星川 康

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.

【目的】難治性気胸の術後合併症リスク評価．【対象と方法】高齢者難治性気胸手術症例43例に対し，術前背景因子，術前臓器機能因子，術前評価可能な麻酔手術侵襲等について比較検討し，単変量解析によるリスク評価を行った．続いて多変量解析を行い，高齢気胸術後合併症リスク評価を試みた．【結果】男性41例女性2例で，術後合併症は10例（23.3％）で認められた．諸因子別網羅的解析では，全25項目中血清TP，Alb，chE，Na^＋低値群およびPS，酸素投与群，麻酔スコア値で有意であった．すべての因子による多変量解析ではPS低値群にて有意に合併症が発生した（odds比：73.7，P＝0.003）．【結語】高齢者難治性気胸ではperformance status不良，低栄養状態，低Na群および酸素吸入群は全身麻酔手術ハイリスク群である．

【目的】難治性気胸の術後合併症リスク評価．【対象と方法】高齢者難治性気胸手術症例43例に対し，術前背景因子，術前臓器機能因子，術前評価可能な麻酔手術侵襲等について比較検討し，単変量解析によるリスク評価を行った．続いて多変量解析を行い，高齢気胸術後合併症リスク評価を試みた．【結果】男性41例女性2例で，術後合併症は10例（23.3％）で認められた．諸因子別網羅的解析では，全25項目中血清TP，Alb，chE，Na^＋低値群およびPS，酸素投与群，麻酔スコア値で有意であった．すべての因子による多変量解析ではPS低値群にて有意に合併症が発生した（odds比：73.7，P＝0.003）．【結語】高齢者難治性気胸ではperformance status不良，低栄養状態，低Na群および酸素吸入群は全身麻酔手術ハイリスク群である．

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.

骨髄移植後閉塞性細気管支炎に起因した再発性難治性気胸の一例を経験したので報告する．症例は４０歳男性．２００３年急性骨髄性白血病にて骨髄移植施行半年後，骨髄移植後閉塞性細気管支炎を発症した．２００４年より右自然気胸を合計３回発症．２００５年に両側気胸発症し，手術目的にて当科紹介となる．４回の手術後，最終的には両側気胸に対し，病巣切除およびポリグリコール酸シート＋フィブリン糊にて胸膜被覆術を施行した．現在再発を認めていない．

血清（1→3）-β-D-グルカン値の測定による深在性真菌症の血清学的診断は，広く利用されているが，その測定値は真菌症以外の種々の因子による影響を受け，偽陽性を示すことがある．我々は肺リンパ脈管筋腫症の患者に対し，脳死両側肺移植術を施行した．術翌日の血清（1→3）-β-D-グルカン値は2964 pg/mlと異常高値を示した．原因を検討した結果，術中の人工心肺中のポンプ吸引使用により，ガーゼに浸み込んだ血液が体内へ送血されたことが原因である可能性が疑われた．それを踏まえ，我々は生理食塩水とガーゼを使用した（1→3）-β-D-グルカン値の実験的測定を行ったところ，ガーゼから生理食塩水への（1→3）-β-D-グルカン成分の溶出を示唆する結果を得た．ガーゼの大量使用，および人工心肺中にポンプ吸引を行った症例では血清（1→3）-β-D-グルカン値の異常高値を示す可能性があり，注意を要すると考えられた．

骨髄移植後閉塞性細気管支炎に起因した再発性難治性気胸の一例を経験したので報告する．症例は４０歳男性．２００３年急性骨髄性白血病にて骨髄移植施行半年後，骨髄移植後閉塞性細気管支炎を発症した．２００４年より右自然気胸を合計３回発症．２００５年に両側気胸発症し，手術目的にて当科紹介となる．４回の手術後，最終的には両側気胸に対し，病巣切除およびポリグリコール酸シート＋フィブリン糊にて胸膜被覆術を施行した．現在再発を認めていない．

症例は42歳女性。喫煙指数420。CT検診で両側上肺野に最大7mmの空洞性病変を多数認めた。気管支肺胞洗浄液中のCD1a陽性細胞数が高値であり、病理組織学的に気道周囲の線維化包巣内にS-100陽性細胞を認め、Pulmonary Langerhans Cell Histiocytosis(以下PLCH)と診断した。禁煙を励行し、3ヵ月後には瘢痕を残し空洞性病変は消失した。禁煙による画像所見の改善に伴い、気管支肺胞洗浄液中のCD1a陽性細胞数は減少し(4.9%→1.8%)、CD4/CD8比は上昇した(1.66→6.16)。PLCHの禁煙後のBAL経過の報告はなく、病態理解上、興味深い所見であった。(著者抄録)

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.