Evidence map›Paper›PMID 42367489›Full record

ArticleCureus2026

Metabolic and Inflammatory Markers of Fatty Liver As Associated Factors of Hepatic Metastatic Spread in Colorectal Cancer.

Syed Umar Farooq, Yasir Khan, Muhammad Sameer Khan, Umair Ali, Zhou Li, Reena Kumari Sunil

Abstract read
In one paragraph

Article in Cureus, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

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2 · The registry

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

6 authors.

Syed Umar FarooqGeneral Surgery, Southern Medical University, Guangzhou, CHN.
Yasir KhanPublich Health and Preventive Medicine, Guangdong Pharmaceutical University, Guangzhou, CHN.
Muhammad Sameer KhanNeurology, Medical School of Yangtze University, Jingzhou, CHN.
Umair AliMedicine, Medical School of Nanchang University, Nanchang, CHN.
Zhou LiGeneral Surgery, Zhujiang Hospital of Southern Medical University, Guangzhou, CHN.
Reena Kumari SunilMedicine, Dr. Ziauddin University Hospital, Karachi, PAK.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background Colorectal cancer is a leading cause of cancer-related morbidity and mortality worldwide, and the development of hepatic metastasis significantly worsens patient prognosis. The liver is the most common site of metastatic spread in colorectal cancer due to portal venous drainage. Increasing evidence suggests that metabolic disorders and fatty liver disease may influence tumour progression by altering the hepatic microenvironment. However, the significance of metabolic and inflammatory markers associated with fatty liver in determining hepatic metastasis remains inadequately explored. Methods This observational analytical study was conducted at the Dr. Ziauddin University Hospital (Karachi, PAK) over one year from February 4, 2025, to February 3, 2026. A total of 200 patients with histologically confirmed colorectal adenocarcinoma were included using consecutive sampling. Fatty liver was assessed by abdominal ultrasonography and graded according to standard criteria. Metabolic parameters, including fasting glucose, fasting insulin, homeostatic model assessment for insulin resistance (HOMA-IR), and lipid profile, were measured. Inflammatory biomarkers, including total leukocyte count, neutrophil-to-lymphocyte ratio, platelet-to-lymphocyte ratio, and high-sensitivity C-reactive protein (hs-CRP), were evaluated. Hepatic metastasis was determined using contrast-enhanced imaging. Logistic regression analysis was performed to identify factors associated with hepatic metastatic spread. Results Among the 200 patients included in the study, hepatic metastasis was identified in 62 (31.0%). Patients with hepatic metastasis had a significantly higher BMI, waist circumference, and prevalence of diabetes mellitus. Moderate-to-severe fatty liver was significantly associated with metastatic disease (p < 0.001). Metabolic markers, including fasting glucose, insulin levels, HOMA-IR, triglycerides, and liver enzymes, were significantly elevated in the metastatic group. Inflammatory markers such as the neutrophil-to-lymphocyte ratio and hs-CRP were also significantly higher. Multivariable logistic regression analysis revealed that moderate-to-severe fatty liver (adjusted OR = 2.18), HOMA-IR (adjusted OR = 1.31), triglycerides (adjusted OR = 1.01), hs-CRP (adjusted OR = 1.15), neutrophil-to-lymphocyte ratio (adjusted OR = 1.54), and advanced tumour stage (adjusted OR = 2.47) were associated with hepatic metastatic spread. Conclusion Metabolic dysfunction, fatty liver severity, and systemic inflammatory markers are significantly associated with hepatic metastasis in colorectal cancer. These parameters may serve as a potential association for identifying patients at increased risk of metastatic spread and may assist in improving risk stratification and surveillance strategies.

Indexed as

colorectal cancerfatty liverhepatic metastasisinflammatory biomarkersinsulin resistance

Identifiers

PMID42367489
PMCPMC13304909

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.