Introduction: It has long been known that COPD causes elevation in BNP level caused by hypoxia present
in cases of pulmonary hypertension in COPD.
The aim of this study: This study was carried out to evaluate the changes in BNP level in COPD patients
without pulmonary hypertension or cor pulmonale during exacerbation and after remission.
Subjects and methods: This study was created on 50 subjects, 30 COPD patients according to inclusion and
exclusion criteria (BNP level will be measured during exacerbation and after remission) plus 20 age
matched apparently healthy control subjects, ten of them are non smokers and ten are asymptomatic
smokers. For all subjects, history taking, full clinical exam done. PFT (spirometry), BNP level measurement
on human serum by ELIZA, routine labs (CBC, liver and renal function). ECG. echocardiography.
Results: Levels of BNP were significantly higher in COPD patients with mean (60.52 ± 30.98 pg/mL) than
control with mean (21.13 ± 4.61 pg/mL) and higher during exacerbation (60.52 ± 30.9 pg/mL) than during
remission (35.65 ± 16.54 pg/mL), BNP was significantly higher in grade (III, IV) with mean (86.94 ± 40.19,
pg/mL) than grade (II) (56.76 ± 6.2 pg/mL) and grade (II) was significantly higher than grade (I) with mean
(37.86 ± 8.81 pg/mL) and it was a significantly inversely related to post FEV1% and post FEF 25–75% and
significantly direct correlated to paco2 and non significant negative correlation to pao2.
Conclusion: Plasma BNP can be used as a useful prognostic biomarker of COPD and a good predictor of
exacerbation, As BNP level was significantly higher in COPD patients than in control groups, (p < 0.005)
and also significantly higher in grade (IV, III) than grade (II) and was significantly higher in grade (II) than
grade (I) COPD patients, BNP level significantly higher (p < 0.005) during exacerbation than during remission
of COPD patients |
