[Evaluation of povidone abdominal washing for prevention of peritoneal cancer cell seeding: experimental study in the rat].
ABSTRACT The aim of the study was to evaluate the in vitro cytototoxicity of diluted povidone iodine on colon cancer cells and its in vivo antitumoral effect in a model of peritoneal carcinomatosis in the rat.
Cell cytotoxicity of a povidone iodine diluted solution was assessed, in vitro, on rat colon cancer cells (DHD/K12/PROb) and human colon cancer cells (HT29). The antitumoral effect of diluted povidone iodine washing was measured in BDIX rats after the intraperitoneal inoculation of 10(6) DHD/K12/PROb cells. Results were compared to an abdominal washing within a 9 g/l salinel solution. In one experiment, peritoneal scars and a colocolic anastomosis were performed after the injection of cancer cells.
A short 10 min incubation of human and rat colon cancer cells with diluted povidone iodine resulted in a complete cell killing. In animals, a peritoneal washing with 1% diluted povidone iodine completely inhibited the tumor growth in parietal peritoneum. However, development of peritoneal tumor nodules was not inhibited in the omentum, in scarified peritoneum or in intestinal anastomosis.
Despite its high in vitro efficacy, diluted povidone iodine has an incomplete effect in the prevention of peritoneal carcinomatosis, with only a partial inhibition in scarred peritoneum epiploïc area and intestinal anastomosis. In contrary, it procures a complete inhibition of tumor growth in normal peritoneum.
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ABSTRACT: A tumor model in the rat was used to study peritoneal tumor growth and abdominal wall metastases after carbon dioxide (CO2) pneumoperitoneum, gasless laparoscopy, and laparotomy. The role of laparoscopic resection of cancer is under debate. Insufflation of the peritoneal cavity with CO2 is believed to be a causative factor in the development of abdominal wall metastases after laparoscopic resection of malignant tumors. In the solid tumor model, a lump of 350-mg CC-531 tumor cells was placed intraperitoneally in rats having CO2 pneumoperitoneum (n = 8), gasless laparoscopy (n = 8), or conventional laparotomy (n = 8). After 20 minutes, the solid tumor was removed through a laparoscopic port or through the laparotomy. In the cell seeding model, 5 x 10(5) CC-531 cells were injected intraperitoneally before CO2 pneumoperitoneum (n = 12), gasless laparoscopy (n = 12), or laparotomy (n = 12). All operative procedures lasted 20 minutes. After 6 weeks, in the solid tumor model and after 4 weeks in the cell seeding model, tumor growth was scored semiquantitatively. All results were analyzed using the analysis of variance. In the solid tumor model, peritoneal tumor growth in the laparotomy group was greater than in the CO2 pneumoperitoneum group (p < 0.01). Peritoneal tumor growth in the CO2 group was greater than in the gasless group (p < 0.01). The size of abdominal wall metastases was greater at the port site of extraction of the tumor than at the other port sites (p < 0.001). In the cell seeding model, peritoneal tumor growth was greater after laparotomy in comparison to CO2 pneumoperitoneum (p < 0.02). Peritoneal tumor growth in the CO2 group was greater than in the gasless group (p < 0.01). The port site metastases in the CO2 group were greater than in the gasless group (p < 0.01). The following conclusions can be made: 1) that direct contact between solid tumor and the port site enhances local tumor growth, 2) that laparoscopy is associated with less intraperitoneal tumor growth than laparotomy, and 3) that insufflation of CO2 promotes tumor growth at the peritoneum and is associated with greater abdominal wall metastases than gasless laparoscopy.Annals of Surgery 12/1996; 224(6):694-700; discussion 700-1. · 6.33 Impact Factor
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ABSTRACT: The natural history of surgically treated intraabdominal malignancy is such that a large proportion of patients present tumor recurrence at wound sites. Numerous factors operating within the wound environment are important determinants in tumor cells arrest or growth at these sites. This article describes the interactions between the traumatized tissues and tumor cells, and attempts to understand the important factors that may have an impact on implantation of cancer cells in wound sites. Modifications of these biologic factors may represent new perspectives for preventing tumor recurrence in intraabdominal wound sites.Journal de Chirurgie 07/1996; 133(4):175-82. · 0.50 Impact Factor
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ABSTRACT: The majority of patients with colorectal cancer present at a stage when the primary cancer can be resected with curative intent. However, despite the high resectability rate, about 30-50% of these patients subsequently develop metastatic disease. In these patients, neoplastic cells were disseminated either before or during surgery of the primary cancer. Due to the lack of appropriate detection systems, the extent of pre- and intraoperative hematogenic tumor cell dissemination has not yet been determined. Using a reverse transcription-PCR assay to amplify cytokeratin 20 transcripts, we were able to detect 10 colorectal cancer cells in 10 ml of blood. Blood samples were taken from 65 patients undergoing resection of primary colorectal cancer or liver metastasis of colorectal cancer pre-, intra-, and postoperatively. Circulating tumor cells were detected in 24 of 58 patients with colorectal resections in correlation to the tumor stage and in 6 of 7 patients who underwent hemihepatectomy for liver metastasis. In 8 of 58 patients with colorectal resection and in 5 of 7 patients with hemihepatectomy, tumor cells could only be detected during or during and after surgery. These results demonstrate that hematogenic tumor cell dissemination is a frequent and early event in colorectal cancer. Surgery enhances the release of tumor cells into the circulation. The long-term follow-up of our patient cohort will provide data on the prognostic relevance of circulating tumor cells and might lead to new therapeutic concepts for perioperative prophylaxis of tumor cell implantation or postoperative adjuvant therapy regimens.Clinical Cancer Research 03/1998; 4(2):343-8. · 7.84 Impact Factor