Systemic and tumor level iron regulation in men with colorectal cancer: a case control study

Nutrition & Metabolism

Carol Braunschweig⁷  Julia Clark³  Damond Ng⁶  Rose Linzmeier⁶  Robert J Cabay⁴  Lisa Tussing-Humphreys¹  Sally Freels⁵  Xavier Llor³  Giamila Fantuzzi⁷  Elizabeta Nemeth⁶  Cenk K Pusatcioglu² 

[1] Department of Medicine, University of Illinois at Chicago, 1747 W Roosevelt Rd, Chicago, IL 60608, USA;Division of Gastroenterology, Hepatology, and Nutrition, Ann & Robert H. Lurie Children’s Hospital of Chicago, 225 E Chicago Ave, Chicago, IL 60611, USA;Section of Digestive Disease and Nutrition, University of Illinois at Chicago, 840 S Wood St, Chicago, IL 60612, USA;Department of Pathology, University of Illinois at Chicago, 840 S Wood St, Chicago, IL 60612, USA;Division of Epidemiology and Biostatistics, University of Illinois at Chicago, 1603 W Taylor St, Chicago, IL 60612, USA;Department of Medicine, University of California, Los Angeles, 10833 Le Conte Ave, Los Angeles, CA 90095, USA;Department of Kinesiology and Nutrition, University of Illinois at Chicago, 1919 W Taylor St, Chicago, IL 60612, USA

关键词: Colorectal cancer;    Anemia;    Inflammation;    Hepcidin;    Iron metabolism;   

Others  :  801323
DOI  :  10.1186/1743-7075-11-21

 received in 2014-01-24, accepted in 2014-04-29,  发布年份 2014

【 摘 要 】

Background

Increased cellular iron exposure is associated with colorectal cancer (CRC) risk. Hepcidin, a liver peptide hormone, acts as the primary regulator of systemic iron status by blocking iron release from enterocytes into plasma. Concentrations are decreased during low iron status and increased during inflammation. The role of hepcidin and the factors influencing its regulation in CRC remains largely unknown. This study explored systemic and tumor level iron regulation in men with CRC.

Methods

The participants were 20 CRC cases and 20 healthy control subjects. Colonic tissue (adenocarcinoma [cases] healthy mucosa [controls]) was subjected to quantitative PCR (hepcidin, iron transporters and IL-6) and Perls’ iron staining. Serum was analyzed using ELISA for hepcidin, iron status (sTfR) and inflammatory markers (CRP, IL-6, TNF-α). Anthropometrics, dietary iron intake and medical history were obtained.

Results

Cases and controls were similar in demographics, medication use and dietary iron intake. Systemically, cases compared to controls had lower iron status (sTfR: 21.6 vs 11.8 nmol/L, p < 0.05) and higher marker of inflammation (CRP: 8.3 vs 3.4 μg/mL, p < 0.05). Serum hepcidin was mildly decreased in cases compared to controls; however, it was within the normal range for both groups. Within colonic tissue, 30% of cases (6/20) presented iron accumulation compared to 5% of controls (1/20) (χ² = 5.0; p < 0.05) and higher marker of inflammation (IL-6: 9.4-fold higher compared to controls, p < 0.05). Presence of adenocarcinoma iron accumulation was associated with higher serum hepcidin (iron accumulation group 80.8 vs iron absence group 22.0 ng/mL, p < 0.05).

Conclusions

While CRC subjects had serum hepcidin concentrations in the normal range, it was higher given their degree of iron restriction. Inappropriately elevated serum hepcidin may reduce duodenal iron absorption and further increase colonic adenocarcinoma iron exposure. Future clinical studies need to assess the appropriateness of dietary iron intake or iron supplementation in patients with CRC.

【 授权许可】

   
2014 Pusatcioglu et al.; licensee BioMed Central Ltd.

【 图 表 】

Figure 1.

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