10 results found
Allinson JP, Chaturvedi N, Wong A, et al., 2023, Early childhood lower respiratory tract infection and premature adult death from respiratory disease in Great Britain: a national birth cohort study., Lancet
BACKGROUND: Lower respiratory tract infections (LRTIs) in early childhood are known to influence lung development and lifelong lung health, but their link to premature adult death from respiratory disease is unclear. We aimed to estimate the association between early childhood LRTI and the risk and burden of premature adult mortality from respiratory disease. METHODS: This longitudinal observational cohort study used data collected prospectively by the Medical Research Council National Survey of Health and Development in a nationally representative cohort recruited at birth in March, 1946, in England, Scotland, and Wales. We evaluated the association between LRTI during early childhood (age <2 years) and death from respiratory disease from age 26 through 73 years. Early childhood LRTI occurrence was reported by parents or guardians. Cause and date of death were obtained from the National Health Service Central Register. Hazard ratios (HRs) and population attributable risk associated with early childhood LRTI were estimated using competing risks Cox proportional hazards models, adjusted for childhood socioeconomic position, childhood home overcrowding, birthweight, sex, and smoking at age 20-25 years. We compared mortality within the cohort studied with national mortality patterns and estimated corresponding excess deaths occurring nationally during the study period. FINDINGS: 5362 participants were enrolled in March, 1946, and 4032 (75%) continued participating in the study at age 20-25 years. 443 participants with incomplete data on early childhood (368 [9%] of 4032), smoking (57 [1%]), or mortality (18 [<1%]) were excluded. 3589 participants aged 26 years (1840 [51%] male and 1749 [49%] female) were included in the survival analyses from 1972 onwards. The maximum follow-up time was 47·9 years. Among 3589 participants, 913 (25%) who had an LRTI during early childhood were at greater risk of dying from respiratory disease by age 73 years than those with
Allinson JP, Patel PH, Donaldson GC, 2022, Obesity, Insulin Resistance, and Asthma, AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, Vol: 206, Pages: 1057-1058, ISSN: 1073-449X
- Author Web Link
- Citations: 1
Allinson JP, Afzal S, Colak Y, et al., 2022, Changes in lung function in European adults born between 1884 and 1996 and implications for the diagnosis of lung disease: a cross-sectional analysis of ten population-based studies, LANCET RESPIRATORY MEDICINE, Vol: 10, Pages: 83-94, ISSN: 2213-2600
- Author Web Link
- Citations: 5
Allinson JP, Hardy R, Donaldson GC, et al., 2018, Childhood exposures, asthma, smoking, interactions and the catch-up hypothesis, Annals of the American Thoracic Society, Vol: 15, Pages: 1241-1242, ISSN: 2329-6933
Allinson JP, Wedzicha JA, 2017, Update in Chronic Obstructive Pulmonary Disease 2016, AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, Vol: 196, Pages: 414-424, ISSN: 1073-449X
Chronic obstructive pulmonary disease (COPD) describes a predominantly smoking-induced small airway and/or emphysematous disease associated with airflow limitation. Considered progressive, irreversible, and responsible for substantial morbidity and mortality worldwide, COPD remains the subject of vigorous study, and advances made during 2016 are already reflected in the Global Initiative for Chronic Obstructive Lung Disease (GOLD) 2017 guidelines (1). Researchers continue to explore strategies, pharmacological or otherwise, to improve the lives of those who have developed this condition; and it is hoped, by improving phenotyping of this heterogeneous disease, that we might ultimately deliver personalized medicine. Debate remains over how to identify undiagnosed COPD in individuals who would benefit from intervention, while avoiding overdiagnosis, and these controversies perhaps highlight shortcomings in accepted disease definitions. Not unrelatedly, renewed interest has emerged in explaining why some individuals develop COPD and identifying the formative stages of COPD development.
Allinson JP, Hardy R, Donaldson GC, et al., 2017, Combined impact of smoking and early life exposures on adult lung function trajectories, American Journal of Respiratory and Critical Care Medicine, Vol: 195, Pages: 1021-1030, ISSN: 1073-449X
BACKGROUND: Both adverse early life exposures and adult smoking can negatively influence adult lung function trajectory but few studies consider how the impact of early life exposures may be modified by subsequent smoking. METHODS: The Medical Research Council National Survey of Health and Development is a nationally representative cohort, initially of 5362 individuals, followed since enrolment at birth in March 1946. Using data collected prospectively across life and multilevel modelling we investigated how the relationships between early life exposures (infant lower respiratory infection, manual social class, home overcrowding and pollution exposure) and FEV1 and FVC trajectories between ages 43 and 60-64 were influenced by smoking behaviour. RESULTS: Among 2172 individuals, there were synergistic interactions of smoking with infant respiratory infection (P=0.04) and early life home overcrowding (P=0.009), for FEV1 at 43 years. Within smoker-stratified models, there were FEV1 deficits among ever-smokers associated with infant lower respiratory infection (-108.2ml; P=0.001) and home overcrowding (-89.2ml; P=0.002) which were not evident among never-smokers (-15.9ml; P=0.69 and -13.7ml; P=0.70 respectively). FVC modelling, including 1960 individuals, yielded similar results. FEV1 decline was greater in smokers (P<0.001) but there was no effect of any early life exposure on FEV1 decline. Neither smoking nor early life exposures were associated with FVC decline. CONCLUSIONS: Besides accelerating adult FEV1 decline, cigarette smoking also modifies how early life exposures impact upon both mid-life FEV1 and FVC. These findings are consistent with smoking impairing pulmonary development during adolescence or early adulthood thereby preventing catch-up from earlier acquired deficits.
Brill S, Law M, El-Emir E, et al., 2015, Effects of different antibiotic classes on airwaybacteria in stable COPD using culture and molecularQ1 techniques: a randomised controlled trial, Thorax, Vol: 70, Pages: 930-938, ISSN: 1468-3296
BackgroundLong term antibiotic therapy is used to prevent exacerbations of chronic obstructive pulmonary disease (COPD) but there is uncertainty over whether this reduces airway bacteria. The optimum antibiotic choice remains unknown. We conducted an exploratory trial in stable patients with COPD comparing three antibiotic regimens against placebo. MethodsThis was a single-centre, single-blind, randomised placebo-controlled trial (clinicaltrials.gov number NCT01398072). Patients ≥45 years with COPD, FEV1<80% predicted and chronic productive cough were randomised to receive either moxifloxacin 400mg daily for 5 days/4 weeks, doxycycline 100mg/day, azithromycin 250mg 3x/week or one placebo tablet daily for 13 weeks. The primary outcome was the change in total cultured bacterial load in sputum from baseline; secondary outcomes included bacterial load by 16S qPCR, sputum inflammation and antibiotic resistance. Results99 patients were randomised; 86 completed follow-up, were able to expectorate sputum and were analysed. After adjustment, there was a mean reduction in bacterial load of 0.42 log10 cfu/ml (95% CI -0.08, 0.91, p=0.10) with moxifloxacin, 0.11 (-0.33, 0.55, p=0.62) with doxycycline, and 0.08 (-0.38, 0.54, p=0.73) with azithromycin from placebo, respectively. There were also no significant changes in bacterial load measured by 16S qPCR or in airway inflammation. More treatment-related adverse events occurred with moxifloxacin. Of note, mean inhibitory concentrations of cultured isolates increased by at least 3 times over placebo in all treatment arms.ConclusionsTotal airway bacterial load did not decrease significantly after three months of antibiotic therapy. Large increases in antibiotic resistance were seen in all treatment groups and this has important implications for future studies.
Donaldson GC, Law M, Kowlessar B, et al., 2015, Impact of prolonged exacerbation recovery in chronic obstructive pulmonary disease, American Journal of Respiratory and Critical Care Medicine, Vol: 192, Pages: 943-950, ISSN: 1535-4970
INTRODUCTION: COPD exacerbations are important and heterogeneous events, but the consequences of prolonged exacerbation recovery are unknown. METHODS: A cohort of 384 COPD patients (FEV1 % predicted 45.8 (SD 16.6) and a median exacerbation rate of 2.13 per year (IQR 1.0-3.2)) were followed for 1039 days (IQR 660-1814) between October 1995 and January 2013. Patients recorded daily worsening of respiratory symptoms and peak expiratory flow (PEF), and when stable underwent 3-monthly spirometry, and completed the St. George's Respiratory Questionnaire (SGRQ) annually. Exacerbations were diagnosed as two consecutive days with one major symptom plus another respiratory symptom. Exacerbation duration was defined as the time from onset to the day preceding two consecutive symptom-free and recovery in PEF as return to pre-exacerbation levels. RESULTS: 351 patients had 1 or more exacerbations. Patients with a longer symptom duration (mean 14.5 days) had a worse SGRQ total score (0.2 units per 1 day; p=0.040). A longer symptomatic duration was associated with a shorter interval between exacerbation recovery and onset of the next exacerbation (Hazard Ratio=1.004; p=0.013). For 257 (7.3%) exacerbations, PEF did not recover within 99 days. These exacerbations were associated with symptoms of a viral infection (cold and sore throat). Patients with these non-recovered exacerbations showed a 10.8 ml/year (p<0.001) faster decline in FEV1. CONCLUSION: Prolonged exacerbation symptomatic duration is associated with poorer health status and a greater risk of a new event. Exacerbations where lung function does not recover are associated with symptoms of viral infections and accelerated decline in FEV1.
Alahmari AD, Mackay AJ, Patel ARC, et al., 2015, Influence of weather and atmospheric pollution on physical activity in patients with COPD, Respiratory Research, Vol: 16, ISSN: 1465-993X
RationaleInformation concerning how climate and atmospheric pollutants affects physical activity in COPD patients is lacking and might be valuable in determining when physical activity should be encouraged.MethodsSeventy-three stable COPD patients recorded on daily diary cards worsening of respiratory symptoms, peak expiratory flow rate, hours spent outside the home and the number of steps taken per day. Pedometry data was recorded on 16,478 days, an average of 267 days per patient (range 29-658). Daily data for atmospheric PM 10 and ozone (O 3 ) were obtained for Bloomsbury Square, Central London from the Air Quality Information Archive databases. Daily weather data were obtained for London Heathrow from the British Atmospheric Data Archive.ResultsColder weather below 22.5 °C, reduced daily step count by 43.3 steps day per°C (95 % CI 2.14 to 84.4; p = 0.039) and activity was lower on rainy than dry days (p = 0.002) and on overcast compared to sunny days (p < 0.001). Daily step count was 434 steps per day lower on Sunday than Saturday (p < 0.001) and 353 steps per day lower on Saturday than Friday (p < 0.001). After allowance for these effects, higher O 3 levels decreased activity during the whole week (-8 steps/ug/m3; p = 0.005) and at weekends (-7.8 steps/ug/m3; p = 0.032). Whilst, during the week PM 10 reduced activity (p = 0.018) but not during the weekend.ConclusionsInactivity of COPD patients is greatest on cold, wet and overcast days and at the weekends. This study also provides evidence of an independent effect of atmospheric pollution at high levels.Keywords: COPD; Atmospheric pollution; Weather; Daily step-count; Physical activity; Daily monitoring
Huerta A, Donaldson G, Singh R, et al., 2015, Upper respiratory symptoms worsen over time and relate to clinical phenotype in COPD., Annals of the American Thoracic Society, Vol: 12, Pages: 997-1004, ISSN: 2329-6933
RATIONALE: How nasal symptoms in patients with COPD change over time and resolve during natural occurring exacerbation have never been described. METHODS: Patients in the London COPD cohort were asked about the presence of nasal symptoms (nasal discharge, sneezing, post-nasal drip (PND), blocked nose and anosmia) over an 8-year period (2005-2013) every three months at routine clinic visits at stable state and daily during exacerbations with the use of diary cards. Data was prospectively collected and in a subgroup of patients COPD Assessment Test (CAT) and human rhinovirus (HRV) identification by PCR was available. Patients were also defined as infrequent/frequent exacerbators (<2 or ≥2 exacerbations/year). RESULTS: On 4368 visits, 209 patients with COPD were asked about their nasal symptoms. On 2033 visits, when the patients were stable, the odds ratio (OR) for nasal discharge increased by 1.32% per year (95% CI 1.19-1.45; p<0.001); sneezing 1.16% (1.05-1.29; p=0.005); PND 1.18% (1.03-1.36; p=0.016) and anosmia 1.19% (1.03-1.37; p=0.015). At exacerbation, nasal discharge was present for 7-daysand blocked nose, sneezing and PND increased for just 3 days; anosmia did not change. Nasal discharge was more likely in frequent exacerbators; OR 1.96 (1.17-3.28; p=0.011) and when present, CAT scores were higher by 1.06 units (0.32-1.80; p=0.005) when stable and 1.30 units (0.05 to 2.57; p=0.042) at exacerbation. CONCLUSION: Upper airway symptoms increase over time in COPD patients and are related to the frequent exacerbator phenotype. These longitudinal changes may be due to increasing airway inflammation or the disease progression.
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