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| 1 | Treating inflammatory bowel disease by adsorptive leucocytapheresis:A desire to treat without drugs显示文摘Ulcerative colitis and Crohn’s disease are the major phenotypes of the idiopathic inflammatory bowel disease(IBD),which afflicts millions of individuals throughout the world with debilitating symptoms,impairing function and quality of life.Current medications are aimed at reducing the symptoms or suppressing exacerbations.However,patients require life-long medications,and this can lead to drug dependency,loss of response together with adverse side effects.Indeed,drug side effects become additional morbidity factor in many patients on long-term medications.Nonetheless,the efficacy of anti-tumour necrosis factors(TNF)-αbiologics has validated the role of inflammatory cytokines notably TNF-αin the exacerbation of IBD.However,inflammatory cytokines are released by patients’own cellular elements including myeloid lineage leucocytes,which in patients with IBD are elevated with activation behaviour and prolonged survival.Accordingly,these leucocytes appear logical targets of therapy and can be depleted by adsorptive granulocyte/monocyte apheresis(GMA)with an Adacolumn.Based on this background,recently GMA has been applied to treat patients with IBD in Japan and in the European Union countries.Efficacy rates have been impressive as well as disappointing.In fact the clinical response to GMA seems to define the patients’disease course,response to medications,duration of active disease,and severity at entry.The best responders have been first episode cases(up to 100%)followed by steroid nave and patients with a short duration of active disease prior to GMA.Patients with deep ulcers together with extensive loss of the mucosal tissue and cases with a long duration of IBD refractory to existing medications are not likely to benefit from GMA.It is clinically interesting that patients who respond to GMA have a good long-term disease course by avoiding drugs including corticosteroids in the early stage of their IBD.Additionally,GMA is very much favoured by patients for its good safety profile.GMA in 21st century reminds us of phlebotomy as a major medical practice at the time of Hippocrates.However,in patients with IBD,there is a scope for removing from the body the sources of proinflammatory cytokines and achieve disease remission.The bottom line is that by introducing GMA at an early stage following the onset of IBD or before patients develop extensive mucosal damage and become refractory to medications,many patients should respond to GMA and avoid pharmacologics.This should fulfill the desire to treat without drugs. | Abbi R Saniabadi Tomotaka Tanaka Toshihide Ohmori Koji Sawada Takayuki Yamamoto Hiroyuki Hanai | 2014 | World Journal of Gastroenterology2014，20，29： | 11 |
| 2 | Effects of adacolumn selective leukocytapheresis on plasma cytokines during active disease in patients with active ulcerative colitis显示文摘瞄准:调查在临床的活动索引的 ulcerative (UC )( 蔡) 和 IL-1ra, IL-10, IL-6 和 IL-18 的传播层次之间的关系。方法:IL-1ra, IL-10, IL-6 和 IL-18 的血层次与活跃 UC 在 31 个病人被测量,吝啬的蔡是 11.1,从 5-25 ;并且是的 12 个健康个人控制。病人们与 Adacolumn 被给粒细胞和单核白血球 adsorptive 词首字母的脱落(GMA ) 。忍受 FcgammaR 并且补充受体的白细胞被吸附到列 leucocytapheresis 搬运人。每个病人能在 8 wk 上收到多达 11 个 GMA 会议。结果:我们发现了在蔡和 IL-10 之间的强壮的关联(r = 0.827, P <
0.001 ) , IL-6 (r = 0.785, P <
0.001 ) 并且 IL-18 (r = 0.791, P <
0.001 ) 。IL-1ra 没与蔡一起被相关。后面的 GMA 治疗, 31 个病人中的 24 个完成了宽恕,所有 4 cytokines 的层次掉在健康控制里到层次。进一步, IL-1ra 和 IL-10 的血层次在从遵守了搬运人的白细胞建议版本的 60 min 在列流出和流入增加了。 | Hiroyuki Hanai Takayuki Iida Masami Yamada Yoshihiko Sato Ken Takeuchi Tatsuo Tanaka Kenji Kondo Masataka Kikuyama Yasuhiko Maruyama Yasushi Iwaoka Akiko Nakamura Kazuhisa Hirayama Abby R Saniabadi Fumitoshi Watanabe | 2006 | World Journal of Gastroenterology2006，12，21： | 8 |
| 3 | Elevated plasma cryofibrinogen in patients with active inflammatory bowel disease is morbigenous显示文摘瞄准:在活跃的煽动性的肠疾病(IBD ) 调查冷沉纤维蛋白(CF ) 的角色。方法:CF 是在 284 个题目的 assayed:61 与活跃并且 63 与不活跃的 ulcerative (UC ) , 45 有 proctocolectomy, 35 与活跃并且 20 与不活跃的 Crohn 的疾病(CD ) , 40 与另外的疾病和 20 健康控制。胰岛素禁止者(TI ) 和 TI 抗体(TI-Ab ) 被 ELISA 在血浆和 CF 建筑群测量。结果:在活跃 UC 的 CF 与所有另外的组(c2<0.001 ) 相比惊人地高。同样, CF 比在不活跃的 CD 或在控制(c2<0.01 ) 在活跃 CD 是显著地更高的。在 UC,高 CF 和 TI-Ab 与对操作的需要被联系。进一步,在血浆的高 CF, CF/fibrinogen 比率,低 TI 和高 TI-Ab 与疾病活动或倔强被联系到药。提高的 CF 没与相似 C 反应的蛋白质和白血房间除了红细胞沉降率数的尖锐反应物被联系,建议那提高的 CF 不是急性炎的后果。结论:在活跃 IBD 的提高的 CF 看起来是致病。CF 经由二主要机制支持 IBD, TI (一种反煽动性的物质) 熄灭并且损害由形成蛋白质总数的微脉管的灌注。CF 可以也用作长期的 IBD 的一个简历标记。另外的研究被保证充分在 IBD 评估 CF 的角色,结果应该贡献 IBD 的致病的更好的理解。 | Koji Sawada Ryouki Takahashi Abbi R Saniabadi Maiko Ohdo Takashi Shimoyama | 2006 | World Journal of Gastroenterology2006，12，10： | 7 |
| 4 | Apoptosis in the failing human heart显示文摘 | Olivetti G Abbi R Quaini F | 1997 | N Engl J Med1997，336，： | 1 |
| 5 | Effect of the fat content of the diet on the carcinogenic activity of 4-(methylnitrosamino)-1-(3-pyri-dyl)-l-butanone in F344 rats显示文摘 | HOFFMANN D RIVENSON A ABBI R | | 0，，： | 1 |
| 6 | Apoptosis in the failing human heart 显示文摘 | Quaini F Abbi R | 1997 | N Engl J Med1997，336，： | 1 |
| 7 | Apoptosis in the failing hman heart显示文摘 | Abbi R Quaini F | 1997 | N Engl J Med1997，336，16： | 1 |
| 8 | Apoptosis in the failing human heart显示文摘 | Olivetti G Abbi R Quaini F | 1997 | N Engl J Med1997，336，16： | 1 |
| 9 | Apoptosis in the failing human heart显示文摘 | Olivetti G Abbi R Quaini F | 1997 | N Engl J Med1997，336，： | 1 |
| 10 | Apoptosis in the failing human heart显示文摘 | Abbi R Quaini F | 1997 | N Eng Med1997，336，16： | 1 |
| 11 | Apoptosis in the failure hu man heart显示文摘 | Olivetti G Abbi R Quaini F | 1997 | N Engl J Med1997，336，16： | 1 |
| 12 | Apoptosis in the failing human heart显示文摘 | Olivetti G Abbi R Quaini F | 1997 | N Eng J Med1997，336，16： | 1 |
| 13 | Apoptosis in the failing human heart显示文摘 | OLIVETTI G ABBI R QUAINI F | 1997 | N Engl J Med1997，336，16： | 1 |
| 14 | Apoptosis in the failing human heart显示文摘 | Olivetti G Abbi R Quaini F | 1996 | N Eng J Med1996，336，： | 1 |
| 15 | Apoptosis in the failing human heart显示文摘 | Olivetti G Abbi R Quaini F | 1997 | N Engl J Med1997，336，： | 1 |
| 16 | Apoptosis in the failing human heart显示文摘 | Abbi R Quaini F | 1997 | N Engl J Med1997，336，： | 1 |
| 17 | Apoptosis in the failing human heart显示文摘 | Olivetti G Abbi R Quaini F | 1997 | N Engl J Marl1997，336，： | 1 |
| 18 | Apoptosis in the failing human heart显示文摘 | Abbi R Quaini F Kajstura J Cheng W Nitahara JA | 1996 | N Eng J Med1996，336，16： | 1 |
| 19 | Apptosis in the failing human heart 显示文摘 | Olivetti G Abbi R Quaini F | 1997 | NEng1 J Med1997，336，： | 1 |
| 20 | Apoptosis in the failing human heart显示文摘 | Abbi R Quaini F | 1997 | N Engl J1997，336，： | 1 |
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