Showing papers by "Martin J. Connolly published in 2006"
TL;DR: Inpatient and 90 day mortality is approximately three times higher in very elderly patients with a COPD exacerbation than in younger patients, and recommended standards of care should be applied equally to elderly Patients with an exacerbation of COPD.
Abstract: Background: Exacerbations of chronic obstructive pulmonary disease (COPD) have a high rate of mortality which gets worse with advancing age. It is unknown whether this is due to age related deficiencies in process of care. A study was undertaken in patients with COPD exacerbations admitted to UK hospitals to assess whether there were age related differences in the process of care that might affect outcome, and whether different models of care affected process and outcome. Methods: 247 hospital units audited activity and outcomes (inpatient death, death within 90 days, length of stay (LOS), readmission within 90 days) for 40 consecutive COPD exacerbation admissions in autumn 2003. Logistic regression methods were used to assess relationships between process and outcome at p Results: 7514 patients (36% aged ⩾75 years) were included. Patients aged ⩾75 years were less likely to have blood gases documented, to have FEV 1 recorded, or to be given systemic corticosteroids. Those admitted under care of the elderly (CoE) physicians were less likely to enter early discharge schemes or to receive non-invasive ventilation when acidotic. Overall inpatient and 90 day mortality was 7.4% and 15.3%, respectively. Inpatient and 90 day adjusted odds mortality rates for those aged ⩾85 years (versus ⩽65 years) were 3.25 and 2.54, respectively. Mortality was unaffected by admitting physician (CoE v general v respiratory). Age predicted LOS but not readmission. Age related deficiencies in process of care did not predict inpatient or 90 day mortality, readmission, or LOS. Conclusions: Management of COPD exacerbations varies with age in UK hospitals. Inpatient and 90 day mortality is approximately three times higher in very elderly patients with a COPD exacerbation than in younger patients. Age related deficiencies in the process of care were not associated with mortality, but it is likely that they represent poorer quality of care and patient experience. Recommended standards of care should be applied equally to elderly patients with an exacerbation of COPD.
81 citations
TL;DR: There is little data regarding aetiological mechanisms leading to depression in COPD, however, disability and handicap are powerful predictors of depression and are likely to be the major determinants in COPd.
Abstract: Chronic obstructive pulmonary disease (COPD) is a major cause of morbidity, disability and mortality in old age [1]. It has been predicted that COPD will be the world’s fifthranking cause of disability by 2020 [2]. Co-morbid psychological impairments (depression and anxiety) are common in COPD and are often associated with increased disability and morbidity. They also impair quality of life in COPD and are often not fully explored in the clinical management of COPD patients. In the UK, the National Institute of Clinical Excellence COPD Guidelines [1] estimates the prevalence of depression in COPD to be 40% (36–44%) and suggests that anxiety symptoms may have a prevalence of 36% (31–41%) [3]. With such a high prevalence, why is depression so often undetected and untreated? First, recognition of co-morbid depression is difficult, because some of the physical symptoms of COPD may mimic the core symptoms of depression, for example, poor sleeping pattern, anorexia and loss of enjoyment due to breathlessness. Second, screening tools for depression and anxiety symptoms are not routinely employed by health care professionals caring for COPD patients. Third, patients often deny that they are suffering from anxiety and depression, perhaps because of perceptions of the stigma attached to these problems [4]. Unrecognised and untreated depression has major implications in compliance with medical treatment and may increase the frequency of consultation with health services, for example, in primary care [5]. In COPD, it increases the likelihood of hospital admission in those most severely disabled [4]. Anxiety is common in patients with COPD. It is often associated with clinical depression, and a study from our centre identified that 37% of depressed COPD patients had clinical anxiety compared with 5% of non-depressed COPD patients [4]. COPD is among a number of medical disorders associated with a high rate of depression. The wide range of conditions suggest that the aetiology is multifactorial. Suggested mechanisms include cerebrovascular and microangiopathy (heart disease, diabetes), localised disruption to frontostriatal brain circuits (stroke), social adversity (diabetes) and neurodegenerative brain disease (Alzheimer’s disease, idiopathic Parkinson’s disease), pain (arthritis, cancer) and oncological therapy (cancer) [6]. Furthermore, there is robust evidence that depression worsens the outcome and mortality of many of these conditions [6], and this has been demonstrated for COPD too [7]. There is little data regarding aetiological mechanisms leading to depression in COPD. However, disability and handicap are powerful predictors of depression and are likely to be the major determinants in COPD [8]. Whether biological mechanisms play a significant role has not been clarified.
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TL;DR: The Dutch Hypothesis suggests that asthma and chronic obstructive pulmonary disease may share some pathogenic mechanisms and it is hypothesized that β2 adrenoceptor polymorphisms would have similar disease modifying roles in patients with COPD.
Abstract: Aims: The Dutch Hypothesis suggests that asthma and chronic obstructive pulmonary disease may share some pathogenic mechanisms. There is considerable evidence that polymorphisms of the β2 adrenoceptor have disease-modifying roles in juvenile onset asthma, determining severity and response to β agonists, but not determining disease susceptibility. There is evidence from family and twin studies to suggest that chronic obstructive pulmonary disease (COPD) also has a significant genetic component. We therefore hypothesized that β2 adrenoceptor polymorphisms would have similar disease modifying roles in patients with COPD.
Methods: One hundred and ninety-five COPD subjects and 142 matched controls were recruited. All had detailed clinical phenotyping. Subjects were genotyped for the Agr Gly polymorphism at codon 16, the Gln Glu polymorphism at codon 27, and the SNPC/T-47 promoter polymorphism.
Results: In patients with COPD (mean age 67, 57% male), individuals with the homozygous Gly16/homozygous Glu27/homozygous SNP −47*C genotype had significantly worse lung function as measured by forced expiratory volume 1, expressed as a percentage of its predicted value (39.2 compared with 45.8, P = 0.004), and for forced vital capacity (FVC) percent predicted (77.2 compared with 70.4, P = 0.02). The polymorphisms had no effect on disease susceptibility.
Conclusion: The Arg16, Gln27, SNPC/T-47 β2 adrenoceptor polymorphisms may have disease modifying roles in patients with COPD.