929; 95% CI: 1.530-5.607; P = 0.001), and SH (OR, 2.316; 95% CI: 1.267-4.241; P = 0.007). Among patients with SH and corresponding Tyrosine Kinase Inhibitor Library controls, gender, preoperative chemotherapy treatment, liver resection approach, extent of liver resection, and underlying SH were associated with any hepatic-related morbidity on univariable analysis (Table 5). On multivariable logistic regression, resection of four or more segments (OR, 9.493; 95% CI: 4.177-21.577; P < 0.001), male gender (OR, 3.252; 95% CI: 1.448-7.303; P = 0.004), and SH (OR, 2.722; 95% CI: 1.201-6.168; P = 0.016) were independently associated with

any hepatic-related morbidity. The relative low numbers of PHI, postoperative hepatic decompensation, and surgical hepatic complication events precluded corresponding multivariable analyses. The aim of this retrospective study was to determine whether simple hepatic steatosis or SH worsens outcomes after liver resection. To achieve this aim, we individually matched patients with either underlying histopathology to control patients based upon extent and approach of liver resection. Controls GSK126 datasheet were then further selected based upon similar diagnoses and potential etiologies of SH or simple steatosis—including alcohol use, MetS, and preoperative chemotherapy

(Table 1). Moreover, the incidence of patients with “two-hits” predisposing to SH (e.g., preoperative chemotherapy treatment and MetS) was similar between SH patients and corresponding controls. Thus, our study accounts for the morbidity derived from factors, such as DM, morbid obesity, and preoperative chemotherapy treatment,

separate from underlying liver injury.41-43 We excluded patients with bridging fibrosis, cirrhosis, cholestasis, or other CLDs in the underlying liver and those who underwent concomitant major extrahepatic procedures (including bile duct resection and bilioenteric Lepirudin anastomosis) to eliminate potential confounding variables that may influence postoperative outcomes. This study design thus avoids the flaws present in other reports that cloud conclusions regarding the association of underlying liver pathology and postoperative outcomes.18, 24-32 Only those with at least moderate underlying steatosis (defined by greater than 33% of liver parenchymal involvement by the NAS)34 were included in the group of patients with simple hepatic steatosis. This relatively high threshold for simple steatosis was selected to maximize the likelihood of detecting differences in postoperative morbidity, when compared to corresponding controls with no underlying liver pathology. Patients with SH in the underlying liver had higher overall (56.9% versus 37.3%; P = 0.008) and any hepatic-related (28.4% versus 15.7%; P = 0.043) morbidity after liver resection, compared to corresponding controls. SH was associated with both outcomes on multivariable logistic regression—indicating that SH leads to higher morbidity after liver resection independent of etiology.