Comparison Accuracy of the Use Carcinoma Embryonic Antigen (CEA) and Lactate Dehidrogenase (LDH) Level to Predict Colorectal Carcinoma Recurrency in Abdul Moeloek Hospital Bandar Lampung
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Abstract
Background: Colorectal cancer is a malignancy that originates from the colon tissue, which consists of the colon and rectum. The incidence of colorectal cancer worldwide is the third largest and is the fourth leading cause of death, accounting for 11% of all cancers in human. In general, the development of colorectal cancer is an interaction between environmental factors and genetic factors. Environmental factors are divided into modifiable factors and non-modifiable factors. The recurrence rate of colorectal cancer is still very high, so it requires a precise and accurate early detection of the recurrency.
Method: Comparing the accuracy of the Carcinoma Embryonic Antigen (CEA) tumor marker examination with Lactate Dehydrogenase (LDH) levels to detect colorectal cancer recurrency by using Spearman correlation analysis between two variables at Abdul Moeloek Hospital Bandar Lampung during the study period of October 2019 to September 2020.
Results: Twenty one samples are obtained, 11 samples did not experience any recurrency and the other 10 samples had colorectal cancer recurrence. The mean CEA level was 139.64 U / mL and the mean LDH level was 353.10 U / L. The relationship between CEA levels and colorectal cancer recurrence was significant with a correlation coefficient of 0.663, while the relationship between LDH levels and colorectal cancer recurrence was insignificant with a correlation coefficient of 0.213.
Conclusion: CEA is more accurate than LDH to predict the recurrency of colorectal cancer, so that in clinical practice CEA is better used to predict colorectal cancer recurrence.
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References
References
Amarican Cancer Society. Colorectal Cancer Facts & Figures 2014-2016.Color Cancer Facts Fig 2014; 1–32.
Bray F, Ferlay J, Soerjomataram I, et al. Global cancer statistics 2018: GLOBOCAN estimates of incidence and mortality worldwide for 36 cancers in 185 countries. CA Cancer J Clin. 2018;68:394–424.
Ahsan H, Neugut A, Garbowski G. Family history of colorectal adenomatous polyps and increased risk for colorectal cancer. Ann Intern Med 1998; 128: 900–5.
Hemminki K, Eng C. Clinical genetic counselling for familial cancers requires reliable data on familial cancer risks and general action plans. J Med Genet2004; 41: 801–7.
Chen K, Qiu JL, Zhang Y, et al. Meta analysis of risk factors for colorectal cancer. World J Gastroenterol2003; 9: 1598–1600.
Johnson CM, Wei C, Ensor JE, et al. Meta-analyses of colorectal cancer risk factors. 2014; 24: 1207–1222.
Chao A, Thun M, Connell C, et al. Meat consumption and risk of colorectal cancer. JAMA 2005; 293: 172–82.
Cross AJ, Ferrucci LM, Risch A, et al. A large prospective study of meat consumption and colorectal cancer risk: an investigation of potential mechanisms underlying this association. Cancer Res2010; 70: 2406–2414.
Topolcan O, Fuchsova R, Svobodova S, et al. Vitamin D and cancer. Tumor Biol 2012; 33: S61.
Gold P, Freedman So."Demonstration Of Tumor-Specific Antigens In Human Colonic Carcinomata By Immunological Tolerance And Absorption Techniques". Gold P, Freedman So. J Exp Med 1965 Mar 1;121(3):439-62. doi: 10.1084/jem.121.3.439.
Valvona CJ, Fillmore HL, Nunn PB, and Pilkington GJ.2015 The Regulation and Function of Lactate, Cellular & Molecular Neuro-oncology Research Group, University of Portsmouth, School of Pharmacy & Biomedical Sciences, Portsmouth, UK. doi:10.1111/bpa.12299