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- Lepzien, Rico, et al.
(author)
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Mononuclear phagocytes in lungs, lymph nodes and blood of sarcoidosis patients
- 2018
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In: European Respiratory Journal. - : European Respiratory Society. - 0903-1936 .- 1399-3003. ; 52
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Journal article (other academic/artistic)abstract
- Introduction: Sarcoidosis is characterized by granuloma formation primarily in the lung and lung-draining lymph nodes (LN). The disease can present with an acute onset (usually Löfgren’s syndrome (LS)) or a gradual onset (non-LS). Mononuclear phagocytes (MNPs) - macrophages, monocytes and dendritic cells (DC) - are likely critical in sarcoidosis as they initiate and maintain T cell activation and contribute to granuloma formation by production of cytokines. MNPs in lung tissue and LN are poorly studied in both, non-LS and LS sarcoidosis patients.Aim: To characterise the distribution and phenotype of MNPs in BAL, endobronchial biopsies (EBB), LN sampled by endobronchial ultrasound-guided transbronchial needle aspiration (EBUS-TBNA) and blood from the same non-LS or LS sarcoidosis patients.Results: We identified MNPs from all four anatomical compartments in non-LS (n=7) and LS (n=4) sarcoidosis patients. Blood, BAL and LN contained all MNP subsets while EBB only harboured one of three monocyte subsets. Frequencies, maturation and migratory status were different between the compartments as well as between non-LS and LS patients. Our results suggest heterogeneity in distribution and function of MNPs within organs typically affected in sarcoidosis and their potential involvement in the disease course.Conclusions: We show that cells from BAL fluid do not necessarily reflect cells from EBB, a tissue primarily affected by granuloma formation. Our work provides a foundation for future investigations of MNPs in non-LS and LS sarcoidosis patients, allowing improved stratification to identify patients at risk of developing severe disease and provide early treatment to slow down disease progression.
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- Nilsson, Ulf, et al.
(author)
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Elevated cardiac troponin predicts 11-year mortality in COPD
- 2020
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In: European Respiratory Journal. - : European Respiratory Society (ERS). - 0903-1936 .- 1399-3003. ; 56:Suppl 64
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Journal article (other academic/artistic)abstract
- Background: Ischemic heart disease (IHD) is a common multimorbidity in individuals with COPD. High sensitive cardiac troponin I (hs-cTnI) has been shown to predict short-term mortality, but longer follow-ups has rarely been performed in population-cohorts.Aim: To evaluate the predictive value of elevated hs-cTnI on mortality among individuals with COPD compared with normal lung function (NLF).Methods: In 2002-04, subjects with FEV1/VC <0.70 (COPD, n=993) and age and sex-matched referents withoutCOPD were identified from OLIN’s population-based cohorts. In 2005, structured interviews, post-bronchodilator spirometry, blood sampling and ECG were performed in individuals with COPD (n=599) and NLF (n=756). Hs-cTnI was analysed in serum and concentrations ≥5 ng/L were defined as elevated. Mortality data were collected until 2016.Results: In 2005, the prevalence of reported IHD and elevated hs-cTnI was higher in COPD than NLF (16.2% vs 11.9% p=.02 and 31.1% vs 25.0% p=.01). The cumulative mortality was higher in COPD than NLF, both overall (36.5% vs 19.2% p<.001), and when restricting comparison to individuals with hs-cTnI≥5 (59.1% vs 34.9% p<.001). In a Cox-regression model adjusting for common confounders including reported IHD and ischemic ECG changes, hs-cTnI≥5 was associated with an increased risk for death in COPD (HR 1.41, 95%CI 1.03-1.93), but not in NLF (HR 0.84 95%CI 0.58-1.22). The increased risk remained after adjusting for FEV1% predicted.Conclusion: Elevated hs-cTnI was associated with increased mortality over a 11 -year follow-up among individuals with COPD, but not among those with NLF in this population-based study. The use of troponin could identify individuals with stable COPD at the highest risk of death.
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- Ghorbani, Ramin, 1981-
(author)
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Real-time breath gas analysis of carbon monoxide : laser-based detection and pulmonary gas exchange modeling
- 2018
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Doctoral thesis (other academic/artistic)abstract
- Breath gas analysis is a promising approach for non-invasive medical diagnostics and physiological monitoring. Real-time, breath-cycle resolved biomarker detection facilitates data interpretation and has the potential to improve the diagnostic value of breath tests as exhalation profiles carry spatiotemporal information about biomarker origin and gas exchange in the respiratory tract. This thesis presents and scrutinizes a novel methodology for the analysis of real-time breath data, where single-exhalation profiles are simulated using a pulmonary gas exchange model and least-squares fitted to measured expirograms to extract airway and alveolar contributions and diffusing capacities. The methodology is demonstrated on exhaled breath carbon monoxide (eCO), a candidate biomarker for oxidative stress and respiratory diseases. The thesis mainly covers (1) the construction of a compact optical sensor based on tunable diode laser absorption spectroscopy (TDLAS) in the mid-infrared region (4.7 μm) for selective and precise real-time detection of CO in breath and ambient air (detection limit 9 ± 5 ppb at 0.1 s), (2) the design of an advanced online breath sampling system, (3) the implementation of a trumpet model with axial diffusion (TMAD) to simulate the CO gas exchange, and (4) the application of extended eCO analysis in clinical studies to establish the healthy non-smoker baseline of the eCO parameters and to study the response to CO and wood smoke exposure. It is shown that the TMAD adequately describes the gas exchange during systemic CO elimination for different breathing patterns, and that there is no difference between eCO parameters from mouth- and nose exhalations. Expirogram shape and eCO parameters exhibit a dependence on the exhalation flow rate, but for a given breathing maneuverer, the parameters lie in a narrow range. Airway CO is close to and correlates with ambient air CO, indicating negligible airway production in the healthy population. The alveolar diffusing capacity is independent of endogenous CO, even after exposure to elevated exogenous CO, and could be used to assess lung diffusion abnormalities. Compared to CO exposure, no clear additional effect of exposure to wood smoke particles on eCO is observed. The discrimination between endogenous and exogenous CO sources remains a challenge.
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