Platelet activation and cardiovascular co-morbidities in patients with chronic obstructive pulmonary disease.

Objective: Platelet activation in COPD patients is associated with an increased risk of cardiovascular events. Aim of the study: to assess the mean platelet volume (MPV), as an index of platelet activation, in patients with COPD both when stable or during exacerbation. Research design and methods: 478 patients with COPD (75 with exacerbation) and 72 age-matched healthy controls were enrolled. Medical history, co-morbidities, medications, pulmonary function tests, MPV and blood cell count, erythrocyte sedimentation rate (ERS) and C reactive protein (CRP) were recorded. Results: MPV was higher in COPD patients than in controls (8.7 \ub1 1.1 fL and 8.4 \ub1 0.8 fL respectively, p = 0.025) and increased across the severity of the diseases as assessed by the GOLD post bronchodilator FEV1 categorized I to IV (p>0.05). MPV was higher in COPD patients during acute exacerbation as compared with stable condition (8.7 \ub1 1.0 fL and 8.9 \ub1 1.0 fL, p = 0.021). MPV 65 10.5 fL correlated with the presence of at least one co-existing cardiovascular disease (p = 0.008) . No correlation was observed between MPV and CRP or ERS in patients or in controls. An inverse significant correlation was found between platelets count and MPV in COPD patients. Conclusions: Elevated MPV is associated with lower platelet count and with cardiovascular co-morbidity in COPD patients. MPV value is higher in more severe COPD and during acute exacerbation. Present findings warrant future studies to confirm a possible clinically relevant role for platelet activation and cardiovascular risk in the population of COPD

Decreased humoral immune response in the bronchi of rapid decliners with chronic obstructive pulmonary disease

Background: Identification of COPD patients with a rapid decline in FEV1 is of particular interest for prognostic and therapeutic reasons. Objective: To determine the expression of markers of inflammation in COPD patients with rapid functional decline in comparison to slow or no decliners. Methods: In COPD patients monitored for at least 3 years (mean ± SD: 5.8 ± 3 years) for lung functional decline, the expression and localization of inflammatory markers was measured in bronchial biopsies of patients with no lung functional decline (FEV1% + 30 ± 43 ml/year, n = 21), slow (FEV1% ml/year, − 40 ± 19, n = 14) and rapid decline (FEV1% ml/year, − 112 ± 53, n = 15) using immunohistochemistry. ELISA test was used for polymeric immunoglobulin receptor (pIgR) quantitation “in vitro”. Results: The expression of secretory IgA was significantly reduced in bronchial epithelium (p = 0.011) and plasma cell numbers was significantly reduced in the bronchial lamina propria (p = 0.017) of rapid decliners compared to no decliners. Bronchial inflammatory cell infiltration, CD4, CD8, CD68, CD20, NK, neutrophils, eosinophils, mast cells, pIgR, was not changed in epithelium and lamina propria of rapid decliners compared to other groups. Plasma cells/mm2 correlated positively with scored total IgA in lamina propria of all patients. “In vitro” stimulation of 16HBE cells with LPS (10 μg/ml) and IL-8 (10 ng/ml) induced a significant increase while H2O2 (100 μM) significantly decreased pIgR epithelial expression. Conclusion: These data show an impaired humoral immune response in rapid decliners with COPD, marked by reduced epithelial secretory IgA and plasma cell numbers in the bronchial lamina propria. These findings may help in the prognostic stratification and treatment of COPD