Publications by authors named "Sansores R"

Background: COPD due to biomass exposure (COPD-B) is highly prevalent in low- and middle-income countries, and there are no clinical trials designed to evaluate the effectiveness of the treatments currently recommended for patients with COPD due to cigarette smoking (COPD-C). The purpose of the study was to compare the efficacy of fluticasone furoate/vilanterol (FF/V) 100/25 μg and umeclidinium/vilanterol (UMEC/VI) 62.5/25 μg on the rate of exacerbations, the time to first exacerbation, on dyspnoea, health-related quality of life (HRQL), forced expiratory volume in 1 s (FEV) and inspiratory capacity (IC) during a period of 6 months in patients with COPD-B and COPD-C, at a third level referral centre in Mexico City.

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Unlabelled: Chronic Obstructive Pulmonary Disease (COPD) is a disease characterized by local and systemic inflammation independently of the risk factor; during the exacerbations, such inflammation is accentuated and amplified. A practical inflammatory marker and one with an applicable predictive value in the follow-up has been sought. FeNO has shown an excellent performance in that respect within the context of asthma and has also been studied in tobacco-smoke COPD (COPD-TS).

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Article Synopsis
  • The study investigates the relationship between certain genetic variants (rs2071288, rs3134940, rs184003, and rs2070600) and soluble-RAGE levels in patients with chronic obstructive pulmonary disease (COPD) related to biomass-burning smoke (BBS) and tobacco smoking.
  • Researchers analyzed 2189 subjects divided into four groups to determine if these variants and RAGE levels were linked to COPD, but found no strong associations, except a marginal one for rs3134940 with COPD-BBS.
  • The findings revealed that sRAGE plasma and sputum levels were lower in COPD patients compared to non-COPD individuals, with rs3134940 influencing these levels, but the genetic variants themselves did
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Introduction: One of the major concerns with post-acute sequelae of COVID-19 (PASC) is the development of pulmonary fibrosis, for which no approved pharmacological treatment exists. Therefore, the primary aim of this open-label study was to evaluate the safety and the potential clinical efficacy of a prolonged-release pirfenidone formulation (PR-PFD) in patients having PASC-pulmonary fibrosis.

Methods: Patients with PASC-pulmonary fibrosis received PR-PFD 1800 mg/day (1200 mg in the morning after breakfast and 600 mg in the evening after dinner) for three months.

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  • Lung microbiome dysbiosis can lead to immune system imbalances and lung inflammation, prompting a study comparing the lung bacteriome and cytokine profiles of women with normal lung function exposed to either tobacco smoke or biomass-burning smoke.
  • The research involved analyzing induced sputum from two groups: women exposed to biomass-burning smoke and current smokers, focusing on the composition of bacteria and measurement of cytokine levels.
  • Results indicated that current smokers had a higher concentration of IL-1β and a different bacteriome composition but did not show statistically significant differences in specific bacteria after adjustments, highlighting potential negative effects of smoking on lung health compared to biomass exposure.
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Chronic obstructive pulmonary disease (COPD) is the third leading cause of death worldwide; the main risk factors associated with the suffering are tobacco smoking (TS) and chronic exposure to biomass-burning smoke (BBS). Different biological pathways have been associated with COPD, especially xenobiotic or drug metabolism enzymes. This research aims to identify single nucleotide polymorphisms (SNPs) profiles associated with COPD from two expositional sources: tobacco smoking and BBS.

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Background: Patients with biomass exposure-related COPD (BE-COPD) is a prevalent disease in developing countries and requires a detailed study of its clinical and inflammatory characteristics, specifying interventions that may differ from tobacco exposure-related COPD (TE-COPD). The objective was to describe clinical characteristics, biomarkers of inflammation, T-helper cells, and microbiological agents during a COPD exacerbation in BE-COPD in comparison with TE-COPD.

Methods: A prospective observational study in patients with moderate or severe exacerbation was recruited either in the emergency room or the COPD clinic.

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Article Synopsis
  • BE-COPD patients, exposed to biomass, may be more vulnerable to COVID-19 than TE-COPD patients, who are affected by tobacco smoke.
  • The study found an 11% prevalence of COVID-19 in both groups, with no significant differences in infection rates or risk factors like housing or knowledge about COVID-19.
  • Poor socioeconomic status was noted in the BE-COPD group, and around 40% of patients had inadequate risk perception and adherence to health guidelines during the pandemic.
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Article Synopsis
  • COPD is an inflammatory disease mainly affecting smokers and those exposed to biomass-burning smoke (BBS), with certain gene variants linked to its risk.
  • Researchers studied 1549 participants to identify associations between two specific single-nucleotide polymorphisms (SNPs) in the heat shock protein (HSP) genes and COPD.
  • Findings showed that certain SNPs were linked to a decreased risk of COPD in individuals exposed to BBS and those with severe forms of the disease among smokers.
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Tobacco smoking results in a multifactorial disease involving environmental and genetic factors; epigenome-wide association studies (EWAS) show changes in DNA methylation levels due to cigarette consumption, partially reversible upon tobacco smoking cessation. Therefore, methylation levels could predict smoking status. This study aimed to evaluate the DNA methylation level of cg05575921 () and cg23771366 () and their correlation with lung function variables, cigarette consumption, and nicotine addiction in the Mexican smoking population.

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Although different trajectories in lung function decline have been identified in patients with COPD associated to tobacco exposure (TE-COPD), genetic, environmental, and infectious factors affecting lung function throughout life have not been fully elucidated in patients with COPD associated to biomass (BE-COPD). In this review, we present current epidemiological findings and notable advances in the natural history of lung decline in BE-COPD, as well as conditions modeling the FEV trajectory, such as health insults, during the first years of childhood. Evidence shows that women exposed to biomass smoke reach adult life with a lower FEV than expected.

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The tobacco industry promotes electronic nicotine delivery systems (ENDS) and heated tobacco products (HTP) as a safer alternative to conventional cigarettes with misleading marketing sustained by studies with conflict of interest. As a result, these devices sell without regulations and warnings about their adverse effects on health, with a growing user base targeting young people. This systematic review aimed to describe the adverse effects on the respiratory system in consumers of these devices.

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Cigarette smoking is influenced by nicotine's effects on dopaminergic activity, which appear to be moderated by genetic variation, particularly a variable number tandem repeat (VNTR, 48 bp) polymorphism in the third exon of the dopamine receptor gene (). Smokers with the VNTR ≥7 repeats (long, L allele) report markedly increased participation in some smoking behaviors; hence, our aim was to evaluate the association of the L allele in Mexican Mestizo smokers with and without COPD. The VNTR 48 bp was genotyped in 492 Mexican Mestizo smokers: 164 COPD patients (≥20 cigarettes per day, cpd), 164 heavy smokers without COPD (HS, ≥20 cpd) and 164 light smokers without COPD (LS, 1-10 cpd).

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Introduction: The efficacy of long-acting bronchodilators for COPD associated with biomass (BE-COPD) has not been properly evaluated.

Objective: To determine the acute effect of indacaterol (IND) 150 μg q.d and tiotropium (TIO) 18 μg q.

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This article contains data on the allele and genotype frequency for single nucleotide polymorphisms (SNPs) in candidate genes (rs16969968, rs17408276, rs680244) (rs6495307, rs12914385) (rs10865246, rs1882296, rs985919) and (rs6311, rs6313) previously evaluated as genetic risk variants for cigarette smoking at an early age and relapse to smoking cessation treatment Pérez-Rubio et al., 2018. These SNPs were selected due to previous associations in other populations, including Mexican Mestizos.

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Chronic obstructive pulmonary disease (COPD) is a complex and heterogeneous entity that may result from different causative agents and risk factors and may follow diverse clinical courses, including COPD secondary to biomass smoke exposure. At present, this phenotype is becoming more important for two reasons: first, because at least almost half of the world's population is exposed to biomass smoke, and second, because the possibility of it being diagnosed is increasing. Biomass smoke exposure COPD affects primarily women and is related with insults to the airways occurred during early life.

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Objectives: Tobacco smoking is a complex and multifactorial disease involving both environmental and genetic factors. In the Mexican mestizo population, single-nucleotide polymorphisms (SNPs) associated with cigarette smoking and a greater degree of nicotine addiction have been identified; however, no possible roles have been explored in regard to the age of onset of smoking or in the success of quitting.

Methods: In this study, 151 Mexican mestizo, who smoke cigarettes, were included.

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Background: Quitting smoking is key for patients with Chronic Obstructive Pulmonary Disease (COPD). Standard recommendations for quitting smoking are implemented for COPD as well. Varenicline Tartrate (VT) is the most effective drug to help quit smoking, but few studies have analysed its effectiveness.

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Introduction: Biomass smoke exposure (BSE) is a recognized cause of COPD particularly in rural areas. However, little research has been focused on BSE in suburban areas.

Objective: The aim of this study was to determine the prevalence of COPD, respiratory symptoms (RS) and BSE in women living in a suburban area of Mexico City exposed to BSE.

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This article contains data on the single nucleotide polymorphisms (SNPs) rs1137115, rs1801272 and rs28399433 rs4105144 in associated to smoking related variables in Mexican Mestizo smokers (Pérez-Rubio et al., 2017) [1]. These SNPs were selected due to previous associations with other populations.

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Nicotine is the main component of cigarettes that causes addiction, which is considered a complex disease, and genetic factors have been proposed to be involved in the development of addiction. The CYP2A6 gene encodes the main enzyme responsible for nicotine metabolism. Depending on the study population, different genetic variants of CYP2A6 associated with cigarette smoking have been described.

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The ALAT and SEPAR Treatment and Control of Smoking Groups have collaborated in the preparation of this document which attempts to answer, by way of PICO methodology, different questions on health interventions for helping COPD patients to stop smoking. The main recommendations are: (i)moderate-quality evidence and strong recommendation for performing spirometry in COPD patients and in smokers with a high risk of developing the disease, as a motivational tool (particularly for showing evidence of lung age), a diagnostic tool, and for active case-finding; (ii)high-quality evidence and strong recommendation for using intensive dedicated behavioral counselling and drug treatment for helping COPD patients to stop smoking; (iii)high-quality evidence and strong recommendation for initiating interventions for helping COPD patients to stop smoking during hospitalization with improvement when the intervention is prolonged after discharge, and (iv)high-quality evidence and strong recommendation for funding treatment of smoking in COPD patients, in view of the impact on health and health economics.

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