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BACKGROUND: Eczema is common in infancy; however, there is little evidence about its natural history to adulthood. OBJECTIVES: To study the natural history of eczema from birth to young adult life with particular reference to its relation to atopy. METHODS: A birth cohort of children with atopic family histories was followed for 23 years. Clinical examinations were conducted until the age of 7 years, skin-prick tests and serum total IgE were recorded in infancy and at ages 7 and 23 years, and questionnaires about eczema symptoms were completed at 15 and 23 years. RESULTS: Information was obtained on 497 subjects at birth, 482 at 1 year, 440 at 7 years, 363 at 15 years and 304 at 23 years. Eczema usually remitted from age 1 to 7 years but became more persistent from the age of 15 years, especially in those who were atopic. The prevalence of eczema rose in women from age 15 to 23 years but declined in men. Adults with eczema had higher IgE than those without at 3 months (geometric mean 3·0 vs. 1·7 kU L(-1); P=0·01), 7 years (107·9 vs. 45·2 kU L(-1); P=0·01) and 23 years (123·4 vs. 42·3 kU L(-1); P=0·01), and were more likely to have had positive skin-prick tests at 1 year of age. Current eczema was associated with raised IgE in infancy and adulthood but not in childhood. CONCLUSIONS: Predisposed infants and children with eczema usually grow out of the disease, but in adolescence it is more likely to persist. Adult eczema is related to atopy from the age of 3 months.

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BACKGROUND: It is not clear whether associations between respiratory symptoms and indoor mould are causal. A randomised controlled trial was conducted to see whether asthma improves when indoor mould is removed. METHODS: Houses of patients with asthma were randomly allocated into two groups. In one group, indoor mould was removed, fungicide was applied and a fan was installed in the loft. In the control group, intervention was delayed for 12 months. Questionnaires were administered and peak expiratory flow rate was measured at baseline, 6 months and 12 months. RESULTS: Eighty-one houses were allocated to the intervention group and 83 to the control group; 95 participants in 68 intervention houses and 87 in 63 control houses supplied follow-up information. Peak expiratory flow rate variability declined in both groups, with no significant differences between them. At 6 months, significantly more of the intervention group showed a net improvement in wheeze affecting activities (difference between groups 25%, 95% CI 3% to 47%; p = 0.028), perceived improvement of breathing (52%, 95% CI 30% to 74%; p<0.0001) and perceived reduction in medication (59%, 95% CI 35% to 81%; p<0.0001). By 12 months the intervention group showed significantly greater reductions than the controls in preventer and reliever use, and more improvement in rhinitis (24%, 95% CI 9% to 39%; p = 0.001) and rhinoconjunctivitis (20%, 95% CI 5% to 36%; p = 0.009). CONCLUSIONS: Although there was no objective evidence of benefit, symptoms of asthma and rhinitis improved and medication use declined following removal of indoor mould. It is unlikely that this was entirely a placebo effect.

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BACKGROUND: A study was undertaken to see whether the prevalence of asthma has changed since a survey was conducted in 1988, using the same methods that showed an increase during the previous 15 years. METHODS: A survey of 12 year old children was conducted in schools in South Wales where surveys had taken place in 1973 and 1988. The survey comprised a parentally completed questionnaire and an exercise challenge test, performed when no bronchodilator had been recently used. RESULTS: In 1973, 1988, and 2003, questionnaires were obtained for 817, 965 and 1148 children, respectively; the exercise test was performed by 812, 960 and 1019 children, respectively. The prevalence of reported wheeze in the last year rose during each 15 year period (9.8%, 15.2%, 19.7%), with an even steeper rise in reported asthma ever (5.5%, 12.0%, 27.3%). There was a continued increase in wheeze attributed to running, in terms of all children (5.8%, 10.5%, 16.0%) and also as the proportion of those with a history of wheeze (34.1%, 47.0%, 57.3%). The use of inhaled corticosteroids (not available in 1973) increased fourfold between 1988 and 2003. The prevalence of exercise induced bronchoconstriction rose between 1973 and 1988 but had declined by 2003. CONCLUSIONS: The rise in the prevalence of asthmatic symptoms has continued since 1988. This appears to conflict with a reported recent decline, unless asthma prevalence peaked in the 1990s. The decline in exercise induced bronchoconstriction is probably attributable to better control of the disease as more children are now using inhaled corticosteroids as preventive treatment.

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Two successive randomized trials examined the effect of an increased intake of fatty fish, or the use of fish oil supplements, in reducing mortality in men with heart disease. The Diet and Reinfarction Trial (DART) was conducted in 2033 men who were recovering from acute myocardial infarction (MI). Those who were advised to eat fatty fish (or who opted to take fish oil capsules instead) had a 29% reduction in all-cause mortality over the following two years compared with those not so advised. The effect appeared in the first few months of the trial. The Diet and Angina Randomized Trial (DART 2) involved 3114 men with stable angina. Advice to eat fatty fish did not reduce mortality, and taking fish oil capsules was associated with a higher risk of cardiac and sudden death. The adverse effects of fish or fish oil were restricted to men not taking beta-blockers or dihydropyridine calcium-channel blockers, and were greater in those taking digoxin. Evidence from other sources strongly suggests an anti-arrhythmic action of fish oil, particularly after MI or in the presence of acute ischemia. The apparently conflicting results of the two trials may reflect different actions of n-3 fatty acids in acute and chronic conditions, together with different effects of eating fish and taking fish oil capsules. A mechanism is proposed that could account for these findings.

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OBJECTIVE: To investigate the effects of laboratory testing policies, particularly selective testing, rule-based reporting and isolate identification, on estimates of community antimicrobial resistance. MATERIALS AND METHODS: Antibiotic resistance estimates were analysed from an all-Wales dataset for approximately 300 000 community isolates of common pathogens. RESULTS: Selective testing policies were often associated with markedly increased resistance, particularly for second-line testing. Site-specific testing tended to yield variant resistance estimates for eye and ear isolates. Estimates from rule-based reporting deviated markedly from test-result-based reporting. Urinary isolates reported as Escherichia coli showed greater susceptibility than those reported as undifferentiated urinary 'coliforms'. The proportion of isolates tested for an antibiotic by a laboratory was a useful indicator of selective testing in this dataset. Selective testing policies had invariably been applied where the proportion of isolates of a species tested against an antibiotic was <90%. As this proportion fell with increasingly selective policies, divergence from pooled-all-Wales non-selective estimates tended to increase, with a bias to increased resistance. CONCLUSIONS: Selective testing, rule-based reporting and urinary coliform identification policies all had significant effects upon resistance estimates. Triage based upon the proportion of isolates tested seemed a useful tool in assigning analysis resources. Where <20% of isolates were tested, selective policies with inherent bias to increased resistance were common, the low number of isolates gave high potential sampling errors, and little confidence could be placed in the resistance estimate. Where 20-90% of isolates were tested, detailed analysis sometimes revealed resistance estimates that might be usefully retrieved. Where >/=90% of isolates were tested, there was no evidence of selective testing, and inter-laboratory variation in estimates appeared to be safely ascribable to other effects, e.g. methodology or real variation in resistance levels.

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BACKGROUND: In a previous study we examined the changes in the median multiple of the median (MoM) with gestation of free beta human chorionic gonadotrophin (F beta-hCG), total human chorionic gonadotrophin (ThCG), alpha-fetoprotein (AFP) and pregnancy-associated plasma protein A (PAPP-A) in a large series of Down's syndrome pregnancies. Results showed that there was a significant temporal variation of the MoM for each marker. In this paper, we assess the impact of this temporal shift on the estimation of patient-specific risks and the detection rates (DRs) for Down's syndrome pregnancies. METHODS: Individual patient-specific risks, DRs and false positive rates were estimated using statistical modelling techniques and computer simulations. The data for these simulations were the regressed mean log(10) analyte MoMs, marker standard deviations (as log(10) MoM) and correlation coefficients derived from the analysis of over 1000 cases of Down's syndrome and 150,000 unaffected pregnancies between 6 and 20 weeks of gestation reported in our previous study. Two models were compared: the classical constant median separation model, which assumes no variation in median shift with gestation (model 1), and a variable median separation model (model 2), which takes account of the changes in median shift with gestation as described in our previous study. RESULTS: When individual patient-specific risks calculated for various MoM values using model 1 were compared with those derived from model 2, considerable differences in risk estimates were observed for all marker combinations, particularly in the first trimester. Using a 1 in 250 cut-off risk, DRs at each gestation in the second trimester for the AFP+F beta-hCG combination were maximized at 14-17 weeks of gestation and were virtually identical at 63-65% for model 1 and model 2. A similar trend was observed for the AFP+ThCG combination, with an optimum gestational range of 15-18 weeks and DRs of 66-68%. In the first trimester, using a 1 in 250 cut-off risk, DRs were more variable with gestation for the prime marker combination of F beta-hCG+PAPP-A, varying from 73% at 8 weeks to 65% at 13 weeks with model 1 and from 75% to 66% with model 2. CONCLUSION: Risk algorithms should take into account temporal variation in marker MoMs in order to produce accurate patient-specific risks. This also helps to maximize DRs, particularly when samples are taken out with the optimal gestational range.

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OBJECTIVE: To see whether mortality among men with angina can be reduced by dietary advice. DESIGN: A randomized controlled factorial trial. SETTING: Male patients of general practitioners in south Wales. SUBJECTS: A total of 3114 men under 70 y of age with angina. INTERVENTIONS: Subjects were randomly allocated to four groups: (1) advised to eat two portions of oily fish each week, or to take three fish oil capsules daily; (2) advised to eat more fruit, vegetables and oats; (3) given both the above types of advice; and (4) given no specific dietary advice. Mortality was ascertained after 3-9 y. RESULTS: Compliance was better with the fish advice than with the fruit advice. All-cause mortality was not reduced by either form of advice, and no other effects were attributable to fruit advice. Risk of cardiac death was higher among subjects advised to take oily fish than among those not so advised; the adjusted hazard ratio was 1.26 (95% confidence interval 1.00, 1.58; P=0.047), and even greater for sudden cardiac death (1.54; 95% CI 1.06, 2.23; P=0.025). The excess risk was largely located among the subgroup given fish oil capsules. There was no evidence that it was due to interactions with medication. CONCLUSIONS: Advice to eat more fruit was poorly complied with and had no detectable effect on mortality. Men advised to eat oily fish, and particularly those supplied with fish oil capsules, had a higher risk of cardiac death. This result is unexplained; it may arise from risk compensation or some other effect on patients' or doctors' behaviour.

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BACKGROUND: Many maternal serum markers show concentration changes in Down's syndrome pregnancies but the magnitude of the change in median marker levels varies with gestation. To date these changes have not been accurately specified. METHODS: The trends in marker median levels between 6 and 20 weeks of gestation were examined for alphafetoprotein (AFP), free beta human chorionic gonadotrophin (Fbeta-hCG), total human chorionic gonadotrophin (ThCG) and pregnancy-associated plasma protein A (PAPP-A) by a meta-analysis of data obtained from our collaborative studies and routine screening programmes for Down's syndrome over a 10-year period. Data were available from between 709 and 1082 Down's syndrome pregnancies and from between 14607 and 153909 unaffected pregnancies for each marker. The median multiple of the median (MoM) and mean log10MoM for each marker at each completed week of gestation were estimated and the trend with gestation smoothed using a weighted least squares regression model. RESULTS: The gestational ages at which maximum separation of marker levels occurred, comparing affected and unaffected pregnancies, and the respective regressed median MoMs and mean log10MoMs, were: for AFP at 16 weeks, 0.72 MoM, -0.14288log10MoM; for Fbeta-hCG at 15 weeks, 2-24MoM, 0.35034 log10MoM; for ThCG at 16 weeks, 1.93 MoM, 0.28548 log10MoM, as well as before 8 weeks (<0.65 MoM, -0.18853 log10MoM); and for PAPP-A before 8 weeks, <0.33 MoM, -0.47727 log10MoM. CONCLUSION: There is significant temporal variation in mean log10MoM values for the screening markers investigated. Screening algorithms, modified to take account of this variation, should allow more accurate gestation-specific risks to be calculated in individual pregnancies.

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