Background-We have previously reported the use of a hospital based respiratory nurse service (Acute Respiratory Assessment Service, ARAS) to support home treatment of patients with exacerbations of chronic obstructive pulmonary disease (COPD). A controlled trial was undertaken to compare early discharge with home treatment supported by respiratory nurses with conventional hospital management of patients admitted with exacerbations of COPD. Methods-Patients with COPD admitted as emergencies were identified the next working day. They were eligible for inclusion in the study if the diVerential diagnosis included an exacerbation of COPD, but were excluded if other medical conditions or acidotic respiratory failure required inpatient investigation or management. Of 360 patients reviewed, 209 were being assessed for other active medical problems and were excluded, 33 potential participants were already involved in research studies and so were ineligible, and 37 did not wish to participate in the study. Eighty one patients were randomised to receive conventional inpatient care (n=40) or to planned early discharge the next working day (n=41). Those discharged early continued treatment at home under the supervision of specialist respiratory nurses. Outcome measures were readmission, additional hospital days, and deaths within 60 days of initial admission. Process measures included number of visits, duration of follow up by the respiratory nurse, and additional treatment provided to support early discharge. Results-On an intention to treat basis, a policy of early discharge reduced inpatient stay from a mean of 6.1 (range 1-13) days with conventional management to 3.2 (1-16) days with an early discharge policy. Twelve patients (30% conventional management, 29.3% early discharge) were readmitted in each group giving a mean diVerence in readmission of 0.7% (95% CI of the diVerence -19.2 to 20.6). In the conventional management group readmitted patients spent a mean of 8.75 additional days in hospital compared with 7.83 days in the early discharge group, giving a mean diVerence of 0.92 days (95% CI of the diVerence -6.5 to 8.3). There were two deaths (5%) in the conventional management group and one (2.4%) in the early discharge group, a mean diVerence of 2.6% (95% CI of the diVerence -5.7 to 10.8). Conclusions-Patients with acute exacerbations of COPD uncomplicated by acidotic respiratory failure or other medical problems can be discharged home earlier than is current practice with support by visiting respiratory nurses. No diVerence was found in the subsequent need for readmission. (Thorax 2000;55:902-906)

The value of an inflammation-based prognostic score (Glasgow Prognostic score, GPS) was compared with performance status (ECOG-ps) in a longitudinal study of patients (n ¼ 101) with inoperable non-small-cell lung cancer (NSCLC). At diagnosis, stratified for treatment, only the GPS (HR 2.32, 95% CI 1.52 -3.54, Po0.001) was a significant predictor of survival. In contrast, neither the GPS nor ECOG-ps measured at 3 -6 months follow-up were significant predictors of residual survival. This study confirms the prognostic value of the GPS, at diagnosis, in patients with inoperable NSCLC. However, the role of the GPS and ECOG-ps during follow-up has not been established.

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The renin-angiotensin system is activated in acute severe asthma, although not in all asthmatics [1,2]. The mechanism of this activation is unclear, but recent evidence has shown elevation of renin and angiotensin II in response to nebulized and intravenous salbutamol [3,4]. A wide variation in plasma β 2 -agonist levels has been found in acute asthmatics in previous studies [5], and could, therefore, account for the variation in renin and angiotensin II levels.However, the degree of activation of the renin-angiotensin system following administration of β 2 -agonists is less than that seen in acute asthma, suggesting an additional mechanism. The generation of angiotensin II via an "alternative" pathway, through the action of inflammatory proteases [6] either circulating or locally within the airways, could occur in addition to the "classical" activation of the renin-angiotensin system. Endogenous catecholamines released during an acute attack of asthma [7] could stimulate adrenoceptors on juxtaglomerular cells in the kidney [8] resulting in renin release, and may act synergistically with systemically absorbed albuterol.Serum angiotensin-converting enzyme (ACE) levels vary between individuals and correlate with a genetic polymorphism of the ACE gene [9]. Homozygotes for the deletion polymorphism have a higher ACE activity [10], and, therefore, the capacity to produce greater levels of angiotensin II in response to activation of the renin-angiotensin system. Thus, serum ACE activity could contribute to the variation seen in angiotensin II levels in acute asth-ma.We hypothesize that activation of the renin-angiotensin system in acute severe asthma is partly due to high levels of circulating β 2 -agonists in some asthmatics, and that other factors, as suggested above, may also contribute, possibly with a synergistic effect. Thus, we have examined the associations between renin, angiotensin II and multiple factors during acute attacks of asthma, with particular emphasis on the mechanisms outlined above. Materials and methods PatientsForty adult asthmatic patients (26 females and 14 males; mean (SD) age 45 (17) yrs) were recruited into the study. All presented nonconsecutively at the accident and emergency department, with acute exacerbations of asthma unresponsive to their regular medication and requiring hospital admission for treatment. Admission parameters were measured with peak expiratory flow rate (PEFR) 35 (18) % predicted, oxygen saturation 94 (4) %, cardiac frequency 108 (16) beats·min -1 , systolic blood pressure 139.5Investigations on the renin-angiotensin system in acute severe asthma. S.G. Ramsay, K.D. Dagg, I.C. McKay, B.J. Lipworth, C. McSharry, N.C. Thomson. ERS Journals Ltd 1997. ABSTRACT: The renin-angiotensin system is activated in acute severe asthma. The precise mechanism of activation is at present unknown, but may involve, β 2 -agonists, catecholamines or proteases released in airway inflammation.This study aims to identify potential factors involved in the activation of the reninangiotensin ...