Metabolic comorbidity burden and oncologic features of early-onset colorectal cancer stratified by hepatic steatosis.

Abstract

e15696 Background: Early-onset colorectal cancer (EO-CRC) incidence is rising, and emerging evidence links EO-CRC with metabolic dysfunction and hepatic steatosis. As CRC staging routinely includes abdominal imaging, this setting offers an opportunity to quantify pre-treatment hepatic steatosis. We report the prevalence of metabolic comorbidities in EO-CRC and compare clinicopathologic features stratified by hepatic steatosis status in a single institution cohort. Methods: We performed a retrospective review of patients aged 18-49 diagnosed with CRC (2019-2025). Records were abstracted for demographics, comorbidities, and tumor characteristics. Hepatic steatosis was assessed using radiology and pathology reports and compared to ICD-9/10 codes. Group comparisons utilized nonparametric tests for continuous variables and chi-square or Fisher’s exact tests for categorical variables. Results: A total of 613 patients were identified (median age 44.0 years [IQR 40.0–48.0]; 50.7% female). Metabolic comorbidities were common: obesity in 38.5%, hypertension in 37.7%, hyperlipidemia in 26.4%, and type 2 diabetes in 16.5%. Adenocarcinoma was the predominant histology (96.8%). Among patients with available staging, advanced disease was frequent with 70.4% presenting with stage III–IV disease, 71.5% were left-sided, and 7.6% exhibited deficient mismatch repair. In the tumor registry subset with comprehensive chart review (n = 258 after exclusions), hepatic steatosis was identified in 45.0% (116/258). Notably, 75.9% (88/116) of patients with steatosis lacked a corresponding ICD diagnosis. Steatosis was present at or within three months of cancer diagnosis in 51.7% (60/116) of cases. Compared to patients without steatosis at diagnosis (n = 198), those with steatosis had significantly higher median BMI (33.9 vs 27.3 kg/m²; p < 0.001), obesity (71.7% vs 38.9%; p < 0.001), hypertension (53.3% vs 31.3%; p = 0.003), and obstructive sleep apnea (26.7% vs 8.6%; p < 0.001). Stage at diagnosis differed between groups (p = 0.047), with a lower proportion of stage IV disease observed in the steatosis group (18.3% vs 32.8%; unknown stage 16.7% vs 6.6%). Tumor characteristics (histology, sidedness, and MMR) were similar between groups. Conclusions: Hepatic steatosis is highly prevalent in EO-CRC but remains under-recognized in clinical coding. While patients with steatosis exhibit higher metabolic burden, tumor characteristics are similar. The lower proportion of metastatic disease in the steatosis cohort warrants further investigation. These findings highlight the need for systematic identification of Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD) in EO-CRC for risk stratification and survivorship. Additional analyses, including mutational profiling, sites of metastasis and preliminary survival outcomes are underway and will be presented.