Chest
Volume 130, Issue 2, August 2006, Pages 326-333
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Original Research: COPD
Systemic Inflammation in Patients With COPD and Pulmonary Hypertension

https://doi.org/10.1378/chest.130.2.326Get rights and content

Study objectives

COPD is a systemic disorder that is associated with increases of inflammatory proteins in systemic circulation. However, no data on the potential role of systemic inflammation in pulmonary hypertension secondary to COPD are available. Therefore, our aim was to investigate the degree of systemic inflammation reflected by circulatory levels of C-reactive protein (CRP), tumor-necrosis factor (TNF)-α, and interleukin (IL)-6 in COPD patients with and without pulmonary hypertension.

Design

Cross-sectional study.

Setting

University hospital, tertiary referral setting.

Patients and measurements

In 43 consecutive patients with COPD (mean [± SD] age, 65.0 ± 10.5 years; mean FEV1, 46.2 ± 18.1% predicted), lung function was assessed using body plethysmography; pulmonary artery pressure (Ppa) levels were measured by echocardiography. Serum TNF-α and IL-6 levels were assessed by enzyme-linked immunosorbent assay, and high-sensitivity serum CRP levels were measured by chemiluminescent immunoassay.

Results

Pulmonary hypertension was present in 19 patients and was absent in 24 patients. In patients with pulmonary hypertension, serum CRP and TNF-α levels were significantly higher than in those patients without hypertension (median, 3.6 mg/L [25th to 75th percentile, 1.4 to 13.0 mg/L] vs 1.8 mg/L [25th to 75th percentile, 0.8 to 2.8 mg/L; p = 0.034]; and median, 4.2 pg/mL [25th to 75th percentile, 3.4 to 10.9 pg/mL] vs 3.1 pg/mL [25th to 75th percentile, 2.1 to 4.2 pg/mL]; p = 0.042, respectively). No differences were seen in serum IL-6 (median, 10.4 pg/mL [25th to 75th percentile, 8.8 to 12.2 pg/mL] vs 10.5 pg/mL [25th to 75th percentile, 9.4 to 39.1 pg/mL]; p = 0.651) between the groups. In multiple linear regression analysis, the following two variables were independent predictors of systolic Ppa (R2 = 0.373): Pao2 (p = 0.011); and log-transformed serum CRP level (p = 0.044).

Conclusion

We conclude that increases in Ppa in patients with COPD are associated with higher serum levels of CRP and TNF-α, raising the possibility of a pathogenetic role for low-grade systemic inflammation in the pathogenesis of pulmonary hypertension in COPD patients.

Section snippets

Subjects

Patients with a diagnosis of COPD, determined according to the American Thoracic Society/European Respiratory Society guidelines,19 were consecutively recruited to the study in a university hospital setting. Exclusion criteria were respiratory disorders other than COPD, pulmonary embolism, left ventricular systolic or diastolic dysfunction, malignancy, systemic autoimmune disorders, infectious diseases, recent surgery, and severe endocrine, hepatic, or renal diseases. The study had local ethics

Patient Characteristics

Forty-three patients (29 male and 14 female) with COPD (mean age, 65.0 ± 10.5 years; range, 40 to 82 years; mean smoking history, 28.4 ± 25.9 pack-years) were recruited to the study. Fourteen patients were classified as having stage II COPD, 19 patients as having stage III COPD, and 10 patients as having stage IV COPD.19 None of the patients had a history of exposure to noxious gases (eg, diesel fumes) or biomass exposure. Pulmonary hypertension was present in 19 patients (mean systolic Ppa,

DISCUSSION

The present study provides a novel observation on the potential significance of systemic inflammation in patients with COPD who have pulmonary hypertension. Our data demonstrate that COPD patients with pulmonary hypertension have higher serum CRP and TNF-α levels compared to those with normal Ppa levels. In addition, in multiple linear regression analysis, log-transformed serum CRP level was an independent predictor of systolic Ppa. In previous studies, a relationship between Ppa and the levels

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    Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (http://www.chestjournal.org/misc/reprints.shtml)

    The authors have reported to the ACCP that no significant conflicts of interest exist with any companies/organizations whose products or services may be discussed in this article.

    This study was supported by operating grant 1/2305/05 of the Ministry of Education and by grant 2005/5-FNLPKE-01 of the Ministry of Health, Slovakia.

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