Chemical pleurodesis is a therapeutic procedure applied to create the symphysis between the parietal and visceral pleura by intrapleural administration of various chemical agents (e.g. talk, tetracycline, iodopovidone, etc.). The two major clinical conditions treated with chemical pleurodesis are recurrent pleural effusion (PE) and recurrent spontaneous pneumothorax. Although the history of chemical pleurodesis began over a century ago, detailed data on the mechanisms of action of sclerosing agents are highly incomplete. The following article aims to present the state of knowledge on this subject.It is believed that mesothelial cells are the main structural axis of pleurodesis. In response to sclerosing agents they secrete a variety of mediators including chemokines such as interleukin 8 (IL-8) and monocyte chemoattractant protein (MCP-1), as well as growth factors - vascular endothelial growth factor (VEGF), platelet-derived growth factor (PDGF), basic fibroblast growth factor (bFGF) and transforming growth factor- β (TGF-β). Numerous data suggest that intact mesothelial cells and the above cytokines play a crucial role in the initiation and maintenance of different pathways of pleural inflammation and pleural space obliteration.It seems that the process of pleurodesis is largely nonspecific to the sclerosant and involves the same ultimate pathways including activation of pleural cells, coagulation cascade, fibrin chain formation, fibroblast proliferation and production of collagen and extracellular matrix components. Of these processes, the coagulation cascade with decreased fibrinolytic activity and increased fibrinogenesis probably plays a pivotal role, at least during the early response to sclerosant administration.A better understanding of various pathways involved in pleurodesis may be a prerequisite for more effective and safe use of various sclerosants and for the development of new, perhaps more personalized therapeutic approaches.

The role of bronchoalveolar lavage fluid (BALf) examination in differential diagnosis of interstitial lung diseases (ILD) was established. Currently, functional polarization into M1 (pro-inflammatory) and M2 (anti-inflammatory) subpopulations is emphasized.The aim of our study was to compare the proportion of M1 and M2 in BALf of patients with different ILD.BALf samples were collected from 75 ILD patients: sarcoidosis (SA, 36), hypersensitivity pneumonitis (HP, 10), non-specific interstitial pneumonia (NSIP, 8), idiopathic pulmonary fibrosis (IPF, 6) and other ILD (15). Phenotyping was performed by immunocytochemistry with anti-CD40 and CD163 antibodies (for M1 and M2, respectively).For both, CD40 and CD163, three populations of cells have been specified: small cells with strong (+++), large cells with weak (+) and cells with no (–) reaction. Due to lack of statistically significant differences between patients with HP, NSIP and IPF, they were classified into a common group and compared to the group of patients with sarcoidosis. The median proportion of macrophage population was as follows: for CD40: 61%, 35%, 2% in patients with SA and 49%, 47%, 3% in patients with other ILD and for CD163: 55%, 35%, 5% in SA and 53%, 43%, 1% in ILD patients, respectively. We found a significantly higher proportion of M1 in SA when compared with other ILD.Our study showed no evidence of defined polarization of alveolar macrophages in different types of interstitial lung diseases. However, we emphasized the role of CD40 positive cells in sarcoidosis and the role of CD163 positive cells in fibrotic diffuse lung diseases.

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The use of EBUS to assess BWT in asthma and COPD is feasible and it shows good compatibility with HRCT. A tendency towards lower BWT values in EBUS when compared to HRCT was observed. The finding that EBUS measurements demonstrated the differences between BWT in patients with obstructive lung diseases and controls, may suggest that EBUS is a more sensitive method to study the BWT than HRCT.

Introduction In contrast to tuberculous pleurisy (TP), no accurate and commonly accepted biochemical marker of malignant pleural effusion (MPE) has been established. Objectives We aimed to evaluate the ability of a previously reported cancer ratio (CR) to discriminate between MPEs and non-MPEs; to test whether age may have additional value in differentiating MPEs from non-MPEs; and if so, to combine lactate dehydrogenase (LDH) and age with other TP biomarkers in search of an index useful in the identification of MPEs. Patients and methods A retrospective analysis of data from 140 patients with malignant (n = 74), tuberculous (n = 37), and parapneumonic (n = 29) pleural effusions was performed. The diagnostic performance of a test to discriminate between MPEs and non-MPEs was evaluated using the receiver operating characteristic curve analysis. Results Three ratios showed the largest area under the curve (AUC): serum LDH to pleural fluid soluble Fas ligand, age to pleural fluid adenosine deaminase (ADA), and serum LDH to pleural fluid interleukin 18; moreover, the ratios were characterized by high sensitivity (95%, 93.2%, and 92.9%, respectively) and fair specificity (64.8%, 71.2%, and 58.5%, respectively) for differentiating MPEs from non-MPEs. The AUC for CR was lower and showed a sensitivity of 94.6% and a specificity of 68.2%. Conclusions Our study showed a lower specificity of the CR for discriminating between MPEs and non-MPEs than previously reported. We demonstrated that the combinations of serum LDH with other pleural fluid biomarkers of TP have a similar diagnostic performance. We also found that age might be an important factor differentiating between MPEs and non-MPEs and proposed a new age to pleural fluid ADA ratio which has a discriminative potential similar to that of the CR.