Dataset Information

Relationships of Haptoglobin Phenotypes with Systemic Inflammation and the Severity of Chronic Obstructive Pulmonary Disease.

ABSTRACT: Chronic obstructive pulmonary disease (COPD) is caused by chronic inflammation. Many inflammatory mediators induce the low grade systemic inflammation of COPD. Haptoglobin (Hp) is synthesized in the liver and by lung epithelial and alveolar macrophage cells. However, associations of the serum concentration and phenotype of Hp with COPD are unclear. Therefore, we explored the association of the Hp concentration and Hp phenotype with the inflammatory response and COPD disease severity. We included healthy subjects and COPD patients. The Hp phenotype was categorized by SDS native-PAGE, and concentrations were determined by ELISA. In this trial Hp concentrations in COPD groups were significantly higher than those in healthy controls. There was a significant negative correlation between the Hp concentration and FEV₁(%) (p < 0.001), while IL-6 and 8-isoprostane were positively correlated with the Hp concentration. As to the Hp phenotype, there were significant negative correlations between the FEV₁ and both Hp2-1 and Hp2-2; IL-6 and 8-isoprostane were significantly positively correlated with Hp2-1 and Hp2-2. The ROC curve analysis of the Hp concentration was significantly higher than CRP. Hp concentrations and phenotype were positively correlated with the severity of COPD, especially Hp2-2. In the future, Hp can be considered a novel biomarker for identifying COPD.

SUBMITTER: Lee PL

PROVIDER: S-EPMC6336792 | biostudies-literature | 2019 Jan

REPOSITORIES: biostudies-literature

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Relationships of Haptoglobin Phenotypes with Systemic Inflammation and the Severity of Chronic Obstructive Pulmonary Disease.

Lee Pao-Lin PL Lee Kang-Yun KY Cheng Tsai-Mu TM Chuang Hsiao-Chi HC Wu Sheng-Ming SM Feng Po-Hao PH Liu Wen-Te WT Chen Kuan-Yuan KY Ho Shu-Chuan SC

Scientific reports 20190117 1

Chronic obstructive pulmonary disease (COPD) is caused by chronic inflammation. Many inflammatory mediators induce the low grade systemic inflammation of COPD. Haptoglobin (Hp) is synthesized in the liver and by lung epithelial and alveolar macrophage cells. However, associations of the serum concentration and phenotype of Hp with COPD are unclear. Therefore, we explored the association of the Hp concentration and Hp phenotype with the inflammatory response and COPD disease severity. We included ...[more]

PMID: 30655590

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Project description:BackgroundThe Systemic Immune-Inflammation Index (SII) is a quantitative measurement of the systemic immune-inflammatory response in the human body. The SII has been shown to have prognostic value in various clinical settings, including critical illness, sepsis, and cancer. Its role in chronic obstructive pulmonary disease (COPD) remains unclear and requires further investigation.MethodsWe analyzed demographic data from 16,636 participants in the National Health and Nutrition Examination Survey. Logistic regression analysis was performed to assess the correlation between COPD, lung function, chronic respiratory symptoms and SII. We used Cox proportional hazards (PH) model to analyze the relationship between SII and mortality in COPD patients and healthy individuals. We used propensity score matching (PSM) method to match the COPD population with similar baseline levels with the normal population to further analyze the correlation between SII and COPD.ResultsWe recruited 16,636 participants, ages 40 and above, for the study. A multivariable logistic regression analysis revealed that a higher SII level was independently associated with an elevated likelihood of COPD (Odds Ratio (OR) = 1.449; 95% Confidence Interval (CI): 1.252-1.676, P < 0.0001) after controlling for all other factors. Results of subgroup analysis showed a significant positive correlation between SII and COPD in different age groups, gender, Body Mass Index, smoking status, and those with a history of hypertension. The SII index had positive correlation with COPD after PSM (OR = 1.673; 95%CI: 1.443-1.938). After full adjustment, an increase in the SII is associated with a higher all-cause mortality rate. The hazard ratio (HR) with a 95% CI in the general population, COPD patients, and healthy individuals are 1.161 (1.088, 1.239), 1.282 (1.060, 1.550), and 1.129 (1.055, 1.207), respectively.ConclusionsHigher SII levels are linked to higher prevalence of COPD. COPD patients with a higher SII levels have a higher risk of all-cause mortality. Additional large-scale, long-term studies are necessary to confirm these results.

Project description:BackgroundPatients with chronic obstructive pulmonary disease (COPD) can experience 'exacerbations' of their conditions. An exacerbation is an event defined in terms of subjective descriptors or symptoms, namely dyspnoea, cough and sputum that worsen sufficiently to warrant a change in medical management. There is a need for reliable markers that reflect the pathological mechanisms that underlie exacerbation severity and that can be used as a surrogate to assess treatment effects in clinical studies. Little is known as to how existing study variables and suggested markers change in both the stable and exacerbation phases of COPD. In an attempt to find the best surrogates for exacerbations, we have reviewed the literature to identify which of these markers change in a consistent manner with the severity of the exacerbation event.MethodsWe have searched standard databases between 1966 to July 2004 using major keywords and terms. Studies that provided demographics, spirometry, potential markers, and clear eligibility criteria were included in this study. Central tendencies and dispersions for all the variables and markers reported and collected by us were first tabulated according to sample size and ATS/ERS 2004 Exacerbation Severity Levels I to III criteria. Due to the possible similarity of patients in Levels II and III, the data was also redefined into categories of exacerbations, namely out-patient (Level I) and in-patient (Levels II & III combined). For both approaches, we performed a fixed effect meta-analysis on each of the reported variables.ResultsWe included a total of 268 studies reported between 1979 to July 2004. These studies investigated 142,407 patients with COPD. Arterial carbon dioxide tension and breathing rate were statistically different between all levels of exacerbation severity and between in out- and in-patient settings. Most other measures showed weak relationships with either level or setting, or they had insufficient data to permit meta-analysis.ConclusionArterial carbon dioxide and breathing rate varied in a consistent manner with exacerbation severity and patient setting. Many other measures showed weak correlations that should be further explored in future longitudinal studies or assessed using suggested mathematical modelling techniques.

Dataset Information

Relationships of Haptoglobin Phenotypes with Systemic Inflammation and the Severity of Chronic Obstructive Pulmonary Disease.

Publications

Relationships of Haptoglobin Phenotypes with Systemic Inflammation and the Severity of Chronic Obstructive Pulmonary Disease.

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