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1.
肝硬化门静脉高压症为全球性疾病,国内一般采用脾切除联合断流术治疗脾亢和(或)食管胃底曲张静脉破裂出血。脾切除术不仅丧失脾脏免疫功能,而且对肝硬化门静脉高压症肝功能的进—步损害较其他条件下的切脾更为严重。我们采用随机对照的方法,研究了腹膜后自体脾移植对保留脾脏免疫功能的作用。临床资料1.一般资料:收集1979年7月至2001年8月入住我院的肝硬化门静脉高压症病人20例,男19例,女1例,年龄33~80岁(平均37.8岁),肝功能Child A~B级。术前均有不同程度的脾肿大及脾功能亢进或食管胃底曲张静脉破裂出血症状。随机分为2组,每组各10例。…  相似文献   

2.
自体脾移植联合食管横断吻合术治疗肝硬化门静脉高压症   总被引:1,自引:0,他引:1  
目的 探讨腹膜后自体脾移植联合食管横断吻合术治疗肝硬化门静脉高压症的临床疗效.方法 将2003年1月至2006年12月收治的36例肝硬化门静脉高压症患者随机分为自体脾移植组(n=18)和脾切除组(n=18),自体脾移植组接受脾切除、食管横断吻合及自体脾移植术,脾切除组接受脾切除、食管横断吻合术.于术前及术后2~6个月定期观察两组患者的一般情况、行脾脏放射性核素扫描,同时检测肝功能、血清促吞噬素(Tuftsin)及IgM水平,并行组间及手术前后比较分析.结果 自体脾移植组患者术后2个月血清Tuftsin和IgM水平与术前比较无明显差异(P0.05),而脾切除组患者术后2个月血清Tuftsin和IgM水平较术前明显降低(P<0.05);自体脾移植术对患者肝功能无明显影响;术后2个月放射性核素扫描证实移植脾于腹膜后存活.结论 自体脾移植对保留机体脾脏免疫功能具有重要价值,腹膜后自体脾移植联合食管横断吻合术治疗肝硬化门静脉高压症的临床效果确切,值得推广应用.  相似文献   

3.
目的探讨肝炎后肝硬化门脉高压症腹膜后单个核细胞移植对门静脉压力的影响。方法随机对肝炎后肝硬化并门静脉高压症上消化道出血的70例病人分为治疗组和对照组。治疗组36例病人行脾切除、门—奇静脉断流的同时在腹膜后植入自体骨髓单个有核细胞。对照组34例行脾切除、门—奇静脉断流。观察术后再出血率及门静脉压力变化情况,用SAS统计软件分析处理。结果 36例在手术后12个月测门静脉压力降低,随访5a无再出血病例。结论肝硬变并门静脉高压症上消化道出血病人在行脾切除,门-奇断流的同时,在腹膜后植入自体骨髓单个核细胞可以增加门静脉侧支循环,降低门静脉压力,预防再上消化道出血的发生。  相似文献   

4.
目的 观察腹膜后自体脾移植联合食管下段横断术治疗肝硬变门静脉高压症的临床效果。方法 将20例肝功能Child A、B级的肝硬变门静脉高压症患者随机均分为自体脾移植组和切脾组。自体脾移植组采用自体带蒂脾组织腹膜后移植联合改良的食管下段横断术,切脾组则采用脾切除联合改良的食管下段横断术。以患者术前的情况为对照,在术后2~6 个月观察患者的一般情况、脾扫描、肝功能、血清促吞噬素(tuftsin)及IgM水平。结果 术后第6天切脾组死亡1例,术后第10天脾移植组出现再出血1 例。自体脾移植组术后血清tuftsin、IgM水平高于切脾组,差异有显著性意义(P<0.01),而对肝功能无明显影响。结论 腹膜后自体脾移植能维持脾脏的基本免疫功能,且能长期存活,在临床上推广应用是可行的。  相似文献   

5.
目的探讨带蒂脾段腹膜后固定术联合改良Sugiura术治疗肝硬化门静脉高压症的可行性。方法对18例门静脉高压症行带蒂脾段腹膜后固定术联合改良Sugiura术患者临床资料及手术过程进行回顾性分析。结果术后止血效果确切,无术后带蒂脾段坏死,术后所有患者食管下段静脉曲张消失或者明显好转,无术后门静脉系统血栓形成。吻合口狭窄发生1例。结论带蒂脾段腹膜后固定术联合改良Sugiura术治疗门静脉高压症是一种合理可取的治疗方法,其疗效满意,操作并不复杂。  相似文献   

6.
门静脉高压常合并门脉高压性胃病(portal hypertensive gastropathy,PHG),治疗门脉高压症的各种手术必然对PHG产生影响。我院自1990年6月至2001年3月,采用脾次全切除腹膜后移位加断流术治疗肝硬化门脉高压症病人48例,术后因肠系膜静脉血栓形成而死亡1例,参与临床随访者47例,随访2~13年,平均91个月,观察此术式对PHG的影响。  相似文献   

7.
在门静脉高压症中,肝外型门静脉高压症占全部门静脉高压症的5%~10%.区域性门静脉高压症亦称为左侧门静脉高压症、局限性门静脉高压症等,占肝外型门静脉高压症的5%,是引起上消化道出血的罕见原因.根据病因,区域性门静脉高压症可分为胰源性、脾源性(如脾动脉瘤、脾动静脉瘘等)和腹膜后源性(如来自腹膜后组织的肿瘤、炎症等)3类.  相似文献   

8.
目的采用随机对照研究的方法观察用自体脾移植联合食管下段横断术治疗肝硬化门脉高压症的临床效果.方法将肝功能ChildA、B级的肝硬化门脉高压症患者随机分为自体脾移植组和切脾组,脾移植组采用自体带蒂脾组织腹膜后移植联合改良的食管下段横断术,切脾组则采用脾切除联合改良的食管下段横断术;以患者术前的情况为对照,在术后2~8个月观察患者的一般情况、脾扫描、肝功能、血清Tuftsin、IgM水平.结果术后第六天切脾组死亡1例,脾移植组出现再出血1例;两组血清Tuftsin、IgM水平有显著性差异(P<0.05),在对肝功能的影响上无明显差异.结论脾自体移植后能够长期存活,并能够维持脾脏的基本免疫功能,是可以在临床上推广应用的.  相似文献   

9.
目的 采用随机对照研究的方法观察用自体脾移植联合食管下段横断术治疗肝硬化门脉高压症的临床效果。方法 将肝功能ChildA、B级的肝硬化门脉高压症患者随机分为自体脾移植组和切脾组 ,脾移植组采用自体带蒂脾组织腹膜后移植联合改良的食管下段横断术 ,切脾组则采用脾切除联合改良的食管下段横断术 ;以患者术前的情况为对照 ,在术后 2~ 8个月观察患者的一般情况、脾扫描、肝功能、血清Tuftsin、IgM水平。结果 术后第六天切脾组死亡 1例 ,脾移植组出现再出血 1例 ;两组血清Tuftsin、IgM水平有显著性差异 (P <0 .0 5 ) ,在对肝功能的影响上无明显差异。结论 脾自体移植后能够长期存活 ,并能够维持脾脏的基本免疫功能 ,是可以在临床上推广应用的。  相似文献   

10.
目的 总结139例采用食管吻合器的断流术经验,并观察治疗门静脉高压症的疗效。方法 对139例肝硬化性门静脉高压症采用食管吻合器的联合断流术治疗。结果 无手术死亡。腹腔内继发性出血2例(1.44%),肺不张和肺部感染各1例(0.72%),脾静脉血栓3例(2.16%),无食管吻合口瘘和吻合口狭窄。肝性脑病发生率0.72%(1/139);再了血率2.16%(3/139);手术1-3个月后,97例术前肝功能属Child-Pugh B级者有,76例转为A组;71例于术后半年接受过胃镜或食管吞钡检查,食管胃底曲张静脉消失者43例(60.56%),显著改善者27例(38.03%),无变化者1例(1.41%)。结论 应用食管吻合器的联合断流术治疗肝硬化性门静脉高压症的疗效较好,再出血率低,并发症少,是一种值得推广的治疗门静脉高压症的方法。  相似文献   

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杭州健康女性定量骨超声测定原发性骨质疏松   总被引:1,自引:0,他引:1       下载免费PDF全文
目的 评价杭州健康女性骨超声速度(SOS)值随增龄减少和骨质疏松患病率,建立杭州地区女性骨超声速度值参考数据库。方法 定量超声法测定1208例杭州地区健康女性桡骨远端(RAD),第3指骨近节(PLX),第V跖骨(MTR)和胫骨中段(TIB)的超声速度值。结果 RAD、PLX、MTR和TIBSOS峰值(Peak of SOS)均出现在40-45岁,TJB的SOS峰值出现在35—40岁,此后随年龄增长而下降。绝经后妇女在绝经后早期和晚期各有1个SOS快速减少期,前见于桡骨近端,平均年减少率为2.4%,后见于胫骨中段,平均年减少率为1.8%。各部位骨SOS累积减少率随年龄增长而增加,到85岁4部位累积减少为13%-18%。60岁以后骨质疏松性症(OP)检出率为45%-70%,OP检出率以桡骨远端最高,60-70岁平均为67%,第3指骨近端次之约50%,胫骨中段最低为36%;75岁以后分别为70%,65%和45%。结论 全身各部位骨超声速度值到达峰值的年龄不同,峰值也各有差异。绝经后妇女骨超声速度值随年龄增加减少较快,应予激素和补钙治疗,桡骨远端为本地区SOS检测和OP检出的敏感部位。  相似文献   

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The authors propose to use more often echocardiography (EchoCG) in examination of elderly (over 60 years) of age patients with cholecystitis that permits to increase surgical activity to 92.4%. Left ventricular ejection fraction is the most informative. When this fraction is lower than 45% surgery must be recommended on vital indications only. EchoCG was used in 155 patients with cholecystitis, 131 of them were operated. 2 (1.52%) patients died due to acute cardio-vascular insufficiency and pulmonary artery thromboembolism.  相似文献   

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Objective To evaluate the role of gliocyte in the spinal cord in the development of bone cancer pain (BCP) in mice. Methods Forty male C3H/He mice aged 8-10 weeks weighing 18-22 g were randomly divided into 4 groups ( n = 10 each) : group I sham operation (group S) , group II BCP, group Ⅲ PBS and group IV minocyline (group M) . In group BCP, PBS and M, bone cancer pain was produced by injection of NCTC2472 fibrosarcoma cell suspension (2 x 105 cells) 10 μl into medullary cavity of calcaneus bone, while in group S, PBS solution 10 μl was injected instead of cancer cell suspension. In group PBS and M, PBS 5 μl and minocyline 5 μl (dissolved to 0.2 mmol/L in PBS)_were given IT immediately before cancer cell inoculation once a day for 11 consecutive days respectively. Mechanical pain threshold was measured at 1 d before cancer cell inoculation, and at 0, 3, 5, 7, 9 and 11d after cancer cell inoculation. Cold pain threshold was measured at 3, 7, 9 and 11d after cancer cell inoculation. The animals were killed after measurement of pain threshold and L4-6, segment of spinal cord was removed for determination of GFAP and CD11b expression by Western blot. Results Compared with group S, mechanical pain threshold was significantly increased at 3-11 d after cancer cell inoculation in group BCP and PBS, and at 3 and S d after cancer cell inoculation in group M, and cold pain threshold was significantly increased at 7-11 d after cancer cell inoculation, and expression of CD11b and GFAP was up-regulated in group BCP, PBS and M ( P < 0.05) . Compared with group BCP, mechanical pain threshold was significantly decreased at 3-11 d after cancer cell inoculation, cold pain threshold was significantly decreased at 7-11 d after cancer cell inoculation, and expression of CD11b and GFAP was down-regulated in group M ( P <0.05) . ConclusionThe activiton of gliocyte in the spinal cord is involved in the development of bone cancer pian in mice.  相似文献   

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目的 评价脊髓胶质细胞在小鼠骨癌痛形成中的作用.方法 健康雄性C3H/He小鼠40只,周龄8~10周,体重18~22 g,随机分为4组(n=10):假手术组(S组)、骨癌痛组(B组)、PBS组(P组)和米诺环素组(M组).S组跟骨骨髓腔内注射PBS 10 μl;余3组跟骨骨髓腔内注射含2×105个骨纤维肉瘤细胞的PBS 10 μl制备骨癌痛模型,于造模前即刻开始PBS组鞘内注射PBS 5μl,M组鞘内注射米诺环素(用PBS溶解为0.2 mmol/L)5μl,1次/d,连续11 d.于造模前1 d、造模后即刻、3、5、7、9、11 d时测定机械痛阈;于造模后3、7、9、11 d机械痛阈测定结束后测定冷痛阈.痛阈测定结束后处死小鼠,取脊髓组织,测定神经胶质纤维酸性蛋白(GFAP)和CD11b的表达水平.结果 与S组比较,B组和P组造模后3-11 d时、M组造模后3、5 d时机械痛阈升高,B组、P组和M组造模后7~11 d时冷痛阈升高,脊髓CD11b和GFAP表达上调(P<0.05).与B组比较,M组造模后3-11 d时机械痛阈降低,造模后7-11 d时冷痛阈降低,脊髓CD11b和GFAP表达下调(P<0.05).结论 脊髓胶质细胞(星形胶质细胞和小胶质细胞)的激活参与了小鼠骨癌痛的形成.  相似文献   

16.
Objective To evaluate the role of gliocyte in the spinal cord in the development of bone cancer pain (BCP) in mice. Methods Forty male C3H/He mice aged 8-10 weeks weighing 18-22 g were randomly divided into 4 groups ( n = 10 each) : group I sham operation (group S) , group II BCP, group Ⅲ PBS and group IV minocyline (group M) . In group BCP, PBS and M, bone cancer pain was produced by injection of NCTC2472 fibrosarcoma cell suspension (2 x 105 cells) 10 μl into medullary cavity of calcaneus bone, while in group S, PBS solution 10 μl was injected instead of cancer cell suspension. In group PBS and M, PBS 5 μl and minocyline 5 μl (dissolved to 0.2 mmol/L in PBS)_were given IT immediately before cancer cell inoculation once a day for 11 consecutive days respectively. Mechanical pain threshold was measured at 1 d before cancer cell inoculation, and at 0, 3, 5, 7, 9 and 11d after cancer cell inoculation. Cold pain threshold was measured at 3, 7, 9 and 11d after cancer cell inoculation. The animals were killed after measurement of pain threshold and L4-6, segment of spinal cord was removed for determination of GFAP and CD11b expression by Western blot. Results Compared with group S, mechanical pain threshold was significantly increased at 3-11 d after cancer cell inoculation in group BCP and PBS, and at 3 and S d after cancer cell inoculation in group M, and cold pain threshold was significantly increased at 7-11 d after cancer cell inoculation, and expression of CD11b and GFAP was up-regulated in group BCP, PBS and M ( P < 0.05) . Compared with group BCP, mechanical pain threshold was significantly decreased at 3-11 d after cancer cell inoculation, cold pain threshold was significantly decreased at 7-11 d after cancer cell inoculation, and expression of CD11b and GFAP was down-regulated in group M ( P <0.05) . ConclusionThe activiton of gliocyte in the spinal cord is involved in the development of bone cancer pian in mice.  相似文献   

17.
Objective To evaluate the role of gliocyte in the spinal cord in the development of bone cancer pain (BCP) in mice. Methods Forty male C3H/He mice aged 8-10 weeks weighing 18-22 g were randomly divided into 4 groups ( n = 10 each) : group I sham operation (group S) , group II BCP, group Ⅲ PBS and group IV minocyline (group M) . In group BCP, PBS and M, bone cancer pain was produced by injection of NCTC2472 fibrosarcoma cell suspension (2 x 105 cells) 10 μl into medullary cavity of calcaneus bone, while in group S, PBS solution 10 μl was injected instead of cancer cell suspension. In group PBS and M, PBS 5 μl and minocyline 5 μl (dissolved to 0.2 mmol/L in PBS)_were given IT immediately before cancer cell inoculation once a day for 11 consecutive days respectively. Mechanical pain threshold was measured at 1 d before cancer cell inoculation, and at 0, 3, 5, 7, 9 and 11d after cancer cell inoculation. Cold pain threshold was measured at 3, 7, 9 and 11d after cancer cell inoculation. The animals were killed after measurement of pain threshold and L4-6, segment of spinal cord was removed for determination of GFAP and CD11b expression by Western blot. Results Compared with group S, mechanical pain threshold was significantly increased at 3-11 d after cancer cell inoculation in group BCP and PBS, and at 3 and S d after cancer cell inoculation in group M, and cold pain threshold was significantly increased at 7-11 d after cancer cell inoculation, and expression of CD11b and GFAP was up-regulated in group BCP, PBS and M ( P < 0.05) . Compared with group BCP, mechanical pain threshold was significantly decreased at 3-11 d after cancer cell inoculation, cold pain threshold was significantly decreased at 7-11 d after cancer cell inoculation, and expression of CD11b and GFAP was down-regulated in group M ( P <0.05) . ConclusionThe activiton of gliocyte in the spinal cord is involved in the development of bone cancer pian in mice.  相似文献   

18.
Objective To evaluate the role of gliocyte in the spinal cord in the development of bone cancer pain (BCP) in mice. Methods Forty male C3H/He mice aged 8-10 weeks weighing 18-22 g were randomly divided into 4 groups ( n = 10 each) : group I sham operation (group S) , group II BCP, group Ⅲ PBS and group IV minocyline (group M) . In group BCP, PBS and M, bone cancer pain was produced by injection of NCTC2472 fibrosarcoma cell suspension (2 x 105 cells) 10 μl into medullary cavity of calcaneus bone, while in group S, PBS solution 10 μl was injected instead of cancer cell suspension. In group PBS and M, PBS 5 μl and minocyline 5 μl (dissolved to 0.2 mmol/L in PBS)_were given IT immediately before cancer cell inoculation once a day for 11 consecutive days respectively. Mechanical pain threshold was measured at 1 d before cancer cell inoculation, and at 0, 3, 5, 7, 9 and 11d after cancer cell inoculation. Cold pain threshold was measured at 3, 7, 9 and 11d after cancer cell inoculation. The animals were killed after measurement of pain threshold and L4-6, segment of spinal cord was removed for determination of GFAP and CD11b expression by Western blot. Results Compared with group S, mechanical pain threshold was significantly increased at 3-11 d after cancer cell inoculation in group BCP and PBS, and at 3 and S d after cancer cell inoculation in group M, and cold pain threshold was significantly increased at 7-11 d after cancer cell inoculation, and expression of CD11b and GFAP was up-regulated in group BCP, PBS and M ( P < 0.05) . Compared with group BCP, mechanical pain threshold was significantly decreased at 3-11 d after cancer cell inoculation, cold pain threshold was significantly decreased at 7-11 d after cancer cell inoculation, and expression of CD11b and GFAP was down-regulated in group M ( P <0.05) . ConclusionThe activiton of gliocyte in the spinal cord is involved in the development of bone cancer pian in mice.  相似文献   

19.
Objective To evaluate the role of gliocyte in the spinal cord in the development of bone cancer pain (BCP) in mice. Methods Forty male C3H/He mice aged 8-10 weeks weighing 18-22 g were randomly divided into 4 groups ( n = 10 each) : group I sham operation (group S) , group II BCP, group Ⅲ PBS and group IV minocyline (group M) . In group BCP, PBS and M, bone cancer pain was produced by injection of NCTC2472 fibrosarcoma cell suspension (2 x 105 cells) 10 μl into medullary cavity of calcaneus bone, while in group S, PBS solution 10 μl was injected instead of cancer cell suspension. In group PBS and M, PBS 5 μl and minocyline 5 μl (dissolved to 0.2 mmol/L in PBS)_were given IT immediately before cancer cell inoculation once a day for 11 consecutive days respectively. Mechanical pain threshold was measured at 1 d before cancer cell inoculation, and at 0, 3, 5, 7, 9 and 11d after cancer cell inoculation. Cold pain threshold was measured at 3, 7, 9 and 11d after cancer cell inoculation. The animals were killed after measurement of pain threshold and L4-6, segment of spinal cord was removed for determination of GFAP and CD11b expression by Western blot. Results Compared with group S, mechanical pain threshold was significantly increased at 3-11 d after cancer cell inoculation in group BCP and PBS, and at 3 and S d after cancer cell inoculation in group M, and cold pain threshold was significantly increased at 7-11 d after cancer cell inoculation, and expression of CD11b and GFAP was up-regulated in group BCP, PBS and M ( P < 0.05) . Compared with group BCP, mechanical pain threshold was significantly decreased at 3-11 d after cancer cell inoculation, cold pain threshold was significantly decreased at 7-11 d after cancer cell inoculation, and expression of CD11b and GFAP was down-regulated in group M ( P <0.05) . ConclusionThe activiton of gliocyte in the spinal cord is involved in the development of bone cancer pian in mice.  相似文献   

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