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直腸癌の患者において，癌性心膜炎による心タンポナーデを来した症例を経験したので報告する．症例は54歳の男性で，2006年6月，進行直腸癌，大動脈周囲および縦隔リンパ腺腫大を認め，化学療法を選択した．同年7月，直腸狭窄が強くなり直腸切断術を施行した．化学療法継続中の2007年7月，著明な顔面浮腫および労作時呼吸困難を自覚．大量の心嚢水貯留を認め，心タンポナーデと診断した．剣状突起下経皮的心嚢ドレナージを行った．同年10月，大量の心嚢水の再貯留あり，再度心嚢ドレナージを行った．Adriamycin30 mg，OK-432 10KEを心嚢内に注入した．その後，4か月経過した現在，心嚢水貯留の再発なく日常生活に復帰している．癌性心膜炎に対し，チューブドレナージ法と心嚢内へのadriamycin，OK-432注入療法を行い優れた効果を得た．進行直腸癌においては，全身化学療法により効果的な延命が期待できるゆえ，積極的に局所コントロールを行う意義がある．

胃癌術後直腸転移および虫垂転移をきたした症例を経験したので報告する．症例は57歳，男性．平成15年8月，胃癌に対し幽門側胃切除を施行した．病理組織学的検査所見はpor，se，n2(+)，ly1，v0，stageIIIA，根治度Bであった．平成18年6月，歯状線直上の直腸前壁に粘膜下を浸潤する形態の隆起性病変を認めた．病理組織学的には，胃癌と同等な低分化型腺癌が粘膜下層を中心に増殖しており，胃癌の直腸転移と診断した．免疫染色組織像においても胃および直腸の組織像で同様の所見を得た．その後，化学療法継続するも徐々に直腸狭窄をきたしたため，平成19年1月，人工肛門を造設した．同年4月，内ヘルニアによる絞扼性イレウスのため緊急手術を施行．その際虫垂切除し，虫垂口より便汁を減圧した．切除虫垂は胃癌，直腸と同様の組織像を呈し胃癌虫垂転移と診断された．その後，化学療法を継続するも，胃癌術後より52カ月目（直腸転移診断より17カ月，虫垂転移診断より8カ月）に癌死した．直腸および虫垂への転移形式はリンパ行性であると示唆された．

Some of our patients showed a recurrence of adhesive small bowel obstruction (ASBO) with nonoperative management. The aim of this study was to evaluate the parameters predicting the recurrence of ASBO in patients managed with a long tube. Of 234 patients with ASBO admitted from April 1998 to September 2002, a total of 91 who recovered with nonoperative management after long tube placement were enrolled in this retrospective clinical study. We divided them into two groups for follow-up: the recurrence group and the no-recurrence group. We compared baseline characteristics, the number of previous ASBO admissions, the number of abdominal operations, the interval from the onset of symptoms to long-tube insertion, the duration of long-tube placement, the type of the contrasted intestine through the long tube, the location of the long-tube tip, and the drainage volume through the long tube between the two groups. We then examined the cumulative recurrence rate. A significant difference was found in the number of previous ASBO admissions, the duration of long-tube placement (77 hours vs. 43 hours), the contrasted intestine through the long tube, and the location of the long-tube tip. By multivariate analysis, the duration of long-tube placement was an independent parameter predicting the recurrence of ASBO. These results suggest that the duration of long-tube placement might serve as a parameter for predicting recurrence of ASBO in patients managed with a long tube.

高齢者における後術癒着性イレウスに対して,イレウス管留置の功罪について検討した.術後癒着性イレウス症例234例で,イレウス管による保存的治療を行った147症例のうち,イレウス管造影を施行した97症例を年齢により75歳以上(15症例), 75歳未満(82症例)に分けた.そして,発症からの経過時間,イレウス管の造影所見,進行状況,排液量,留置期間,手術率,イレウス管留置中の合併症,死亡率に着目して比較検討した.高齢者群では非高齢者群に比してイレウス管の進行が不良であり,排液量も遷延化する傾向にあった.保存的治療継続中に合併症が有意に多く発症した(P

目的: 術後癒着性イレウスを対象としてイレウス管の管理と手術のタイミングについて検討した. 方法: 入院2日以内の軽快例または緊急手術例を除き, 入院3日目以降に保存的治療のみで改善した23症例と手術を行った56症例 (79症例すべて入院より24時間以内にイレウス管留置) について, イレウス発症からイレウス管挿入までの時間, イレウス管の造影所見, 進行状況, 排液量に着目して比較検討した. また, 両群の予後についても検討した. 結果: 入院3日目以降までイレウス管留置を必要とした症例において, 保存的治療有効群では発症からイレウス管挿入までの時間が平均35時間で手術群の44時間に比べて有意に短かった. イレウス管造影所見では小腸閉塞, 停滞型は手術へ移行する傾向が高く, またイレウス管先端部の進行状況が良好な症例は有意に保存的改善となった. 排液量の検討では3日目の排液量500ml以上の症例は有意に手術へ移行していた. また, 3日目以降に保存的に改善した23症例は3年以内70%が再発し, その半数が手術を施行されていた. 考察: 術後癒着性イレウスの保存的治療においてはイレウス管の迅速な挿入を考慮し, 挿入後は排液量推移の観察が重要である. 3日目以降にイレウスが改善せず, 3日目の排液量が500ml 以上の症例では手術を考慮すべきである.

閉鎖孔ヘルニアは男性では非常に稀な疾患である.今回われわれは男性の閉鎖孔ヘルニアを2例経験した.症例1, 79歳男性,腹痛,嘔吐を主訴に来院.原因不明の腸閉塞にてイレウス管留置された.イレウス症状改善せず, 4日後の腹部CTにて閉鎖孔ヘルニアによる腸閉塞と診断し手術施行した.症例2, 82歳男性.数日前からの大腿部痛,嘔吐を主訴に来院.即日,腹部CTにて閉鎖孔ヘルニアによる腸閉塞と診断し,緊急手術施行した.自験例を含め男性報告例では自然解除例はなく,骨盤CTによる早期の診断,手術が特に重要である.男性発症例の特徴についての検討を加えて報告する.

転移性脈絡膜腫瘍の原発巣の大部分は乳癌と肺癌であり,消化器癌が原発である症例は非常に少ない.今回われわれは上行結腸癌根治術後7カ月で両肺転移をきたしたために全身化学療法を施行した結果,肺病変に関してはCRを得られていた患者が,その後に転移性脈絡膜腫瘍をきたした症例を経験した.症例は79歳,男性で主訴は右目の霧視である.平成11年3月に上行結腸癌の診断で結腸右半切除を施行.同年10月末には両肺に腫瘤性病変を認めた.平成12年1月よりUFT内服と5-FUの24時間持続静注による全身化学療法を行ったところ両肺の腫瘤性病変は消失し,その後も引き続き化学療法を施行した.平成12年9月に右目の霧視を自覚したため,精査を行ったところ転移性脈絡膜腫瘍と診断された.眼病変に対して放射線治療を行ったところ腫瘍性病変は縮小したが,視力の回復は得られなかった.

To test the hypothesis that plasminogen activator inhibitor-1 (PAI-1) may serve as a candidate marker for the malignancy of colorectalcancer (CRC), we performed a quantitative RT–PCR for PAI-1 gene and evaluated the possible relationship between PAI-1 geneexpression levels and clinicopathological findings in CRC. A significant increase in PAI-1 expression scores was observed in lymphnode metastasis-positive CRCs (2.1970.43) compared to negative ones (0.3570.42) (P¼0.0037) as well as in distant metastasis-positive CRCs (3.5071.18) compared to negative ones (0.9970.30). The PAI-1 expression score markedly increased with thetumour stage (P¼0.0063; ANOVA test). Moreover, multivariate analysis revealed the PAI-1 expression score to be a strong andindependent prognostic factor for CRC (P¼0.0432). These results suggested that PAI-1 might serve as a new parameter for theprediction of prognoses in CRC.British Journal of Cancer (2005) 93, 799–803. doi:10.1038/sj.bjc.6602743 www.bjcancer.comPublished online 9 August 2005& 2005 Cancer Research UKKeywords: plasminogen activator inhibitor-1; colorectal cancer; quantitative RT–PCRThere is now good evidence that a series of genetic alterations inboth dominant oncogenes and tumour suppressor genes areinvolved in the pathogenesis of human colorectal cancer (CRC).Activation of oncogenes such as the ras gene, and inactivation oftumour suppressor genes such as the APC and p53 genes, havebeen identified in CRC (Bos et al, 1987; Baker et al, 1990; Nishishoet al, 1991). In addition, we found that several other genes arerelated to the pathogenesis of this disease (Hibi et al, 1996, 1997,2002, 2004; Yamazaki et al, 2002). An investigation of geneticchanges is important to clarify the tumorigenic pathway of CRC(Vogelstein et al, 1988).Plasminogen activator inhibitor-1 (PAI-1), a 45-kDa serineproteinase inhibitor with a reactive peptide bond, Arg345–Met346,is a multifaceted proteolytic inhibitor that not only functions as afibrinolytic inhibitor, but also plays an important role in signaltransduction, cell adherence, and cell migration. There is clinicalevidence implicating PAI-1 as a key factor in tumour invasion andmetastasis (Potempa et al, 1994; Lijnen, 2005). Moreover, PAI-1has been linked to a poor prognosis in several cancers (Nekardaet al, 1994; Cantero et al, 1997; Chambers et al, 1998; Foekens et al,2000; Konecny et al, 2001). Previously, we also demonstrated thatPAI-1 expression was significantly correlated with a poorprognosis in esophageal squamous carcinoma (Sakakibara et al,2004). These results prompted us to examine the PAI-1 expressionlevel in other cancers, especially in CRC.To test the hypothesis that PAI-1 may serve as a candidatemarker for the malignancy of CRC, we performed a quantitativereverse transcription-PCR (RT–PCR) and evaluated the relation-ship between the PAI-1 gene expression levels and clinicopatho-logical findings in CRC.

Purpose and Experimental Design: To test whether plasminogen activator inhibitor-1 (PAI-1) can serve as a candidate marker for the malignancy of esophageal squamous cell carcinoma (SCC), we performed a quantitative reverse transcription-PCR for PAI-1 gene and evaluated the possible relationship between PAI-1 gene expression levels and clinicopathological findings in esophageal SCC. Results: Significant increases in PAI-1 scores were observed in metastasis-positive esophageal SCCs (3.08 ± 0.80) compared with metastasis-negative ones (−0.31 ± 0.62; P = 0.0042). PAI-1 expression scores significantly increased with tumor stage (P = 0.05, ANOVA). Conclusions: These results suggested that PAI-1 might serve as a new parameter for prediction of prognosis in esophageal SCC.

A successful surgical repair of a right hepatic hydrothorax in the absence of ascites is reported. A technetium-99m scintigram that was injected intraperitoneally provided evidence of a one-way flow of fluid from the peritoneal to pleural cavity. To identify and possible minute defects in the diaphragm, carbon dioxide was insufflated into the peritoneal cavity during the operation. We performed a direct suture of the defect observed on the diaphragm. The pleural effusion subsequently vanished after the operation.

10094 Background: We performed a quantitative RT-PCR for Plasminogen Activator Inhibitor-1 (PAI-1) gene in 55 surgical specimens of colorectal cancer (CRC) and corresponding normal mucosa. To test the hypothesis that PAI-1 may serve as a candidate marker for the malignant potential of CRC, we evaluated the possible relationship between PAI-1 gene expression levels and clinicopathological findings in CRC. Next, to investigate the mechanism of PAI-1 overexpression in CRC, we compared the PAI-1 expression levels in these cancers with those in the corresponding normal tissues. Results: A significant increase in PAI-1 expression scores was observed in node-positive CRCs (2.19Å}0.43) compared to negative ones (0.35Å}0.42) (P=0.0037) as well as in CRCs with distant metastasis (3.50Å}1.18) compared to negative ones (0.99Å}0.30). A significant increase in PAI-1 expression scores was observed in lymph node metastasis-positive CRCs (2.19Å}0.43) compared to negative ones (0.35Å}0.42) (P=0.0037) as well as in distant metastasis-positive CRCs (3.50Å}1.18) compared to negative ones (0.99Å}0.30). The PAI-1 expression score markedly increased with the tumor stage (P=0.0063; ANOVA test). Moreover, multivariate analysis revealed the PAI-1 expression score to be a strong and independent prognostic factor for CRC (P=0.0432). There was a significant correlation between CRC and corresponding normal PAI-1 expressions with a Spearman’s rank correlation coefficient of 0.81 (P < 0.0001). Conclusion: These results suggested that PAI-1 might serve as a new parameter for the prediction of prognoses in CRC. Taken together, PAI-1 overexpression in CRCs might originate from higher PAI-1 expression in the corresponding normal tissues and result in a malignant phenotype of these cancers. No significant financial relationships to disclose.