After conventional and local pancreatic resections for benign and premalignant neoplasms, metabolic dysfunctions and steatohepatitis were assessed. Studies presenting measured data on metabolic activities following PD, left pancreatic resection (PLR), duodenum-sparing pancreatic head resection (DPPHR), pancreatic middle segment resection (PMSR), and tumor enucleation (TEN) were searched in the Medline, Embase, and Cochrane libraries. A total of 40 cohort studies with 2,729 people were included. After a mean follow-up of 32 months, PD for the benign tumor was related with postoperative new-onset diabetes mellitus (pNODM) in 46 of 327 patients (14.1%) and postoperative new-onset pancreatic exocrine insufficiency in 109 of 243 patients (44.9%). pNODM was found in 32 of 204 patients (15.7%) after PD and in 10 of 200 patients (5%) after DPPHR [P<0.01; OR: 0.33; (95% -CI: 0.15–0.22). PEI was detected in 77 of 174 patients (44.3%) after PD and in 7 of 104 patients (6.7%) after DPPHR (P<0.01;OR: 0.15; 95% -C: 0.07–0.32). PNODM was found in 107 of 459 patients (23.3%) after PLR and in 23 of 412 patients (5.6%) after PMSR (P<0.01; OR: 0.20; 95% CI: 0.12–0.32). New onset of pancreatic exocrine insufficiency occurred in 17% of patients after PLR and 8% after PMSR (P<0.01). Patients with pNODM after PPPD and tumor enucleation were found in 19.7% and 5.7% (P<0.03) of cases. Following a mean follow-up of 30.4 months after PD/PPPD, 145 of 608 patients (23.8%) developed nonalcoholic fatty liver disease. DPPHR resulted in steatohepatitis in 2 of 66 (3%) patients, which was substantially lower than PPPD (P<0.01). Standard pancreatic resections for benign tumors carry a significant risk of new-onset diabetes, pancreatic exocrine insufficiency, and steatohepatitis following PD. Local resections that spare the parenchyma were linked to low-grade metabolic dysfunctions.
