Role of serum and induced sputum surfactant protein D in predicting the response to treatment in chronic obstructive pulmonary disease
Author(s) -
Wei Liu,
Chunrong Ju,
RONG-CHANG CHEN,
Zhiguang Liu
Publication year - 2014
Publication title -
experimental and therapeutic medicine
Language(s) - English
Resource type - Journals
eISSN - 1792-1015
pISSN - 1792-0981
DOI - 10.3892/etm.2014.1865
Subject(s) - sputum , copd , medicine , gastroenterology , pulmonary disease , respiratory system , immunology , pathology , tuberculosis
This study was designed to determine the expression of serum and sputum surfactant protein D (SP-D) in chronic obstructive pulmonary disease (COPD) and its association with treatment response. Sixty-five treatment-naive patients with COPD and 26 normal control subjects were recruited in the study. The concentrations of serum and sputum SP-D were measured, and the associations of SP-D with pulmonary function and the modified Medical Research Council dyspnea scale (mMRC) and the St. George's Respiratory Questionnaire (SGRQ) scores before and after three months of treatment with an inhaled corticosteroid and a long-acting β2-agonist were analyzed. The concentrations of serum and sputum SP-D in the COPD group (45.46±37.78 and 173.23±186.93 ng/ml, respectively) were significantly higher than those of the normal control group (31.68±12.04 and 89.59±70.29 ng/ml, respectively). After three months of treatment, serum SP-D levels were reduced to 30.7±13.9 ng/ml and were significantly lower than the baseline levels (t=2.217, P=0.031). However, no significant reduction in sputum SP-D levels was observed following the treatment (P>0.05). A significant association between baseline sputum SP-D and change in SGRQ activity scores (r=-0.652, P=0.012) was observed; however no association was established with the changes in other clinical profiles following the treatment (P>0.05). This result suggested that an increased baseline sputum SP-D may be a weak predictive indicator of response to treatment with inhaled corticosteroids and long-acting β2-agonists in patients with COPD.
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