Objective: To evaluate the association of colorectal adenoma with metabolic syndrome (MS) and relevant parameters.
Methods: Clinical data of 289 subjects who underwent screening colonoscopy in the University of Hong Kong-Shenzhen Hospital from January 2014 to June 2015 were retrospectively analyzed, including 130 normal subjects (normal group) and 159 cases with colorectal adenoma confirmed by pathology(adenoma group). Levels of MS-associated parameters were compared between the two groups, and the association of metabolic diseases with colorectal adenoma was examined.
Results: The gender, smoking and drinking habit, regular physical activity, family history of colorectal cancer, and consumption history of long-term non-steroidal anti-inflammatory drugs were not significantly different between two groups (all P>0.05). As compared to normal group, adenoma group had higher body mass index (BMI) [(23.5±3.2) kg/m(2) vs. (22.7±2.8) kg/m(2), t=1.97, P=0.050], larger abdominal circumference [(83.4±10.3) cm vs. (79.6±13.8) cm, t=2.46, P=0.015], higher serum high-density lipoprotein level [(1.3±0.3) mmol/L vs. (1.2±0.3) mmol/L, t=2.03, P=0.044], and higher serum cholesterol [(5.4±1.0) mmol/L vs. (5.0±1.1) mmol/L, t=2.39, P=0.018]. No significant difference was demonstrated in comparing hip circumference and waist-hip ratio, as well as serum fasting glucose and triglyceride(all P>0.05). Higher incidence of colorectal adenoma was found in subjects with MS [69.8%(37/53) vs. 1.7%(122/236), P=0.017], overweight or obesity [65.1% (56/86) vs. 50.7%(103/203), P=0.025], hypertension [67.3%(37/55) vs. 52.1%(122/234), P=0.046] and hypercholesterolemia [66.7%(64/96) vs. 49.2%(95/193), P=0.005].
Conclusions: Metabolic syndrome increased the risk of developing colorectal adenoma. The mechanism may be related to higher serum cholesterol and high density lipoprotein, which may lead to the elevated catabolism of serum cholesterol. Screening colonoscopy should be performed for patients diagnosed as metabolic syndrome, especially for those with central obesity and hypercholesterolemia, thus early diagnosis and treatment of colorectal adenoma may be available.
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Hered Cancer Clin Pract
January 2025
First Department of Medicine, Hamamatsu University School of Medicine, Hamamatsu, 431-3192, Japan.
Background: Familial adenomatous polyposis (FAP) is an autosomal dominant colorectal tumour syndrome characterised by the formation of multiple adenomatous polyps throughout the colon. It is important to understand the extracolonic phenotype that characterizes FAP. Most previous case reports of patients with both FAP and intellectual disability (ID) have described deletions in all or part of chromosome 5q, including the APC locus.
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January 2025
Department of Gastroenterology, National Clinical Research Center for Digestive Diseases, State Key Laboratory of Digestive Health, Beijing Digestive Disease Center, Beijing Key Laboratory for Precancerous Lesion of Digestive Diseases, Beijing Friendship Hospital, Capital Medical University, Beijing, 100050, China.
Nature
January 2025
Department of Medical Oncology and Center for Functional Cancer Epigenetics, Dana-Farber Cancer Institute, Boston, MA, USA.
Oncogenic mutations that drive colorectal cancer can be present in healthy intestines for long periods without overt consequence. Mutation of Adenomatous polyposis coli (Apc), the most common initiating event in conventional adenomas, activates Wnt signalling, hence conferring fitness on mutant intestinal stem cells (ISCs). Apc mutations may occur in ISCs that arose by routine self-renewal or by dedifferentiation of their progeny.
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January 2025
Internal Medicine, National Taiwan University Hospital, Taipei, Taiwan.
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January 2025
Department of Biomedical Sciences, Humanitas University, Milan, Italy.
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