Evaluation of the relationship between WBC, HS.CRP and secondary pulmonary hypertension in patients with COPD

authors:

avatar Khalil Ansarin 1 , avatar Farid Rashidi 2 , * , avatar Mohammad Reza Ghaffari 1 , avatar Hossein Namdar 3 , avatar Akbar Sharifi 1

Dept. of Internal Medicine, Tuberculosis and Lung Disease Research Center, Tabriz University of Medical Sciences, Tabriz, Iran
Dept. of Internal Medicine, Imam Reza Hospital, Kermanshah University of Medical Sciences, Kermanshah, Iran
Dept. of Cardiology, Cardiovascular Research Center, Tabriz University of Medical Sciences, Tabriz, Iran
Journal of Kermanshah University of Medical Sciences: Vol.17, issue 10; e74331
published online: January 29, 2014
article type: Research Article
received: June 10, 2013
accepted: October 29, 2013
DOI: https://doi.org/10.22110/jkums.v17i10.1213

how to cite: Ansarin K, Rashidi F, Ghaffari M R, Namdar H, Sharifi A. Evaluation of the relationship between WBC, HS.CRP and secondary pulmonary hypertension in patients with COPD. J Kermanshah Univ Med Sci. 2014;17(10):e74331. https://doi.org/10.22110/jkums.v17i10.1213.

Abstract

Background: Inflammatory mechanisms appear to play a major role in pathogenesis of various types of pulmonary hypertension such as idiopatic PAH (iPAH). Although inflammatory factors such as IL6 and TNFa play an important role in IPAH, there is limited information about the relationship between acute phase reactants and pulmonary hypertension occurring secondary to pulmonary diseases such as chronic obstructive pulmonary diseases (COPD).
Methods: This cross-sectional study was carried out on 94 patients with COPD. Patients with a recent history of systemic corticosteroid use, infection, trauma or surgery, and gastrointestinal bleeding were excluded. Body plethysmography and transthoracic echocardiography were  performed. Blood samples were taken from all patients and sent for complete blood count (CBC) and hsCRP tests.
Results: Twenty patients (28.6%) had pulmonary hypertension. There was a significant difference between the mean of WBC in patients with and without pulmonary hypertension (8505 mic/lit vs. 7044 mic/lit) (p=0.04). There was also a significant difference between the hs.CRP in patients with and without pulmonary hypertension (8.8pg/ml vs. 4.07pg/ml) (p=0.032). After adjustment of age, sex, serum  hemoglobin, hematocrit, O2sat, FEV1 and FVC, the relationship between the IL6, white blood cell count, HS.CRP and pulmonary hypertension remained significant (p=0.018, p=0.022).
Conclusion: Inflammatory factors such as white blood cell and HS.CRP are independent risk factors of pulmonary hypertension in COPD patients.

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References

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