Yasushi Hoshikawa

Objective: Postoperative acute interstitial pneumonia is a subset of post-surgical. acute respiratory distress syndrome (ARDS) and is responsible for one third of in-hospital deaths following lung resection in patients with primary lung cancer. We evaluated the usefulness of computed tomography (CT) for detection of interstitial pneumonia (IP) as a risk factor of postoperative ARDS. Methods: Preoperative chest CT of patients who underwent thoracotomy for primary lung cancer was reviewed retrospectively and IP findings in the chest CT were detected. Results: A total of 1148 patients with primary lung cancer underwent thoracotomy. Fifteen patients (1.3%) developed postoperative ARDS. Eleven of these 15 patients died of ARDS. Three of 41 patients who received induction therapy developed postoperative ARDS. Induction therapy was a risk factor of postoperative ARDS (p < 0.01). Eleven out of the 15 patients who developed postoperative ARDS had IP findings (10: localized, 1: diffuse) in their chest CT Two of three patients who had postoperative ARDS after induction therapy also had IP findings. Chest CTs of 834 patients were retrospectively analyzed; 91 patients (10.9%) had IP-findings (diffuse 1.8%, localized 9.1%). Postoperative ARDS occurred in 8.8% of IP-positive patients, and in 0.4% of IP-negative patients (p < 0.0011. Conclusion: Detection of IP by chest CT is useful for the selection of high-risk patients who may have postoperative ARDS following thoracotomy. (C) 2008 European Association for Cardio-Thoracic Surgery. Published by Elsevier B.V. All rights reserved.

Objective: Postoperative acute interstitial pneumonia is a subset of post-surgical. acute respiratory distress syndrome (ARDS) and is responsible for one third of in-hospital deaths following lung resection in patients with primary lung cancer. We evaluated the usefulness of computed tomography (CT) for detection of interstitial pneumonia (IP) as a risk factor of postoperative ARDS. Methods: Preoperative chest CT of patients who underwent thoracotomy for primary lung cancer was reviewed retrospectively and IP findings in the chest CT were detected. Results: A total of 1148 patients with primary lung cancer underwent thoracotomy. Fifteen patients (1.3%) developed postoperative ARDS. Eleven of these 15 patients died of ARDS. Three of 41 patients who received induction therapy developed postoperative ARDS. Induction therapy was a risk factor of postoperative ARDS (p < 0.01). Eleven out of the 15 patients who developed postoperative ARDS had IP findings (10: localized, 1: diffuse) in their chest CT Two of three patients who had postoperative ARDS after induction therapy also had IP findings. Chest CTs of 834 patients were retrospectively analyzed; 91 patients (10.9%) had IP-findings (diffuse 1.8%, localized 9.1%). Postoperative ARDS occurred in 8.8% of IP-positive patients, and in 0.4% of IP-negative patients (p < 0.0011. Conclusion: Detection of IP by chest CT is useful for the selection of high-risk patients who may have postoperative ARDS following thoracotomy. (C) 2008 European Association for Cardio-Thoracic Surgery. Published by Elsevier B.V. All rights reserved.

Thoracotomy for the management of intractable secondary pneumothorax is associated with a high perioperative risk related to the presence of underlying lung disease. This study was undertaken to determine factors associated with in-hospital morbidity among patients after general thoracic surgery for intractable secondary pneumothorax and to construct a risk model. PATIENTS AND METHODS: A total of 60 patients were included, of which 43 underwent elective surgery. Predicted morbidity rates were calculated using univariate analysis and multivariate logistic regression analysis. RESULTS: Of the 43 original patients, 10 (23%) developed postoperative complications. The following factors were found to be significantly associated with the occurrence of postoperative complications on univariate analysis: total protein, albumin, sodium ions, chorine esterase, O₂ inhalation, performance status, and the anesthesic score. On multivariate analysis, these factors were the performance status (95% confidence interval: 1.41-3850, odds ratio: 73.66, p=0.033). Conclusion: These results suggest that postoperative complications of secondary pneumothorax in elderly patients can be predicted by preoperative examinations. Poor performance status, nutrition, low sodium levels, and respiratory failure are dependent risk factors for postoperaive complications of secondary pneumothorax in elderly patients.

Thoracotomy for the management of intractable secondary pneumothorax is associated with a high perioperative risk related to the presence of underlying lung disease. This study was undertaken to determine factors associated with in-hospital morbidity among patients after general thoracic surgery for intractable secondary pneumothorax and to construct a risk model. PATIENTS AND METHODS: A total of 60 patients were included, of which 43 underwent elective surgery. Predicted morbidity rates were calculated using univariate analysis and multivariate logistic regression analysis. RESULTS: Of the 43 original patients, 10 (23%) developed postoperative complications. The following factors were found to be significantly associated with the occurrence of postoperative complications on univariate analysis: total protein, albumin, sodium ions, chorine esterase, O₂ inhalation, performance status, and the anesthesic score. On multivariate analysis, these factors were the performance status (95% confidence interval: 1.41-3850, odds ratio: 73.66, p=0.033). Conclusion: These results suggest that postoperative complications of secondary pneumothorax in elderly patients can be predicted by preoperative examinations. Poor performance status, nutrition, low sodium levels, and respiratory failure are dependent risk factors for postoperaive complications of secondary pneumothorax in elderly patients.

Background. Transferring genes with immunoregulatory capacity to transplanted organs has the potential to modify allograft rejection (AR). We examined the effect of ex vivo lipid-mediated transbronchial human interieukin-10 (hIL-10) gene transfer on acute AR in a rat model of lung transplantation. Methods. Left single lung transplantations were performed between a highly histoincompatible rat combination: Brown Norway to Lewis. The extracted donor left lung was intrabronchially instilled with a plasmid encoding hIL-10 or Escherichia coli P-galactosidase (control), mixed with a cationic lipid. On day 6 posttransplantation, the degree of AR was graded histologically (stages 1-4) based upon pathological categories of inflammation: perivascular, peribronchial, and peribronchiolar lymphocytic infiltrates, edema, intraalveolar hemorrhage, and necrosis. Results. The stage of AR in the IL-10 group (3.1 +/- 0.4) was significantly lower than the control group (3.8 +/- 0.4). Pathological scores for ederna, intraalveolar hemorrhage, and necrosis in the IL-10 group (2.3 +/- 0.8, 0.3 +/- 0.5, and 0.3 +/- 0.5, respectively) were also significantly decreased compared with those in the control group (3.2 +/- 0.4, 2.2 +/- 0.8, and 1.2 +/- 0.4, respectively). Conclusion. Ex vivo lipid-mediated transbronchial hIL-10 gene transfer attenuated acute inflammation associated with AR in a rat model of lung transplantation.

Background. Transferring genes with immunoregulatory capacity to transplanted organs has the potential to modify allograft rejection (AR). We examined the effect of ex vivo lipid-mediated transbronchial human interieukin-10 (hIL-10) gene transfer on acute AR in a rat model of lung transplantation. Methods. Left single lung transplantations were performed between a highly histoincompatible rat combination: Brown Norway to Lewis. The extracted donor left lung was intrabronchially instilled with a plasmid encoding hIL-10 or Escherichia coli P-galactosidase (control), mixed with a cationic lipid. On day 6 posttransplantation, the degree of AR was graded histologically (stages 1-4) based upon pathological categories of inflammation: perivascular, peribronchial, and peribronchiolar lymphocytic infiltrates, edema, intraalveolar hemorrhage, and necrosis. Results. The stage of AR in the IL-10 group (3.1 +/- 0.4) was significantly lower than the control group (3.8 +/- 0.4). Pathological scores for ederna, intraalveolar hemorrhage, and necrosis in the IL-10 group (2.3 +/- 0.8, 0.3 +/- 0.5, and 0.3 +/- 0.5, respectively) were also significantly decreased compared with those in the control group (3.2 +/- 0.4, 2.2 +/- 0.8, and 1.2 +/- 0.4, respectively). Conclusion. Ex vivo lipid-mediated transbronchial hIL-10 gene transfer attenuated acute inflammation associated with AR in a rat model of lung transplantation.

Pulmonary arterial hypertension (PAH) is characterized by abnormal proliferation of smooth muscle cells (SMCs), leading to occlusion of pulmonary arterioles, right ventricular (RV) hypertrophy, and death. We investigated whether mycophenolate mofetil (MMF), a potent inummosuppresssant, prevents the development of monocrotaline (MCT)-induced PAH in rats. MMF effectively decreased RV systolic pressure and RV hypertrophy, and reduced the medial thickness of pulmonary arteries. MMF significantly inhibited the number of proliferating cell nuclear antigen (PCNA)-positive cells, infiltration of macrophages, and expression of P-selectin and interleukin-6 on the endothelium of pulmonary arteries. The infiltration of T cells and mast cells was not affected by MMF. In vitro experiments revealed that mycophenolic acid (MPA), an active metabolite of MMF, dose-dependently inhibited proliferation of human pulmonary arterial SMCs. MMF attenuated the development of PAH through its anti-inflammatory and anti-proliferative properties. These findings provide new insight into the potential role of immunosuppressants in the treatment of PAR (c) 2006 Elsevier Inc. All rights reserved.

Pulmonary arterial hypertension (PAH) is characterized by abnormal proliferation of smooth muscle cells (SMCs), leading to occlusion of pulmonary arterioles, right ventricular (RV) hypertrophy, and death. We investigated whether mycophenolate mofetil (MMF), a potent inummosuppresssant, prevents the development of monocrotaline (MCT)-induced PAH in rats. MMF effectively decreased RV systolic pressure and RV hypertrophy, and reduced the medial thickness of pulmonary arteries. MMF significantly inhibited the number of proliferating cell nuclear antigen (PCNA)-positive cells, infiltration of macrophages, and expression of P-selectin and interleukin-6 on the endothelium of pulmonary arteries. The infiltration of T cells and mast cells was not affected by MMF. In vitro experiments revealed that mycophenolic acid (MPA), an active metabolite of MMF, dose-dependently inhibited proliferation of human pulmonary arterial SMCs. MMF attenuated the development of PAH through its anti-inflammatory and anti-proliferative properties. These findings provide new insight into the potential role of immunosuppressants in the treatment of PAR (c) 2006 Elsevier Inc. All rights reserved.

A 40-year-old man, diagnosed as acute myelogenic leukemia underwent a HLA-identical sibling peripheral blood stem cell transplant following an off treatment relapse. He subsequently developed chronic graft-versus-host disease (GVHD) and bronchiolitis obliterans caused recurrent pneumothorax. In order to control the recurrent medical-treatment-resistant pneumothorax, four surgeries (three left, one right) were necessary. It was thought important to reinforce the whole visceral pleura by covering it with an absorbable material sheet and fibrin glue in surgical treatment for recurrent pneumothorax.

The determination of plasma (1→3)-β-D-glucan is widely used for the diagnosis of deep mycosis, but it is often affected by various factors. We experienced a case with markedly increased plasma (1→3)-β-D-glucan after bilateral lung transplantation for pulmonary lymphangiomyomatosis. The patient's plasma (1→3)-β-D-glucan increased up to 2964 pg/ml the day after transplantation. We searched for the reason for this increase and it was suspected that blood from the surgical field, which contained gauze, returning to the circulation through a heart-lung machine might have caused the increase in plasma (1→3)-β-D-glucan. To examine this hypothesis, we experimentally measured the (1→3)-β-D-glucan level in saline in which gauze had been immersed. The result implies that (1→3)-β-D-glucan might have been eluted from the gauze. If large amounts of gauze are used in the surgical field and the blood aspirated is returned to the circulation, the postoperative plasma (1→3)-β-D-glucan level should be carefully interpreted.

A 40-year-old man, diagnosed as acute myelogenic leukemia underwent a HLA-identical sibling peripheral blood stem cell transplant following an off treatment relapse. He subsequently developed chronic graft-versus-host disease (GVHD) and bronchiolitis obliterans caused recurrent pneumothorax. In order to control the recurrent medical-treatment-resistant pneumothorax, four surgeries (three left, one right) were necessary. It was thought important to reinforce the whole visceral pleura by covering it with an absorbable material sheet and fibrin glue in surgical treatment for recurrent pneumothorax.

Empyema associated with bronchopleural fistula (BPF) is one of the serious complications after pulmonary resection.(1) Various methods (eg, direct suture of BPF, omental and muscular transposition, thoracoplasty, or a combination of them) have been indicated to treat empyema. However, these treatments often fail because of the recurrent BPFs.(1-4) In these treatments, complete obliteration of residual pleural space is important to prevent the recurrence of BPF. Here we report a successful treatment for a patient with persistent BPF. The patient was lean and did not have enough muscles for pleural space obliteration, so we devised a new method-muscle transposition combined with an endobronchial plug.

Empyema associated with bronchopleural fistula (BPF) is one of the serious complications after pulmonary resection.(1) Various methods (eg, direct suture of BPF, omental and muscular transposition, thoracoplasty, or a combination of them) have been indicated to treat empyema. However, these treatments often fail because of the recurrent BPFs.(1-4) In these treatments, complete obliteration of residual pleural space is important to prevent the recurrence of BPF. Here we report a successful treatment for a patient with persistent BPF. The patient was lean and did not have enough muscles for pleural space obliteration, so we devised a new method-muscle transposition combined with an endobronchial plug.

Background: Tranilast is an anti-allergic agent known to inhibit the release of histamine, interleukin-1beta, transforming growth factor beta1, and platelet-derived growth factor from various cells and currently is used to treat allergic diseases, keloids, and hypertrophic scars. We evaluated the ability of tranilast to inhibit the development of obliterative airway disease (OAD) in a rat model of heterotopic tracheal transplantation. Methods: We transplanted tracheal segments from donor rats (Brown Norway) into subcutaneous pouches in major histocompatibility complex-incompatible recipient rats (Lewis). At Days 21 and 28 after transplantation, we histologically assessed the harvested allografts scored the degree of OAD, on a scale from zero to 4 as previously described, caused by fibroproliferative tissue. Results: Recipient animals treated orally with 400 mg/kg/day tranilast throughout the experiment showed significantly decreased OAD compared with control animals, with a histologic score of 1.1 +/- 0.4 vs 3.0 +/- 1.3, respectively (mean +/- SD, p = 0.007), at Day 21 after transplantation and 2.0 +/- 1.4 vs 3.9 +/- 0. 4, respectively (mean +/- SD, p = 0.017), at Day 28 after transplantation. Conclusion: These results showed that treatment with tranilast significantly decreased fibroproliferative airway changes associated with allograft rejection in a rat model of tracheal transplantation, suggesting that tranilast may be useful in preventing bronchiolitis obliterans after lung transplantation. Copyright (C) 2004 by the International Society for Heart and Lung Transplantation.

Background: Tranilast is an anti-allergic agent known to inhibit the release of histamine, interleukin-1beta, transforming growth factor beta1, and platelet-derived growth factor from various cells and currently is used to treat allergic diseases, keloids, and hypertrophic scars. We evaluated the ability of tranilast to inhibit the development of obliterative airway disease (OAD) in a rat model of heterotopic tracheal transplantation. Methods: We transplanted tracheal segments from donor rats (Brown Norway) into subcutaneous pouches in major histocompatibility complex-incompatible recipient rats (Lewis). At Days 21 and 28 after transplantation, we histologically assessed the harvested allografts scored the degree of OAD, on a scale from zero to 4 as previously described, caused by fibroproliferative tissue. Results: Recipient animals treated orally with 400 mg/kg/day tranilast throughout the experiment showed significantly decreased OAD compared with control animals, with a histologic score of 1.1 +/- 0.4 vs 3.0 +/- 1.3, respectively (mean +/- SD, p = 0.007), at Day 21 after transplantation and 2.0 +/- 1.4 vs 3.9 +/- 0. 4, respectively (mean +/- SD, p = 0.017), at Day 28 after transplantation. Conclusion: These results showed that treatment with tranilast significantly decreased fibroproliferative airway changes associated with allograft rejection in a rat model of tracheal transplantation, suggesting that tranilast may be useful in preventing bronchiolitis obliterans after lung transplantation. Copyright (C) 2004 by the International Society for Heart and Lung Transplantation.