Expert Review of Respiratory Medicine最新文献

Introduction: Dyspnea is a complex symptom, which largely results from an imbalance between an afferent sensory stimulus and the corresponding efferent respiratory neuromuscular response. In addition, it is heavily influenced by the patient's prior experiences and sociocultural factors.

Areas covered: The diagnostic approach to these patients requires a graded, systematic, and often multidisciplinary approach to determine what is the underlying pathophysiologic process. Utilization of objective data obtained through lab testing, imaging, and advanced testing, such as cardiopulmonary exercise testing, is often required to help identify underlying pathology contributing to a patient's symptoms. This article will review dyspnea's underlying pathophysiological mechanisms and standardized approaches to diagnoses. In the expert opinion section, we will discuss our own clinical approach to evaluating patients with persistent dyspnea.

Expert opinion: Unexplained dyspnea is a challenging diagnosis that occurs in patients with and without underlying cardiopulmonary diseases. It requires a systematic approach, which initially uses clinical evaluation in addition to standard imaging and clinical biomarkers. When diagnoses are not made during the initial evaluation, subsequent tests can include cardiopulmonary exercise test and methacholine challenge. To be certain of the correct diagnosis, It is imperative that the clinician determines dyspnea's response to a particular therapeutic intervention.

Introduction: Pulmonary fibrosis is an age-related, progressive, and fatal disease with a median survival of 3-5 years after diagnosis; idiopathic pulmonary fibrosis (IPF) is the most common type. It is characterized by fibroblast proliferation and accumulation of excessive extracellular matrix. Patients with IPF are at increased risk for lung cancer. Epigenetic mechanisms are involved in lung fibrosis and cancer, and DNA methylation is critical in disease pathogenesis and progression. Therefore, studies of DNA methylation contribute to better understanding of the underlying mechanisms of these two respiratory diseases, and can offer novel diagnostic and treatment options.

Areas covered: This review discusses the latest advances in our understanding of epigenetic factors related to DNA methylation that impact development of lung cancer and pulmonary fibrosis, discusses the role of DNA methylation in promoting or inhibiting these diseases, and proposes its potential clinical significance in disease diagnosis and treatment.

Expert opinion: DNA methylation plays a critical role in lung cancer and fibrosis pathogenesis. DNA methylation offers a new biomarker for disease diagnosis or monitoring, and provides a new therapeutic target for treatment.

Introduction: Occupational chronic obstructive pulmonary disorder, i.e. work-related asthma (WRA) and occupational chronic obstructive pulmonary disease (COPD), are the most common occupational lung diseases in the last decades worldwide. As in the case of the other occupational disorders, these diseases may be prevented.

Areas covered: WRA is a heterogeneous entity that includes three subtypes, immunologic occupational asthma (OA), irritant-induced asthma (IIA), and work-exacerbated asthma (WEA), depending on the role of occupational exposures as a causing or aggravating factor of the disease. In addition, there is consistent evidence that a substantial proportion of COPD cases can be explained by exposure to noxious particles and gases other than tobacco smoke, such as workplace dusts, gases, fumes, and vapors. The articles cited in this paper were searched by keywords in several databases in the period up to May-July 2021.

Expert opinion: The development of occupational chronic obstructive disorder is a matter of prevention. WRA and occupational COPD contribute significantly to the overall burden of asthma and COPD. Activities and measures targeted to elimination or reduction of harmful workplace exposures, as well as to early detection and early intervention in the course of the lung damage, can significantly reduce the burden caused by these diseases.

Background: Due to the disagreement in studies, the present study performed a systematic review and meta-analysis to investigate the relationship between childhood asthma and the development of chronic obstructive pulmonary disease (COPD) in adulthood.

Methods: Literature search was performed in Medline and Embase databases until the end of 2019. Data were recorded as adjusted odds ratio (OR) and 95% confidence interval (95%CI). Analyses were performed on STATA 14.0 and an overall OR was reported. Subgroup analysis was performed to determine the source of heterogeneity.

Results: Data from 11 articles were included in the meta-analysis. Overall, the odds of developing adulthood COPD in children with asthma were 3.0 times higher than that in non-asthmatic children (OR = 3.00; 95%CI: 2.25-4.00; p < 0.001). The relationship between childhood asthma and COPD in adulthood was reported somewhat greater in random sampling method studies than consecutive sampling method studies (OR = 2.89; 95% CI: 1.72-4.86; p = 0.001).

Conclusion: Asthma in childhood could be considered as an independent risk factor for COPD in adulthood. Since type of study, sampling method, sample size of study and COPD prevalence are the main sources of heterogeneity, further prospective high-quality studies assessing the relationship of childhood asthma and adulthood COPD are recommended to be performed.

Objective: To date, some studies revealed that HHIP gene polymorphisms may be associated with the risk of chronic obstructive pulmonary disease (COPD). Therefore, this meta-analysis explored the association between single-nucleotide polymorphisms (SNPs) of the human hedgehog interacting protein (HHIP) gene and susceptibility to COPD.

Methods: Seven Chinese and English electronic databases were searched for eligible studies up to 30 May 2020. After the inclusion criteria were strictly followed, the Newcastle-Ottawa Scale (NOS) was used to evaluate the quality of the included studies. The pooled odds ratio (OR) of the 95% confidence interval (CI) under four different genetic models was calculated to evaluate the association strength between the SNPs and COPD. Egger's test was used to evaluate publication bias.

Results: This meta-analysis was registered at PROSPERO (CRD42021235708). In total, 12 studies involving 6623 COPD patients and 11,373 healthy controls were included. Regarding rs13118928 and rs1828591, an A > G mutation increased the risk of COPD in Asian and Caucasian individuals, and the rs13147758 A > G mutation and rs10519717 C > T mutation increased the risk of COPD only in Asian people. No significant publication bias was observed.

Conclusion: This meta-analysis provides a theoretical basis suggesting that HHIP gene polymorphisms may be associated with the risk of COPD.

Introduction: A novel virus, Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) was reported via nucleic acid identification in December, 2019. 'Asymptomatic cases' have arised as an obstacle for an accurate diagnosis, curtailing the elimination of the ongoing pandemic.

Areas covered: In this review, we analyze the definition of symptoms and the principles of diagnosing COVID-19. Also, we explore the major reasons for cases presenting a phenotype with mild symptoms. Host, viral and environmental aspects for a COVID-19 leading to mild symptoms are being highlighted. A final aspect regarding a rational asymptomatic COVID-19 is presumed.

Expert opinion: Diagnosing a pandemic via a sole test can be risky. Epidemiological administration should be more accurate and precise, not only for the societal pandemic levels and following policies, but for the same scientific community, that studies SARS-CoV-2 and its mutants. Several other issues should be answered before analyzing human genome for the asymptomatic scenario.

Objective: To develop a predictive model for COPD patients admitted for COVID-19 to support clinical decision-making.

Method: Retrospective cohort study of 1313 COPD patients with microbiological confirmation of SARS-CoV-2 infection. The sample was randomly divided into two subsamples, for the purposes of derivation and validation of the prediction rule (60% and 40%,respectively). Data collected for this study included sociodemographic characteristics, baseline comorbidities, baseline treatments, and other background data. Multivariable logistic regression analysis was used to develop the predictive model.

Results: Male sex, older age, hospital admissions in the previous year, flu vaccination in the previous season, a Charlson Index>3 and a prescription of renin-angiotensin aldosterone system inhibitors at baseline were the main risk factors for hospital admission. The AUC of the categorized risk score was 0.72 and 0.69 in the derivation and validation samples, respectively. Based on the risk score, four groups were identified with a risk of hospital admission ranging from 21% to 80%.

Conclusions: We propose a classification system to identify COPD people with COVID-19 with a higher risk of hospitalization, and indirectly, more severe disease, that is easy to use in primary care, as well as hospital emergency room settings to help clinical decision-making.

Clinicaltrials.gov identifier: NCT04463706.

Introduction: Although polycythemia has been considered a common adverse event in COPD, anemia is reported more often and has gained more importance than polycythemia over the last thirty years.

Areas covered: Factors considered to be associated with the development of anemia in COPD have included: Aging and kidney dysfunction with erythropoietin deficiency and bone marrow suppression due to uremic toxins; heart failure (HF), often encountered in COPD and accompanied by anemia in one-third of the cases; Low-grade chronic inflammation, directly suppressing bone marrow and diminishing iron absorption and utilization via increased hepcidin levels; long-term oxygen therapy (LTOT), ameliorating chronic hypoxia, and most important, RAS inhibitors, which are widely used for the comorbidities associated with COPD (hypertension, HF, CKD, diabetes) and have previously been shown to lower hematocrit values or cause anemia in various clinical conditions.

Expert opinion: Introduction of LTOT in COPD and especially the established use of RAS inhibitors form the basis for the shift from polycythemia to anemia in COPD. Interestingly, when the SGLT2 inhibitors are introduced for cardiorenal protection in COPD, one could anticipate correction of anemia or even reemergence of polycythemia, since this new class of drugs can augment erythropoietin secretion and increase hematocrit values.