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Targeted metabolomics in colorectal cancer: a strategic approach using standardized laboratory tests of the blood and urine
Targeted metabolomics in colorectal cancer: a strategic approach using standardized laboratory tests of the blood and urine
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Targeted metabolomics in colorectal cancer: a strategic approach using standardized laboratory tests of the blood and urine
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Targeted metabolomics in colorectal cancer: a strategic approach using standardized laboratory tests of the blood and urine
Targeted metabolomics in colorectal cancer: a strategic approach using standardized laboratory tests of the blood and urine
Journal Article

Targeted metabolomics in colorectal cancer: a strategic approach using standardized laboratory tests of the blood and urine

2017
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Overview
Glycolytic markers have been detected in colorectal cancer (CRC) using advanced analytical methods. Using commercially available assays, by-products of anaerobic metabolism were prospectively measured in the blood and urine of 20 patients with metastatic colorectal cancer (mCRC) and 20 patients with local disease. Twenty-four-hour urine citrate, plasma lactate, ketones, venous blood gas, anion gap, and osmolar gap were investigated. Results of patients with metastatic and local CRC were compared using two-sample -tests or equivalent nonparametric tests. In addition, plasma total CO concentrations in our local hospital (5,931 inpatients and 1,783 outpatients) were compared retrospectively with those in our dedicated cancer center (1,825 outpatients) over 1 year. The average venous pCO was higher in patients with mCRC (50.2 mmHg; standard deviation [SD]=9.36) compared with those with local disease (42.8 mmHg; SD=8.98), =0.045. Calculated serum osmolarity was higher in mCRC and attributed to concomitant sodium and urea elevations. In our retrospective analysis, plasma total CO concentrations (median=27 mmol/L) were higher in cancer patients compared to both hospital inpatients (median=23 mmol/L) and outpatients (median=24 mmol/L), <0.0001. Patients with mCRC had higher venous pCO levels than those with local disease. Although causation cannot be established, we hypothesize that pCO elevation may stem from a perturbed metabolism in mCRC.

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