Correlations of gastrointestinal hormones with inflammation and intestinal flora in patients with gastric cancer.
2019
PURPOSE: To investigate the correlations of gastrointestinal hormones with inflammation and intestinal flora in patients with gastric cancer. METHODS: The data of patients with gastric cancer in the Department of Oncology and people with normal physical examination in our hospital were included. All patients received FOLFOX4 chemotherapy. The expression levels of gastrointestinal hormones and inflammatory cytokines were compared between the two groups, and the changes in the intestinal flora spectrum were analyzed. Two-sample t-test was used for the comparison between groups. Pearson's test was used for correlation analysis. P<0.05 showed statistical significance. RESULTS: The levels of serum gastrin-17 (G17) and pepsinogen II (PG II) detected in gastric cancer patients were higher than those in the control group, and the higher the tumor stage, the higher the expression levels. After therapy with PG I, the G17 and PG II levels increased. Moreover, the levels of serum interleukin-6 (IL-6) and IL-17 in patients with gastric cancer were higher than those in normal controls, and the higher the tumor stage, the higher the expression levels. After therapy with IL-6, the IL-6 and IL-7 levels were reduced. In addition, in gastric cancer patients, the numbers of Bifidobacteria, Lactobacilli and bacilli or cocci were apparently decreased, and were markedly increased after therapy, while those of Escherichia coli, Staphylococci, Enterococci and Peptostreptococci were significantly increased, and were evidently decreased after therapy. The results revealed that G17 had positive correlations with IL-6 and IL-17, PG II was positively correlated with IL-17, and G17 was negatively related to the numbers of Bifidobacteria and Lactobacilli. CONCLUSIONS: Gastrointestinal hormones are involved in the occurrence and development of gastric cancer, and they have certain correlations with the inflammation and intestinal flora leading to the tumor genesis.
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