COPD: Iron Deficiency and Clinical Characteristics in Patients With and Without Chronic Respiratory Failure.

Background: The prevalence of iron deficiency in patients with chronic obstructive pulmonary disease (COPD) varies in previous studies. We aimed to assess its prevalence according to 3 well-known criteria for iron deficiency, its associations with clinical characteristics of COPD, and mortality. Methods: In a cohort study consisting of 84 COPD patients, of which 21 had chronic respiratory failure, and 59 were non-COPD controls, ferritin, transferrin saturation (TSat), and mortality across 6.5 years were assessed. Associations between clinical characteristics and iron deficiency were examined by logistic regression, while associations with mortality were assessed in mixed effects Cox regression analyses. Results: The prevalence of iron deficiency in the study population was 10%-43% according to diagnostic criteria, and was consistently higher in individuals with COPD, peaking at 71% in participants with chronic respiratory failure. Ferritin < cutoff was significantly associated with forced expiratory volume in 1 second (FEV1) (odds ratio [OR] 0.33 per liter increase), smoking (OR 3.2), and cardiovascular disease (OR 4.7). TSat < 20% was associated with body mass index (BMI) (OR 1.1 per kg/m2 increase) and hemoglobin (OR 0.65 per g/dL increase). The combined criterion of low ferritin and TSat was only associated with FEV1 (OR 0.39 per liter increase). Mortality was not significantly associated with iron deficiency (hazard ratio [HR] 1.2-1.8). Conclusion: The prevalence of iron deficiency in the study population increased with increasing severity of COPD. Iron deficiency, defined by ferritin < cutoff, was associated with bronchial obstruction, current smoking, and cardiovascular disease, while TSat < 20% was associated with reduced levels of hemoglobin and increased BMI. Iron deficiency was not associated with increased mortality.

It is unlikely that oxygen supplementation in COPD patients with chronic respiratory failure reduce cardiac troponin level.

BACKGROUND: Cardiac troponin T (cTnT) is a biomarker of myocardial injury frequently elevated in COPD patients, potentially because of hypoxemia. This non-randomised observational study investigates whether long-term oxygen treatment (LTOT) reduces the cTnT level. METHODS: We compared cTnT between COPD patients who were candidates for LTOT (n = 20) with two reference groups. Patients from both reference groups were matched with the index group using propensity score.Reference groups consists of institutional pulmonary rehabilitation patients (short-term group) (n = 105 after matching n = 11) and outpatients at a pulmonary rehabilitation clinic (long-term group)(n = 62 after matching n = 10). Comparison was done within 24 h after LTOT initiation in first reference group and within 6 months after inclusion in the second group. RESULTS: The geometric mean of (standard deviation in parentheses) cTnT decreased from 17.8 (2.3) ng/L (between 8 and 9 a.m.) to 15.4 (2.5) ng/L between 1 and 2 p.m. in the LTOT group, and from 18.4 (4.8) ng/L to15.4 (2.5) ng/L in group (1) The corresponding long-term results were 17.0 (2.9) ng/L at inclusion (between 10 and 12 a.m.) to 18.4 (2.4) ng/L after 3 months in the LTOT-group, and from 14.0 (2.4) ng/L to 15.4 (2.5) ng/L after 6 months in group (2) None of the differences in cTnT during the follow-up between the LTOT-group and their matched references were significant. CONCLUSION: Initiation of LTOT was not associated with an early or sustained reduction in cTnT after treatment with oxygen supplementation.

Systemic inflammation induced by exacerbation of COPD or pneumonia in patients with COPD induces cardiac troponin elevation.

BACKGROUND: Troponin is a biomarker of myocardial injury. In chronic obstructive pulmonary disease (COPD), troponin is an important determinant of mortality after acute exacerbation. Whether acute exacerbation of COPD (AECOPD) causes troponin elevation is not known. Here, we investigated whether troponin is increased in AECOPD compared to stable COPD. METHODS: We included 320 patients with COPD in the stable state and 63 random individuals from Akershus University hospital's catchment area. All participants were ≥40 years old (mean 65·1 years, SD 7·6) and 176 (46%) were females. The geometric mean of high-sensitivity cardiac troponin T (hs-cTnT) was 6·9 ng/L (geometric-SD 2·6). They were followed regarding hospital admission for the subsequent 5 years. RESULTS: During the 5-year follow-up, we noted 474 hospitalisations: Totally, 150 and 80 admissions were due to AECOPD or pneumonia, respectively. The geometric mean ratio with geometric SE (GSE) between cTnT at admission and stable state in AECOPD and pneumonia was 1·27 (GSE=1.11, p=0·023) and 1·28 (GSE=1.14, p=0·054), respectively. After inclusion of blood leucocyte count and C reactive protein at hospitalisation, these ratios attenuated to zero. However, we estimated an indirect of AECOPD and pneumonia on the ratio between hs-cTnT at admission and the stable state to 1·16 (p=0·022) and 1·22 (p=0·008), representing 91% (95% CI 82% to 100%) and 95% (95% CI 83% to 100%) of the total effects, respectively. CONCLUSION: AECOPD and pneumonia in patients with COPD is associated with higher cTnT levels. This association appears to be mediated by systemic inflammation.

Annual decline in forced expiratory volume and airway inflammatory cells and mediators in a general population-based sample.

BACKGROUND: Few studies have examined the relationships between sputum inflammatory markers and subsequent annual decline in forced expiratory volume in 1 s (dFEV1). This study investigated whether indices of airway inflammation are predictors of dFEV1 in a general population-based sample. METHODS: The study, conducted from 2003 to 2005, included 120 healthy Norwegian subjects aged 40 to 70 years old. At baseline, the participants completed a self-administered respiratory questionnaire and underwent a clinical examination that included spirometry, venous blood sampling, and induced sputum examination. From 2015 to 2016, 62 (52%) participants agreed to a follow-up examination that did not include induced sputum examination. Those with a FEV1/forced vital capacity (FVC) ratio <  0.70 underwent a bronchial reversibility test. The levels of cytokines, pro-inflammatory M1 macrophage phenotypes were measured in induced sputum using bead-based multiplex analysis. The associations between cytokine levels and dFEV1 were then analysed. RESULTS: The mean dFEV1 was 32.9 ml/year (standard deviation 26.3). We found no associations between dFEV1 and the baseline indices of sputum inflammation. Seven participants had irreversible airflow limitation at follow-up. They had lower FEV1 and gas diffusion at baseline compared with the remaining subjects. Moreover, two of these individuals had a positive reversibility test and sputum eosinophilia at baseline. CONCLUSIONS: In this cohort of presumably healthy subjects, we found no associations between sputum inflammatory cells or mediators and dFEV1 during 10 years of follow-up.

The prognostic value of measurement of high-sensitive cardiac troponin T for mortality in a cohort of stable chronic obstructive pulmonary disease patients.

BACKGROUND: Cardiovascular disease (CVD) is a common comorbidity in chronic obstructive pulmonary disease (COPD). Cardiac troponin (cTn) elevation, indicating myocardial injury, is frequent during acute COPD exacerbations and associated with increased mortality. The prognostic value of circulating cTnT among COPD patients in the stable state of the disease is still unknown. The purpose of the present study was to assess the association between circulating cTnT measured by a high sensitive assay (hs-cTnT) and all-cause mortality among patients with stable COPD without overt CVD. METHODS: In a prospective cohort study we included 275 patients from the Akershus University Hospital's outpatient clinic and from Glittre, a pulmonary rehabilitation clinic. COPD-severity and cardiovascular risk factors were assessed, and time to all-cause death was recorded during a mean follow-up time of 2.8 years. RESULTS: One hundred-eighty patients (65%) had hs-cTnT concentrations ≥ the level of detection (5.0 ng/L) and 66 patients (24%) had hs-cTnT above the normal range (≥14.0 ng/L). In total, 47 patients (17%) died. hs-cTnT concentrations in the ranges <5.0, 5.0-13.9 and ≥14 ng/L were associated with crude mortality rates of 2.8, 4.4 and 11.0 per 100 patient-years, respectively. In adjusted analyses the hazard ratios (95% confidence intervals) for death were 1.7 (0.8-3.9) and 2.9 (1.2-7.2) among patients with hs-cTnT concentrations 5.0-13.9 and ≥14 ng/L, respectively, compared to patients with hs-cTnT <5.0 ng/L. CONCLUSIONS: hs-cTnT elevation is frequently present in patients with stable COPD without overt CVD, and associated with increased mortality, independently of COPD-severity and other cardiovascular risk factors.

Sense of coherence in patients treated for depression with ECT.

OBJECTIVE: The purpose of the study was to investigate whether the Antonovsky Sense of Coherence test administered before and after electroconvulsive treatment (ECT) can contribute more information pertinent to outcome than a test of depression. METHOD: Twenty patients with a severe unipolar or bipolar depression underwent a series of unipolar ECT under standard conditions. As part of the routine of the department, the patients filled in, before and after ECT, the following questionnaires: Beck Depression Inventory (Beck), 20-item version and Antonovsky Sense of Coherence test (SOC), 13-item version. Mean age was 40.3, somewhat less for women. RESULTS: A reduction was obtained from 35 to 17 in total score on Beck, i.e., to mild depression. The SOC value increased to the normal range from a mean of 2.5 to 3.2, indicating a better manageability, comprehensibility and meaningfulness in life. Four patients had an invalidity pension. Ten of the 16 remaining patients attained work after ECT, and scored better than those not starting to work on both tests, SOC > Beck. A low SOC value may indicate increased mortality risk. CONCLUSIONS: Patients who are favorably treated with ECT against any depression, but who do not show a considerable improvement in SOC, would need special follow-up on factors not directly related to mental illness to reduce relapse and mortality risk.