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经导管动脉栓塞术联合肝动脉诱导内源性肿瘤坏死因子治疗肝细胞癌

[Transcatheter arterial embolization with hepatic arterial induction of endogenous TNF in hepatocellular carcinoma].

作者信息

Takekoshi H, Oyama R

机构信息

Dept. of Internal Medicine, Saiseikai Central Hospital.

出版信息

Gan To Kagaku Ryoho. 1989 Aug;16(8 Pt 2):2845-8.

PMID:2476966
Abstract

Antitumor effect and reduction of tumor size by some cytokines as Biological Response Modifier have been demonstrated by various studies. Endogenous tumor necrosis factor is produced from macrophage. To increase the antitumor effect of transcatheter arterial embolization (TAE) in hepatocellular carcinoma (HCC), we treated 7 HCC patients with endogenous tumor necrosis factor (ETNF) which was induced by hepatic arterial injection of gamma-IFN (1.0-3.0 X 10(6) IU) as priming agent and OK-432 (2-5 KE) as triggering agent. TAE was performed with Lipiodol, ADM and gelatin sponge on 3-10 days after the induction of ETNF. TNF activity was detected in 2 cases and suspected to depend on the dose of gamma-IFN and OK-432. Serum alpha-Fetoprotein levels after the injection of ETNF began to decrease from 3-30 days in 5 patients and remained unchanged in 2 cases. Serum alpha-Fetoprotein levels after TAE with the induction of ETNF were decreased 1-5 months in 5 cases. Reduced size and low-density area on CT scan in 3 advanced cases after these procedures were no different from those of HCC patients treated with TAE alone. In one of two inoperable cases with a single mass lesion in the liver, CT scan after one more added TAE following these procedures showed a low-density area around the Lipiodol uptaking tumor, indicating obstruction of the peripheral portal vein. CT scan of another case revealed low density around Lipiodol in the tumor, which showed complete necrotic change. In all cases, middle-grade fever and hypotension were seen transiently, but these subsided by symptomatic treatment. The antitumor effect of TAE in HCC might be enhanced with ETNF induced by hepatic arterial injection of a low dose of gamma-INF and OK-432.

摘要

多项研究已证实,某些作为生物反应调节剂的细胞因子具有抗肿瘤作用并能使肿瘤缩小。内源性肿瘤坏死因子由巨噬细胞产生。为增强经导管动脉栓塞术(TAE)对肝细胞癌(HCC)的抗肿瘤效果,我们对7例HCC患者进行了治疗,通过肝动脉注射γ-干扰素(1.0 - 3.0×10⁶IU)作为启动剂和OK - 432(2 - 5KE)作为触发剂来诱导内源性肿瘤坏死因子(ETNF)。在诱导ETNF后3 - 10天,使用碘油、阿霉素和明胶海绵进行TAE。在2例患者中检测到TNF活性,怀疑其取决于γ-干扰素和OK - 432的剂量。注射ETNF后,5例患者的血清甲胎蛋白水平在3 - 30天开始下降,2例患者保持不变。诱导ETNF后进行TAE,5例患者的血清甲胎蛋白水平在1 - 5个月下降。在这些操作后,3例晚期病例CT扫描显示的肿瘤大小缩小和低密度区域与单纯接受TAE治疗的HCC患者无异。在2例肝脏有单个肿块病变的不可手术病例中,其中1例在这些操作后再进行一次TAE,CT扫描显示碘油摄取肿瘤周围有低密度区域,提示外周门静脉阻塞。另一例患者的CT扫描显示肿瘤内碘油周围有低密度区域,呈现完全坏死改变。所有病例均短暂出现中度发热和低血压,但经对症治疗后消退。肝动脉注射低剂量γ-干扰素和OK - 432诱导的ETNF可能增强TAE对HCC的抗肿瘤效果。

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