Adenocarcinoma of stomach has a high capability of sending peritoneal deposits. The benefit of surgery in the term of cure or improving survival in these cases was very limited. Unfortunately, many cases were discovered to have peritoneal deposits only during surgery in spite of negative imaging findings regarding peritoneal deposits, making theses surgeries invaluable and conducting laparoscopy for all patients with gastric cancer is costly and maybe unavailable in all centers especially in healthcare system of limited resources and hence the importance of the conducting study which aimed to identify the factors which make the biology and the stage of gastric cancer have higher incidence of sending peritoneal deposits and so limiting the laparoscopic exploration for only this cases. An important finding of the current study was the association of a tumor in middle part (body) of stomach with higher incidence of peritoneal deposits in contrast to tumors originating from the cardia or pylorus. This may be attributable to the low incidence of obstructive symptoms of gastric cancer associated with body tumors compared with tumors originating from other parts of the stomach, delaying patient presentation to late stages of the disease. Irene Thomasson et al. reported that, in contrast to tumors located in only one region of the stomach, tumors which occupied more than one anatomical part of stomach were associated with higher incidences of peritoneal metastasis [4]. Diffuse infiltration morphology which usually present in linitis plastica and aggressive pathology like undifferentiated carcinoma were associated with higher incidence of peritoneal carcinomatosis. This is concomitant with C Honoré et al. findings which showed the same results [5, 6]. In concordance with Florian Seyfried et al. findings, high grade tumor (G3) had higher incidence of peritoneal metastasis (P value = 0.018).
Rosenberg R., et al. explained that peritoneal carcinomatosis develops through the penetration of tumor cells into the serosa, followed by their shedding into the peritoneal cavity [7]. In addition, the deeper the penetration of tumor cells into the layers of stomach, the more these tumor cells have access to the lymphatic system, leading to higher incidences of peritoneal metastasis. The conducting study showed higher trend of the percent of the cases with peritoneal deposits in advanced T stage (T3, T4) in comparison to T2 but statistically insignificant. In Literature, Michael D’ Angelica et al. reported peritoneal recurrence in 37% of the cases of completely resected T3 and T4 gastric carcinomas versus a recurrence rate of only 13% of cases diagnosed with T0, T1, and T2 tumors [8].
Detailed interactions between tumor and inflammatory cells have not, to date, been fully delineated. Neutrophils could possibly have a role in the promotion of tumor formation through the production of vascular endothelial growth factor and matrix metalloproteinase-9 [9, 10]. In addition, the neutrophils are believed to have inhibitory effects on natural killer cells and lymphocytes, possibly promoting the progression of tumors [11, 12]. It has also been proposed that activated platelets may have a role in the progression of tumors through the secretion of growth factors [13]. Conversely, the role of the adaptive immune system, especially lymphocytes, in the eradication of cancer cells has been extensively studied and further affirmed after the finding of increase incidence of cancer in patients receiving immunosuppressants after organ transplantation [14]. Robert Schreiber reported an increased incidence of sarcomas in mice which lacked an adaptive immune system [15]. In the present study, lymphocytic count below or equal 1.9 × 103 per microliter was a found to be risk factor for peritoneal spread of a gastric carcinoma.
A large number of studies have attempted to create a comprehensive model of the role of immune factors in cancer development and spread in order to better predict prognosis and recurrence. Such immune factors have included a number of ratios, including neutrophils/lymphocytes, platelets/lymphocytes, and monocytes/lymphocytes [16, 17]. Nakayama et al. reported that a neutrophil/lymphocytic ratio > 2.37 was an independent predictor of peritoneal metastasis of gastric origin [18]. Inoue, et al. reported higher peritoneal recurrence rate and lower overall survival after gastrectomy in cases with a high preoperative systemic immune inflammation index of S II (with a cut-off 395, P value = 0.028). The index is computed as follows: platelet count × neutrophil count/lymphocyte count [19].
The conducted study highlighted the impact of different factors on the presence or absence of peritoneal metastasis of gastric origin but it has some limitations regarding the retrospective design and some missing data like exactly T and N stage of the tumors for some patients. But its results are valuable as it showed that the site ,morphology and grading of tumor as well as low lymphocytic count and higher CA 19-9 were predictors for peritoneal metastasis from gastric cancer. Further studies needed to be conducted comparing laparoscopic exploration findings regarding presence or absence of peritoneal deposits with the predicting factors and discuss the interaction between them aiming to exactly identify the exact patients who will benefit from laparoscopy.