Associations between Systemic Immune-Inflammation Index and Diabetes Mellitus Secondary to Pancreatic Ductal Adenocarcinoma

Abstract

Background: There is a high prevalence of diabetes mellitus (DM) in patients with pancreatic ductal adenocarcinoma (PDAC). An inflammatory response is considered as a potential mechanism involved in the process. The systemic immune-inflammation (SII) index is an integrated and novel inflammatory indicator developed in recent years. The purpose of this study was to determine the relationship between the SII and DM secondary to PDAC. Method: Patients with a confirmed diagnosis of PDAC were analyzed in this cross-sectional study. Anthropometric measures, glucose-related data (including fasting glucose, 2 h OGTT, glycated hemoglobin, fasting insulin, and fasting c-peptide), tumor characteristics (tumor volumes, location and stages), and the periphery blood inflammatory index (white blood cell count, neutrophil-to-lymphocyte ratio, platelet-to-lymphocyte ratio, and SII) were recorded. The inflammation index was analyzed for its association with glucose-related parameters. Multivariable logistic regression analysis was used to analyze the association between SII levels and DM secondary to PDAC. Results: Blood cell results showed that the white blood cell count, neutrophils, lymphocytes, monocytes, platelets, the neutrophil-to-lymphocyte ratio, and platelet-to-lymphocyte ratio were higher in patients with diabetes. It was worth noting that SII significantly increased in patients with diabetes secondary to PDAC (4.41 vs. 3.19, p < 0.0001). Multivariable logistic regression analysis showed that SII (OR: 2.024, 95%CI: 1.297, 3.157, p = 0.002) and age (OR: 1.043, 95%CI: 1.01, 1.077, p = 0.011) were the risk factors for DM secondary to PDAC after adjusting for covariates. According to Spearmen correlation analysis, SII was positively correlated with fasting glucose (r = 0.345, p < 0.0001), 2 h OGTT (r = 0.383, p < 0.0001), HbA1c (r = 0.211, p = 0.005), fasting insulin (r = 0.435, p < 0.0001), fasting C-peptide (r = 0.420, p < 0.0001), and HOMA2-IR (r = 0.491, p < 0.0001). Conclusions: In conclusion, SII is significantly increased among patients with DM secondary to PDAC and is associated with the DM in patients with PDAC (OR: 2.382, 95% CI: 1.157, 4.903, p = 0.019). Additionally, SII is significantly correlated with insulin resistance. We are the first to investigate the relationship between SII and diabetes secondary to PDAC and further confirm the role of an inflammatory response in this process. More studies need to be designed to clarify how inflammatory responses participate.