单纯肝动脉化疗和肝动脉栓塞化疗治疗原发性肝癌

经导管行肝动脉化疗 (ＨＡＩ)和肝动脉栓塞化疗(ＨＡＥ)治疗原发性肝癌已取得了显著疗效 ,尤其对无手术指征的中晚期肝癌是目前首选的治疗方法。现将我院自 1992～ 1996年 12月收治并取得随访结果的 58例行单纯肝动脉化疗和肝动脉栓塞化疗治疗原发性肝癌的情况总结如下。1　资料与方法1 1　一般资料　 58例中男 51例 ,女 7例 ;年龄 2 5～ 71岁 ,平均 4 6.5岁。全部病例均经临床体检、甲胎蛋白(ＡＦＰ)测定、Ｂ超、ＣＴ或ＭＲＩ检查和肝动脉造影诊断为原发性肝癌 ,符合 1977年全国制定的肝癌分型、分期标准。所有病例初诊时 ,均已失去外科手…     

原发性肝癌行肝动脉化疗栓塞介入治疗的临床观察

目的观察介入治疗对原发性肝癌不同类型的临床疗效。方法介入化疗栓塞（TACE）治疗原发性肝癌25例,其中结节型14例,弥漫型6例,巨块型5例。根据不同类型采用化疗＋栓塞和灌注化疗的治疗方式。结果结节型一年存活率7例;巨块型一年存活率2例,弥漫性一年存活率0例。结论结节型、巨块型行肝动脉化疗栓塞治疗效果明显,弥漫型仅在短期内减轻患者痛苦有效。结果表明肝癌越小介入治疗栓塞效果越好。介入治疗对肝癌有明显的辅助治疗作用,减轻患者的痛苦,提高患者的生存时间。     

经肝动脉化疗栓塞治疗原发性肝癌观察

目的:观察中晚期原发性肝癌经肝动脉化疗栓塞术治疗的疗效及不良反应。方法:65例中晚期原发性肝癌患者,接受TACE治疗,评估疗效和不良反应。结果:经治疗后38.4%(25/65)的患者部分缓解:58.4%(38/65)病情稳定:生存期明显延长,1、2、3年生存率分别为46.1%(30/65)、21.5%(14/65)、7.6%(5/65)。结论:TACE是治疗中晚期肝癌的有效方法,明显提高生存期。     

肝动脉灌注化疗联合栓塞介入治疗原发性肝癌的价值

目的 探讨将肝动脉灌注化疗与栓塞联合介入治疗应用于原发性肝癌的价值.方法 90例原发性肝癌患者,采用随机数字表的方式分为实验组和对照组,每组45例.实验组患者在接受肝动脉单纯栓塞介入治疗的同时进行肝动脉灌注化疗,对照组患者只接受肝动脉单纯栓塞介入治疗.对比两组患者的治疗效果及身体恢复状况.结果 实验组治疗良好率97.7...     

肝动脉化疗栓塞对原发性肝癌术后的影响

目的：评价经导管肝动脉化疗栓塞对原发性肝细胞癌术后的疗效。方法：将术前诊断为能手术切除的88例原发性肝细胞癌患者随机分为两组。A组(n＝44)术前4—8周进行1—2次化疗栓塞后手术切除．B组(n＝44)诊断成立后即手术切除。结果：无严重手术并发症或化疗栓塞相关并发症。术后6、12、18、24、36个月复发率差异不显著(P＞0．05)，12、24、36个月生存率相差不显著(P＞0．05)，术中平均出血量、手术并发症发生率及联合脏器切除相差显著(P＜0．05)。结论：能手术切除的原发性肝细胞癌术前不宜行经导管肝动脉化疗栓塞。     

原发性肝癌肝动脉灌注化疗及栓塞术12例分析

我科自2002～2003年共收治原发性肝癌12例，进行肝动脉灌注化疗及栓塞术(TACE)治疗，收到良好疗效，现报道如下。     

肝动脉栓塞化疗术治疗原发性肝癌65例

目的探讨肝动脉栓塞化疗术治疗原发性肝癌的方法和疗效。方法对驻马店市第一人民医院收治的65例不适宜手术的原发性肝癌患者,采用Seldinger技术,经肝固有动脉或肝左、右动脉,注入超液化碘油抗癌药混悬剂进行栓塞治疗。结果大多数患者的肿瘤呈明显缩小,占总数的81.5%。AFP大多也恢复到正常水平或者有不同程度的降低。患者的生存期超过6个月者占90.8%,12个月以上占66.2%,24个月以上占26.2%。结论 TACE作为介入治疗肝癌的有效方法之一,可大大提高患者的临床生存率,值得在临床上推广。     

肝动脉化疗栓塞治疗原发性肝癌围术期的护理

目的：探讨肝动脉化疗栓塞治疗原发性肝癌的护理干预方法。方法：回顾性分析66例行肝动脉化疗栓塞的中晚期原发性肝癌患者的临床资料,重点是术前心理护理、社会支持、术前评估和准备,术中配合和护理,术后一般护理、并发症的观察和护理、心理支持等。结果：手术顺利完成,避免和减轻了患者在治疗中的不良反应。结论：围术期护理是肝癌患者进行肝动脉化疗栓塞术手术安全的重要保证,确保了肝动脉化疗栓塞术治疗的效果。     

肝动脉灌注化疗加化疗栓塞治疗原发性肝癌48例护理体会

我院肿瘤科于 1998年 2月至 2 0 0 2年 12月对原发性肝癌病人行动脉灌注化疗加明胶海绵栓塞治疗原发性肝癌 48例 ,取得了良好的疗效。现将护理体会总结如下。1　临床资料男 3 9例 ,女 9例 ,中位年龄 47岁。其中原发性肝癌伴其他部位转移者 3 0例。经肝动脉灌注化疗加化疗栓塞治疗后取得良好疗效 ,病人生活质量明显改善。2　术前护理2 1　心理护理　了解病人的病情 ,协助医师做好病人及家属的思想工作。对于初次接受治疗的病人 ,由于病人缺乏对灌注化疗的了解 ,担心插管失败 ,甚至会有生命危险 ,护士应介绍此项技术治疗的优点及注意事项 ,并…     

含药微球肝动脉末梢栓塞治疗原发性肝癌的初步观察

原发性肝癌在无普查条件下的切除率仍徘徊在20％左右,对80％左右不能手术切除的病例的治疗仍然是今后治疗的重点课题。本文为1989年12月～1991年4月期间所做的前瞻性观察。用含甲氨喋呤白蛋白微球肝动脉末梢栓塞治疗不能手术切除的中晚期肝癌19例,从癌灶大小、甲胎蛋白动态变化等临床资料初步总结,肯定了这一治疗方法的优越性。     

阿霉素脂质体犬肝动脉栓塞后的体内分布与药代动力学研究

用阿霉素脂质体与碘油混合后对大经导管肝动脉栓塞,用反相高效液相色谱法研究了阿霉素在犬体内的分布及药代动力学。结果显示,阿霉素脂质体－碘油栓塞组大血浆阿霉素浓度显著低于阿霉素灌注组（P＜0.01）和阿霉素－碘油栓塞组（P＜0．05）,而其血浆阿霉素消除半衰期和肝组织中阿霉素浓度与后两组相比则显著增加（p＜0．01及p＜0．05）。说明阿霉素脂质体与碘油混合肝动脉栓塞后可显著提高阿霉素对肝脏的靶向性,延长阿霉素消除半衰期．     

肝动脉栓塞微球的动物药动学和药效学研究

肝动脉栓塞微球是用于治疗中晚期肝癌的新剂型。通过动脉插管即可将微球栓塞肝癌邻近的末梢动脉血管,起阻断血流和在局部缓释药物的双重作用。本文结合几年来对甲氨蝶吟(MTX),羟基喜树碱明胶微球和顺铂-乙基纤维素微球的基础研究工作,综述微球栓塞后在动物的体内过程和药效学。     

靶向给药系统——甲氨蝶呤肝动脉栓塞微球特征及其对大鼠肝癌的实验治疗

本文介绍用乳化—冻凝技术制备甲氨蝶吟—明胶微球的方法。实验结果证实,包裹在微球内的MTX对⁶⁰钻幅射、温度和光照射是稳定的。微球的体外溶出试验、明胶微球在介质中不同时间的溶胀度试验也在文中介绍。微球肝动脉栓塞实验治疗用大鼠移植性肝癌进行,结果表明MTX微球治疗组的大鼠在肿瘤抑制率、促使肿瘤坏死程度以及延长荷瘤动物存活期方面比肝动脉灌注生理盐水、MTX溶液和明胶微球为佳.由于MTX微球具有阻断肿瘤血供和在其局部缓释化疗药物等双重功用,故治疗肝癌的效果明显优于动脉化疗或单纯栓塞方法。     

经动脉灌注药物并栓塞治疗高龄中晚期肝癌的临床分析

目的　经导管肝动脉灌注化疗药物及栓塞 (TAE)作为晚期肝癌首选的姑息疗法 ,其临床价值已得到肯定。本文为探讨老年性肝癌采用此法的效果及并发症。方法　已确诊的 72例 70岁以上老年性肝癌 ,采用经皮肝动脉插管灌注化疗药物 ,一般为三联 ,并以碘化油乳化剂及明胶海绵碎屑沿导管注入 ,进行肝动脉栓塞。结果　 72例病人共进行介入治疗 2 2 4例次 ,其中进行栓塞 5 1例次 ,最多 13例次 ,最少 2例次 ,平均 4 8例次。生存期最长 18个月 ,最短 4个月 ,平均生存 6 5个月。CR 7例 ,PR 43例 ,NC 17例 ,PD 5例 ,总有效率 (CR PR)为 6 9 4% ( 5 0 72 )。经治疗后患者肝区疼痛减轻、腹水明显消退 ,食欲增加 ,免疫指标提高。结论　高龄中晚期肝癌采用肝动脉化疗药物灌注并栓塞术不失为一种有效的姑息方法。     

选择性肝左、右动脉阻断联合控制性低中心静脉压在肝叶切除手术的应用研究

目的观察选择性肝左、右动脉阻断联合控制性低中心静脉压术中出血量的影响。方法择期全麻下行肝叶切除术患者24例。分为2组:低中心静脉压组(LCVP组)和选择性肝左、右动脉阻断联合控制性低中心静脉压组(S组)。二组病人均为12人。二组在肝实质完全离断过程中CVP控制在0～0.49kPa水平。测量两组病人术中出血量。结果选择性肝左、右动脉阻断联合控制性低中心静脉压组和LCVP组术中出血量分别为(313±167)ml和(474±222)ml(P<0.05)。结论选择性肝左、右动脉阻断联合控制性低中心静脉压较单存低中心静脉压可减少肝叶切除手术术中出血量。     

Hepatic modeling of metabolite kinetics in sequential and parallel pathways: Salicylamide and gentisamide metabolism in perfused rat liver

Previous data on salicylamide (SAM) metabolism in the perfused rat liver had indicated that SAM was metabolized by three parallel (competing) pathways: sulfation, glucuronidation, and hydroxylation, whereas sequential metabolism of the hydroxylated metabolite, gentisamide (GAM), was solely via 5-glucuronidation to form GAM-5G. However, under comparable conditions, preformed GAM formed mainly two monosulfate conjugates at the 2- and 5-positions (GAM-2S and GAM-5S); 5-glucuronidation was a minor pathway. In the present study, the techniques of normal (N) and retrograde (R) rat liver perfusion with SAM and mathematic modeling on SAM and GAM metabolism were used to explore the role of enzymic distributions in determining the dissimilar fates of GAM, as a generated metabolite of SAM or as preformed GAM. Changes in the steady-state extraction ratio of SAM (E) and metabolite formation ratios between N and R perfusions were used as indices of the uneven distribution of enzyme activities. Two SAM concentrations (134 and 295 M) were used for single-pass perfusion: the lower SAM concentration exceeded the apparent K_m for SAM sulfation but was less than those for SAM glucuronidation and hydroxylation; the higher concentration exceeded the apparent K_m 's for SAM sulfation and glucuronidation but was less than the K_m for hydroxylation. Simulation of SAM metabolism data was carried out with various enzyme distribution patterns and extended to include GAM metabolism. At both input concentrations, E washigh (0.94 at 134 Mand 0.7 at 295 M) and unchanged during N and R, with SAM-sulfate (SAM-S) as the major metabolite and GAM-5G as the only detectable metabolite of GAM. Saturation of SAM sulfation occurred at the higher input SAM concentration as shown by a decrease in Eand a proportionally less increase in sulfation rates and proportionally more than expected increases in SAM hydroxylation and glucuronidation rates. At both SAM concentrations, the steady-state ratio of metabolite formation rates for SAM-S/SAM-G decreased when flow direction changed from N to R. An insignificant decrease in SAM-S/SAM-OH was observed at the low input SAM concentration, due to the small amount of SAM-OH formed and hence large variation in the ratio among the preparations, whereas at the high input SAM concentration, the decrease in SAM-S/SAM-OH with a change in flow direction from N to R was evident. The metabolite formation ratio, SAM-G/SAM-OH, however, was unchanged at both input concentrations and flow directions. The observed data suggest an anterior SAM sulfation system in relation to the glucuronidation and hydroxylation systems, which are distributed similarly. When the observations were compared to predictions from the enzyme-distributed models, the best prediction on SAM metabolism was given by a model which described sulfation activities anteriorly, glucuronidation activities evenly, and hydroxylation activities posteriorly (perivenous). When the model was used to predict data for SAM and GAM metabolism in once-through perfused rat livers at different input SAM concentrations, in the absence or presence of the sulfation inhibitor, 2,6-dichloro-4-nitrophenol (DCNP), the predictions were in close agreement with previously observed SAM data but failed to predict the exclusive formation of GAM-SG; rather, GAM-2S and GAM-5S were predicted as major sequential metabolites of SAM. The poor correlation for GAM metabolic data may be explained on the basis of subcellular enzyme localizations: the cytochromes P-450 and UDP-glucuronyltransferases, being membrane-bound enzymes, are more coupled for GAM formation and glucuronidation, when GAM was generated intracellularly. The present study suggests that subcompartmentalization of enzymes may need to be considered in hepatic modeling for better prediction of metabolic events.This work was presented in part at the ASPET meeting, Montreal, 1988, and was conducted in partial fulfilment of Xin Xu's Ph.D. thesis. This work was supported by the Medical Research Council of Canada and a grant from the Canadian Liver Foundation.     

Effects of Probenecid on Hepatic and Renal Disposition of Hexadecanedioate,an Endogenous Substrate of Organic Anion Transporting Polypeptide 1B in Rats

The aim of the present study was to investigate changes in plasma concentrations and tissue distribution of endogenous substrates of organic anion transporting polypeptide (OATP) 1B, hexadecanedioate (HDA), octadecanedioate (ODA), tetradecanedioate (TDA), and coproporphyrin-III, induced by its weak inhibitor, probenecid (PBD), in rats. PBD increased the plasma concentrations of these four compounds regardless of bile duct cannulation, whereas liver-to-plasma (K_p,liver) and kidney-to-plasma concentration ratios of HDA and TDA were reduced. Similar effects of PBD on plasma concentrations and K_p,liver of HDA, ODA, and TDA were observed in kidney-ligated rats, suggesting a minor contribution of renal disposition to the overall distribution of these three compounds. Tissue uptake clearance of deuterium-labeled HDA (d-HDA) in liver was 16-fold higher than that in kidney, and was reduced by 80% by PBD. This was compatible with inhibition by PBD of d-HDA uptake in isolated rat hepatocytes. Such inhibitory effects of PBD were also observed in the human OATP1B1-mediated uptake of d-HDA. Overall, the disposition of HDA is mainly determined by hepatic OATP-mediated uptake, which is inhibited by PBD. HDA might, thus, be a biomarker for OATPs minimally affected by urinary and biliary elimination in rats.