Left ventricular dysfunction can be improved with angiotensin-converting-enzyme inhibition started 1 week after myocardial infarction or later. To see whether earlier intervention may confer greater benefit, a double-blind study was carried out in which 100 patients with Q wave myocardial infarction, but without clinical heart failure, were randomly allocated treatment with captopril 50 mg twice daily or placebo starting 24-48 h after onset of symptoms. Left ventricular volumes were measured regularly during 3 months of treatment and after a 48 h withdrawal period by means of two-dimensional echocardiography. The placebo group showed significant increases in left ventricular end-diastolic (LVEDVI) and end-systolic (LVESVI) volume indices, with the ejection fraction unchanged. By contrast, the captopril group showed a slight but not significant rise in LVEDVI and a significant reduction in LVESVI with ejection fraction increased significantly. At 3 months there was a 4.6% difference in the change in ejection fraction from baseline between the groups (p less than 0.0001). Most of the treatment benefit was evident at 1 month and there were no changes in left ventricular volumes after 48 h withdrawal of treatment at 3 months. Heart failure requiring treatment with frusemide developed in 7 patients in each group during the study period; 3 of these (1 captopril-treated, 2 placebo-treated) had to be withdrawn from the trial with severe heart failure requiring open treatment. Thus early treatment with captopril is effective in preventing the ventricular dilatation that can occur after Q wave myocardial infarction.

The prevalence, rate, and degree of memory impairment for next-day activities during a short, intermittent course of bedtime doses of triazolam, temazepam, and placebo were assessed in a double-blind parallel-group study. 5 of the 6 subjects in the triazolam group reported at least one episode of next-day memory impairment/amnesia, with a total of 12 episodes being reported for the 30 subject-drug nights (a rate of 40%). In the temazepam group there were no such episodes of memory impairment. Immediate and delayed recall were also tested and related to whether active drug or placebo had been taken the night before. Impairment of delayed recall was significantly and several times greater than that in the temazepam or placebo groups. Next-day memory impairment/amnesia after a bedtime dose of triazolam tended to increase with continued or intermittent drug use. Cognitive impairments associated with triazolam probably represent a spectrum of organic brain dysfunction, with memory impairment/amnesia and confusion being the commonest, and milder manifestations and hallucinations and delusions the more severe and less common, features.

The hypotheses that patients with chronic fatigue syndrome (CFS) have low red blood cell magnesium and that magnesium treatment would improve the wellbeing of such patients were tested in a case-control study and a randomised, double-blind, placebo-controlled trial, respectively. In the case-control study, 20 patients with CFS had lower red cell magnesium concentrations than did 20 healthy control subjects matched for age, sex, and social class (difference 0.1 mmol/l, 95% confidence interval [CI] 0.05 to 0.15). In the clinical trial, 32 patients with CFS were randomly allocated either to intramuscular magnesium sulphate every week for 6 weeks (15 patients) or to placebo (17). Patients treated with magnesium claimed to have improved energy levels, better emotional state, and less pain, as judged by changes in the Nottingham health profile. 12 of the 15 treated patients said that they had benefited from treatment, and in 7 patients energy score improved from the maximum to the minimum. By contrast, 3 of the 17 patients on placebo said that they felt better (difference 62%, 95% CI 35 to 90), and 1 patient had a better energy score. Red cell magnesium returned to normal in all patients on magnesium but in only 1 patient on placebo. The findings show that magnesium may have a role in CFS.

To see whether the introduction of screening tests for post-transfusion non-A, non-B hepatitis (NANBH) in the UK would be worth while, the incidence of such hepatitis was assessed among patients receiving blood during operations at five hospitals served by the North London Blood Transfusion Centre. 387 patients, who each received blood or blood components from an average of 3 donors were followed up prospectively and blood samples were taken every 2 weeks for 3 months and then each month for a further 3 months. 229 patients also provided a sample at 12 months. All available patient and donor samples were tested for alanine aminotransferase concentrations and for antibody to hepatitis C virus (anti-HCV) by ELISA. Repeatedly anti-HCV positive samples were submitted to supplementary HCV assays. 1 of the 387 patients showed biochemical evidence of acute post-transfusion NANBH after exclusion of non-viral causes. Anti-HCV developed in this patient and the seroconversion was confirmed by recombinant immunoblot assay and polymerase chain reaction. Serum from 1 of the 8 donors whose blood he received was positive for anti-HCV by all three methods. In another patient HCV seroconversion was shown by ELISA but alanine aminotransferase concentrations remained normal throughout follow-up. His samples and those of his 2 donors were negative for HCV by the polymerase chain reaction. A third patient showed rises in alanine aminotransferase compatible with post-transfusion NANBH, but serology and polymerase chain reaction assays for HCV were negative for her samples and those of her donors. Anti-HCV reactivity likely to be false positive (negative by both confirmatory tests and no adverse effects in recipients) was seen in 6 of 1283 donors. This study, despite its being carried out in the part of the UK with the highest frequency of infectious markers in blood donations, has shown a very low incidence of post-transfusion NANBH.

358 children in the Gambian villages of Keneba and Manduar, where hepatitis B virus (HBV) infection is endemic, were vaccinated with plasma-derived vaccine against HBV according to one of four regimens and followed for up to 4 years. Two regimens by which vaccine was injected intradermally into children between 0 and 4 years old led to peak geometric mean (95% CI) concentrations of antibody against HBV surface antigen of 270 (202-358) and 555 (418-748) mlU/ml. The third regimen--intramuscular vaccination of children aged between 0 and 4 years--gave geometric mean peak antibody concentrations of 926 (765-1122) mlU/ml. A fourth regimen was intramuscular vaccination of children between 1 and 9 months old, which gave geometric mean antibody concentrations of 5431 (3903-75,456) mlU/ml. Despite these widely divergent responses and a 89% decay in antibody over the first 2 years, vaccination against HBV was 97% effective in preventing chronic infection. Vaccination was less effective in preventing uncomplicated infection: 5.3% of 264 vaccinees in Keneba and 19.1% of 94 vaccinees in Manduar tested positive for antibody to HBV core antigen. These "breakthrough infections" did not differ in frequency between regimens, and were associated with low initial antibody responses and chronic maternal carriage of HBV.

The effects of a highly selective leukotriene D4 receptor antagonist, ICI 204.219, on allergen-induced bronchoconstriction and changes in airway reactivity were evaluated in a double-blind, placebo-controlled, crossover trial. Ten atopic subjects were selected for the study on the basis of an immediate fall in forced expiratory volume in 1 s (FEV1) of at least 15% and a least a doubling dose fall in their PC20-histamine (the concentration of histamine needed to reduce FEV1 by 20%) after antigen challenge. Baseline PC20-histamine was determined before the ingestion of a single oral 40 mg dose of ICI 204.219 or matched placebo. 2 h later subjects were challenged with aerosolised allergen; FEV1 was measured for the next 6 h then PC20-histamine was remeasured. Two subjects did not complete the study for reasons not related to the trial medication. ICI 204.219 significantly attenuated the early and late phase bronchoconstriction to inhaled allergen (mean treatment difference in area under the FEV1-time curves 2529 [95% Cl 1085-3972] delta %FEV1.min; p less than 0.005: and 3537 [528-6545] delta %FEV1.min; p less than 0.03) and suppressed the allergen-induced increase in non-specific bronchial reactivity (mean treatment difference 1.03 [0.34-1.71] doubling dilutions of histamine; p less than 0.01). These findings suggest that ICI 204.219 may be a disease-modifying agent in asthma. Further studies are under way to evaluate its clinical efficacy.

To assess how an isolated change in the pattern of care influences outcome of care and hospital use, a randomised prospective 2-year study was done in which 31 of 61 consecutive children with newly diagnosed insulin-dependent diabetes mellitus (IDDM) were admitted to hospital at disease onset for about a week and compared with the other 30 children who were admitted for about 4 weeks. Insulin treatment and education about diabetes were similar in the two groups. Duration of initial stay in hospital had no effect on metabolic control during the 2 years but time since diagnosis was significant with respect to effect on haemoglobin A1 (p = 0.001), haemoglobin A1c (p = 0.004), and insulin dose (p less than 0.001). At 2 years, 45% of the children in the short-term group and 29% in the long-term group were C-peptide positive (p = NS); C-peptide positivity correlated with age. A change in the pattern of care of children with IDDM, led to a pronounced decrease in hospital use by this patient group. Irrespective of the length of initial stay in hospital, equally good metabolic control was obtained in both groups for 2 years.