Pathogenesis Of Primary Spontaneous Pneumothorax Research Articles

Excessive aggregation of fine particles may play a crucial role in adolescent spontaneous pneumothorax pathogenesis.

The pathogenesis of primary spontaneous pneumothorax (PSP) is unclear. Fine particles aggregated in the lung can be phagocytosed by alveolar macrophages (AMs) to induce an inflammatory reaction and damage local pulmonary tissue, which could be a mechanism of PSP. This project aimed to explore the pathological association between fine particulate matter and PSP. Thirty pulmonary bullae tissues were obtained from surgery of PSP patients (B group). The adjacent normal tissues of the lungs were defined as the control S group. Another 30 normal lung tissues with nonpneumothorax disease (NPD) were applied as the control N group. Hematoxylin and eosin (H & E), Wright-Giemsa (W-G), Victoria blue, and immunohistochemical (IHC) staining experiments were performed to measure the levels of fine particulate matter, alveolar macrophages (AMs), pulmonary elastic fibers, monocyte chemoattractant protein-1 (MCP-1), and matrix metalloproteinase-9 (MMP-9) in the lung tissues. The serum levels of MCP-1 and MMP-9 were prospectively analyzed as well. Histopathological examinations revealed obvious deposition of fine particulate matter and inflammatory reactions (proliferation of AMs) in the B group, compared with those in the S group and the N group. These alterations were significantly associated with PSP. The numbers of AMs and pulmonary elastic fibers, the positive area of the H-score, as well as the concentrations of MCP-1 and MMP-9 in the lungs of the experimental group were obviously raised compared with the controls (P < 0.05). Fine particulate matter aggregation, inflammation (macrophage hyperplasia), and overexpression of MCP-1 and MMP-9 may contribute to the pathogenesis of PSP. The overaccumulation of fine particulate matter may play a crucial part in the occurrence of adolescent and young adult PSP. This project was enrolled on the Chinese Clinical Trial Registry: ChiCTR2100051460.

CASE REPORT: TREATMENT EXPERIENCE OF A RECURRENT PRIMARY SPONTANEOUS PNEUMOTHORAX

Primary spontaneous pneumothorax (PSP) is a condition characterized as accumulation of air in the pleural cavity without the cause of underlying lung disease. The symptoms of this pathology range from asymptomic to severe hemodynamic disorders. Though the pathogenesis of PSP has been gradually uncovered, there is still a lack of consensus in the diagnostic approach and treatment strategies for this disorder. Different authors offer a broad variety of treatment recommendations, that could still result in reoccurrence of PSP. We present a case report of our experience in treating a 4 time PSP recurrence.

Expression of TGF-beta receptor 1 and Smads in the tissues of primary spontaneous pneumothorax.

Primary spontaneous pneumothorax (PSP) is a common disease which is often caused by the rupture of bullae in the lungs. The underlying pathogenesis of PSP remains unclear. Some molecules may be involved in the development of PSP potentially. The aim of this study was to investigate the expression of TGF-beta receptor 1 (TβR1), Smad2, Smad3 and Smad4 in the resected bullae of patients with PSP. From May 2015 to May 2016, 34 patients with PSP underwent video-assisted thoracoscopic surgery (VATS) bullectomy. Immunohistochemistry was performed to identify the expression of TβR1, Smad2, Smad3 and Smad4 in the resected pulmonary bullae tissues. The levels of these cytokines were calculated by immunoreactivity scoring system (IRS). Ten patients without pneumothorax associated disease were selected as the control group. The analysis showed that the expression levels of TβR1, Smad2 and Smad4 were significantly higher in bullae tissues of patients with PSP than that in normal lung tissues (P=0.012, 0.031, 0.000 respectively). There was no significant difference between the expression level of Smad3 in bullae tissue of PSP patients and that in normal lung tissues of the control group (P=0.140). However, the absolute quantity of Smad3 expression in PSP bullae tissues was (4.2529±1.7193), scored by the IRS, which is higher than that in the control lung tissues (3.2600±2.2132). Also, the expression of TβR1, Smad2, Smad3 and Smad4 were not showed correlation with the clinical characteristics of PSP patients, such as age, sex, body mass index (BMI), recurrence and side of pneumothorax. TβR1, Smad2 and Smad4 highly expressed in bullae tissues of PSP patients. Our findings suggested that TβR1, Smad2 and Smad4 may be related to the development of PSP bullae.

Pneumothorax in a young man with anorexia nervosa

Primary spontaneous pneumothorax (PSP) is defined as a pneumothorax that occurs in the absence of an external cause in an individual without underlying generalized lung disease. A number of factors are important and should be carefully considered in the pathogenesis of PSP. This is the first case report of a PSP in a severely malnourished adolescent male with anorexia nervosa (AN) who was involved in excessive physical activity. Clinicians caring for adolescents with AN and vigorous exercise need to be aware of the risk factors associated with the development of a PSP. © 2016 Wiley Periodicals, Inc.(Int J Eat Disord 2016; 49:895-898).

Preliminary Study of Expression of KL-6, FGF-10 and MMP-9 in the Primary Spontaneous Pneumothorax

Objective: Pathogenesis of primary spontaneous pneumothorax (PSP) is unclear and has been rarely reported in the literature. Thus, we measured expression of Krebs Vonden Lungen-6 (KL-6), fibroblast growth factor-10 (FGF-10), and matrix metalloproteinase-9 (MMP-9) in PSP samples and evaluated their significance on the development and progress of the disease. Methods: Immunohistochemical staining and ELISA were used to measure expression of KL-6, FGF-10, and MMP-9 in the pulmonary bullae and the peripheral normal lung tissue in 24 cases of PSP. Statistical results were analyzed using the Student’s paired t-test. Results: Immunohistochemical data revealed that KL-6 and FGF10 expression in the pulmonary bullae was significantly higher than in peripheral normal lung tissue, but MMP-9 expression did not differ. ELISA confirmed that KL-6 and FGF-10 expression in the pulmonary bullae was significantly higher than the peripheral normal lung tissue (P 0.05). Conclusion: Expression of KL-6 and FGF-10 in pulmonary bullae of PSP patients was significantly higher than in the peripheral normal lung tissue, suggesting that KL-6-mediated pulmonary fibrosis and abnormal FGF-10 expression-induced congenital abnormalities in development of bronchi may be associated with PSP. MMP-9 was not different in both groups, suggesting that further correlation between MMP-9-mediated inflammation and PSP remains unclear.

Overexpression of Matrix Metalloproteinases in Lung Tissue of Patients with Primary Spontaneous Pneumothorax

Background: Although blebs and bullae are frequently found in the apexes of lungs of patients with primary spontaneous pneumothorax (PSP), its pathogens remain unclear. Objectives: To examine the role of proteases [matrix metalloproteinase (MMP)-2, MMP-7 and MMP-9] and antiproteases [tissue inhibitors of metalloproteinase (TIMP)-1, TIMP-2, TIMP-3 and TIMP-4] in the pathogenesis of PSP. Method: Fifty consecutive PSP patients who received standard surgical care were enrolled in the study. Lung tissues from 20 patients with stage I non-small cell lung cancer were used as a control. Immunohistochemistry (IHC), reverse transcription-polymerase chain reaction (RT-PCR) and gelatin zymography were used to evaluate the expression of MMP and TIMP in the lung tissue of patients with PSP. Results: Overexpression of MMP-2, MMP-7 and MMP-9 was found in the afflicted lung by IHC, zymography and RT-PCR. By IHC, higher expression of MMP-2 and MMP-9 in PSP patients was identified in alveolar macrophages and type II pneumocytes (88 and 92% of patients in macrophages, and 72 and 70% of patients in type II pneumocytes, respectively). MMP-2, MMP-7 and MMP-9 expression in patients was higher in mesothelial cells (66, 76 and 76%). Overexpression of TIMP-2 was detected in the extracellular matrix around bullae and blebs. Expression levels of TIMP-1, TIMP-3 and TIMP-4 were negligible (<10% of cells) in both PSP patients and controls. Conclusions: MMP-2, MMP-9, MMP-7 and TIMP-2 were upregulated in PSP lesions. These results suggest that an imbalance between the expression of proteases and antiproteases may be involved in the pathogeneses of PSP.

Diagnosis and treatment of primary spontaneous pneumothorax

Primary spontaneous pneumothorax (PSP) commonly occurs in tall, thin, adolescent men. Though the pathogenesis of PSP has been gradually uncovered, there is still a lack of consensus in the diagnostic approach and treatment strategies for this disorder. Herein, the literature is reviewed concerning mechanisms and personal clinical experience with PSP. The chest computed tomography (CT) has been more commonly used than before to help understand the pathogenesis of PSP and plan further management strategies. The development of video-assisted thoracoscopic surgery (VATS) has changed the profiles of management strategies of PSP due to its minimal invasiveness and high effectiveness for patients with these diseases.