Real-life burden of hospitalisations due to COPD exacerbations in Spain

Patients with chronic obstructive pulmonary disease (COPD) often suffer episodes of exacerbation of symptoms (ECOPD) that may eventually require hospitalisation due to several, often overlapping, causes. We aimed to analyse the characteristics of patients hospitalised because of ECOPD in a real-life setting using a "big data" approach.The study population included all patients over 40 years old with a diagnosis of COPD (n=69 359; prevalence 3.72%) registered from 1 January 2011 to 1 March 2020 in the database of the public healthcare service (SESCAM) of Castilla-La Mancha (Spain) (n=1 863 759 subjects). We used natural language processing (Savana Manager version 3.0) to identify those who were hospitalised during this period for any cause, including ECOPD.During the study 26 453 COPD patients (38.1%) were hospitalised (at least once). Main diagnoses at discharge were respiratory infection (51%), heart failure (38%) or pneumonia (19%). ECOPD was the main diagnosis at discharge (or hospital death) in 8331 patients (12.0% of the entire COPD population and 31.5% of those hospitalised). In-hospital ECOPD-related mortality rate was 3.11%. These patients were hospitalised 2.36 times per patient, with a mean hospital stay of 6.1 days. Heart failure was the most frequent comorbidity in patients hospitalised because of ECOPD (52.6%).This analysis shows that, in a real-life setting, ECOPD hospitalisations are prevalent, complex (particularly in relation to heart failure), repetitive and associated with significant in-hospital mortality.Copyright ©The authors 2022

Polymorphisms within inflammatory genes and colorectal cancer

BACKGROUND: Chronic inflammation is a risk factor for colorectal cancer and polymorphisms in the inflammatory genes could modulate the levels of inflammation. We have investigated ten single nucleotide polymorphisms (SNPs) in the following inflammation-related genes: TLR4 (Asp299Gly), CD14 (-260 T>C), MCP1 (-2518 A>G), IL12A (+7506 A>T, +8707 A>G, +9177 T>A, +9508 G>A), NOS2A (+524T>C), TNF (-857C>T), and PTGS1 (V444I) in 377 colorectal (CRC) cancer cases and 326 controls from Barcelona (Spain). RESULTS: There was no statistically significant association between the SNPs investigated and colorectal cancer risk. CONCLUSION: The lack of association may show that the inflammatory genes selected for this study are not involved in the carcinogenic process of colorectum. Alternatively, the negative results may derive from no particular biological effect of the analysed polymorphisms in relation to CRC. Otherwise, the eventual biological effect is so little to go undetected, unless analysing a much larger sample size

Gene Expression Patterns in Peripheral Blood Correlate with the Extent of Coronary Artery Disease

Systemic and local inflammation plays a prominent role in the pathogenesis of atherosclerotic coronary artery disease, but the relationship of whole blood gene expression changes with coronary disease remains unclear. We have investigated whether gene expression patterns in peripheral blood correlate with the severity of coronary disease and whether these patterns correlate with the extent of atherosclerosis in the vascular wall

CD14 and toll-like receptor 4: a link between infection and acute coronary events?

The CD14 receptor is a pattern recognition molecule in the innate immune response against microorganisms and other exogenous and endogenous stress factors. The most important CD14 signalling co-receptor is toll-like receptor 4 (TLR4), which activates, among others, the nuclear factor κB (NF-κB) inflammatory pathway. Besides its role in innate immunity and host defence, the proinflammatory cytokines expressed upon TLR4/NF-κB pathway activation exert proatherogenic effects. The CD14 C(–260)T promoter and TLR4 Asp299Gly functional polymorphisms have been recently implicated in the development of cardiovascular events, suggesting that the genetically determined inflammatory response against pathogens or their antigens may have a major role in atherogenesis and subsequent acute events. Is the association of these polymorphisms with cardiovascular disease more evidence for the implication of infection, especially by Gram negative bacteria, in the development of acute coronary events? This article reviews the molecular basis, biological functions, and clinical implications of the CD14/TLR4 polymorphisms in the development of cardiovascular events

C-reactive protein elevation and disease activity in patients with coronary artery disease

AIMS: We sought to assess (1) whether C-reactive protein (CRP) is an independent predictor of future cardiovascular events after adjustment for coronary artery disease (CAD) severity and (2) whether CRP levels correlate with number of angiographically complex coronary artery stenosis. METHODS AND RESULTS: We studied 825 consecutive angina patients (mean age 63+/-10 years, 74% men), 700 with chronic stable angina (CSA) and 125 with acute coronary syndromes without ST-segment elevation (ACS). The composite endpoint of non-fatal acute myocardial infarction, hospital admission with class IIIb unstable angina and cardiac death was assessed at one year follow-up. Hs-CRP level was higher in CSA patients with the combined end-point (P=0.03) after adjustment for number of diseased coronary arteries. Hs-CRP was also significantly higher in patients with ACS compared to CSA ( P=0.004) and correlated with number of complex angiographic stenoses (r=0.36, P=0.01). Hs-CRP was also increased in patients with NYHA functional class III or IV compared to those in class I or II (p<0.0001). CONCLUSIONS: CRP levels predict future cardiovascular events independently of CAD severity and correlate with number of angiographically complex coronary artery stenosis in patients with ACS. Thus, CRP levels are a marker of atheromatous plaque vulnerability and CAD activ

Markers of inflammation and multiple complex stenoses (pancoronary plaque vulnerability) in patients with non-ST segment elevation acute coronary syndromes

Objective: To assess the relation between markers of inflammation and the presence of multiple vulnerable plaques in patients with non-ST segment elevation acute coronary syndromes. Design: Prospective cohort study of 55 patients with non-ST segment elevation acute coronary syndromes and angiographically documented coronary disease. Blood samples were obtained at study entry for the assessment of high sensitivity C reactive protein (CRP), neopterin, and neutrophil count. Coronary stenoses were assessed by quantitative computerised angiography and classified as “complex” (irregular borders, ulceration, or filling defects) or “smooth” (absence of complex features). Extent of disease was also assessed by a validated angiographic score. Results: Neutrophil count (r  =  0.36, p  =  0.007), CRP concentration (r  =  0.33, p  =  0.02), and neopterin concentration (r  =  0.45, p < 0.001) correlated with the number of complex stenoses. Patients with multiple (three or more) complex stenoses, but not patients with multiple smooth lesions, had a higher neutrophil count (5.9 (1.4) × 10(9)/l v 4.8 (1.4) × 10(9)/l, p  =  0.02), CRP concentration (log transformed) (1.08 (0.63) v 0.6 (0.6), p  =  0.03), and neopterin concentration (log transformed) (0.94 (0.18) v 0.79 (0.15), p  =  0.002). Multiple regression analysis showed that neopterin concentration (B  =  4.8, 95% confidence interval (CI) 1.9 to 7.7, p  =  0.002) and extent of coronary artery disease (B  =  0.6, 95% CI 0.03 to 1.2, p  =  0.04) were independently associated with the number of complex stenoses. Conclusions: Acute inflammatory markers such as high neutrophil count, CRP concentration, and neopterin concentration correlate with the presence of multiple angiographically complex coronary stenoses. Neopterin concentration was a stronger predictor of multiple complex plaques than were neutrophil count and CRP concentration. These findings suggest that a relation exists between inflammation and pancoronary plaque vulnerability