Impaired TRIM16-Mediated Lysophagy in Chronic Obstructive Pulmonary Disease Pathogenesis.

Insufficient autophagic degradation has been implicated in accelerated cellular senescence during chronic obstructive pulmonary disease (COPD) pathogenesis. Aging-linked and cigarette smoke (CS)-induced functional deterioration of lysosomes may be associated with impaired autophagy. Lysosomal membrane permeabilization (LMP) is indicative of damaged lysosomes. Galectin-3 and tripartite motif protein (TRIM) 16 play a cooperative role in recognizing LMP and inducing lysophagy, a lysosome-selective autophagy, to maintain lysosome function. In this study, we sought to examine the role of TRIM16-mediated lysophagy in regulating CS-induced LMP and cellular senescence during COPD pathogenesis by using human bronchial epithelial cells and lung tissues. CS extract (CSE) induced lysosomal damage via LMP, as detected by galectin-3 accumulation. Autophagy was responsible for modulating LMP and lysosome function during CSE exposure. TRIM16 was involved in CSE-induced lysophagy, with impaired lysophagy associated with lysosomal dysfunction and accelerated cellular senescence. Airway epithelial cells in COPD lungs showed an increase in lipofuscin, aggresome and galectin-3 puncta, reflecting accumulation of lysosomal damage with concomitantly reduced TRIM16 expression levels. Human bronchial epithelial cells isolated from COPD patients showed reduced TRIM16 but increased galectin-3, and a negative correlation between TRIM16 and galectin-3 protein levels was demonstrated. Damaged lysosomes with LMP are accumulated in epithelial cells in COPD lungs, which can be at least partly attributed to impaired TRIM16-mediated lysophagy. Increased LMP in lung epithelial cells may be responsible for COPD pathogenesis through the enhancement of cellular senescence.

Chaperone-Mediated Autophagy Suppresses Apoptosis via Regulation of the Unfolded Protein Response during Chronic Obstructive Pulmonary Disease Pathogenesis.

Cigarette smoke (CS) induces accumulation of misfolded proteins with concomitantly enhanced unfolded protein response (UPR). Increased apoptosis linked to UPR has been demonstrated in chronic obstructive pulmonary disease (COPD) pathogenesis. Chaperone-mediated autophagy (CMA) is a type of selective autophagy for lysosomal degradation of proteins with the KFERQ peptide motif. CMA has been implicated in not only maintaining nutritional homeostasis but also adapting the cell to stressed conditions. Although recent papers have shown functional cross-talk between UPR and CMA, mechanistic implications for CMA in COPD pathogenesis, especially in association with CS-evoked UPR, remain obscure. In this study, we sought to examine the role of CMA in regulating CS-induced apoptosis linked to UPR during COPD pathogenesis using human bronchial epithelial cells (HBEC) and lung tissues. CS extract (CSE) induced LAMP2A expression and CMA activation through a Nrf2-dependent manner in HBEC. LAMP2A knockdown and the subsequent CMA inhibition enhanced UPR, including CHOP expression, and was accompanied by increased apoptosis during CSE exposure, which was reversed by LAMP2A overexpression. Immunohistochemistry showed that Nrf2 and LAMP2A levels were reduced in small airway epithelial cells in COPD compared with non-COPD lungs. Both Nrf2 and LAMP2A levels were significantly reduced in HBEC isolated from COPD, whereas LAMP2A levels in HBEC were positively correlated with pulmonary function tests. These findings suggest the existence of functional cross-talk between CMA and UPR during CSE exposure and also that impaired CMA may be causally associated with COPD pathogenesis through enhanced UPR-mediated apoptosis in epithelial cells.

[Elastofibroma Dorci;Report of a Case].

Elastofibroma is a relatively rare tumor that occurs commonly at the apex of scapula in elderly people. We report a case of elastofibroma of a female in her seventies. She visited our hospital with complaints of painful mass in her back, which was increasing in size. On the magnetic resonance imaging (MRI),the T1 and the T2-weighted images showed the same signal intensity as the muscle between the right scapula and the intercostal muscles. The internal fat component was cord-like, with high signal intensity. Based on the site of the tumor and characteristic findings on imaging, it was diagnosed as elastofibroma and resection was performed. Pathological findings revealed bundle-like proliferation of fibrous and spherical hyaline substances, together with collagen fibers. The hyaline substance stained in black on Elastica van Gieson staining and was confirmed to be elastic fiber. Thus, it was diagnosed as elastofibroma. The patient is on regular follow-up, with no recurrence after surgery.

[Rapidly Developing Pulmonary Cyst Complicated by Pneumothorax Occurred in the Early Post-operative Period after Lung Segmentectomy].

The patient was a 74-year-old man who had undergone surgery for rectal cancer 9 years before and had developed left lung metastasis(S3)3 years and 4 months prior to admission. He had received video assisted left lung wedge resection. He presented with a growing nodular lesion close to the remaining left lung margin and elevated serum carcinoembryonic antigen(CEA)levels, and underwent open extended segmentectomy. The chest drain tube was removed on 3rd post-operative day, but he developed left pneumothorax on 4th post-operative day and a computed tomography(CT)scan revealed a cystic lesion 5.0 cm in size at the base of his left lung. Revision surgery was performed on 8th post-operative day. A pulmonary cyst on the diaphragmatic surface of the lung(S10)was found and location of the air leak was confirmed in the same area. Following wedge resection of the cyst-containing region, the leak ceased completely. Rapid manifestation of a newly formed pulmonary cyst during the acute post-operative period is rare.

[Pulmonary Cryptcoccosis Mimicking Malignant Tumor;Report of a Case].

Pulmonary cryptococcosis is difficult to distinguish from lung cancer clinically, and is often diagnosed by surgery. A 72-year-old woman, who underwent distal pancreatectomy and splenectomy for pancreatic carcinoma. Four months after surgery, a tumor shadow was detected in the left lung as a groundglass nodule (GGN)of 12 mm in diameter, which was found to change to 15 mm with increased density by the computed tomography(CT)scan after 2 months. The nodule showed positive accumulation of fluorodeoxyglucose(FDG)by positron emission tomography(PET), and was suspected of malignant tumor. She underwent a partial resection of the left lung under thoracoscopy.

Autophagy induction by SIRT6 through attenuation of insulin-like growth factor signaling is involved in the regulation of human bronchial epithelial cell senescence.

Cigarette smoke (CS)-induced cellular senescence has been implicated in the pathogenesis of chronic obstructive pulmonary disease, and SIRT6, a histone deacetylase, antagonizes this senescence, presumably through the attenuation of insulin-like growth factor (IGF)-Akt signaling. Autophagy controls cellular senescence by eliminating damaged cellular components and is negatively regulated by IGF-Akt signaling through the mammalian target of rapamycin (mTOR). SIRT1, a representative sirtuin family, has been demonstrated to activate autophagy, but a role for SIRT6 in autophagy activation has not been shown. Therefore, we sought to investigate the regulatory role for SIRT6 in autophagy activation during CS-induced cellular senescence. SIRT6 expression levels were modulated by cDNA and small interfering RNA transfection in human bronchial epithelial cells (HBECs). Senescence-associated ß-galactosidase staining and Western blotting of p21 were performed to evaluate senescence. We demonstrated that SIRT6 expression levels were decreased in lung homogenates from chronic obstructive pulmonary disease patients, and SIRT6 expression levels correlated significantly with the percentage of forced expiratory volume in 1 s/forced vital capacity. CS extract (CSE) suppressed SIRT6 expression in HBECs. CSE-induced HBEC senescence was inhibited by SIRT6 overexpression, whereas SIRT6 knockdown and mutant SIRT6 (H133Y) without histone deacetylase activity enhanced HBEC senescence. SIRT6 overexpression induced autophagy via attenuation of IGF-Akt-mTOR signaling. Conversely, SIRT6 knockdown and overexpression of a mutant SIRT6 (H133Y) inhibited autophagy. Autophagy inhibition by knockdown of ATG5 and LC3B attenuated the antisenescent effect of SIRT6 overexpression. These results suggest that SIRT6 is involved in CSE-induced HBEC senescence via autophagy regulation, which can be attributed to attenuation of IGF-Akt-mTOR signaling.

Insufficient autophagy in idiopathic pulmonary fibrosis.

Autophagy, a process that helps maintain homeostatic balance between the synthesis, degradation, and recycling of organelles and proteins to meet metabolic demands, plays an important regulatory role in cellular senescence and differentiation. Here we examine the regulatory role of autophagy in idiopathic pulmonary fibrosis (IPF) pathogenesis. We test the hypothesis that epithelial cell senescence and myofibroblast differentiation are consequences of insufficient autophagy. Using biochemical evaluation of in vitro models, we find that autophagy inhibition is sufficient to induce acceleration of epithelial cell senescence and myofibroblast differentiation in lung fibroblasts. Immunohistochemical evaluation of human IPF biospecimens reveals that epithelial cells show increased cellular senescence, and both overlaying epithelial cells and fibroblasts in fibroblastic foci (FF) express both ubiquitinated proteins and p62. These findings suggest that insufficient autophagy is an underlying mechanism of both accelerated cellular senescence and myofibroblast differentiation in a cell-type-specific manner and is a promising clue for understanding the pathogenesis of IPF.

Apoptosis inhibitor of macrophage (AIM) expression in alveolar macrophages in COPD.

BACKGROUND: Marked accumulation of alveolar macrophages (AM) conferred by apoptosis resistance has been implicated in pathogenesis of chronic obstructive pulmonary disease (COPD). Apoptosis inhibitor of macrophage (AIM), has been shown to be produced by mature tissue macrophages and AIM demonstrates anti-apoptotic property against multiple apoptosis-inducing stimuli. Accordingly, we attempt to determine if AIM is expressed in AM and whether AIM is involved in the regulation of apoptosis in the setting of cigarette smoke extract (CSE) exposure. METHODS: Immunohistochemical evaluations of AIM were performed. Immunostaining was assessed by counting total and positively staining AM numbers in each case (n = 5 in control, n = 5 in non-COPD smoker, n = 5 in COPD). AM were isolated from bronchoalveolar lavage fluid (BALF). The changes of AIM expression levels in response to CSE exposure in AM were evaluated. Knock-down of anti-apoptotic Bcl-xL was mediated by siRNA transfection. U937 monocyte-macrophage cell line was used to explore the anti-apoptotic properties of AIM. RESULTS: The numbers of AM and AIM-positive AM were significantly increased in COPD lungs. AIM expression was demonstrated at both mRNA and protein levels in isolated AM, which was enhanced in response to CSE exposure. AIM significantly increased Bcl-xL expression levels in AM and Bcl-xL was involved in a part of anti-apoptotic mechanisms of AIM in U937 cells in the setting of CSE exposure. CONCLUSIONS: These results suggest that AIM expression in association with cigarette smoking may be involved in accumulation of AM in COPD.

Insulin-dependent phosphatidylinositol 3-kinase/Akt and ERK signaling pathways inhibit TLR3-mediated human bronchial epithelial cell apoptosis.

TLR3, one of the TLRs involved in the recognition of infectious pathogens for innate and adaptive immunity, primarily recognizes viral-associated dsRNA. Recognition of dsRNA byproducts released from apoptotic and necrotic cells is a recently proposed mechanism for the amplification of toxicity, suggesting a pivotal participation of TLR3 in viral infection, as well as in lung diseases where apoptosis plays a critical role, such as asthma and chronic obstructive pulmonary disease. In addition to metabolic control, insulin signaling was postulated to be protective by inhibiting apoptosis. Therefore, we explored the role of insulin signaling in protecting against TLR3-mediated apoptosis of human bronchial epithelial cells. Significant TLR3-mediated apoptosis was induced by polyinosinic-polycytidylic acid, a dsRNA analog, via caspase-8-dependent mechanisms. However, insulin efficiently inhibited TLR3/polyinosinic-polycytidylic acid-induced human bronchial epithelial cell apoptosis via PI3K/Akt and ERK pathways, at least in part, via upregulation of cellular FLIPs and through protein synthesis-independent mechanisms. These results indicate the significance of TLR3-mediated dsRNA-induced apoptosis in the pathogenesis of apoptosis-driven lung disease and provide evidence for a novel protective role of insulin.

Involvement of creatine kinase B in cigarette smoke-induced bronchial epithelial cell senescence.

Cigarette smoke induces damage to proteins and organelles by oxidative stress, resulting in accelerated epithelial cell senescence in the lung, which is implicated in chronic obstructive pulmonary disease (COPD) pathogenesis. Although the detailed molecular mechanisms are not fully understood, cellular energy status is one of the most crucial determinants for cell senescence. Creatine kinase (CK) is a constitutive enzyme, playing regulatory roles in energy homeostasis of cells. Among two isozymes, brain-type CK (CKB) is the predominant CK in lung tissue. In this study, we investigated the role of CKB in cigarette smoke extract (CSE)-induced cellular senescence in human bronchial epithelial cells (HBECs). Primary HBECs and Beas2B cells were used. Protein carbonylation was evaluated as a marker of oxidative protein damage. Cellular senescence was evaluated by senescence-associated ß-galactosidase staining. CKB inhibition was examined by small interfering RNA and cyclocreatine. Secretion of IL-8, a hallmark of senescence-associated secretary phenotype, was measured by ELISA. CKB expression levels were reduced in HBECs from patients with COPD compared with that of HBECs from nonsmokers. CSE induced carbonylation of CKB and subsequently decreased CKB protein levels, which was reversed by a proteasome inhibitor. CKB inhibition alone induced cell senescence, and further enhanced CSE-induced cell senescence and IL-8 secretion. CSE-induced oxidation of CKB is a trigger for proteasomal degradation. Concomitant loss of enzymatic activity regulating energy homeostasis may lead to the acceleration of bronchial epithelial cell senescence, which is implicated in the pathogenesis of COPD.

Analysis of postoperative weight loss associated with prognosis after lobectomy for lung cancer.

OBJECTIVES: Weight assessment is an easy-to-understand method of health checkup. The present study investigated the association between weight loss (WL) after lung cancer (LC) surgery and short-mid-term prognosis. METHODS: The data of patients who underwent radical lobectomy for primary LC were assessed between December 2017 and June 2021. Percentage weight gain or loss was determined at 3, 6 and 12 months postoperatively based on preoperative weight. The timing of decreased weight was divided into 0-3, 3-6 and 6-12 months. We also evaluated the relationship between severe WL (SWL) and prognosis. RESULTS: We reviewed 269 patients, of whom 187 (69.5%) showed WL within 1 year after surgery. The interquartile range for maximal WL was 2.0-8.2% (median 4.0%). Furthermore, we defined SWL as WL ≥8%. Twenty-five patients (9.3%) died: 9 from primary LC and 16 from non-LC causes. Cancer recurrences occurred in 45 patients (16.7%). WL occurred from 6 to 12 months postoperatively was associated with poor overall survival and recurrence-free survival (P < 0.05, both). Body mass index <18.5 kg/m2 and idiopathic pulmonary fibrosis were predictive factors (P < 0.05, all). In the SWL group, overall survival, recurrence-free survival and non-cancer-specific were worse (P = 0.001, 0.005 and 0.019, respectively). Age ≥70 years and severe postoperative complications were predictive factors for SWL (P < 0.05, all). CONCLUSIONS: WL from 6 to 12 months postoperatively and SWL were associated with poor prognosis. Ongoing nutritional management is important to prevent life-threatening WL in patients with predictive factors.

Esophagobronchial fistula successfully managed with a self-expandable metallic stent followed by fixation using a silicon Y stent.

Esophagobronchial fistula (EBF) formation is a severe complication of advanced thoracic malignancies, that affects the prognosis and quality of life of patients. This study reports the case of an 80-year-old man with advanced esophageal cancer, complicated by EBF formation in the left main bronchus proximal to the carina following chemoradiation therapy. A fully covered stent was placed in the left main bronchus but was dislocated on the oral side. The attempt to place a partially covered self-expandable metallic stent (SEMS) also failed due to stent dislocation on the oral side. To avoid stent dislocation, a partially covered SEMS with a length of 40 mm and a diameter of 16 mm was placed to cover the EBF in the left main bronchus. Then, a silicone Y stent (16 × 13 × 13 mm in outer diameter) was inserted to support the SEMS from the inside. After placing the SEMS and Y stent, the position of the SEMS was stabilized. The patient remained stable with adequate oral intake.

Effect of resected lung lobe on the prediction of postoperative pulmonary function.

OBJECTIVES: This study examined whether a resected lung lobe can affect the accuracy of postoperative forced expiratory volume in 1 s (FEV1) predicted using the subsegment counting method and three-dimensional computed tomography (3D-CT) volumetry. METHODS: Overall, 125 patients who underwent lobectomy through video-assisted thoracic surgery were enrolled in this retrospective study. Pulmonary function tests were performed preoperatively and postoperatively at 3 months. We defined the accuracy index as the ratio of predicted postoperative FEV1 to measured postoperative FEV1 and compared the accuracy index of the subsegment counting method and 3D-CT volumetry. Factors affecting the accuracy index were also examined. RESULTS: The accuracy index of the subsegment counting method was 0.94 ± 0.12, versus 0.93 ± 0.11 for 3D-CT volumetry (P = 0.539). There was a significant difference among the resected lobes in the accuracy index of the subsegment counting method (P < 0.001) but not in that of 3D-CT volumetry (P = 0.370). The resected lobe, the number of staples used for interlobar dissection and interstitial pneumonia were significantly associated with the accuracy index of the subsegment counting method (all P < 0.001). The number of staples and interstitial pneumonia were significantly associated with the accuracy index of 3D-CT volumetry (P < 0.001, respectively), whereas the resected lobe was not a significant factor (P = 0.240). CONCLUSIONS: The resected lobe affected the accuracy of the subsegment counting method but not that of 3D-CT volumetry. Furthermore, 3D-CT volumetry predicted postoperative FEV1 independent of the resected lobe.

Thoracoscopic resection of a mediastinal venous hemangioma: Report of a case.

Mediastinal hemangioma is a rare tumor, accounting for 0.5% or fewer of all mediastinal tumors in most reports. We herein report a case of thoracoscopic resection of venous hemangioma in the middle mediastinum. A 48-year-old man was referred to our hospital for dysphagia. A chest computed tomography scan showed the mass to have a smooth surface and heterogeneous contents. Magnetic resonance imaging demonstrated the morphology of the vascular tumor to be a hyperintense mass on a T2-weighted image. Using thoracoscopic surgery, the tumor was completely extirpated and confirmed histologically to be a venous hemangioma. In this case, thoracoscopic surgery provided a satisfactory view and facilitated correct handling for the mediastinal venous hemangioma.

Catamenial pneumothorax with partial liver herniation due to diaphragmatic laceration: a case report and literature review.

BACKGROUND: Catamenial pneumothorax is generally uncommon, with an incidence of less than 3-6% in women with spontaneous pneumothorax. As few cases of catamenial pneumothorax with diaphragmatic defect and liver herniation have been reported, this case report may be useful for understanding the cause and treatment. This case highlights the importance of the approach for liver hernia in patients with catamenial pneumothorax and endometriosis. CASE PRESENTATION: We report a case of catamenial pneumothorax in a 43-year-old woman with diaphragmatic partial liver hernia who was treated with thoracoscopic surgery. She was diagnosed with a right pneumothorax at menstruation onset. Chest computed tomography showed a nodule protruding above the right diaphragm. We performed thoracoscopic surgery to treat the persistent air leak and biopsied the nodule on the right diaphragm. There were blueberry spots on the diaphragm; the nodule was found to be the herniated liver. The diaphragmatic defect was sutured. Histological examination of the tissue near the partial prolapsed liver revealed endometrial tissue. CONCLUSIONS: It is speculated that ectopic endometrial tissue in the diaphragm will periodically necrose to become a diaphragmatic tear, which is a pathway for air to enter the thoracic cavity and eventually a herniated liver. Thoracoscopic surgery should be considered in patients with catamenial pneumothorax when a diaphragmatic lesion is suspected.

Clinical Efficacy and Safety of Nivolumab in Japanese Patients With Malignant Pleural Mesothelioma: 3-Year Results of the MERIT Study.

INTRODUCTION: We examined the long-term efficacy and safety of nivolumab, a human monoclonal antibody that inhibits interactions between the programmed cell death protein-1 receptor and its ligands (programmed death-ligand 1 and programmed death-ligand 2), in Japanese patients with malignant pleural mesothelioma (MPM). METHODS: Japanese patients with previously treated MPM (one or two regimens) were enrolled in a single-arm, phase 2 study and received nivolumab intravenously 240 mg every 2 weeks until progressive disease or unacceptable toxicity. The primary end point was the centrally assessed objective response rate. Other end points included overall survival (OS), progression-free survival (PFS), treatment-related adverse events, and patient-reported outcomes (Lung Cancer Symptom Scale for mesothelioma and EuroQOL visual analog scale). Patient enrollment started on June 16, 2016. Here, we report 3-year follow-up data (cutoff date: November 12, 2019). RESULTS: Thirty-four patients were enrolled. The centrally assessed objective response rate was previously reported (29.4%). The 2- and 3-year OS rates were 35.3% and 23.5%, respectively, and the corresponding PFS rates were 17.0% and 12.7%. Median OS and PFS were 17.3 and 5.9 months, respectively. Eight patients were alive at 3 years of follow-up. Nivolumab was well tolerated and no new safety signals were found. The patient-reported outcomes were maintained without marked deteriorations during the study. CONCLUSIONS: Our results reveal clinically relevant long-term efficacy and safety of nivolumab for the treatment of MPM.

A successful case of complete surgical resection via left upper and right lower lobectomy for bilateral lung metastases of a perivascular epithelioid cell tumor in the colon: a case report.

BACKGROUND: Perivascular epithelioid cell tumors (PEComas) are rare mesenchymal neoplasms with malignant potential. No effective treatment other than surgical resection has been established for lung metastases of PEComas. We describe a patient who underwent complete surgical resection via bilateral lobectomy involving a two-step procedure for lung metastases 8 years after undergoing radical surgery for a colonic PEComa. CASE PRESENTATION: A 53-year-old woman underwent partial colectomy for a PEComa in the transverse colon 8 years ago. She presented with an abnormal chest shadow during a health examination. Chest computed tomography (CT) revealed a solid nodule 2 cm in diameter located centrally in the right lower lobe and a solid nodule 3 cm in diameter located centrally in the left upper lobe. Positron emission tomography revealed 18F-fluorodeoxyglucose uptake in these nodules. These nodules were suspected to be metastatic tumors of the colonic PEComa and were considered for complete surgical resection. Segmentectomy could not be performed because of the anatomical location of the tumors straddling the segments; therefore, bilateral lobectomy was required for complete surgical resection. Therefore, we performed two-step lobectomy safely with the expectation of pulmonary function recovery. Microscopically, the tumors were diagnosed as lung metastases of the PEComa. One year after the last surgery, no recurrence was detected, and the patient's pulmonary function improved. CONCLUSIONS: This case indicates that even if multiple lung metastases of a PEComa require bilateral lobectomy, complete resection with a two-step surgery may be considered.

Localized pleural metastasis without other organ metastases after nephrectomy for renal cell carcinoma.

We present a case of a 69-year-old man who had localized pleural metastasis without other organ metastases after nephrectomy for right renal cell carcinoma (RCC). He complained of respiratory symptoms for more than two years after the operation and was confirmed to have right pleural effusion and multiple pleural masses on computed tomography (CT). There were no abnormal findings in the other organs, but the pleural mass gradually increased in size on CT. We suspected malignant tumors such as malignant pleural mesothelioma and synovial sarcoma in addition to RCC metastasis. Finally, we performed surgical resection of the pleural mass under general anesthesia, and we diagnosed pathologically as metastasis from RCC. Distant metastases of RCC are common in the lungs, bones, brain, and liver. To our knowledge, localized pleural metastases from RCC is rare.

Measured versus predicted postoperative pulmonary function at repeated times up to 1 year after lobectomy.

OBJECTIVES: Postoperative pulmonary function is difficult to predict accurately, because it changes from the time of the operation and is also affected by various factors. The objective of this study was to assess the accuracy of predicted postoperative forced expiratory volume in 1 s (FEV1) at different postoperative times after lobectomy. METHODS: This retrospective study enrolled 104 patients who underwent lobectomy by video-assisted thoracic surgery. Pulmonary function tests were performed preoperatively and postoperatively at 3, 6 and 12 months. We investigated time-dependent changes in FEV1. In addition, the ratio of measured to predicted postoperative FEV1 calculated by the subsegmental method was evaluated to identify the factors associated with variations in postoperative FEV1. RESULTS: Compared with the predicted postoperative FEV1, the measured postoperative FEV1 was 8% higher at 3 months, 11% higher at 6 months and 13% higher at 12 months. The measured postoperative FEV1 significantly increased from 3 to 6 months (P = 0.002) and from 6 to 12 months (P = 0.015) after lobectomy resected lobe, smoking history and body mass index were significant factors associated with the ratio of measured to predicted postoperative FEV1 at 12 months (P < 0.001, P = 0.036 and P = 0.025, respectively). CONCLUSIONS: Postoperative FEV1 increased up to 12 months after lobectomy by video-assisted thoracic surgery. The predicted postoperative pulmonary function was underestimated after 3 months, particularly after lower lobectomy.

Optimal timing of video-assisted thoracic surgery for acute pyothorax: a retrospective study.

OBJECTIVE: Although the value of video-assisted thoracic surgery for acute pyothorax is becoming widely recognized, the optimal timing of surgery has not been established. Therefore, we aimed to determine the optimal timing of video-assisted thoracic surgery in acute pyothorax. METHODS: We retrospectively reviewed 38 consecutive video-assisted thoracic surgeries performed for acute pyothorax between January 2013 and December 2017 at our institution. Data were analyzed using the independent samples t test and Mann-Whitney U test. A receiver-operating characteristic curve was used to identify the optimal time for intervention. RESULTS: The average time from disease onset to surgery was 17.9 days, and the average preoperative drainage period was 8.3 days. The operation was completed in all patients with video-assisted thoracic surgery curettage and drainage under general anesthesia; single lung ventilation was administered, and one or two thoracic drains were placed. The average postoperative drainage period was 10.8 days. Intraoperative complications were observed in two cases; no perioperative death occurred. Additional surgery was performed in four cases because of poor treatment response. There was no recurrence of pyothorax over a mean postoperative follow-up period of 42.5 months. A receiver-operating characteristic curve showed that the cut-off time from disease onset to surgery was 21.0 days; complication rates were 14.3% and 25.0% for patients operated on before and after 21 days, respectively. CONCLUSIONS: Thoracoscopic surgery for acute pyothorax is safe and curative, and should be performed within 21 days of disease onset to avoid postoperative complications.