Iwanaka T, Arya G, Ziegler M M
Division of Pediatric Surgery, Children's Hospital Medical Center Cincinnati, Ohio 45229, USA.
J Pediatr Surg. 1998 Mar;33(3):457-61. doi: 10.1016/s0022-3468(98)90088-4.
BACKGROUND/PURPOSE: Although minimally invasive surgery (MIS) has been broadly applied in patients with cancer of the gastrointestinal tract, the etiology of port-site tumor recurrence (PSR) after laparoscopic cancer surgery remains unclear. The authors report here an analysis of PSR in a model of murine neuroblastoma after laparoscopic tumor biopsy and propose a mechanism for this complication as well as a potential treatment.
Immature 5- to 7-week old male A/J mice (18-23 g) were subcutaneously inoculated with the minimally immunogenic TBJ-neuroblastoma (TBJ-NB) in the left flank and divided into three treatment groups. The following operations were performed 14 days after tumor inoculation: group 1, additional intraperitoneal or intravenous injection of TBJ-NB during CO2 pneumoperitoneum; group 2, simulated transperitoneal tumor biopsy using MIS techniques during either CO2 pneumoperitoneum or gasless suspension; Group 3, intraperitoneal (IP) or intravenous (IV) administration of cyclophosphamide on postoperative days 0 and 3 to prevent PSR after simulated tumor biopsy during CO2 pneumoperitoneum.
In group 1, the incidence of PSR was 0% in the intravenously injected mice versus 63% in mice injected intraperitoneally with TBJ-NB. In group 2, no significant difference in the incidence of PSR was seen between simulated tumor biopsy (89%) animals with CO2 pneumoperitoneum versus animals with gasless suspension (81%). In group 3, mice that did not receive any chemotherapy had an 89% incidence of PSR. Administration of cyclophosphamide via either the IP or IV route effectively prevented PSR, although there was no difference in the incidence of PSR between the two routes (IP 12% versus IV 13%).
The data suggest that PSR in tumor-bearing hosts may be caused by direct seeding of exfoliated tumor cell, and not by hematogenous metastases. Contrary to the other reports, CO2 pneumoperitoneum was not found to be essential for the development of PSR. Furthermore, the authors conclude that postoperative chemotherapy may be useful in preventing PSR after MIS in patients bearing chemotherapy-sensitive tumors such as neuroblastoma.
背景/目的：尽管微创手术（MIS）已广泛应用于胃肠道癌患者，但腹腔镜癌症手术后穿刺孔部位肿瘤复发（PSR）的病因仍不清楚。作者在此报告对小鼠神经母细胞瘤模型腹腔镜肿瘤活检后PSR的分析，并提出这种并发症的机制以及潜在的治疗方法。
将5至7周龄未成熟雄性A/J小鼠（18 - 23克）左侧腹皮下接种免疫原性极低的TBJ - 神经母细胞瘤（TBJ - NB），并分为三个治疗组。肿瘤接种14天后进行以下操作：第1组，在二氧化碳气腹期间额外腹腔内或静脉内注射TBJ - NB；第2组，在二氧化碳气腹或无气悬吊期间使用MIS技术模拟经腹肿瘤活检；第3组，在术后第0天和第3天腹腔内（IP）或静脉内（IV）给予环磷酰胺，以预防二氧化碳气腹期间模拟肿瘤活检后的PSR。
在第1组中，静脉注射小鼠的PSR发生率为0%，而腹腔内注射TBJ - NB的小鼠为63%。在第2组中，二氧化碳气腹的模拟肿瘤活检（89%）动物与无气悬吊（81%）动物之间的PSR发生率无显著差异。在第3组中，未接受任何化疗的小鼠PSR发生率为89%。通过IP或IV途径给予环磷酰胺均有效预防了PSR，尽管两种途径之间的PSR发生率无差异（IP为12%，IV为13%）。
数据表明，荷瘤宿主中的PSR可能是由脱落肿瘤细胞的直接种植引起的，而非血行转移。与其他报告相反，未发现二氧化碳气腹对于PSR的发生是必不可少的。此外，作者得出结论，术后化疗可能有助于预防对化疗敏感的肿瘤（如神经母细胞瘤）患者MIS后的PSR。
