Chest最新文献

Case presentation: A 72-year-old man who underwent bilateral orthotropic lung transplantation for interstitial lung disease 6 months ago presented to the clinic with a 2-week history of cough, shortness of breath, and mid-back pain. The donor was negative for cytomegalovirus (CMV) and positive for Epstein-Barr virus (EBV), and the recipient was positive for both CMV and EBV. He also reported headaches but denied any fever, chills, weight loss, night sweats, chest pain, orthopnea, paroxysmal nocturnal dyspnea, or leg swelling. His other medical history included renal cell carcinoma, for which he had undergone partial right nephrectomy 6 years earlier. The patient lived in central Florida and denied any recent travel to the fungal endemic areas or international travel. He never suffered from TB or had any exposure to patients with TB. His immunosuppressive regimen consisted of tacrolimus, mycophenolate mofetil, and prednisone. The targeted tacrolimus trough level was 10 to 12 ng/mL, and the patient was generally in the therapeutic range.

Background: Patients with OSA are at increased risk of postoperative cardiorespiratory complications and death. Attempts to stratify this risk have been inadequate, and predictors from large, well-characterized cohort studies are needed.

Research question: What is the relationship between OSA severity, defined by various polysomnography-derived metrics, and risk of postoperative cardiorespiratory complications or death, and which metrics best identify such risk?

Study design and methods: In this cohort study, 6,770 consecutive patients who underwent diagnostic polysomnography for possible OSA and a procedure involving general anesthesia within a period of 2 years before and at least 5 years after polysomnography. Participants were identified by linking polysomnography and health databases. Relationships between OSA severity measures and the composite primary outcome of cardiorespiratory complications or death within 30 days of hospital discharge were investigated using univariable and multivariable analyses.

Results: The primary outcome was observed in 5.3% (n = 361) of the cohort. Although univariable analysis showed strong dose-response relationships between this outcome and multiple OSA severity measures, multivariable analysis showed its independent predictors were: age older than 65 years (OR, 2.67 [95% CI, 2.03-3.52]; P < .0001), age 55.1 to 65 years (OR, 1.47 [95% CI, 1.09-1.98]; P = .0111), time between polysomnography and procedure of ≥ 5 years (OR, 1.32 [95% CI, 1.02-1.70]; P = .0331), BMI of ≥ 35 kg/m² (OR, 1.43 [95% CI, 1.13-1.82]; P = .0032), presence of known cardiorespiratory risk factor (OR, 1.63 [95% CI, 1.29-2.06]; P < .0001), > 4.7% of sleep time at an oxygen saturation measured by pulse oximetry of < 90% (T90; OR, 1.91 [95% CI, 1.51-2.42]; P < .0001), and cardiothoracic procedures (OR, 7.95 [95% CI, 5.71-11.08]; P < .0001). For noncardiothoracic procedures, age, BMI, presence of known cardiorespiratory risk factor, and percentage of sleep time at an oxygen saturation of < 90% remained the significant predictors, and a risk score based on their ORs was predictive of outcome (area under receiver operating characteristic curve, 0.7 [95% CI, 0.64-0.75]).

Interpretation: These findings provide a basis for better identifying high-risk patients with OSA and determining appropriate postoperative care.

Background: Sarcoidosis staging primarily has relied on the Scadding chest radiographic system, although chest CT imaging is finding increased clinical use.

Research question: Whether standardized chest CT scan assessment provides additional understanding of lung function beyond Scadding stage and demographics is unknown and the focus of this study.

Study design and methods: We used National Heart, Lung, and Blood Institute study Genomics Research in Alpha-1 Antitrypsin Deficiency and Sarcoidosis (GRADS) cases of sarcoidosis (n = 351) with Scadding stage and chest CT scans obtained in a standardized manner. One chest radiologist scored all CT scans with a visual scoring system, with a subset read by another chest radiologist. We compared demographic features, Scadding stage and CT scan findings, and the correlation between these measures. Associations between spirometry and diffusing capacity of the lungs for carbon monoxide (Dlco) results and CT scan findings and Scadding stage were determined using regression analysis (n = 318). Agreement between readers was evaluated using Cohen's κ value.

Results: CT scan features were inconsistent with Scadding stage in approximately 40% of cases. Most CT scan features assessed on visual scoring were associated negatively with lung function. Associations persisted for FEV₁ and Dlco when adjusting for Scadding stage, although some CT scan feature associations with FVC became insignificant. Scadding stage was associated primarily with FEV₁, and inclusion of CT scan features reduced significance in association between Scadding stage and lung function. Multivariable regression modeling to identify radiologic measures explaining lung function included Scadding stage for FEV₁ and FEV₁ to FVC ratio (P < .05) and marginally for Dlco (P < .15). Combinations of CT scan measures accounted for Scadding stage for FVC. Correlations among Scadding stage and CT scan features were noted. Agreement between readers was poor to moderate for presence or absence of CT scan features and poor for degree and location of abnormality.

Interpretation: In this study, CT scan features explained additional variability in lung function beyond Scadding stage, with some CT scan features obviating the associations between lung function and Scadding stage. Whether CT scan features, phenotypes, or endotypes could be useful for treating patients with sarcoidosis needs more study.

Background: Although evidence has documented the associations of ambient air pollution with chronic respiratory diseases (CRDs) and lung function, the underlying metabolic mechanisms remain largely unclear.

Research question: How does the metabolomic signature for air pollution relate to CRD risk, respiratory symptoms, and lung function?

Study design and methods: We retrieved 171,132 participants free of COPD and asthma at baseline from the UK Biobank, who had data on air pollution and metabolomics. Exposures to air pollutants (particulate matter with diameter ≤ 2.5 μm [PM_2.5], particulate matter with a diameter ≤ 10 μm, nitrogen oxide [NO_X], and NO₂) were assessed for 4 years before baseline considering residential address histories. We used 10-fold cross-validation elastic net regression to identify air pollution-associated metabolites. Multivariable Cox models were used to assess the associations between metabolomic signatures and CRD risk. Mediation and pathway analysis were conducted to explore the metabolic mechanism underlying the associations.

Results: During a median follow-up of 12.51 years, 8,951 and 5,980 incident COPD and asthma cases were recorded. In multivariable Cox regressions, air pollution was positively associated with CRD risk (eg, hazard ratio per interquartile range increment in PM_2.5, 1.09; 95% CI, 1.06-1.13). We identified 103, 86, 85, and 90 metabolites in response to PM_2.5, particulate matter with a diameter ≤ 10 μm, NO_X, and NO₂ exposure, respectively. The metabolomic signatures showed significant associations with CRD risk (hazard ratio per SD increment in PM_2.5 metabolomic signature, 1.11; 95% CI, 1.09-1.14). Mediation analysis showed that peripheral inflammatory and erythrocyte-related markers mediated the effects of metabolomic signatures on CRD risk. We identified 14 and 12 perturbed metabolic pathways (energy metabolism and amino acid metabolism pathways, etc) for PM_2.5 and NO_X metabolomic signatures.

Interpretation: Our study identifies metabolomic signatures for air pollution exposure. The metabolomic signatures showed significant associations with CRD risk, and inflammatory- and erythrocyte-related markers partly mediated the metabolomic signatures-CRD links.