ABSTRACT
The relationship between adiposity and respiratory function is poorly understood. Most studies investigating this have used indirect measures of body fat and few have assessed how changes in adiposity influence lung function.Body fat measured by bio-electrical impedance analysis, body mass index, waist circumference, spirometry, body plethysmography and transfer factor were measured at ages 32 and 38â years in 361 non-smoking, non-asthmatic participants from a population-based birth cohort.Higher percentage body fat was associated with lower spirometric and plethysmographic lung volumes, but not with airflow obstruction, or transfer factor at 32â years. Changes in adiposity between ages 32 and 38â years were inversely associated with changes in lung volumes. These associations were generally stronger in men than women, but an association between increasing adiposity and lower airway function (forced expiratory volume in 1â s/forced vital capacity) was only found in women. Similar associations were found for body mass index and waist circumference.Higher percentage body fat is associated with lower lung volumes. Direct and indirect measures of adiposity had similar associations with lung function. Adiposity had a greater effect on lung volumes in men than women but was associated with airway function only in women. There was little evidence that adiposity influenced transfer factor.
Subject(s)
Adipose Tissue/physiopathology , Adiposity , Forced Expiratory Volume , Respiration , Adult , Anthropometry , Asthma/diagnosis , Body Mass Index , Cohort Studies , Cross-Sectional Studies , Electric Impedance , Female , Follow-Up Studies , Humans , Male , New Zealand , Plethysmography , Respiratory Function Tests , Smoking , Spirometry , Vital Capacity , Waist CircumferenceABSTRACT
INTRODUCTION: Interstitial lung abnormalities (ILA) are relatively common incidental findings in participants undergoing low-dose CT screening for lung cancer. Some ILA are transient and inconsequential, but others represent interstitial lung disease (ILD). Lung cancer screening therefore offers the opportunity of earlier diagnosis and treatment of ILD for some screening participants. METHODS: The prevalence of ILA in participants in the baseline screening round of the Yorkshire Lung Screening Trial is reported, along with the proportion referred to a regional ILD service, eventual diagnoses, outcomes and treatments. RESULTS: Of 6650 participants undergoing screening, ILA were reported in 169 (2.5%) participants. Following review in a screening review meeting, 56 participants were referred to the ILD service for further evaluation (0.8% of all screening participants). 2 participants declined referral, 1 is currently awaiting review and the remaining 53 were confirmed as having ILD. Eventual diagnoses were idiopathic pulmonary fibrosis (n=14), respiratory bronchiolitis ILD (n=4), chronic hypersensitivity pneumonitis (n=2), connective tissue disease/rheumatoid arthritis-related ILD (n=4), asbestosis (n=1), idiopathic non-specific interstitial pneumonia (n=1), sarcoidosis (n=1) and pleuroparenchymal fibroelastosis (n=1). Twenty five patients had unclassifiable idiopathic interstitial pneumonia. Overall, 10 people received pharmacotherapy (7 antifibrotics and 3 prednisolone) representing 18% of those referred to the ILD service and 0.15% of those undergoing screening. 32 people remain under surveillance in the ILD service, some of whom may require treatment in future. DISCUSSION: Lung cancer screening detects clinically significant cases of ILD allowing early commencement of disease-modifying treatment in a proportion of participants. This is the largest screening cohort to report eventual diagnoses and treatments and provides an estimate of the level of clinical activity to be expected by ILD services as lung cancer screening is implemented. Further research is needed to clarify the optimal management of screen-detected ILD. TRIAL REGISTRATION NUMBER: ISRCTN42704678.
Subject(s)
Alveolitis, Extrinsic Allergic , Idiopathic Pulmonary Fibrosis , Lung Neoplasms , Humans , Early Detection of Cancer , Lung , Lung Neoplasms/diagnosis , Lung Neoplasms/diagnostic imagingABSTRACT
RATIONALE: Symptoms and respiratory function tests may be difficult to assess and interpret in obese patients with asthma, particularly if the asthma is severe. It is unclear whether the dynamic changes that occur during bronchoconstriction differ between obese versus nonobese patients with asthma. OBJECTIVES: To explore whether the changes in airway caliber and lung volumes that occur with acute bronchoconstriction are different in obese and nonobese patients with asthma and whether any differences contribute to the quality and intensity of symptoms. METHODS: Thirty female patients with asthma were studied. Spirometry, lung volume measurements, and dyspnea scores were obtained before and immediately after bronchoconstriction induced by methacholine, aiming to provoke a reduction in FEV1 of 30%. MEASUREMENTS AND MAIN RESULTS: Body mass index was independently associated with changes in lung volume after adjustment for baseline airway caliber and hyperresponsiveness. Increases in functional residual capacity and decreases in inspiratory capacity were significantly greater in obese participants (P < 0.001 and P = 0.003, respectively). CONCLUSIONS: Changes in respiratory function, notably dynamic hyperinflation, are greater in obese individuals with bronchoconstriction. This may potentially alter the perception and assessment of asthma severity in obese patients with asthma.
Subject(s)
Asthma/physiopathology , Bronchoconstriction/physiology , Obesity/complications , Pulmonary Emphysema/physiopathology , Adult , Asthma/complications , Body Mass Index , Female , Forced Expiratory Volume/physiology , Humans , Middle Aged , Obesity/physiopathology , Prognosis , Pulmonary Emphysema/etiology , Severity of Illness IndexABSTRACT
RATIONALE: Both obesity and asthma are common conditions, and both are characterized by the presence of inflammation. Animal studies suggest that the development of airway hyperresponsiveness with antigen challenge is exaggerated with obesity. However, clear evidence for either an additive or a synergistic pathologic interaction between obesity and asthma is lacking in humans. OBJECTIVES: To identify whether an interaction between systemic and local inflammation occurs in obese subjects with asthma in a controlled observational study. METHODS: We studied 79 women: obese patients with asthma (n = 20), normal-weight patients with asthma (n = 19), obese patients without asthma (n = 20), and normal-weight patients without asthma (n = 20). After corticosteroid withdrawal, between-group differences in spirometric values, lung volumes, exhaled nitric oxide, induced sputum cell counts, and biomarkers of inflammation in sputum supernatant and blood were measured, and interactions explored. MEASUREMENTS AND MAIN RESULTS: Markers of systemic inflammation were increased with obesity, and Th2 cytokines were increased with asthma, but no important interactions were identified. Obesity adversely affected lung function with increases in functional residual capacity and residual volume in obese but not normal-weight patients with asthma, with a significant obesity by asthma interaction. CONCLUSIONS: The link between obesity and asthma is unlikely to be explained by enhancement of the "classical" forms of airway inflammation resulting from the systemic inflammatory effects of obesity itself. Other mechanisms, possibly related to innate immunity, may explain the relationship between obesity and asthma.
Subject(s)
Asthma/physiopathology , Obesity/physiopathology , Adult , Asthma/epidemiology , Biomarkers/metabolism , Case-Control Studies , Comorbidity , Cytokines/blood , Female , Humans , Inflammation , Middle Aged , New Zealand/epidemiology , Obesity/epidemiologyABSTRACT
BACKGROUND AND OBJECTIVE: In New Zealand, lung cancer is the commonest cause of cancer death in men and is projected to become the commonest cause in women by 2011. Rates of survival from lung cancer are among the lowest in the developed world. There are discrepancies between health outcomes according to patients' ethnicity and socioeconomic status in many diseases. This study determined the incidence of lung cancer, duration of survival and treatment according to ethnicity and socioeconomic status in a health district in New Zealand. METHODS: A retrospective review was conducted of patients diagnosed with lung cancer in the period 1997-1999. Data were collected on ethnicity, gender, socioeconomic status and cancer stage at diagnosis. Treatment and 5-year survival were recorded. RESULTS: A total of 102 eligible patients were identified. Maori had 3-4 times the incidence of lung cancer compared with New Zealand Europeans and patients from the more socially deprived areas had nearly double the incidence. More than one half of the patients presented with widespread disease, with a disproportionate number of these being from Maori and socially deprived groups. Only 9.8% of cases were considered to be potentially curative. Survival at 1 year was 24% and at 5 years, 6%. No Maori were alive at 5 years. CONCLUSIONS: Lung cancer disproportionately affects Maori and socially disadvantaged persons in New Zealand society. Survival at 5 years is low, especially in these groups.
Subject(s)
Lung Neoplasms/epidemiology , Adult , Aged , Aged, 80 and over , Female , Humans , Incidence , Lung Neoplasms/ethnology , Male , Middle Aged , New Zealand/epidemiology , Retrospective Studies , Social Class , White People/statistics & numerical dataABSTRACT
BACKGROUND: Obesity is thought to increase the risk of asthma, especially in women. It has been proposed that this association could be due to the immune-modulating effect of adipokines secreted by adipose tissue. OBJECTIVE: To investigate whether aspects of the asthma phenotype are associated with higher levels of the proinflammatory adipokine leptin and lower levels of the anti-inflammatory adipokine adiponectin in a cross-sectional analysis of a group of young adults. METHODS: Associations between leptin and adiponectin and a diagnosis of asthma, symptoms of wheeze, bronchodilator response, airflow obstruction, and exhaled nitric oxide were evaluated by logistic or linear regression in a population-based birth cohort of approximately 1,000 men and women aged 32 years. Further analyses adjusted for smoking and body fat. RESULTS: There were no significant associations between leptin and any of the markers of the asthma phenotype in either men or women. In men, higher levels of adiponectin were associated with lower levels of exhaled nitric oxide but an increased risk of bronchodilator responsiveness. The inverse association with exhaled nitric oxide remained significant after adjustment for body fat, but the association with bronchodilator responsiveness did not. Adiponectin levels were not associated with any markers of asthma in women. CONCLUSIONS: The inverse association between adiponectin and exhaled nitric oxide in men warrants further investigation. However, the findings indicate that levels of leptin and adiponectin are unlikely to mediate the previously observed association between obesity and asthma.
Subject(s)
Asthma/blood , Leptin/blood , Adiponectin/blood , Adult , Asthma/complications , Asthma/epidemiology , Asthma/physiopathology , Breath Tests , Bronchial Provocation Tests , Cohort Studies , Female , Forced Expiratory Volume/physiology , Humans , Male , New Zealand/epidemiology , Nitric Oxide/metabolism , Obesity/blood , Obesity/complications , Respiratory Sounds/diagnosis , Sex Characteristics , Smoking/blood , Vital Capacity/physiologyABSTRACT
BACKGROUND: Asthma is an inflammatory condition of the airways, and there is some evidence to suggest that it is associated with a systemic inflammatory response, as measured by C-reactive protein (CRP) and fibrinogen. Exhaled nitric oxide is a noninvasive measure of asthmatic airway inflammation. OBJECTIVE: To determine if there is an association between exhaled nitric oxide and these systemic inflammatory markers. METHODS: The Dunedin Multidisciplinary Health and Development Study is a birth cohort of approximately 1,000 individuals born between April 1, 1972, and March 31, 1973. At the age of 32 years, study members were assessed for diagnosis of asthma, atopy by skin prick testing, smoking, body mass index, exhaled nitric oxide, high-sensitivity serum CRP, and plasma fibrinogen level. RESULTS: There was no significant association between exhaled nitric oxide and CRP (P = .99). There was a trend to an inverse association between exhaled nitric oxide and fibrinogen (P = .049), but this was not significant after adjusting for smoking and use of corticosteroids or after further adjustment for body mass index and atopy (P = .71). CONCLUSION: In this population-based sample of young adults, there was no association between airway inflammation, as measured by exhaled nitric oxide, and systemic inflammation, as measured by either CRP or fibrinogen.
Subject(s)
Asthma/metabolism , C-Reactive Protein/analysis , Fibrinogen/analysis , Nitric Oxide/analysis , Adult , Asthma/immunology , Asthma/pathology , Cohort Studies , Female , Humans , Linear Models , Longitudinal Studies , MaleABSTRACT
BACKGROUND: Asthma is an inflammatory condition of the airways, and there is some evidence to suggest that it is associated with a systemic inflammatory response, as measured by C-reactive protein (CRP) and fibrinogen. Exhaled nitric oxide is a noninvasive measure of asthmatic airway inflammation. OBJECTIVE: To determine if there is an association between exhaled nitric oxide and these systemic inflammatory markers. METHODS: The Dunedin Multidisciplinary Health and Development Study is a birth cohort of approximately 1,000 individuals born between April 1, 1972, and March 31, 1973. At the age of 32 years, study members were assessed for diagnosis of asthma, atopy by skin prick testing, smoking, body mass index, exhaled nitric oxide, high-sensitivity serum CRP, and plasma fibrinogen level. RESULTS: There was no significant association between exhaled nitric oxide and CRP (P = .99). There was a trend to an inverse association between exhaled nitric oxide and fibrinogen (P = .049), but this was not significant after adjusting for smoking and use of corticosteroids or after further adjustment for body mass index and atopy (P = .71). CONCLUSION: In this population-based sample of young adults, there was no association between airway inflammation, as measured by exhaled nitric oxide, and systemic inflammation, as measured by either CRP or fibrinogen.