Kolorektal adenoma ve karsinomlu hastalarda metabolik ve inflamatuvar risk faktörlerinin değerlendirilmesi

Background and Aims: Metabolic syndrome and its related components are thought to be risk factors for developing colorectal neoplasms due to hyperinsulinemia, insulin resistance, and oxidative stress resulting in chronic low-grade inflammation. This study aims to explain the association of colorectal neoplasms (colon adenocarcinoma and colon adenoma) with metabolic syndrome components, non-alcoholic fatty liver disease, and inflammatory markers. Materials and Methods: Data of 151 patients diagnosed with colon adenoma and colorectal adenocarcinoma were retrospectively reviewed. Demographic characteristics, routine blood tests, colonoscopic findings, pathology results, tumor-node-metastasis stages of colorectal adenocancer, and hepatic ultrasonography findings were recorded. The Homeostatic Model Assessment for Insulin Resistance scores were calculated. Results: The study cohort consisted of 71 patients with adenoma and 80 patients with colorectal adenocancer. The number of patients with diabetes mellitus, hypertension, hypertriglyceridemia, metabolic syndrome, severe liver steatosis was significantly higher in the colorectal adenocancer group compared to the colorectal adenoma group. Additionally, neutrophil-lymphocyte ratio, C-reactive protein, and C-reactive protein to albumin ratio were significantly higher in the colorectal adenocancer group compared to the adenoma group. In univariant analysis, patients with diabetes mellitus, hypertension, hypertriglyceridemia, metabolic syndrome, severe liver steatosis were found to have a shorter duration of survival than those who did not have these risk factors. In multivariate analysis, advanced tumor-node-metastasis stage, severe hepatosteatosis, hypertension, and hypertriglyceridemia were found to be independent risk factors for survival of the patients with colorectal adenocancer. Conclusions: Metabolic syndrome, severe liver steatosis, and inflammatory process may be risk factors for the transition from colon adenoma to adenocarcinoma and shorter survival in colorectal cancer patients.