Background: The diagnosis of COPD is based on both clinical signs and functional tests. Although there are different functional tests used to assess COPD, no reliable biomarkers able to provide information on pathogenesis and severity are available. The aim of the present study is to explore the relationship between surfactant protein B (Sp-B) serum levels and clinical, radiological, and functional pulmonary parameters in COPD patients. Methods: Forty COPD patients and twenty smokers without airflow limitations or respiratory symptoms were enrolled. Each patient was given questionnaires (CAT and mMRC) and 6MWT, spirometry, DLCO, and computer tomography (CT) were performed. All participants underwent a venous blood sample drawing, and quantitative detection of their Sp-B plasma levels was performed by an enzyme-linked immunosorbent assay. The spirometry and Sp-B plasma levels were assessed after 12 months. Results: A statistically significant difference was found in the plasma Sp-B levels between COPD patients compared to the other group (4.72 + 3.2 ng/mL vs. 1.78 + 1.5 ng/mL; p < 0.001). The change in FEV1 after 12 months (Delta FEV1) showed a significantly negative correlation with respect to the change in Sp-B levels (Delta SpB) (r = −0.4; p < 0.05). This correlation indicates that increasing the plasma dosage of SpB is a foretoken of functional decline. Conclusions: SpB may be considered as a useful marker in COPD assessment and provides prognostic information on lung functional decline. Despite its usefulness, further studies are needed to define its reliability as a biomarker.

Background: OSAS is characterized by a chronic intermittent hypoxia (CIH) and sleep fragmentation. Polysonnography is the standard diagnostic test. New biomarkers have been proposed. The BDNF is a key mediator of neuronal and synaptic plasticity in cognitive functions. Experimental studies demonstrate changes of serum levels of BDNF following CIH Objectives: To determine serum level of BDNF in patients with severe OSAS compared with a control group and its relationship to neurocognitive function. Changes in BDNF serum levels in OSAS patients after CPAP treatment. Methods: Serum BDNF and the Montreal Cognitive Assestment (MoCA) are evaluated in 12 patients with newly diagnosed severe OSAS and in 8 healthy patients (control group). In OSAS patients serum BDNF and MoCA were reassessed after 45 days of CPAP treatment. Results: BDNF in OSAS patients was significantly higher compared to control group (p=0.01) and showed a positive correlation with ODI (p=0.01, r=0.6). Serum BDNF had a decreasing trend after CPAP treatment. Before the treatment, MoCA scores were lower in OSAS patients than controls and are positively correlated with serum BDNF levels (p=0.02, r=0.57). MoCA is normalized by CPAP therapy Conclusions: OSAS patients showed higher serum BDNF levels and lower MoCA scores compared to controls. The positive correlation between BDNF values and MoCA might reveal a peculiar BDNF-mediated neuroprotective mechanism against neuroinflammation induced by hypoxia.

Background: OSAS is characterized by a chronic intermittent hypoxia (CIH) and sleep fragmentation. PSG is the gold standard for diagnosis. New biomarkers have been proposed. BDNF is a key mediator of cognitive functions. Changes of BDNF serum levels follow CIH. OSAS patients have mucosal upper airways inflammation. BDNF has been identified in various chronic inflammatory airways diseases. Objectives: BDNF serum levels and mucosal expression in severe OSAS patients compared to controls. Relationship of serum BDNF with neurocognitive function. Changes in serum BDNF after CPAP. Methods: Serum BDNF, upper airways mucosal biopsy and Montreal Cognitive Assestment (MoCA) are performed in 12 naïve severe OSAS patients and in 8 controls. In OSAS patients serum BDNF and MoCA were reassessed after 45 days of CPAP treatment. Results: BDNF in OSAS was significantly higher than controls (p=0.01) and showed a positive correlation with ODI (p=0.01, r=0.6). Serum BDNF had a decreasing trend after CPAP treatment. Before the treatment, MoCA scores were lower in OSAS than controls and are positively correlated with serum BDNF levels (p=0.02, r=0.57). MoCA is normalized by CPAP therapy. Immunohistochemistry of mucosal biopsy in OSAS patients showed higher inflammatory infiltrate CD3+ CD79a+ (BDNF positive) than controls. Conclusions: OSAS patients showed higher serum BDNF levels and lower MoCA scores than controls. The positive correlation between BDNF values and MoCA might reveal a peculiar BDNF-mediated neuroprotective mechanism against neuroinflammation induced by hypoxia. OSAS have mucosal upper airway lymphocytic inflammation BDNF positive.