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A 19-year-old patient after previous wedge resection of the right upper pulmonary lobe a year ago urgently admitted with recurrent right-sided spontaneous pneumothorax. According to standard management of spontaneous pneumothorax, we performed diagnostic thoracoscopy and drainage of the right pleural cavity with regular X-ray examinations. However, these measures were ineffective. The patient was scheduled for surgery, and we intraoperatively observed an unusual cause of pneumothorax. Thus, we present spontaneous pneumothorax following right upper lobe pulmonary sequestration. The uniqueness of this case is associated with unusual manifestation and non-standard localization of rare lesion. A few cases of pneumothorax in similar patients are described in the world literature. The key limiting factor in diagnosis of such defects (identification of aberrant vessel supplying abnormal lung parenchyma) is the lack of routine CT angiography in patients diagnosed with pneumothorax. That is why CT changes were interpreted as postoperative ones, and the true cause was established only during redo surgery. A thorough inspection of the pleural cavity and alertness regarding unusual appearance of the right upper pulmonary lobe made it possible to suggest a non-standard diagnosis, avoid complications (bleeding from afferent vessel) and perform adequate lung resection.

The authors of the article prove the need to include a new name for the disease - "Progressive Fibrosing Lung Disease" into clinical practice. Recognition of the fact that some lung diseases end in a fibrosing process, which does not have any significant differences depending on the initial disease that led to fibrosis, will expand the indications for earlier prescription of antifibrotic drugs, which will undoubtedly improve the prognosis in this extremely severe category of patients.

The clinic and pathological anatomy of the infection caused by the SARS-CoV-2 virus (coronavirus infection - CI) with the development of Post-Covid syndrome (PS) have not been studied enough. This also applies to morphofunctional changes in the lungs, one of the most important components of PS. We conducted a histological and bacterioscopic study of lung biopsy specimens in 20 patients of both sexes aged 22-75 years. In many patients, PS developed relatively late - not earlier than 1 year - 1 year 4 months after the onset of acute clinical symptoms of CI. Structural changes in the lungs in PS appear as an inflammatory reaction such as interstitial pneumonia. Most patients had nonspecific interstitial pneumonia with elements of organizing interstitial pneumonia, in some cases complicated by the presence of a specific granulomatous reaction, characteristic of pulmonary tuberculosis. Despite this, according to the results of traditional bacterioscopic and bacteriological studies, the tuberculous etiology of pulmonary fibrosis has not yet been confirmed. Perhaps this is due to the fact that we are talking about an inapparent tuberculosis infection, the causative agent of which is the L-form of Mycobacterium tuberculosis. Patients with PS who have pulmonary fibrosis on x-ray should be under the special supervision of a phthisiatrician or pulmonologist.

The article describes the clinical, radiological and pathological features of epithelioid hemangioendothelioma (EHE) in 27 adult patients, mainly female. In all cases, with the exception of one, there was a benign course of the disease over many years with a tendency to stabilize growth, the morphological sign of which was the development of widespread sclerotic changes. With the help of immunohistochemical method, the endothelial nature of EHE cells and its relatively low proliferative potential were confirmed. Clinical and morphological features of EHE raise the question of the essence of proliferation of endothelial cells with the formation of tumor-like nodes. There is every reason to consider EHE as a pseudotumor of the type of nodose hyperplasia in the nosological group of dyshormonal hyperplasia, similar to benign leiomyoma of the uterus with lung damage, as we have previously proposed.

The paper presents an X-ray morphological differential diagnosis of idiopathic pulmonary fibrosis (IPF) and fibrotic hypersensitivity pneumonitis (FHP). It describes the etiology, pathogenesis, radiological signs, and pathoanatomy of IPF and FHP. For differential diagnosis, radiological and morphological signs were studied in 105 patients with IPF and in 111 patients with FHP. The mean ages of patients with IPF or FHP were 65.0±8.9 and 48.9±12.3 years, respectively. The history of IPF to the moment of its diagnosis ranged from 1 to 18 months, while that of FHP was 35 to 79 days. The authors describe the additional morphological signs of FHP: delicate collagen fibrosis; smooth muscle metaplasia in the interalveolar septa and fibrotic areas; fibroblastic foci mainly in the walls of bronchioles; plasma cell infiltration of interalveolar septa with a touch of neutrophils and eosinophils. A table has been compiled for differential diagnosis according to the morphological signs of IPF and FHP.

The pathogenetic relationship between pulmonary tuberculosis and lung cancer in their concurrence is now still the subject of discussion., Objective: To study the pathogenetic relationship between pulmonary tuberculosis and lung cancer., Material and Methods: The investigators examined surgical material from 51 patients (41 men) aged 41-73 years (mean age, 63.7 years) with pulmonary tuberculosis concurrent with lung cancer. They also studied tumors, tuberculous caverns, infiltrates, and foci with surrounding macroscopically intact lung tissue, as well as fibrotic changes by histological, histochemical and immunohistochemical examinations., Results: Previous tuberculosis can be considered as a risk factor for lung cancer. Central cancer was more common in patients with inactive, chronic tuberculosis with a predominance of fibrotic processes in the root of the lung and in its hilar zones. Fibrous-cavernous tuberculosis and cavernous tuberculosis were more frequently concurrent with central cancer; peripheral tumors mainly occurred in infiltrative tuberculosis and tuberculomas., Conclusion: The findings suggest that in a number of cases, cancer and tuberculosis may be anatomically close, developing in the same anatomical unit - the lung. However, this does not indicate an unambiguous etiopathogenetic relationship between pulmonary tuberculosis and lung cancer. The relationships between pulmonary tuberculosis and lung cancer are much more complex and do not fit into the simple scheme of cause-and-effect relations.

The paper presents the data available in the literature on the pathogenesis, clinical and morphological, histological and immunohistochemical features of pulmonary sclerosing pneumocytoma (SP). The paper gives the detailed histological and immunohistochemical characteristics of 6 SP cases. The need for the differential diagnosis of SP is determined by the features and complexity of their histo- and morphogenesis within a single tumor and a complex diagnostic study.

The effect of the tetrapeptide bronchogen on the structural and functional state of the bronchial epithelium and inflammatory activity in the lungs was studied in the chronic obstructive pulmonary disease (COPD) model, created in rats by a 60-day intermittent exposure to nitrogen dioxide. The cell composition and cytokine-enzyme profile of bronchoalveolar lavage fluid (BALF), the content of secretory immunoglobulin A and surfactant protein B in BALF were determined. Following the course of peptide treatment the decreased activity of neutrophilic inflammation with the normalization of cellular composition and profile of pro-inflammatory cytokines and enzymes in the bronchoalveolar space was observed. The structure of bronchial epithelium, disturbed during formation of COPD model, was restored and accompanied by restoration of its functional activity as evidenced by an increase of secretory immunoglobulin A (local immunity marker) and surfactant protein B, responsible for reducing the alveolar surface tension.

The role of mast cells in contractile bronchial smooth muscle activity has been evaluated in a model of chronic obstructive pulmonary disease induced in rats that were intermittently exposed to nitrogen dioxide (NO 2 ) for 60 days. Starting from the 31st day, one group of rats inhaled sodium cromoglycate before exposure to NO 2 to stabilize mast cell membranes. The second group (control) was not treated. Isometric smooth muscle contraction was analysed in isolated bronchial samples in response to nerve and smooth muscle stimulation. Histological analysis revealed large numbers of mast cells in lung tissue of COPD model rats. The inhibition of mast cell degranulation by sodium cromoglycate prevented the development of nerve-stimulated bronchial smooth muscle hyperactivity in COPD model rats. Histamine or adenosine-induced hyperactivity on nerve stimulation was also inhibited by sodium cromoglycate in bronchial smooth muscle in both control and COPD model rats. This suggests that the mechanism of contractile activity enhancement of bronchial wall smooth muscle cells may be mediated through the activation of resident mast cells transmembrane adenosine receptors resulting in their partial degranulation, with the released histamine acting upon histamine H1-receptors which trigger reflex pathways via intramural ganglion neurons.

Effect of mast cell degranulation blockade on the inflammatory response and character of the lung tissue structure-functional changes were evaluated in the chronic obstructive pulmonary disease model produced in rats by 60-day intermittent exposure to nitrogen dioxide. The membrane stabilizer sodium cromoglicate was used to blockade of mast cell degranulation. Lung tissue sections were stained with toluidine blue to identify mast cells. Bronchoalveolar lavage fluid (BALF) cytogram was determined. The levels of mast cell tryptase and chymase, proinflammatory cytokine TNF-α, surfactant protein B were measured in BALF. Suppression of mast cell degranulation prevented the release of proteases in the bronchoalveolar space and reduced activity of the inflammatory process. The influx of inflammatory cells and TNF-α concentration decreased. There was no interstitial inflammatory infiltration. Bronchoalveolar epithelium structure was recovered that is the basis of its functional usefulness. The results confirm the active involvement of mast cells in the development of the inflammatory process in obstructive pulmonary diseases and allow us to consider them as a possible therapeutic target.

On the model of chronic obstructive pulmonary disease, the effect of therapy with low-molecular-weight peptides on restructuring and functional activity of bronchial epithelium for restoring the immune and barrier function of the lungs and prevention of inflammatory process progression was studied. Chronic obstructive pulmonary disease was modeled in rats by 60-day intermittent exposure to NO2. Administration of tetrapeptide Bronchogen for 1 month eliminates symptoms of remodeling of the bronchial epithelium and lung tissue typical of chronic obstructive pulmonary disease (goblet cell hyperplasia, squamous metaplasia, lymphocytic infiltration and emphysema, and restoration of ciliated cells). Enhanced production of secretory IgA, a local immunity marker, attested to normalization of functional activity of bronchial epithelium, while normalization of cell composition and profile of proinflammatory cytokines in the bronchoalveolar space reflected reduction of neutrophilic inflammation.

Objective: to assess the favorable and unfavorable types of lung tissue fibrotic changes in patients with interstitial lung diseases (ILD) detected by high-resolution computed tomography (HRCT). MATERIAL AND METHODS. The results of examinations were analyzed in 385 patients: 181 with respiratory organ sarcoidosis, 130 with fibrosing alveolitis, 36 with histiocytosis X, and 38 with lymphangiolciomyomatosis. All the patients underwent HRCT; the data were compared with the results of comprehensive functional study of external respiration (CFSER), histological examination (in 70.1%), and the pattern of the disease., Results: Comparison of the clinical and functional course of ILD with the types of lung tissue fibrotic changes detected by HRCT and morphological examination showed that the favorable types of pulmonary fibrosis included stringy central and peripheral interstitial fibrotic changes and the atelectatic type of fibrosis, the occurrence of which failed to affect the development of obvious perfusion and diffusion disorders and to give rise to respiratory failure. The unfavorable types of pulmonary fibrosis included the peripheral pulmonary interstitial fibrotic changes (acinar fibrosis, honeycomb lung), which led to restrictive changes and perfusion disorders, which were accompanied by significant respiratory failure, decreases in quality of life and survival, as well as fibrotic changes in the walls of long-lasting air-containing cysts and a fibrotic Aevity mass that resulted Ind complications (pulmonary hemorrhage, pneumothorax, and pneumomediastinum)., Conclusion: The type of pulmonary fibrosis development is one of the major prognostic criteria for he course of ILD. HRCT makes it possible to assess its clinical picture as a whole and to reveal the type of development of fibrotic changes, their extent, the degree of involvement of the tracheobronchial tree in the process (formation of different types of bronchiectasis), concomitant extrapulmonary changes that may be clinically and functionally relevant (chest bone frame deformation, varying pleural changes, vascular disorders). Estimation of prognosis of the disease is most effective in comparing clinical, morphological, HRCT, and CFSER data.

Pulmonary Alveolar Proteinosis is a rare disease with unknown etiology that is due to an abnormal surfactant metabolism. Retrospective analysis of a consecutive series of 68 patients with PAP who were seen at Pulmonology Clinic of Pavlov State Medical University from 1977-2013 was performed. The mean time since first abnormalities were found until diagnosis establishment was 34 months. During that time, most patients were treated with antibiotics, tuberculostatics, glucocorticoids, and immunosupressants. The most effective PAP treatment method was found to be whole lung lavage procedure: 82% of patients showed improvement after its implementation. Delayed diagnosis and incorrect administration of antibiotics, tuberculostatics etc. reduce the probability of a long symptom-free period after lung lavage and spontaneous resolution of the disease., (© 2014 by the Association of Clinical Scientists, Inc.)

We studied the effect of a non-steroidal anti-inflammatory drug fenspiride on contractive activity of bronchial smooth muscles on the model of chronic obstructive pulmonary disease of rats induced by 60-day exposure to nitrogen dioxide. The administration of fenspiride during the acute stage of the disease (day 15) abolished the constricting effect of the pollutant on the bronchial smooth muscles. Dilatation effect of fenspiride in a low dose (0.15 mg/kg) was mediated by its interaction with nerve endings of bronchial capsaicin-sensitive nerve C-fibers. The interaction of drug with receptors of C-fibers prevented neurogenic inflammation, which was confirmed by the absence of structural changes in the lungs typical of this pathology. The broncholytic effect of fenspiride in a high dose (15 mg/kg) was mediated by not only afferent pathways, but also its direct relaxing action on smooth muscle cells. The observed anti-inflammatory and bronchodilatation effect of fenspiride in very low doses can be used for prevention of chronic obstructive pulmonary disease in risk-group patients contacting with aggressive environmental factors.

A method for experimental reproduction of stages of chronic obstructive pulmonary disease formation (from acute inflammation to bronchopulmonary tissue restructuring characteristic of this disease) is presented. Lung injury and inflammation were induced by nitrogen dioxide. Hyperplasia and hypersecretion of goblet cells, squamous cell metaplasia of the ciliary epithelium, emphysema, and focal fibrosis served as the morphological substrate for the formation of bronchial obstruction. The adequacy of the model is confirmed by signs characteristic of chronic obstructive pulmonary disease: hyperexpression of CD3 lymphocytes in the bronchial wall and parenchyma, manifold increased production of TNFα and TGFβ, high concentrations of circulating pathogenic immune complexes. Persistence of the structural and functional shifts throughout 6 months after exposure to nitrogen dioxide indicated a chronic course of the resultant pathological process.