Atopy in people aged 40 years and over: Relation to airflow limitation.

BACKGROUND: Previous studies have reached conflicting conclusions about the role of atopy as a risk factor for COPD. In part, this is attributable to variation in the definitions of airflow limitation and the treatment of people with asthma. OBJECTIVE: To establish whether there is any independent association between atopy and post-bronchodilator airflow limitation in the general population aged 40 years and over. METHODS: A cross-sectional survey was conducted in a general population sample of 2415 people aged 40 years and over in Australia. A history of ever being diagnosed with asthma was elicited by questionnaire. Atopy was defined as any skin prick test weal to common aeroallergens ≥4 mm. Airflow limitation was defined as post-bronchodilator spirometric (FEV1 /FVC) ratio

An observational study of PM10 and hospital admissions for acute exacerbations of chronic respiratory disease in Tasmania, Australia 1992-2002.

OBJECTIVE: Particulate matter with a diameter below 10 µ (PM10) has been a major concern in the Tamar Valley, Launceston, where wood heaters are extensively used. We examined the relationship between PM10 levels, meteorological variables, respiratory medications and hospital admissions for respiratory disease over the decade 1992-2002. METHODS: PM10 levels were provided by the Department of Primary Industry Water, Parks and Environment, and meteorological variables from the Bureau of Meteorology. We obtained hospital discharge codes for the Launceston General Hospital. Poisson regression was used for statistical analyses. RESULTS: Mean daily PM10 levels declined from 50.7 to 16.5 µg/m(3). Hospitalisations for asthma decreased from 29 to 21 per month, whereas chronic obstructive pulmonary disease (COPD) increased and bronchitis/bronchiolitis remained unchanged. We found a 10 µg/m(3) increase in PM10 to be associated with a 4% increase in admissions for acute bronchitis/bronchiolitis (p0.05), but no association with asthma or COPD was found. All respiratory diseases showed seasonal patterns of hospitalisation. CONCLUSIONS: This is the first long-term study in Australia to demonstrate an association between PM10 levels and respiratory diseases. Reducing exposure to PM10 may decrease hospital admissions for respiratory diseases. IMPLICATION: Better preventive measures, including sustained public health initiatives to combat air pollution, are required to reduce respiratory morbidity.

Cardiovascular effects of methacholine-induced airway obstruction in man.

Cardiovascular disease is the most frequent cause of death in people with chronic respiratory disease. The cause of this association has been attributed to airway obstruction leading to cardiovascular dysfunction (increased central blood pressure (BP) and aortic stiffness). However, this has never been experimentally tested. Methacholine is routinely used to stimulate airway function changes that mimic airway pathology. This study aimed to determine the cardiovascular effects of methacholine-induced airway obstruction. Fifteen healthy young adults (aged 22.9±2.5 years; 4 male; mean±S.D.) underwent a bronchial challenge test (randomized, blinded, cross-over design) in which they received nebulized methacholine inhalation in serially increasing concentrations (from 0.39 to 25 mg/ml) or saline (0.9%; control) on two separate days. Bronchoconstriction was assessed by forced expiratory volume at one second (FEV1) and cardiovascular effects by augmentation index, brachial BP, central BP, heart rate and aortic stiffness. Methacholine significantly decreased FEV1 from baseline to peak inhaled concentration compared with saline (-0.48±0.34 vs. -0.07±0.16 L; p<0.001), but there was no between-group change in augmentation index (1.6±7.0 vs. 3.7±10.2% p=0.49), brachial systolic BP (-3.3±7.6 vs. -4.7±5.7 mmHg; p=0.59), central systolic BP (-1.1±5.2 vs. -0.3±5.5 mmHg; p=0.73), heart rate (0.4±7.1 vs. -0.8±6.6 bpm; p=0.45) or aortic stiffness (0.2±1.3 vs. 0.8±1.8 m/s; p=0.20; n=12). Thus, methacholine induced airway obstruction does not acutely change brachial BP or central haemodynamics. This finding refutes the notion that airway obstruction per se leads to cardiovascular dysfunction, at least in healthy individuals in the acute setting.

Interstitial lung disease due to fumes from heat-cutting polymer rope.

Interstitial lung disease (ILD) due to inhalation of fume/smoke from heating or burning of synthetic polymers has not been reported previously. A fish farm worker developed ILD after cutting rope (polypropylene and nylon) for about 2 hours per day over an extended period using an electrically heated 'knife'. This process produced fume/smoke that entered the workers breathing zone. No other likely cause was identified. This case suggests that exposure to airborne contaminants generated by the heating or burning of synthetic polymers has the potential to cause serious lung disease.

Cardiovascular mortality and morbidity in chronic obstructive pulmonary disease: the impact of bronchodilator treatment.

Chronic obstructive pulmonary disease (COPD) is a substantial health burden. Cardiovascular disease (CVD), the leading cause of death, frequently coexists with COPD, an effect attributed to high individual disease prevalences and shared risk factors. It has long been recognized that COPD, whether stable or during acute exacerbations, is associated with an excess of cardiac arrhythmias. Bronchodilator medications have been implicated in the excess CVD seen in COPD, either as an intrinsic medication effect or related to side-effects. Despite the theory behind increased pro-arrhythmic effects in COPD, the reported results of trials investigating this for inhaled formulations at therapeutic doses are few. Methodological flaws, retrospective analysis and inadequate adjustment for concomitant medications, including short-acting 'relief' bronchodilators and non-respiratory medications with known arrhythmia propensity, mar many of these studies. For most bronchodilators at therapeutic levels in stable COPD, we can be reassured of their safety from current studies. The exception to this is ipratropium bromide, where the current data indicate an association with increased cardiovascular adverse effects. Moreover, there is no proven benefit from combining short-acting beta-agonists with short-acting anticholinergics at high doses in the acute setting, and although this practice is widespread, it is associated with increased cardiovascular risk.

Adherence to asthma management guidelines by middle-aged adults with current asthma.

BACKGROUND: With the increasing burden of asthma worldwide, much effort has been given to developing and updating management guidelines. Using data from the Tasmanian Longitudinal Health Study (TAHS), the adequacy of asthma management for middle-aged adults with asthma was investigated. METHODS: Information about spirometry, medication history and current asthma status was collected by the most recent TAHS when participants were in their mid 40s. Only those who reported ever having asthma were eligible for analysis. RESULTS: Of the 702 participants who reported ever having asthma, 50% had current asthma (n = 351) of whom 71% were categorised as having persistent asthma (n = 98 mild, n = 92 moderate, n = 58 severe). The majority (85.2%) of participants with current asthma had used some form of asthma medication in the past 12 months, but the proportion of the use of minimally adequate preventer medication was low (26%). Post-bronchodilator airflow obstruction increased progressively from mild to severe persistent asthma for those inadequately managed, but not for those on adequate therapy. CONCLUSION: Appropriate use of asthma medication by this middle-aged group of adults with current asthma was inadequate, especially for those with adult-onset moderate or severe persistent disease and without a family history of asthma. These results suggest that proper use of preventer medication could protect against the progressive decline in lung function associated with increasing severity. This has implications not just for poor quality of life, but also for the development of fixed airflow obstruction.

A mixed methods study to compare models of spirometry delivery in primary care for patients at risk of COPD.

BACKGROUND: To increase recognition of airflow obstruction in primary care, we compared two models of spirometry delivery in a target group at risk of chronic obstructive pulmonary disease (COPD). METHODS: A 6 month qualitative/quantitative cluster randomised study in eight practices compared opportunistic spirometry by "visiting trained nurses" (TN) with optimised "usual care" (UC) from general practitioners (GPs) for smokers and ex-smokers, aged over 35 years. Outcomes were: spirometry uptake and quality, new diagnoses of COPD and GPs' experiences of spirometry. RESULTS: In the eligible target population, 531/904 (59%) patients underwent spirometry in the TN model and 87/1130 (8%) patients in the UC model (p < 0.0001). ATS spirometry standards for acceptability and reproducibility were met by 76% and 44% of tests in the TN and UC models, respectively (p < 0.0001). 125 (24%) patients tested with the TN model and 38 (44%) with the UC model reported a pre-existing respiratory diagnosis (p < 0.0001). Three months after spirometry, when the ratio of forced expiratory volume in 1 s/forced vital capacity (FEV(1)/FVC) was < 0.7 and no prior COPD diagnosis was reported, nine (8%) participants had a new doctor recorded COPD diagnosis in practices with the TN model and two (8%) participants in practices with the UC model. Mislabelling of participants with a diagnosis of COPD when FEV(1)/FVC was > or = 0.7 was present in both models prior to and after spirometry. GPs valued high quality spirometry and increased testing of patients at risk of COPD in the TN model. They identified limitations, including the need for better systematic follow-up of abnormal spirometry and support with interpretation, which may explain persisting underdiagnosis of COPD in practice records. CONCLUSIONS: Although opportunistic testing by visiting trained nurses substantially increased and improved spirometry performance compared with usual care, translating increased detection of airflow obstruction into diagnosis of COPD requires further development of the model. TRIAL REGISTRATION NUMBER: Australian Clinical Trials Registry: registration No 12605000019606.

Airway cell and cytokine changes in early asthma deterioration after inhaled corticosteroid reduction.

BACKGROUND: Back-titration of inhaled corticosteroid (ICS) dose in well-controlled asthma patients is emphasized in clinical guidelines, but there are few published data on the airway cell and cytokine changes in relation to ICS reduction. In our study, 20 mild-to-moderate persistent (inspite of low-moderate dose ICS treatment) asthmatic subjects prospectively rendered largely asymptomatic by high-dose ICS were assessed again by clinical, physiological, and airway inflammatory indices after 4-8 weeks of reduced ICS treatment. We aimed at assessing the underlying pathological changes in relation to clinical deterioration. METHODS: Patients recorded daily symptom scores and peak expiratory flows (PEF). Spirometry and airways hyperreactivity (AHR) were measured and bronchoscopy was performed with assessment of airway biopsies (mast cells, eosinophils, neutrophils, and T lymphocytes), bronchoalveolar lavage (BAL) IL-5 and eotaxin levels and cellular profiles at the end of high-dose ICS therapy and again after ICS dose reduction. Baseline data were compared with symptomatic steroid-free asthmatics (n=42) and non-asthmatic controls (n=28). RESULTS: After ICS reduction, subjects experienced a variable but overall significant increase in symptoms and reductions in PEF and forced expiratory volume in 1 s. There were no corresponding changes in AHR or airways eosinophilia. The most relevant pathogenic changes were increased CD4(+)/CD8(+) T cell ratio, and decreased sICAM-1 and CD18 macrophage staining (potentially indicating ligand binding). However, there was no relationship between the spectrum of clinical deterioration and the changes in cellular profiles or BAL cytokines. CONCLUSIONS: These data suggest that clinical markers remain the most sensitive measures of early deterioration in asthma during back-titration of ICS, occurring at a time when AHR and conventional indices of asthmatic airway inflammation appear unchanged. These findings have major relevance to management and to how back-titration of ICS therapy is monitored.

Injectable vaccines for preventing pneumococcal infection in patients with chronic obstructive pulmonary disease.

BACKGROUND: As chronic obstructive pulmonary disease (COPD) progresses, exacerbations can occur with increasing frequency. One goal of therapy in COPD is to try and prevent these exacerbations, thereby reducing disease morbidity and associated healthcare costs. Pneumococcal vaccinations are considered to be one strategy for reducing the risk of infective exacerbations. OBJECTIVES: To determine the safety and efficacy of pneumococcal vaccination in COPD. The primary outcome assessed was acute exacerbations. Secondary outcomes of interest included episodes of pneumonia, hospital admissions, adverse events related to treatment, disability, change in lung function, mortality, and cost effectiveness. SEARCH STRATEGY: We searched the Cochrane Airways Group COPD trials register using pre-specified terms. We also conducted additional handsearches of conference abstracts. The last round of searches were performed in April 2006. SELECTION CRITERIA: Only randomised controlled trials assessing the effects of injectable pneumococcal vaccine in people with COPD were included. DATA COLLECTION AND ANALYSIS: Two review authors independently extracted data and three review authors independently assessed trial quality. MAIN RESULTS: Although 10 studies cited in 11 publications were identified that met the inclusion criteria for this review, only four of these provided data on participants with COPD. The studies which did provide data for this review consisted of two trials using a 14-valent vaccine, and two using a 23-valent injectable vaccine. Data for the primary outcome, acute exacerbation of COPD, was available from only one of the four studies. The odds ratio of 1.43 (95% confidence interval (CI) 0.31 to 6.69) between interventions was not statistically significant. Of the secondary outcomes for which data were available and could be extracted, none reached statistical significance. Three studies provided dichotomous data for persons who developed pneumonia (OR 0.89, 95% CI 0.58 to 1.37, n = 748). Rates of hospital admissions and emergency department visits came from a single study. There was no significant reduction in the odds of all-cause mortality 1 to 48 months post-vaccination (Peto odds ratio 0.94, 95% CI 0.67 to 1.33, n = 888), or for death from cardiorespiratory causes (OR 1.07, 95% CI 0.69 to 1.66). AUTHORS' CONCLUSIONS: There is no evidence from randomised controlled trials that injectable pneumococcal vaccination in persons with COPD has a significant impact on morbidity or mortality. Further large randomised controlled trials would be needed to ascertain if the small benefits suggested by individual studies are real.

Oxygen therapy in the pre-hospital setting for acute exacerbations of chronic obstructive pulmonary disease.

BACKGROUND: Chronic obstructive pulmonary disease (COPD), a leading cause of morbidity and mortality in the developed world, is characterised by acute deterioration in symptoms. During these exacerbations, people are prone to developing alveolar hypoventilation, which may be contributed to by the administration of high inspired oxygen concentrations. OBJECTIVES: The objective of the review was to determine the effect of different inspired oxygen concentrations ("high flow" compared to "controlled") in the pre-hospital setting on outcome for people with acute exacerbations of COPD. SEARCH STRATEGY: We searched the Cochrane Airways Group Specialised Register (August 2005), the Cochrane Central Register of Controlled Trials (The Cochrane Library Issue 3, 2005), MEDLINE (1966 to August 2005), EMBASE (1980 to wk 32, 2005), CINAHL (1982 to August wk 1, 2005) and reference lists of articles. We also contacted authors of identified RCTs for details of other relevant, published and unpublished studies. SELECTION CRITERIA: Randomised controlled trials comparing oxygen therapy at different concentrations or oxygen therapy versus placebo in the pre-hospital setting for treatment of acute exacerbations of COPD were eligible. DATA COLLECTION AND ANALYSIS: Two review authors independently assessed trial quality and extracted data. MAIN RESULTS: The search identified a total of 741 abstracts, of which 18 were selected as potentially relevant, only two of the 18 studies were randomised controlled trials and eligible for inclusion in the review, but were ongoing and had no data available for analysis. AUTHORS' CONCLUSIONS: No relevant trials have been published to date, so there is no evidence to indicate whether different oxygen therapies in the pre-hospital setting have an effect on outcome for people with acute exacerbations of COPD. There is an urgent need for robust, well-designed randomised controlled trials to investigate the effect of oxygen therapies in the pre-hospital setting for people with acute exacerbations of COPD.

Influenza vaccine for patients with chronic obstructive pulmonary disease.

BACKGROUND: Influenza vaccinations are currently recommended in the care of people with COPD, but these recommendations are based largely on evidence from observational studies with very few randomised controlled trials (RCTs) reported. Influenza infection causes excess morbidity and mortality in COPD patients but there is also the potential for influenza vaccination to cause adverse effects or not to be cost effective. OBJECTIVES: To evaluate the evidence from RCTs for a treatment effect of influenza vaccination in COPD subjects. Outcomes of interest were exacerbation rates, hospitalisations, mortality, lung function and adverse effects. SEARCH STRATEGY: We searched the Cochrane Airways Group Specialised Register of trials, and reference lists of articles. References were also provided by a number of drug companies we contacted. SELECTION CRITERIA: RCTs that compared live or inactivated virus vaccines with placebo, either alone or with another vaccine in persons with COPD. Studies of people with asthma were excluded. DATA COLLECTION AND ANALYSIS: Two reviewers extracted data. All entries were double checked. Study authors and drug companies were contacted for missing information. MAIN RESULTS: Eleven trials were included but only six of these were specifically performed in COPD patients. The others were conducted on elderly and high-risk individuals, some of whom had chronic lung disease. Inactivated vaccine in COPD patients resulted in a significant reduction in the total number of exacerbations per vaccinated subject compared with those who received placebo (weighted mean difference (WMD) -0.37, 95% confidence interval -0.64 to -0.11, P = 0.006). This was due to the reduction in "late" exacerbations occurring after three or four weeks (WMD -0.39, 95% CI -0.61 to -0.18, P = 0.0004). In Howells 1961, the number of patients experiencing late exacerbations was also significantly less (odds ratio 0.13, 95% CI 0.04 to 0.45, P = 0.002). Both Howells 1961 and Wongsurakiat 2004 found that inactivated influenza vaccination reduced influenza -related respiratory infections (WMD 0.19, 95% CI 0.07 to 0.48, P = 0.0005). In both COPD patient and in elderly patients (only a minority of whom had COPD), there was a significant increase in the occurrence of local adverse reactions in vaccinees, but the effects were generally mild and transient. There was no evidence of an effect of intranasal live attenuated virus when this was added to inactivated intramuscular vaccination. The studies are too small to have detected any effect on mortality. An updated search conducted in September 2001 did not yield any further studies. A search in 2003 yielded two further reports of the same eligible study Gorse 2003. A search in 2004 yielded two reports of the another eligible study Wongsurakiat 2004. The author informed us of another report of the same study Wongsurakiat 2004/2. AUTHORS' CONCLUSIONS: It appears, from the limited number of studies performed, that inactivated vaccine reduces exacerbations in COPD patients. The size of effect was similar to that seen in large observational studies, and was due to a reduction in exacerbations occurring three or more weeks after vaccination, and due to influenza. There is a mild increase in transient local adverse effects with vaccination, but no evidence of an increase in early exacerbations.

Action plans for chronic obstructive pulmonary disease.

BACKGROUND: The effectiveness of action plans as treatment for chronic obstructive pulmonary disease (COPD) is not known. OBJECTIVES: To assess the efficacy of action plans in the management of COPD. SEARCH STRATEGY: We searched the Cochrane Airways Group Specialised Register, CENTRAL, MEDLINE, CINAHL and the National Research Register of Ongoing Trials. We also searched reference lists of identified studies. The search was completed in August 2004. SELECTION CRITERIA: Randomised controlled trials of action plans in COPD. Studies with a primary diagnosis of asthma excluded. DATA COLLECTION AND ANALYSIS: Two reviewers independently assessed trial quality and extracted data. Investigators were contacted for additional information when necessary. Study results were combined in meta-analyses using the Cochrane Collaboration software RevMan. MAIN RESULTS: There was evidence of a positive effect of action plans on self-management knowledge. The mean difference (MD) for recognition of a severe exacerbation was 2.50; 95% confidence interval 1.04 to 3.96, for self-action in severe exacerbations MD 1.50; 95% confidence interval 0.62 to 2.38 and the use of antibiotics MD 6.00; 95% confidence interval 2.68 to 9.32. There was also evidence of a positive effect on the initiation of antibiotics (odds ratio (OR) 10.16; 95% confidence interval 2.02 to 51.09) and/or oral steroids (OR 6.58; 95% confidence interval 1.29 to 33.62). However, there was no evidence of significant effects on healthcare utilisation, health-related quality of life, lung function, functional capacity, symptom scores, mortality, anxiety, or depression. No trials used as outcomes: number of exacerbations, length of exacerbations, or days lost from work. AUTHORS' CONCLUSIONS: This review shows there is evidence that action plans aid people with COPD in recognising and reacting appropriately to an exacerbation of their symptoms via the self-initiation of antibiotics or steroids. Further research needs to be completed with more comprehensive outcomes measures in order to ascertain whether this results in significantly decreased morbidity and/or mortality.

Oral corticosteroids for stable chronic obstructive pulmonary disease.

BACKGROUND: Chronic obstructive pulmonary disease (COPD) is a common chronic lung disorder, usually related to cigarette smoking, representing a major and increasing cause of morbidity and mortality. It is defined "as a disease state characterized by airflow limitation that is not fully reversible. The airflow limitation is usually both progressive and associated with an abnormal inflammatory response of the lungs to noxious particles or gases". The use of corticosteroids for their anti-inflammatory effects has been suggested. OBJECTIVES: To assess the effects of oral corticosteroids on the health status of patients with stable COPD. SEARCH STRATEGY: Searches of the Cochrane Airways Group Specialised Register and MEDLINE were carried out in December 2003 and 2004. Review articles and bibliographies were searched. SELECTION CRITERIA: Randomised controlled prospective studies in adults with stable COPD ( post-bronchodilator FEV1 <80% of predicted, FEV1/FVC <70%) and a history of smoking, excluding known asthmatics, in which oral steroid use was compared with placebo and use of co-interventions was matched in both groups. DATA COLLECTION AND ANALYSIS: Data was extracted independently by two reviewers. All trials were combined using Review Manager (version 4.2.7). MAIN RESULTS: From 459 titles 24 studies met the inclusion criteria. Treatment lasted three weeks or less in 19 studies, high dose oral steroid was used in 21 studies and subjects had moderate or severe COPD in 15 studies. There was a significant difference in FEV1 after two weeks treatment, WMD 53.30 ml; 95% confidence interval 22.21 to 84.39 favouring oral steroid use compared to placebo when 14 studies with available data (n=396) were combined, with no significant heterogeneity. There was a significant increase in odds for individual patient FEV1 response greater than 20% from baseline with high dose oral steroid treatment compared to placebo, OR 2.71; 95% CI 1.84 to 4.01 (9 studies) . It would be necessary to treat 7 patients (95% CI 5 to 12) with oral corticosteroids to achieve one extra case of increasing FEV1 by more than 20%, with a placebo group risk of 0.13. All differences in health-related quality of life were less than the minimum clinically important difference. There were small statistically significant advantages for functional capacity and respiratory symptom of wheeze with oral steroid treatment but no significant difference in risk of withdrawal from study due to an exacerbation or rate of serious exacerbations over 2 years with low dose oral steroid treatment. There was an increased risk of adverse effects, including increased blood glucose, adrenal suppression and reduced serum osteocalcin. AUTHORS' CONCLUSIONS: There is no evidence to support the long-term use of oral steroids at doses less than 10-15 mg prednisolone though some evidence that higher doses (>/= 30 mg prednisolone) improve lung function over a short period. Potentially harmful adverse effects e.g.. diabetes, hypertension, osteoporosis would prevent recommending long-term use at these high doses in most patients.

Long-acting beta2-agonists in asthma: an overview of Cochrane systematic reviews.

According to major asthma management guidelines, long-acting beta2-agonists (LABAs) should be used only when asthma remains symptomatic in patients already receiving regular inhaled corticosteroids (ICSs). A large Cochrane systematic review provides evidence that LABAs are safe and beneficial in control of asthma; sub-group analyses indicating that this is true when ICSs are used and in their absence. Two other Cochrane systematic reviews have found that LABAs are more effective than regular short-acting beta2-agonists, and are as effective as theophylline with fewer side-effects. These reviews support guidelines in the use of LABA as additional therapy when asthma is inadequately controlled by ICS at moderate dose. However, guidelines may be too conservative, and more studies in stable mild asthma comparing their use and safety with placebo and ICS are required.

Systemic corticosteroids for acute exacerbations of chronic obstructive pulmonary disease.

BACKGROUND: COPD is a common condition, mainly related to smoking. The burden of the disease is increasing and it is projected to rank fifth in 2020 for the world-wide burden of disease. Acute exacerbations of COPD, usually related to superimposed infection occur commonly and systemic corticosteroids are widely used in their management in combination with other treatments including antibiotics, oxygen supplementation and bronchodilators. OBJECTIVES: To determine the efficacy of corticosteroids, administered either parenterally or orally, on the outcome in patients with acute exacerbations of COPD. SEARCH STRATEGY: Searches were carried out using the Cochrane Airways Group COPD RCT register with additional studies sought in the bibliographies of randomised controlled trials and review articles. Authors of identified randomised controlled trials were contacted for other published and unpublished studies. The last search was carried out in August 2004. SELECTION CRITERIA: Randomised controlled trials comparing corticosteroids, administered either parenterally or orally, with appropriate placebo. Other interventions e.g. bronchodilators and antibiotics were standardised. Clinical studies of acute asthma were excluded. DATA COLLECTION AND ANALYSIS: Data was extracted independently by two reviewers. Outcome data was sent to authors for verification. All trials were combined using Review Manager (version 4.2.4) for analyses. MAIN RESULTS: Ten studies were identified that fulfilled the inclusion criteria. There were significantly fewer treatment failures within thirty days in patients given corticosteroid treatment, odds ratio 0.48; 95% confidence interval 0.34 to 0.68 and Hazard Ratio 0.78; 95% confidence interval 0.63 to 0.97. It would have been necessary to treat 9 patients (95%CI 6 to 14) with systemic corticosteroids to avoid one treatment failure in this time period. There was no significant difference in mortality. The early FEV1, up to 72 hours, showed a significant treatment benefit, weighted mean difference 140 mls (95% confidence interval 80-200 mls), although this benefit was not found for later time points. There was a significant improvement in breathlessness and blood gases between 6 - 72 hours after treatment. There was an increased likelihood of an adverse drug reaction with corticosteroid treatment, odds ratio 2.29; 95% confidence interval 1.55 to 3.38. Overall one extra adverse effect occurred for every 6 people treated (95% CI 4 to 10). The risk of hyperglycaemia was significantly increased, odds ratio 5.48; 95% confidence interval 1.58 to 18.96. AUTHORS' CONCLUSIONS: Treatment of an exacerbation of COPD with oral or parenteral corticosteroids significantly reduces treatment failure and the need for additional medical treatment . It increases the rate of improvement in lung function and dyspnoea over the first 72 hours, but at a significantly increased risk of an adverse drug reaction.

Decreased lung capillary blood volume post-exercise is compensated by increased membrane diffusing capacity.

The diffusing capacity of the lung for carbon monoxide (DLCO) decreases to below the pre-exercise value in the hours following a bout of intense exercise. Two mechanisms have been proposed: (1) development of pulmonary oedema and (2) redistribution of central blood volume to peripheral muscles causing a reduction in pulmonary capillary blood volume ( V(c)). In the present study DLCO, V(c) and the membrane diffusing capacity ( D(m)) were measured in nine healthy females using a rebreathing method, in contrast to the single breath technique employed in previous studies. DLCO, V(c) and D(m) were measured before and at 1, 2, 3, 16 and 24 h following maximal treadmill exercise. Compared with pre-exercise values, DLCO was depressed by up to 8.9 (3.0)% ( P<0.05) for the first 3 h following exercise, but had returned to pre-exercise values by 16 h post-exercise. V(c) fell by 21.2 (4.1)% ( P<0.05) at 3 h post-exercise, but at the same time D(m) increased by 14.7 (9.1)%. It was concluded that: (1) the increase in D(m) made it unlikely that the fall in DLCO was due to interstitial oedema and injury to the blood gas barrier; (2) on the other hand, the reduction in DLCO following exercise was consistent with a redistribution of blood away from the lungs; and (3) the trend for D(m) and V(c) to reciprocate one another indicates a situation in which a fall in V(c) nevertheless promotes gas transfer at the respiratory membrane. It is suggested that this effect is brought about by the reorientation of red blood cells within the pulmonary capillaries following exercise.