BMC Gastroenterol. 2026 Jun 29. doi: 10.1186/s12876-026-05059-y. Online ahead of print.
ABSTRACT
BACKGROUND: The incidence of colorectal cancer (CRC) continues to rise, with colorectal adenoma(CRA) being its primary precancerous lesion. Recent studies suggest that hyperlipidemia may promote adenoma development by influencing cell membrane structure, cholesterol metabolism, and inflammatory responses. However, its independent role in the adenoma stage remains unclear.
OBJECTIVE: To investigate the association between hyperlipidemia and colorectal adenoma(CRA) risk and to evaluate the dose-response relationship based on lipoprotein profile stratification.
METHODS: This single-center retrospective case-control study included 180 patients with colorectal adenoma(CRA) and 80 colonoscopy-negative controls. An additional 80 patients with pathologically confirmed colorectal adenocarcinoma (CRAC) were included as a secondary exploratory comparison group. Demographic characteristics and lipid parameters, including total cholesterol (TC), triglycerides (TG), low-density lipoprotein cholesterol (LDL-C), and high-density lipoprotein cholesterol (HDL-C), were collected. Univariate and multivariable unconditional logistic regression analyses were performed to evaluate associations between lipid abnormalities and colorectal adenoma, with adjustment for age, sex, BMI, smoking, alcohol consumption, and family history of colorectal cancer. Variance inflation factors were calculated to assess multicollinearity. Quartile stratification and restricted cubic spline models were used to explore dose-response patterns, and E-value analysis was performed to assess the potential impact of unmeasured confounding.
RESULTS: High TC, high TG, high LDL-C, and low HDL-C were significantly associated with the overall presence of CRA in univariate analysis. After adjustment for potential confounders, these associations remained statistically significant. Quartile stratification showed that higher levels of TC, TG, and LDL-C were associated with progressively higher odds of colorectal adenoma, whereas HDL-C showed an inverse association. The RCS models suggested steeper increases in adenoma odds at higher TC and LDL-C levels, while HDL-C showed an approximately linear inverse association. Although high TG was associated with overall adenoma occurrence, TG levels did not differ significantly across adenoma histological subtypes. Subgroup analyses suggested that smoking, obesity, and family history may modify the associations between dyslipidemia and colorectal adenoma.
CONCLUSION: Hyperlipidemia was independently associated with CRA in this retrospective case-control study. A comprehensive dyslipidemic pattern, characterized by elevated TC, TG, and LDL-C and reduced HDL-C, was observed among patients with CRA. Lipoprotein profiles may serve as accessible clinical indicators for colorectal adenoma risk stratification. However, because of the retrospective case-control design, causal inference and temporal relationships cannot be established, and the possibility of reverse causality should be considered.
PMID:42366352 | DOI:10.1186/s12876-026-05059-y
