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1.
COPD ; 16(5-6): 321-329, 2019 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-31709837

RESUMO

In individuals with chronic obstructive pulmonary disease (COPD), the presence of comorbidities is associated with increased mortality risk. We wanted to study the association between bone mineral density (BMD) and mortality among individuals with COPD in a population-based cohort study. Participants were recruited from the second (1995-1997) and third (2006-2008) surveys of the HUNT Study and followed until February 2019. Hip and forearm BMD were included as continuous T-scores or categorized according to WHO criteria (normal, osteopenia, and osteoporosis). Hazard ratios with 95% confidence intervals were estimated by multivariable Cox regression models. In total, 2076 and 3239 participants were identified as having COPD by FEV1/FVC below lower limit of normal (LLN) or <0.70, respectively, according to Global Lung Initiative (GLI) and Global Initiative for Chronic Obstructive Lung Disease (GOLD). The prevalence of osteoporosis was 15.7% vs. 16.6% in the GLI-COPD vs. GOLD-COPD cohorts. Mean follow-up was 12.7 and 11.9 years. Lower T-scores were associated with a 5% (95% confidence interval (CI) 1.01-1.09) increased mortality in the GLI-COPD and GOLD-COPD cohorts, respectively. However, the presence of osteoporosis (T < -2.5), compared to normal BMD, was not associated with mortality in neither GLI-COPD (HR 1.13, 95% CI 0.91-1.41) nor GOLD-COPD cohorts (HR 1.22, 95% CI 0.99-1.51). Thus, a small positive association was found between decreasing BMD T-score and mortality in both GLI-COPD and GOLD-COPD. However, osteoporosis as defined by WHO was not associated with mortality, probably due to loss of power upon categorization.

3.
Thorax ; 2019 Oct 14.
Artigo em Inglês | MEDLINE | ID: mdl-31611343

RESUMO

BACKGROUND: We aimed to investigate the potential causal associations of adiposity with asthma overall, asthma by atopic status or by levels of symptom control in a large adult population and stratified by sex. We also investigated the potential for reverse causation between asthma and risk of adiposity. METHODS: We performed a bidirectional one-sample Mendelian randomisation (MR) study using the Norwegian Nord-Trøndelag Health Study population including 56 105 adults. 73 and 47 genetic variants were included as instrumental variables for body mass index (BMI) and waist-to-hip ratio (WHR), respectively. Asthma was defined as ever asthma, doctor-diagnosed asthma and doctor-diagnosed active asthma, and was further classified by atopic status or levels of symptom control. Causal OR was calculated with the Wald method. RESULTS: The ORs per 1 SD (4.1 kg/m2) increase in genetically determined BMI were ranged from 1.36 to 1.49 for the three asthma definitions and similar for women and men. The corresponding ORs for non-atopic asthma (range 1.42-1.72) appeared stronger than those for the atopic asthma (range 1.18-1.26), but they were similar for controlled versus partly controlled doctor-diagnosed active asthma (1.43 vs 1.44). There was no clear association between genetically predicted WHR and asthma risk or between genetically predicted asthma and the adiposity markers. CONCLUSIONS: Our MR study provided evidence of a causal association of BMI with asthma in adults, particularly with non-atopic asthma. There was no clear evidence of a causal link between WHR and asthma or of reverse causation.

4.
Eur J Epidemiol ; 34(10): 967-977, 2019 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-31512117

RESUMO

Asthma, a chronic inflammatory airway disease, shares several common pathophysiological mechanisms with acute myocardial infarction (AMI). Our aim was to assess the prospective associations between asthma, levels of asthma control and risk of AMI. We followed 57,104 adults without previous history of AMI at baseline from Nord-Trøndelag health study (HUNT) in Norway. Self-reported asthma was categorised as active asthma (i.e., using asthma medication) and non-active asthma (i.e., not using asthma medication). Levels of asthma control were defined as controlled, partly controlled, and uncontrolled based on the Global Initiative for Asthma guidelines. AMI was ascertained by linking HUNT data with hospital records. A total of 2868 AMI events (5.0%) occurred during a mean (SD) follow-up of 17.2 (5.4) years. Adults with active asthma had an estimated 29% higher risk of developing AMI [adjusted hazard ratio (HR) 1.29, 95% CI 1.08-1.54] compared with adults without asthma. There was a significant dose-response association between asthma control and AMI risk, with highest risk in adults with uncontrolled asthma (adjusted HR 1.73, 95% CI 1.13-2.66) compared to adults with controlled asthma (p for trend < 0.05). The associations were not explained by smoking status, physical activity and C-reactive protein levels. Our study suggests that active asthma and poor asthma control are associated with moderately increased risk of AMI. Further studies are needed to evaluate causal relationship and the underlying mechanisms and to clarify the role of asthma medications in the risk of AMI.


Assuntos
Asma/epidemiologia , Infarto do Miocárdio/epidemiologia , Adulto , Idoso , Asma/fisiopatologia , Asma/terapia , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Infarto do Miocárdio/etiologia , Noruega/epidemiologia , Modelos de Riscos Proporcionais , Estudos Prospectivos , Medição de Risco , Fatores de Risco , Fatores de Tempo
5.
Respirology ; 2019 Jul 24.
Artigo em Inglês | MEDLINE | ID: mdl-31339206

RESUMO

BACKGROUND AND OBJECTIVE: Post-bronchodilator (BD) lung function is recommended for the diagnosis of chronic obstructive pulmonary disease (COPD). However, often only pre-BD lung function is used in clinical practice or epidemiological studies. We aimed to compare the discrimination ability of pre-BD and post-BD lung function to predict all-cause mortality. METHODS: Participants aged ≥40 years with airflow limitation (n = 2538) and COPD (n = 1262) in the second survey of the Nord-Trøndelag Health Study (HUNT2, 1995-1997) were followed up until 31 December 2015. Survival analysis and time-dependent area under the receiver operating characteristic curves (AUC) were used to compare the discrimination ability of pre-BD and post-BD lung function (percent-predicted forced expiratory volume in the first second (FEV1 ) (ppFEV1 ), FEV1 z-score, FEV1 quotient (FEV1 Q), modified Global Initiative for Chronic Obstructive Lung Disease (GOLD) categories or GOLD grades). RESULTS: Among 2538 participants, 1387 died. The AUC for pre-BD and post-BD ppFEV1 to predict mortality were 60.8 and 61.8 (P = 0.005), respectively, at 20 years' follow-up. The corresponding AUC for FEV1 z-score were 58.5 and 60.4 (P < 0.001), for FEV1 Q were 68.7 and 70.1 (P = 0.002) and for modified GOLD categories were 62.3 and 64.5 (P < 0.001). Among participants with COPD, the AUC for pre-BD and post-BD ppFEV1 were 57.0 and 58.8 (P < 0.001), respectively. The corresponding AUC for FEV1 z-score were 53.1 and 55.8 (P < 0.001), for FEV1 Q were 63.6 and 65.1 (P = 0.037) and for GOLD grades were 56.0 and 57.0 (P = 0.268). CONCLUSION: Mortality was better predicted by post-BD than by pre-BD lung function; however, they differed only by a small margin. The discrimination ability using GOLD grades among COPD participants was similar.

6.
Int J Cancer ; 2019 Jul 05.
Artigo em Inglês | MEDLINE | ID: mdl-31276202

RESUMO

Cell-mediated immune suppression may play an important role in lung carcinogenesis. We investigated the associations for circulating levels of tryptophan, kynurenine, kynurenine:tryptophan ratio (KTR), quinolinic acid (QA) and neopterin as markers of immune regulation and inflammation with lung cancer risk in 5,364 smoking-matched case-control pairs from 20 prospective cohorts included in the international Lung Cancer Cohort Consortium. All biomarkers were quantified by mass spectrometry-based methods in serum/plasma samples collected on average 6 years before lung cancer diagnosis. Odds ratios (ORs) and 95% confidence intervals (CIs) for lung cancer associated with individual biomarkers were calculated using conditional logistic regression with adjustment for circulating cotinine. Compared to the lowest quintile, the highest quintiles of kynurenine, KTR, QA and neopterin were associated with a 20-30% higher risk, and tryptophan with a 15% lower risk of lung cancer (all ptrend < 0.05). The strongest associations were seen for current smokers, where the adjusted ORs (95% CIs) of lung cancer for the highest quintile of KTR, QA and neopterin were 1.42 (1.15-1.75), 1.42 (1.14-1.76) and 1.45 (1.13-1.86), respectively. A stronger association was also seen for KTR and QA with risk of lung squamous cell carcinoma followed by adenocarcinoma, and for lung cancer diagnosed within the first 2 years after blood draw. This study demonstrated that components of the tryptophan-kynurenine pathway with immunomodulatory effects are associated with risk of lung cancer overall, especially for current smokers. Further research is needed to evaluate the role of these biomarkers in lung carcinogenesis and progression.

7.
COPD ; 16(1): 8-17, 2019 02.
Artigo em Inglês | MEDLINE | ID: mdl-30870059

RESUMO

The CODEX index was developed and validated in patients hospitalized for COPD exacerbation to predict the risk of death and readmission within one year after discharge. Our study aimed to validate the CODEX index in a large external population of COPD patients with variable durations of follow-up. Additionally, we aimed to recalculate the thresholds of the CODEX index using the cutoffs of variables previously suggested in the 3CIA study (mCODEX). Individual data on 2,755 patients included in the COPD Cohorts Collaborative International Assessment Plus (3CIA+) were explored. A further two cohorts (ESMI AND EGARPOC-2) were added. To validate the CODEX index, the relationship between mortality and the CODEX index was assessed using cumulative/dynamic ROC curves at different follow-up periods, ranging from 3 months up to 10 years. Calibration was performed using univariate and multivariate Cox proportional hazard models and Hosmer-Lemeshow test. A total of 3,321 (87.8% males) patients were included with a mean ± SD age of 66.9 ± 10.5 years, and a median follow-up of 1,064 days (IQR 25-75% 426-1643), totaling 11,190 person-years. The CODEX index was statistically associated with mortality in the short- (≤3 months), medium- (≤1 year) and long-term (10 years), with an area under the curve of 0.72, 0.70 and 0.76, respectively. The mCODEX index performed better in the medium-term (<1 year) than the original CODEX, and similarly in the long-term. In conclusion, CODEX and mCODEX index are good predictors of mortality in patients with COPD, regardless of disease severity or duration of follow-up.

8.
BMC Pulm Med ; 19(1): 2, 2019 Jan 06.
Artigo em Inglês | MEDLINE | ID: mdl-30612551

RESUMO

BACKGROUND: Although dynamic lung volume is not considered a limiting factor of peak oxygen uptake (VO2peak) in healthy subjects, an association between forced expiratory lung volume in one second (FEV1) and VO2peak has been reported in a healthy population aged 69 - 77 years. We hypothesized that a corresponding association could be found in a healthy general population including young and middle-aged subjects. METHODS: In a population-based study in Norway, we investigated the association between FEV1 above the lower limit of normal (LLN) and VO2peak using linear regression and assessed the ventilatory reserve (VR) in healthy subjects aged 20 - 79 years (n = 741). RESULTS: On average, one standard deviation (SD) increase in FEV1 was associated with 1.2 ml/kg/min (95% CI 0.7 - 1.6) higher VO2peak. The association did not differ statistically by sex (p-value for interaction = 0.16) and was similar (0.9 ml/kg/min, 95% CI 0.2 - 1.5) in a sensitivity analysis including only never-smokers (n = 376). In subjects below and above 45 years of age, corresponding estimates were 1.2 ml/kg/min (95% CI 0.5 - 1.8) and 1.2 ml/kg/min (95% CI 0.5 - 1.9), respectively. Preserved VR (≥ 20%) was observed in 66.6% of men and 86.4% of women. CONCLUSIONS: Normal dynamic lung volume, defined as FEV1 above LLN, was positively associated with VO2peak in both men and women, in never-smokers and in subjects below and above 45 years of age. The majority of subjects had preserved VR, and the results suggest that FEV1 within normal limits may influence VO2peak in healthy subjects even when no ventilatory limitation to exercise is evident.


Assuntos
Volume Expiratório Forçado/fisiologia , Pulmão/fisiologia , Consumo de Oxigênio/fisiologia , Adulto , Fatores Etários , Idoso , Teste de Esforço , Feminino , Voluntários Saudáveis , Humanos , Modelos Lineares , Masculino , Pessoa de Meia-Idade , Noruega , Fatores Sexuais , Espirometria , Adulto Jovem
9.
BMJ ; 364: k4981, 2019 01 03.
Artigo em Inglês | MEDLINE | ID: mdl-30606716

RESUMO

OBJECTIVES: To conduct a comprehensive analysis of prospectively measured circulating high sensitivity C reactive protein (hsCRP) concentration and risk of lung cancer overall, by smoking status (never, former, and current smokers), and histological sub-type. DESIGN: Nested case-control study. SETTING: 20 population based cohort studies in Asia, Europe, Australia, and the United States. PARTICIPANTS: 5299 patients with incident lung cancer, with individually incidence density matched controls. EXPOSURE: Circulating hsCRP concentrations in prediagnostic serum or plasma samples. MAIN OUTCOME MEASURE: Incident lung cancer diagnosis. RESULTS: A positive association between circulating hsCRP concentration and the risk of lung cancer for current (odds ratio associated with a doubling in hsCRP concentration 1.09, 95% confidence interval 1.05 to 1.13) and former smokers (1.09, 1.04 to 1.14) was observed, but not for never smokers (P<0.01 for interaction). This association was strong and consistent across all histological subtypes, except for adenocarcinoma, which was not strongly associated with hsCRP concentration regardless of smoking status (odds ratio for adenocarcinoma overall 0.97, 95% confidence interval 0.94 to 1.01). The association between circulating hsCRP concentration and the risk of lung cancer was strongest in the first two years of follow-up for former and current smokers. Including hsCRP concentration in a risk model, in addition to smoking based variables, did not improve risk discrimination overall, but slightly improved discrimination for cancers diagnosed in the first two years of follow-up. CONCLUSIONS: Former and current smokers with higher circulating hsCRP concentrations had a higher risk of lung cancer overall. Circulating hsCRP concentration was not associated with the risk of lung adenocarcinoma. Circulating hsCRP concentration could be a prediagnostic marker of lung cancer rather than a causal risk factor.


Assuntos
Proteína C-Reativa/metabolismo , Carcinoma de Células Grandes/sangue , Carcinoma de Células Pequenas/sangue , Carcinoma de Células Escamosas/sangue , Neoplasias Pulmonares/sangue , Fumar/sangue , Adolescente , Adulto , Idoso , Idoso de 80 Anos ou mais , Biomarcadores/sangue , Biomarcadores Tumorais/sangue , Carcinoma de Células Grandes/epidemiologia , Carcinoma de Células Pequenas/epidemiologia , Carcinoma de Células Escamosas/epidemiologia , Estudos de Casos e Controles , Ex-Fumantes/estatística & dados numéricos , Feminino , Humanos , Neoplasias Pulmonares/epidemiologia , Masculino , Pessoa de Meia-Idade , não Fumantes/estatística & dados numéricos , Razão de Chances , Estudos Prospectivos , Medição de Risco , Sensibilidade e Especificidade , Fumantes/estatística & dados numéricos , Fumar/epidemiologia , Adulto Jovem
10.
Int J Cancer ; 2018 Nov 29.
Artigo em Inglês | MEDLINE | ID: mdl-30499135

RESUMO

Vitamin B supplementation can have side effects for human health, including cancer risk. We aimed to elucidate the role of vitamin B12 in lung cancer aetiology via direct measurements of pre-diagnostic circulating vitamin B12 concentrations in a nested case-control study, complemented with a Mendelian randomization (MR) approach in an independent case-control sample. We used pre-diagnostic biomarker data from 5,183 case-control pairs nested within 20 prospective cohorts, and genetic data from 29,266 cases and 56,450 controls. Exposures included directly measured circulating vitamin B12 in pre-diagnostic blood samples from the nested case-control study, and 8 single nucleotide polymorphisms associated with vitamin B12 concentrations in the MR study. Our main outcome of interest was increased risk for lung cancer, overall and by histological subtype, per increase in circulating vitamin B12 concentrations. We found circulating vitamin B12 to be positively associated with overall lung cancer risk in a dose response fashion (odds ratio for a doubling in B12 [ORlog2B12 ] = 1.15, 95% confidence interval (95%CI) = 1.06-1.25). The MR analysis based on 8 genetic variants also indicated that genetically determined higher vitamin B12 concentrations were positively associated with overall lung cancer risk (OR per 150 pmol/L standard deviation increase in B12 [ORSD ]= 1.08, 95%CI= 1.00-1.16). Considering the consistency of these two independent and complementary analyses, these findings support the hypothesis that high vitamin B12 status increases the risk of lung cancer. This article is protected by copyright. All rights reserved.

11.
Eur J Epidemiol ; 2018 Nov 21.
Artigo em Inglês | MEDLINE | ID: mdl-30465296

RESUMO

Observational studies have shown consistent associations between higher circulating 25-hydroxyvitamin D [25(OH)D] levels and favorable serum lipids. We sought to investigate if such associations were causal. A Mendelian randomization (MR) study was conducted on a population-based cohort comprising 56,435 adults in Norway. A weighted 25(OH)D allele score was generated based on vitamin D-increasing alleles of rs2282679, rs12785878 and rs10741657. Linear regression analyses of serum lipid levels on the allele score were performed to assess the presence of causal associations of serum 25(OH)D with the lipids. To quantify the causal effects, the inverse-variance weighted method was used for calculating MR estimates based on summarized data of individual single-nucleotide polymorphisms. The MR estimate with 95% confidence interval (CI) represents percentage difference in the lipid level per genetically determined 25 nmol/L increase in 25(OH)D. The 25(OH)D allele score demonstrated a clear association with high-density lipoprotein (HDL) cholesterol (p = 0.007) but no association with total or non-HDL cholesterol or triglycerides (p ≥ 0.27). The MR estimate showed 2.52% (95% CI 0.79-4.25%) increase in HDL cholesterol per genetically determined 25 nmol/L increase in 25(OH)D, which was stronger than the corresponding estimate of 1.83% (95% CI 0.85-2.81%) from the observational analysis. The MR estimates for total cholesterol (0.60%, 95% CI - 0.73 to 1.94%), non-HDL cholesterol (0.04%, 95% CI - 1.79 to 1.88%) and triglycerides (- 2.74%, 95% CI - 6.16 to 0.67%) showed no associations. MR analysis of data from a population-based cohort suggested a causal and positive association between serum 25(OH)D and HDL cholesterol.

13.
JAMA Cardiol ; 3(8): 721-728, 2018 Aug 01.
Artigo em Inglês | MEDLINE | ID: mdl-29998294

RESUMO

Importance: Asthma, a chronic inflammatory airway disease, and atrial fibrillation (AF) share several common pathophysiological mechanisms. Research on the association between asthma and atrial fibrillation is lacking, and to our knowledge, no previous studies have assessed the dose-response association between levels of asthma control and AF. Objective: To assess the association between asthma, levels of asthma control, and AF. Design, Setting, and Participants: This prospective population cohort analyzed data on adults from a second and third iteration of the survey-based Nord-Trøndelag Health Study (HUNT) in Norway. All included participants were free from AF at baseline. Atrial fibrillation was ascertained by linking HUNT data with hospital records from the 2 hospitals in Nord-Trøndelag County. Data analysis was completed from May 2017 to November 2017. Exposures: Self-reported asthma was categorized into 3 groups: those who had ever had asthma, those who self-report being diagnosed with asthma, and those who had active asthma. Asthma control was defined according to Global Initiative for Asthma guidelines and was categorized into controlled, partly controlled, and uncontrolled cases. Main Outcomes and Measures: Atrial fibrillation. Results: A total of 54 567 adults were included (of whom 28 821 [52.8%] were women). Of these, 5961 participants (10.9%) reported ever having asthma, 3934 participants (7.2%) reported being diagnosed with asthma, and 2485 participants (4.6%) reported having active asthma. During a mean (SD) follow-up of 15.4 (5.8) years, 2071 participants (3.8%) developed AF. Participants with physician-diagnosed asthma had an estimated 38% higher risk of developing AF (adjusted hazard ratio, 1.38 [95% CI, 1.18-1.61]) compared with participants without asthma. There was a dose-response association between levels of asthma control and risk of AF with the highest risk for AF in participants with uncontrolled asthma (adjusted hazard ratio, 1.74 [95% CI, 1.26-2.42]; P for trend < .001). Conclusions and Relevance: Asthma and lack of asthma control were associated with moderately increased risks of AF in a dose-response manner. Further studies are needed to explore the underlying mechanisms and clarify causal pathways between asthma and AF.

14.
Int J Epidemiol ; 47(6): 1760-1771, 2018 Dec 01.
Artigo em Inglês | MEDLINE | ID: mdl-29901778

RESUMO

Background: Self-reported smoking is the principal measure used to assess lung cancer risk in epidemiological studies. We evaluated if circulating cotinine-a nicotine metabolite and biomarker of recent tobacco exposure-provides additional information on lung cancer risk. Methods: The study was conducted in the Lung Cancer Cohort Consortium (LC3) involving 20 prospective cohort studies. Pre-diagnostic serum cotinine concentrations were measured in one laboratory on 5364 lung cancer cases and 5364 individually matched controls. We used conditional logistic regression to evaluate the association between circulating cotinine and lung cancer, and assessed if cotinine provided additional risk-discriminative information compared with self-reported smoking (smoking status, smoking intensity, smoking duration), using receiver-operating characteristic (ROC) curve analysis. Results: We observed a strong positive association between cotinine and lung cancer risk for current smokers [odds ratio (OR ) per 500 nmol/L increase in cotinine (OR500): 1.39, 95% confidence interval (CI): 1.32-1.47]. Cotinine concentrations consistent with active smoking (≥115 nmol/L) were common in former smokers (cases: 14.6%; controls: 9.2%) and rare in never smokers (cases: 2.7%; controls: 0.8%). Former and never smokers with cotinine concentrations indicative of active smoking (≥115 nmol/L) also showed increased lung cancer risk. For current smokers, the risk-discriminative performance of cotinine combined with self-reported smoking (AUCintegrated: 0.69, 95% CI: 0.68-0.71) yielded a small improvement over self-reported smoking alone (AUCsmoke: 0.66, 95% CI: 0.64-0.68) (P = 1.5x10-9). Conclusions: Circulating cotinine concentrations are consistently associated with lung cancer risk for current smokers and provide additional risk-discriminative information compared with self-report smoking alone.

15.
Respir Med ; 138: 50-56, 2018 05.
Artigo em Inglês | MEDLINE | ID: mdl-29724393

RESUMO

BACKGROUND: COPD is a major cause of morbidity and mortality across the world and new estimates of prevalence and trend are of great importance. We aimed to estimate the prevalence and trend of COPD from 1995-1997 to 2006-2008 in Norwegian adults ≥40 years from the Nord-Trøndelag Health Study. MATERIAL AND METHODS: COPD was assessed using a fixed-ratio and lower limit of normal (LLN) criteria. Pre-bronchodilator spirometry was performed during 1995-1997 (n = 7158) and 2006-2008 (n = 8788). The prevalence of COPD was weighted using the inverse probability of selection and predicted probability of response. RESULTS: The prevalence of pre-bronchodilator COPD was 16.7% in 1995-1997 and 14.8% in 2006-2008 using fixed-ratio criteria, and 10.4% in 1995-1997 and 7.3% in 2006-2008 using LLN criteria. The prevalence of LLN COPD was higher among men (13.0% in 1995-1997, 7.7% in 2006-2008) than women (8.0% in 1995-1997, 6.9% in 2006-2008). From 1995-1997 to 2006-2008, the prevalence decreased among men but remained relatively stable among women. Over the 11-year period, the cumulative incidence of pre-bronchodilator COPD using LLN criteria was 3.3% and 2.7% among men and women respectively. The prevalence of self-reported asthma and respiratory symptoms increased. CONCLUSIONS: The prevalence declined in men but not in women from 1995-1997 to 2006-2008, and was consistently higher among men than women.

16.
EBioMedicine ; 31: 36-46, 2018 May.
Artigo em Inglês | MEDLINE | ID: mdl-29678673

RESUMO

Lung cancer causes >1·6 million deaths annually, with early diagnosis being paramount to effective treatment. Here we present a validated risk assessment model for lung cancer screening. The prospective HUNT2 population study in Norway examined 65,237 people aged >20years in 1995-97. After a median of 15·2years, 583 lung cancer cases had been diagnosed; 552 (94·7%) ever-smokers and 31 (5·3%) never-smokers. We performed multivariable analyses of 36 candidate risk predictors, using multiple imputation of missing data and backwards feature selection with Cox regression. The resulting model was validated in an independent Norwegian prospective dataset of 45,341 ever-smokers, in which 675 lung cancers had been diagnosed after a median follow-up of 11·6years. Our final HUNT Lung Cancer Model included age, pack-years, smoking intensity, years since smoking cessation, body mass index, daily cough, and hours of daily indoors exposure to smoke. External validation showed a 0·879 concordance index (95% CI [0·866-0·891]) with an area under the curve of 0·87 (95% CI [0·85-0·89]) within 6years. Only 22% of ever-smokers would need screening to identify 81·85% of all lung cancers within 6years. Our model of seven variables is simple, accurate, and useful for screening selection.


Assuntos
Neoplasias Pulmonares/epidemiologia , Modelos Biológicos , Sistema de Registros , Fumar , Adulto , Idoso , Idoso de 80 Anos ou mais , Bases de Dados Factuais , Feminino , Seguimentos , Humanos , Masculino , Pessoa de Meia-Idade , Noruega , Valor Preditivo dos Testes , Estudos Prospectivos , Fatores de Risco , Fumar/efeitos adversos , Fumar/epidemiologia
17.
BMC Med ; 16(1): 33, 2018 03 02.
Artigo em Inglês | MEDLINE | ID: mdl-29495970

RESUMO

BACKGROUND: External validations and comparisons of prognostic models or scores are a prerequisite for their use in routine clinical care but are lacking in most medical fields including chronic obstructive pulmonary disease (COPD). Our aim was to externally validate and concurrently compare prognostic scores for 3-year all-cause mortality in mostly multimorbid patients with COPD. METHODS: We relied on 24 cohort studies of the COPD Cohorts Collaborative International Assessment consortium, corresponding to primary, secondary, and tertiary care in Europe, the Americas, and Japan. These studies include globally 15,762 patients with COPD (1871 deaths and 42,203 person years of follow-up). We used network meta-analysis adapted to multiple score comparison (MSC), following a frequentist two-stage approach; thus, we were able to compare all scores in a single analytical framework accounting for correlations among scores within cohorts. We assessed transitivity, heterogeneity, and inconsistency and provided a performance ranking of the prognostic scores. RESULTS: Depending on data availability, between two and nine prognostic scores could be calculated for each cohort. The BODE score (body mass index, airflow obstruction, dyspnea, and exercise capacity) had a median area under the curve (AUC) of 0.679 [1st quartile-3rd quartile = 0.655-0.733] across cohorts. The ADO score (age, dyspnea, and airflow obstruction) showed the best performance for predicting mortality (difference AUCADO - AUCBODE = 0.015 [95% confidence interval (CI) = -0.002 to 0.032]; p = 0.08) followed by the updated BODE (AUCBODE updated - AUCBODE = 0.008 [95% CI = -0.005 to +0.022]; p = 0.23). The assumption of transitivity was not violated. Heterogeneity across direct comparisons was small, and we did not identify any local or global inconsistency. CONCLUSIONS: Our analyses showed best discriminatory performance for the ADO and updated BODE scores in patients with COPD. A limitation to be addressed in future studies is the extension of MSC network meta-analysis to measures of calibration. MSC network meta-analysis can be applied to prognostic scores in any medical field to identify the best scores, possibly paving the way for stratified medicine, public health, and research.


Assuntos
Doença Pulmonar Obstrutiva Crônica/diagnóstico , Idoso , Estudos de Coortes , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Prognóstico , Doença Pulmonar Obstrutiva Crônica/fisiopatologia , Índice de Gravidade de Doença
18.
Respir Med ; 136: 65-70, 2018 03.
Artigo em Inglês | MEDLINE | ID: mdl-29501248

RESUMO

Few studies have investigated the association between serum 25-hydroxyvitamin D (25[OH]D), vitamin D supplement and asthma control among adults. We aimed to examine whether low levels of serum 25(OH)D or not taking vitamin D supplement were associated with an increased risk of poorly controlled asthma among Norwegian adults with asthma. We used a definition of asthma control adapted from the Global Initiative for Asthma. We first examined cross-sectional associations between serum 25(OH)D (n = 806) or vitamin D supplement (n = 1179) and poorly controlled asthma. Next, among those with well controlled asthma at baseline, we examined prospective associations between serum 25(OH)D (n = 147) or vitamin D supplement (n = 208) and poorly controlled asthma at follow-up, approximately 11 years later. We estimated risk ratios (RR) and 95% confidence intervals (CI) with Poisson regression. The adjusted RR for poorly controlled asthma was 1.00 (95% CI, 0.89-1.13) for adults with serum 25(OH)D < 50 nmol/L in cross-sectional and 1.50 (95% CI, 0.46-4.95) in prospective analyses. The adjusted RR for poorly controlled asthma was 1.17 (95% CI 1.00-1.37) for non-users of vitamin D supplement in cross-sectional and 1.66 (95% CI 0.49-5.67) in prospective analyses. Our study did not show strong evidence that among adults with asthma, having a low serum 25(OH)D or being a non-user of vitamin D supplement was associated with an increased risk of poorly controlled asthma. Some point estimates indicated an increased risk, however our estimates were generally imprecise and further evidence is needed.

19.
J Natl Cancer Inst ; 110(8): 831-842, 2018 Aug 01.
Artigo em Inglês | MEDLINE | ID: mdl-29518203

RESUMO

Background: The obesity-lung cancer association remains controversial. Concerns over confounding by smoking and reverse causation persist. The influence of obesity type and effect modifications by race/ethnicity and tumor histology are largely unexplored. Methods: We examined associations of body mass index (BMI), waist circumference (WC), and waist-hip ratio (WHR) with lung cancer risk among 1.6 million Americans, Europeans, and Asians. Cox proportional hazard regression was used to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) with adjustment for potential confounders. Analyses for WC/WHR were further adjusted for BMI. The joint effect of BMI and WC/WHR was also evaluated. Results: During an average 12-year follow-up, 23 732 incident lung cancer cases were identified. While BMI was generally associated with a decreased risk, WC and WHR were associated with increased risk after controlling for BMI. These associations were seen 10 years before diagnosis in smokers and never smokers, were strongest among blacks, and varied by histological type. After excluding the first five years of follow-up, hazard ratios per 5 kg/m2 increase in BMI were 0.95 (95% CI = 0.90 to 1.00), 0.92 (95% CI = 0.89 to 0.95), and 0.89 (95% CI = 0.86 to 0.91) in never, former, and current smokers, and 0.86 (95% CI = 0.84 to 0.89), 0.94 (95% CI = 0.90 to 0.99), and 1.09 (95% CI = 1.03 to 1.15) for adenocarcinoma, squamous cell, and small cell carcinoma, respectively. Hazard ratios per 10 cm increase in WC were 1.09 (95% CI = 1.00 to 1.18), 1.12 (95% CI = 1.07 to 1.17), and 1.11 (95% CI = 1.07 to 1.16) in never, former, and current smokers, and 1.06 (95% CI = 1.01 to 1.12), 1.20 (95% CI = 1.12 to 1.29), and 1.13 (95% CI = 1.04 to 1.23) for adenocarcinoma, squamous cell, and small cell carcinoma, respectively. Participants with BMIs of less than 25 kg/m2 but high WC had a 40% higher risk (HR = 1.40, 95% CI = 1.26 to 1.56) than those with BMIs of 25 kg/m2 or greater but normal/moderate WC. Conclusions: The inverse BMI-lung cancer association is not entirely due to smoking and reverse causation. Central obesity, particularly concurrent with low BMI, may help identify high-risk populations for lung cancer.

20.
Clin Epidemiol ; 10: 83-96, 2018.
Artigo em Inglês | MEDLINE | ID: mdl-29391831

RESUMO

Objective: Biochemical changes associated with obesity may accelerate osteoarthritis beyond the effect of mechanical factors. This study investigated whether metabolic syndrome and its components (visceral obesity, hypertension, dyslipidemia and insulin resistance) were risk factors for subsequent total hip replacement (THR) or total knee replacement (TKR) due to primary osteoarthritis. Design: In this prospective cohort study, data from the second survey of the Nord-Trøndelag Health Study 2 (HUNT2) were linked to the Norwegian Arthroplasty Register for identification of the outcome of THR or TKR. The analyses were stratified by age (<50, 50-69.9 and ≥70 years) and adjusted for gender, body mass index, smoking, physical activity and education. Results: Of the 62,661 participants, 12,593 (20.1%) were identified as having metabolic syndrome, and we recorded 1,840 (2.9%) THRs and 1,111 (1.8%) TKRs during a mean follow-up time of 15.4 years. Cox regression analyses did not show any association between full metabolic syndrome and THR or TKR, except in persons <50 years with metabolic syndrome who had a decreased risk of THR (hazard ratio [HR] 0.58, 95% CI 0.40-0.83). However, when including only participants whose exposure status did not change during follow-up, this protective association was no longer significant. Increased waist circumference was associated with increased risk of TKR in participants <50 years (HR 1.62, 95% CI 1.10-2.39) and 50-69.9 years (HR 1.43, 95% CI 1.14-1.80). Hypertension significantly increased the risk of TKR in participants <50 years (HR 1.38, 95% CI 1.05-1.81), and this risk was greater for men. Conclusion: This study found an increased risk of TKR in men <50 years with hypertension and persons <70 years with increased waist circumference. Apart from this, neither metabolic syndrome nor its components were associated with increased risk of THR or TKR due to primary osteoarthritis.

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