Assessment of platelet activation and phagocytic activity in gastric cancer patients

Abstract

AIM:To assess the activation of platelets and their phagocytic activity in the course of gastric cancer. METHODS:Forty-three gastric cancer patients were recruited to the study. The patients were divided into 3 groups depending on tumor stage. Group E included 6 patients with early gastric cancer; group A 18 patients with locally advanced cancer; and group M-19 with metastatic cancer. The investigations were performed twice, prior to surgery and 12-14 d afterwards. RESULTS:The platelet count and the level of soluble platelet selectin (sP-selectin) were found to increase with the disease progression. The level of sP-selectin was lowest in early cancer and was observed to increase after surgery in all the study patients. Irrespective of tumor stage, a statistically significant decrease was noted in the percentage of phagocytizing platelets and in the phagocytic index in gastric cancer patients as compared to healthy subjects. Despite increased platelet count and stimulation of thrombocytopoiesis, the phagocytic functions of blood platelets were markedly impaired. Tumor development seems to impair metabolic processes. CONCLUSION:A decreasing phagocytic activity can promote both inflammatory processes and cancer growth.

Impact of preoperative immunonutrition on thrombocyte phagocytic activity and early postoperative outcomes in invasive gastric cancer patients.

“…Current work confirms impaired phagocytic activity in patients with gastric cancer. A decreased phagocytic activity can influence inflammatory processes as well as cancer growth [25]. In this study, impact of immunonutrition on phagocytic activity of platelets was In our study in all groups showed severe impairment of thrombocyte phagocytic activity.…”

“…In a previous study of our group, we found elevated levels of interleukin 6 (IL-6) in gastric cancer patients which correlated negatively with the disease stage. Its values were highest in patients with early gastric cancer [25]. Administration of the preoperative parenteral glutamine immunonutrition results in normalization of cholesterol and triglycerides by increasing or decreasing their levels to achieve the normal range.…”

Coagulation and fibrinolysis in gastric cancer

“…VTE has been implicated in GC progression and metastasis, so much so that a coagulation score based on levels of preoperative platelets, FBG, and D‐dimer (DD, a product of fibrin degradation) was recently proposed as a promising predictor for postoperative complications and recurrence after gastrectomy in stage II/III GC patients . During GC progression and metastasis, an increase in platelet number and volume occurs, the number of glycoprotein receptors (CD41a, CD61, and CD62P) increases, and P‐selectin expression on the platelet surface decreases, while levels of soluble P‐selectin (a marker of platelet hyperactivity, endothelial dysfunction, and inflammation) increase in plasma, suggesting platelet activation …”

“…[43][44][45][46] During GC progression and metastasis, an increase in platelet number and volume occurs, the number of glycoprotein receptors (CD41a, CD61, and CD62P) increases, and P-selectin expression on the platelet surface decreases, while levels of soluble P-selectin (a marker of platelet hyperactivity, endothelial dysfunction, and inflammation) increase in plasma, suggesting platelet activation. [47][48][49] VTE occurrence and bleeding complications are heightened by chemotherapeutic treatments. [50][51][52][53] Finally, excessive blood coagulation leading to a decrease in intratumoral perfusion, and thereby drug delivery into the tumor stroma, affects patient responses to chemotherapeutic treatments.…”

Diagnostic Markers for Nonspecific Inflammatory Bowel Diseases

“…It is an important factor in evaluating the changes of platelet functions in a patient with inflammatory bowel disease. Elevated PDMP levels in patients with active IBD and its significant correlation with sP-selectin suggest that platelets play an important role in the pathogenesis of inflammation [ 26 ].…”