Changes in basal insulin secretion capacity after pancreatectomy: a retrospective study

This study evaluated the changes in basal insulin secretion capacity (BISC) after pancreatectomy across two surgical procedures. We also investigated the association between decreased BISC and the introduction of postoperative insulin therapy. The data on 110 patients who underwent pancreatectomy during October 2018-February 2022 at our hospital were analyzed retrospectively. We focused on the C-peptide index (CPI) as an index for BISC. A decreased postoperative BISC was defined as a postoperative CPI (post-CPI) <1.0, which was in turn defined as the event occurrence in our study. The receiver operating characteristic curve for the event occurrence was plotted for factors related to preoperative glucose tolerance. Of the preoperative non-diabetic 73 patients, 44 and 29 who underwent pancreaticoduodenectomy (PD) and distal pancreatectomy (DP), respectively, were examined. A post-CPI of <1.0 was observed in 29 patients (39%). Although the proportion of remnant pancreatic volume was significantly smaller in patients with PD than in patients with DP (38% vs. 68%, p <0.0001), no significant difference was observed in the event rates (39% vs. 41%). In patients with PD, preoperative CPI (area under the curve: 0.75) was used for predicting post-CPI <1.0. Multivariate analysis revealed that preoperative CPI <1.65 (odds ratio: 7.69, 95% confidence interval: 1.87-31.5) was an independent predictor of decreased postoperative BISC. However, in patients with DP, no significant predictors were identified. Induction of insulin therapy was significantly lower in preoperative non-diabetic patients (n=73) after undergoing a pancreatectomy (1.4% vs. 37.5%, p<0.0001) than in preoperative medically treated patients (n=16); there was no significant difference in event (post-CPI <1.0) rates (39.7% vs. 56.2%, p=0.23). Although pancreatectomy reduces BISC after surgery, the coexistence of insulin resistance, which is a pathophysiology of type 2 diabetes mellitus, may play a role in whether postoperative glucose tolerance is reduced to the point where insulin therapy is necessary.