries with a high prevalence of the infection and to previous parenteral treatment and blood transfusions. Infection with hepatitis B virus does not enhance the development of chronic liver disease in heavy drinkers, except in the small number who remain positive for HBsAg.

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Analysis of 51 cases of hepatitis B virus infection in health care workers admitted as patients to the liver unit over seven years showed three healthy carriers of hepatitis B virus, seven cases of fulminant hepatic persistent hepatitis, 17 cases of chronic active hepatitis (of whom 11 had cirrhosis), and five cases of hepatocellular carcinoma. To date 11 of these patients have died. Only 15 of the 51 patients had a history of direct occupational exposure and only three patients could recall specific inoculation injuries. In contrast, the source of infection was apparent in 32 of 50 consecutive cases of fulminant hepatic failure or acute hepatitis B in nonmedical staff. Since specific inoculation injuries are not the usual mode of infection ion medical staff and since only a few of the patients who are hepatitis B virus carriers will be detected by selective screening of "high-risk" patients, the overall risk of infection can be reduced only by stricter precautions in the handling of any patient's blood and by the use of hepatitis B virus vaccines for medical staff at high risk.

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A severely anaemic, but asymptomatic patient, who is a heterozygous carrier of haemoglobin Hammersmith (beta42 (CD1) phenylalanine - Serine), has been studied to elucidate the mechanisms resulting in physiological compensation for the anaemia. Four factors have been investigated: the oxygen affinity of her blood, the cardiac output at rest and during exercise, the blood gas indices, and pulmonary function. It was found that due to the presence of Heinz bodies within the erythrocytes, the level of functional, haemoglobin was considerably less (50 g/l) than that measured by standard methods (87 g/l). In addition a moderate degree of arterial hypoxaemia (arterial oxygen tension = 10.7 kPa (80.4 mmHg) was present which could not be explained on the basis of abnormal pulmonary function. Both of these factors would result in tissue hypoxia, but the finding of consistently normal oxygen tensions ('mixed' venous oxygen tension = 5.4 kPa (40.3 mmHg) in blood obtained from the right atrium, suggested that hypoxia was not present. This was explained by a decreased whole blood oxygen affinity (P50 = 4.6 kPa (34.5 mmHg) at pH 7.4) and an increase in the cardiac index (5.3 L.min.-1m-2). The latter was the result of an increased stroke volume (125 - 135 ml), the heart rate being normal (63/min.). During moderate exercise, further increases at cardiac output were brought about by a change in heart rate alone. It has been calculated that the decrease in whole blood oxygen per se could not account for adequate tissue oxygenation. This is confirmed by the finding of an increased cardiac output in this patient. It is suggested that in any severe haemolytic anaemia, even if the whole blood oxygen affinity is low, cardiac output is probably increased to achieve complete physiological compensation.

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Whole blood cell separators are being used to achieve partial exchange transfusions in patients with hemoglobin S. The rate and extent of the alteration of whole blood oxygen affinity, incurred by this procedure, has been determined in a patient with Hb S/C disease. The implications in terms of oxygen delivery to the tissues are described for this patient and also for patients with the more severe disease associated with Hb S/S. It is concluded that whole blood cell separators should be used with an awareness of the possible detrimental effects of acute increases of whole blood oxygen affinity in these patients.

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The accuracy of the Lex-O2-Con apparatus is compared with the classical method of Van Slyke & Neill (1924) and the inaccuracies introduced by the presence of volatile anaesthetics in the sample are evaluated. The absolute levels of oxygen content depend upon the flow rate of carrier gas through the instrument.

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Fifty patients were examined clinically and neurologically for seven days after pneumoencephalography. Headache was present in 78%, neck stiffness in 34%, pyrexia in 38%, vomiting in 34%, tachycardia in 74%, a change in the level of consciousness in 18%, and abnormal neurological signs in 30%. Of the 13 patients with epilepsy, there was an increased frequency of seizures in four, associated with increased EEG epileptiform activity in three. EEG abnormality either appeared or increased in 74% of cases on the second day after the air study. A mechanism for the production of these sequelae is proposed. It is concluded that these findings indicate that in most cases an organic brain syndrome follows pneumoencephalography.

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