15 research outputs found

    Cohort Profile: Burden of Obstructive Lung Disease (BOLD) study

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    The Burden of Obstructive Lung Disease (BOLD) study was established to assess the prevalence of chronic airflow obstruction, a key characteristic of chronic obstructive pulmonary disease, and its risk factors in adults (≥40 years) from general populations across the world. The baseline study was conducted between 2003 and 2016, in 41 sites across Africa, Asia, Europe, North America, the Caribbean and Oceania, and collected high-quality pre- and post-bronchodilator spirometry from 28 828 participants. The follow-up study was conducted between 2019 and 2021, in 18 sites across Africa, Asia, Europe and the Caribbean. At baseline, there were in these sites 12 502 participants with high-quality spirometry. A total of 6452 were followed up, with 5936 completing the study core questionnaire. Of these, 4044 also provided high-quality pre- and post-bronchodilator spirometry. On both occasions, the core questionnaire covered information on respiratory symptoms, doctor diagnoses, health care use, medication use and ealth status, as well as potential risk factors. Information on occupation, environmental exposures and diet was also collected

    Reduced forced vital capacity is independently associated with, aging, height and a poor socioeconomic status: a report from the Tunisian population-based BOLD study

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    BACKGROUND: Reduced forced vital capacity (FVC) is a risk factor of all-cause mortality; however, the prevalence and determinants of reduced FVC are not available for the Tunisian population. This study investigated the association of reduced FVC with risk factors and health variables in an urban population of subjects aged ≥ 40 years and living in the city of Sousse in Tunisia. METHODS: A cross-sectional survey was performed using data from the Tunisian Burden of Obstructive Lung Disease (BOLD) study. We defined reduced FVC as a post-bronchodilator FVC below the lower limit of normal using National Health and Nutrition Examination Survey (NHANES) values and Global Lung Function Initiative 2012 equations (GLI 2012) and determined the relation between this finding and the potential risk factors (demographic and socioeconomic factors and the presence of chronic diseases), using multivariable regression analysis. RESULTS: The prevalence of reduced FVC was 26.6% (176/661) when using NHANES values for white Americans and 14.2% (94/661) using the GLI 2012 equations. Compared to people with normal FVC, those with a reduced FVC were significantly older, taller, had a lower body mass index (BMI), more respiratory symptoms and a higher prevalence of heart disease and hypertension. Multivariable analysis showed that reduced FVC was essentially driven by exposure to biomass smoke for heating, a number of schooling years lower than or equal to 6 years, a childhood history of hunger for a lack of money, aging and height. CONCLUSIONS: The prevalence of reduced FVC is associated with a poor socioeconomic status aging and height

    Combined Analysis of EPHX1, GSTP1, GSTM1 and GSTT1 Gene Polymorphisms in Relation to Chronic Obstructive Pulmonary Disease Risk and Lung Function Impairment

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    Smoking is considered as the major causal factor of chronic obstructive pulmonary disease (COPD). Nevertheless, a minority of chronic heavy cigarette smokers develops COPD. This suggests important contribution of other factors such as genetic predisposing. Our objective was to investigate combined role of EPHX1, GSTP1, M1 and T1 gene polymorphisms in COPD risk, its phenotypes and lung function impairment. Prevalence of EPHX1, GSTP1, M1 and T1 gene polymorphisms were assessed in 234 COPD patients and 182 healthy controls from Tunisia. Genotypes of EPHX1 (Tyr113His; His139Arg) and GSTP1 (Ile105Val; Ala114Val) polymorphisms were performed by PCR-RFLP, while the deletion in GSTM1 and GSTT1 genes was determined using multiplex PCR. Analysis of combinations showed a significant association of 113His/His EPHX1/null-GSTM1 (OR = 4.07) and null-GSTM1/105Val/Val GSTP1 (OR = 3.56) genotypes with increased risk of COPD (respectively P=0.0094 and P=0.0153). The null-GSTM1/ null-GSTT1, 105Val/Val GSTP1/null GSTT1, 113His/His EPHX1/null-GSTM1 and null-GSTM1/105Val/Val GSTP1 genotypes were related to emphysema (respectively P = 0.01; P = 0.009; P = 0.008 and P = 0.001). Combination of 113His/His EPHX1/null-GSTM1 genotypes showed a significant association with the decrease of ΔFEV1 in patients (P = 0.028)

    Mise au point: déficit en alpha 1 antitrypsine

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    International audienceLe déficit en alpha 1 antitrypsine (AAT) est un désordre génétique commun qui se manifeste principalement par des maladies pulmonaires obstructives et plus rarement par une atteinte hépatique. La découverte de l'alpha 1 antitrypsine en tant qu'inhibiteur de protéases a abouti à la théorie du déséquilibre de la balance protéase-antiprotéase, qui demeure encore la clé de voute de la physiopathologie de l'emphysème pulmonaire. Cet article fait le point sur la pathogénèse, les facteurs de risque environnementaux et les manifestations cliniques du déficit en AAT. Des informations concernant la distribution mondiale, le diagnostic et les stratégies thérapeutiques de la maladie sont également apportées. Nous avons insisté sur l'épidémiologie du déficit en AAT dans les pays du bassin méditerranéen
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