SINDROME METABÓLICO: DEFINICIONES, EPIDEMIOLOGÍA, ETIOLOGÍA, COMPONENTES Y TRATAMIENTO.
Palabras clave:
Síndrome metabólico, obesidad, diabetes mellitus tipo 2, dislipidemia, resistencia a la insulina.
Resumen
El síndrome metabólico (SM) es un desorden clínico que se caracteriza por presentar obesidad abdominal, hipertensión, dislipidemia y resistencia a la insulina. El SM es un estado de inflamación crónica de bajo grado con efectos sistémicos profundos. El SM incrementa el riesgo de diabetes tipo 2 y de enfermedad cardiovascular. El riesgo para resultados adversos en la salud se incrementa sustancialmente con la acumulación de components del SM. En las dos últimas décadas varias organizaciones han propuesto diferentes definiciones usando diferente terminología. Varios factores de riesgo modulan la prevalencia del SM, incluyendo factores del estilo de vida como la calidad nutricional y la ausencia de actividad física. La edad, la etnia y el sexo también contribuyen a la susceptibilidad metabólica. La adiposidad visceral ectópica en exceso es fundamental en la patofisiología del SM. Un enfoque inicial en la terapia del SM incluye una combinación entre la reducción de peso, la modificación dietaria y el incremento en la actividad física, preferiblemente los tres. El tratamiento farmacológico debe considerarse para aquellas personas cuyos factores de riesgo no son reducidos adecuadamente con las medidas preventivas y los cambios en el estilo de vida.
Citas
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10. Blümel, B., Flores, M., González, J. A. y Arraztoa, J. A. (2005). ¿Es el HOMA un instrumento adecuado para el diagnóstico de insulino resistencia en pacientes con síndrome de ovario poliquístico? Rev Chil Obstet Ginecol, 70, 5, 345-351.
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24. Sun, D. L., Wang, J. H., Jiang, B., Li, L. S., Wu, L., Wu, H. Y., He, Y. (2012). Metabolic syndrome vs its components for prediction of cardiovascular mortality: a cohort study in chinese elderly adults. J Geriatric Cardiology, 9, 123- 129.
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31. Monteiro, R. & Azevedo, I. (2010). Chronic inflammation in obesity and the metabolic syndrome. Mediators of Inflammation,: 1-10.
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33. Chandalia, M., Lin, P., Seenivasan, T., Livingston, E., Snell, P., Grundy, S. & Abat, N. (2007). Insulin resistance and body fat distribution in South Asian men compared to Caucasian men. PLOS One, 2, 8, 1-7.
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36. Monteiro, R. & Azevedo, I. (2010). Chronic inflammation in obesity and the metabolic syndrome. Mediators of Inflammation, 1-10.
37. Misra, A. & Shrivastava, U. (2013). Obesity and dyslipidemia in south asians. Nutrients, 5, 2708-2733.
38. Vaziri, N. (2009). Causes of disregulation of lipid metabolism in chronic renal failure. Sem Dial, 22, 6, 644-651
39. Athyros, V., Tziomalos, K., Karagiannis, A. & Mikhailidis, D. (2011). Dyslipidaemia of obesity, metabolic syndrome and type 2 diabetes mellitus: the case for residual risk reduction after statin treatment. Open Cardiovasc Med J, 5, 24-34.
40. Mendizábal, Y., Llorens, S. & Nava E. (2013). Hypertension in metabolic syndrome: vascular Pathophysiology. Int J Hypertension, 1-15.
41. Putnam, K., Shoemaker, R., Yiannikouris, F. & Cassis, L. (2012). The renin-angiotensin system: a target of and contributor to dyslidemias, altered glucose homeostasis, and hypertension of the metabolic syndrome. Ann J Physiol Heart Circ Physiol, 302, H1219-H1230.
42. Malin, S., Finnegan, S., Fealy, C., Filion, J., Rocco, M. & Kirwan, J. (2014). β-cell dysfunction is associated with metabolic syndrome severity in adults. Metabolic Syndrome and Related Disorders, 12,2, 79-85.
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44. Fu, Z., Gilberth, E. & Liu, D. (2013). Regulation of insulin synthesis and secretion and pancreatic beta-cell dysfunction in diabetes. Curr Diabetes Rev, 9, 1, 25-53.
45. Flier, S. N., Kulkarni, R. N. & Kahn, C. R. (2001). Evidence for circulating islet cell growth factor in insulin resistant states. Proc Natl Acad Sci USA, 98, 13, 7475-7480.
46. Jaikaran, E. T. & Clark, A. (2001). Islet amyloid and type 2 diabetes: from molecular misfolding to islet Pathophysiology. Biochim Biophys Acta, 1537, 3, 179-203. [PubMed: 11731221].
47. Kajimoto, Y. & Kaneto, H. (2004). Role of oxidative stress in pancreatic β-cell dysfunction. Annal of the New York Acad Sci, 1011, 168-176.
48. Eizirik, D. L., Cardozo, A. K. & Cnop, M. (2008). The role for endoplasmic reticulum stress in diabetes mellitus. Endocrine Reviews, 29, 1, 42-61.
49. Cai, D. & Liu, T. (2012). Inflammatory cause of metabolic syndrome via brain stress and NF-kB. Aging, 4, 2, 98-115.
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51. Russo, I. (2012). The prothrombotic tendency in metabolic syndrome: focus on the potential mechanisms involved in impaired haemostasis and fibrinolytic balance. Scientifica, 1-17.
52. De Pergola, G., Pannacciulli, N., Coviello, P., et al. (2008). P-selectin plasma levels in obesity: association witj insulin resistance and related metabolic and prothrombotic factors. Nutrition, Metabolism and Cardiovascular Diseases, 18, 3, 227-232.
53. Fuentes, E., Fuentes, F., Vilahur, G., Badimon, L. & Palomo, I. (2013). Mechanism of chronic state of inflammation as mediators that link obese adipose tissue and metabolic syndrome. Mediators of inflammation, 1-11.
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2. Kaur, J. (2014). A comprehensive review on metabolic syndrome. Cardiology Research and Practice, 1-21.
3. Bonomini, F., Rodella, L. F. & Rezzani, R. (2015). Metabolic syndrome, aging and involvement of oxidative stress. Aging and Disease, 6, 2, 109-120.
4. Vykoukal, D. & Davies, M. (2011). Vascular biology of metabolic syndrome. J Vasc Surg, 54(3), 819-831.
5. Sperling, L., Mechanick, J., Neeland, I. J., Herrick, C. J., Després, J. P. Ndumele, C., et al. (2015). The cardiometabolic health Alliance. Working toward a new care model for the metabolic syndrome. J Am Col Cardiol, 66, 9, 1051-1067.
6. Ikun, O. & Boudina S. (2013). Cardiac dysfunction and oxidative stress in the metabolic syndrome: an update on antioxidant therapies. Curr Pharm Des, 19, 27, 4806-4817.
7. Hutcheson, R. & Rocic, P. (2012). The metabolic syndrome, oxidative stress, environment, and cardiovascular disease: the great exploration. Experimental Diabetes Research, 1-13.
8. Yudkin, J. S., Juhan-Vague, I., Hawe, E., Humphries, S. E., Di Minno, G., Margaglione, M., et al. (2004). Low grade inflammation may play a role in the etiology of the metabolic syndrome in patients with coronary Heart disease: the HIFMECH study. Metabolism, 53, 852-857.
9. Shin, J. A., Lee, J. H., Lim, S. Y., Ha, H. S., Kwon, H. S., Park, Y. M., et al. (2013). Metabolic syndrome as a predictor of type 2 diabetes, and its clinical interpretations and usefulness. J Diabetes Invest, 4,4, 334-343.
10. Blümel, B., Flores, M., González, J. A. y Arraztoa, J. A. (2005). ¿Es el HOMA un instrumento adecuado para el diagnóstico de insulino resistencia en pacientes con síndrome de ovario poliquístico? Rev Chil Obstet Ginecol, 70, 5, 345-351.
11. Von Frankenberg. A,, Do Nascimento, F., Gatelli, L. E., Nedel, B. L., Garcia, S. P., Oliveira, C. S., et al. (2014). Major components of metabolic syndrome and adiponectin levels: a cross-sectional study. Diabetology & Metabolic Syndrome, 6, 1-9.
12. Khoo, M., Oliveira, F. & Cheng L. (2013). Understanding the metabolic syndrome: a modelins perspective. Rev Biomed Engl, 6, 143-155.
13. Rodríguez, A., Delgado-Cohen, H., Reviriego, J. & Serrano-Ríos, M. (2011). Risk factors associated with metabolic syndrome in type 2 diabetes patients according to World Health Organization, Third Report National Cholesterol Education Program, and International Diabetes Federation definitions. Diabetes, Metabolic Syndrome and Obesity: Targets and therapy, 4, 1-4.
14. Luksiene, D. L., Baceviciene, M., Tamosiunas, A., Reklaitiene, R. & Radisauskas R. (2012). Comparison of four definitions of the metabolic syndrome and odds of isquemic Heart disese in the Lithuanian urban population. Int J Public Health, 57, 3, 543-550.
15. Wen, J., Yang, J., Shi, Y., Liang, Y., Wang, F., Duan, X., et al. (2015). Comparisons of different metabolic syndrome definitions and associations with coronary heart disease, stroke, and peripheral arterial disease in a rural chinese population. PLOS ONE, 10, 5, 1-15
16. Lijnen, H. R. (2009). Role of fibrinolysis in obesity and thrombosis. Thrombosis Research, 123, 4, S46-S49.
17. Al-Aqeedi, R. F., Abdullatef, W. K., Dabdoob, W., Bener, A., Albinali, H. A. & Gehani, A. (2013). The prevalence of metabolic syndrome components, individually and in combination, in male patients admitted with acute coronary syndrome, without previous diagnosis of diabetes mellitus. Libyan J Med, 8, 1-7.
18. Khosravi-Boroujeni, H., Ahmed, F., Sadeghi, M., Roohafza, H., Talaei, M., Dianatkhah, M., et al. (2015). Does the impact of metabolic syndrome on cardiovascular events vary by using different definitions? BMC Public Health, 15, 1-8.
19. Nishimura, R., Nakagami, T., Tominaga, M., et al. (2007). Prevalence of metabolic syndrome and optimal waist circumference cutoff values in Japan. Diabetes Res Clin Pract, 78, 77-84.
20. Bener, A., Yousafzai, M., Darwish, S., Al-Hamaq, A., Nasralla, E. & Abdul-Ghani, M. (2013). Obesity index that better predict metabolic syndrome: body mass index, waist circumference, waist hip ratio, or waist height ratio. J Obesity, 1-9.
21. Parikh, R. & Mohan, V. (2012). Changing definitions of metabolic syndrome. Indian J Endocrinology and Metabolism, 16, 1, 7-12.
22. Zhou, J-Y., Ge, H., Zhu, M-F., Wan,g L-J., Chen, L., Tan, Y-Z., et al. (2013). Neck circumference as an independent predictive contributor to cardio-metabolic syndrome. Cardiovascular Diabetology, 12: 1-7.
23. Mogre, V., Salifu, Z. & Abedandi, R. (2014). Prevalence, components and associated demographic and lifestyle factors of the metabolic syndrome in type 2 diabetes mellitus. J Diabetes & Metabolic Disorders, 13, 1-7.
24. Sun, D. L., Wang, J. H., Jiang, B., Li, L. S., Wu, L., Wu, H. Y., He, Y. (2012). Metabolic syndrome vs its components for prediction of cardiovascular mortality: a cohort study in chinese elderly adults. J Geriatric Cardiology, 9, 123- 129.
25. Chackrewarthy, S., Gunasekera, D., Pathmeswaren, A., Wijekoon, C. N., Ranawaka, U. K., Kato, N., et al. (2013). A Comparison between revised NCEP ATP III and IDF definitions in diagnosing metabolic syndrome in an urban Sri Lanka population: The Ragama Health Study. ISRN Endocrinology, 1-7
26. Zambon, S., Zanoni, S., Romanato, G., Corti, M. C., Noale, M., Sartori, L., et al. (2009). Metabolic syndrome and all-cause and cardiovascular mortality in an Italian elderly population: the Progetto Veneto Anziani (Pro. V. A.) Study. Diabetes Care, 32, 153-159.
27. Jee, S. H. & Jo, J. (2012). Linkage of epidemiologic evidence with the clinical aspects of metabolic syndrome. Korean Society Cardiology, 42, 6, 371-378.
28. Ivezic-Lalic, D., Bergman, B., Kranjcevic, K., Kern, J., Vrdoljak, D. & Vucak, J. (2013). Diversity of metabolic syndrome criteria in association with cardiovascular diseases-a family medicine-based Investigation. Medical Science Monitor, 19, 571-578.
29. Wilson, P. W., D´Agostino, R. B., Parise, H., et al. (2005). Metabolic syndrome as a precursor of cardiovascular disease and type 2 diabetes mellitus. Circulation, 112, 3066-3072.
30. Nakanishi, N., Takatorige, T., Fukuda, H., et al. (2004). Components of the metabolic syndrome as predictors of cardiovascular disease and type 2 diabetes in middle-aged Japanese men. Diabetes Res Clin Pract, 6, 59-70.
31. Monteiro, R. & Azevedo, I. (2010). Chronic inflammation in obesity and the metabolic syndrome. Mediators of Inflammation,: 1-10.
32. Anand, S. S., Tarnopolsky, M. A., Rashid, S., Schulze, K., Desai, D., Mente, A., et al. (2011). Adipocyte hypertrophy, fatty liver, and metabolic risk factors in South Asians: The Molecular Study of Health and Risk Ethnic Groups (mol.SHARE). PLOS One, 6, 7, 1-8.
33. Chandalia, M., Lin, P., Seenivasan, T., Livingston, E., Snell, P., Grundy, S. & Abat, N. (2007). Insulin resistance and body fat distribution in South Asian men compared to Caucasian men. PLOS One, 2, 8, 1-7.
34. Park, Y. W., Zhu, S., Palaniappan, L., Heshka, S., Carnethon, M. R. & Heymsfield, B. (2003). The metabolic syndrome: prevalence and associated risk factor findings in the US population from the Third National Health and Nutrition Examination Survey, 1988-1994. Archives of Internal Medicine, 163, 4, 427-436.
35. Faloia, E., Grazia, M., De Robertis, M., Luconi, M. P., Furlani, G. & Boscaro, M. (2012). Inflammation as a link between obesity and metabolic syndrome. J Nutrition and Metabolism, 1-7.
36. Monteiro, R. & Azevedo, I. (2010). Chronic inflammation in obesity and the metabolic syndrome. Mediators of Inflammation, 1-10.
37. Misra, A. & Shrivastava, U. (2013). Obesity and dyslipidemia in south asians. Nutrients, 5, 2708-2733.
38. Vaziri, N. (2009). Causes of disregulation of lipid metabolism in chronic renal failure. Sem Dial, 22, 6, 644-651
39. Athyros, V., Tziomalos, K., Karagiannis, A. & Mikhailidis, D. (2011). Dyslipidaemia of obesity, metabolic syndrome and type 2 diabetes mellitus: the case for residual risk reduction after statin treatment. Open Cardiovasc Med J, 5, 24-34.
40. Mendizábal, Y., Llorens, S. & Nava E. (2013). Hypertension in metabolic syndrome: vascular Pathophysiology. Int J Hypertension, 1-15.
41. Putnam, K., Shoemaker, R., Yiannikouris, F. & Cassis, L. (2012). The renin-angiotensin system: a target of and contributor to dyslidemias, altered glucose homeostasis, and hypertension of the metabolic syndrome. Ann J Physiol Heart Circ Physiol, 302, H1219-H1230.
42. Malin, S., Finnegan, S., Fealy, C., Filion, J., Rocco, M. & Kirwan, J. (2014). β-cell dysfunction is associated with metabolic syndrome severity in adults. Metabolic Syndrome and Related Disorders, 12,2, 79-85.
43. Newsholme, E. P., Haber, S. & Hirabara, S. M., et al. (2007). Diabetes associated cell stress and dysfunction: role of mitochondrial and non-mitochondrial ROS production and activity. Journal of Physiology, 583, 1, 9-24.
44. Fu, Z., Gilberth, E. & Liu, D. (2013). Regulation of insulin synthesis and secretion and pancreatic beta-cell dysfunction in diabetes. Curr Diabetes Rev, 9, 1, 25-53.
45. Flier, S. N., Kulkarni, R. N. & Kahn, C. R. (2001). Evidence for circulating islet cell growth factor in insulin resistant states. Proc Natl Acad Sci USA, 98, 13, 7475-7480.
46. Jaikaran, E. T. & Clark, A. (2001). Islet amyloid and type 2 diabetes: from molecular misfolding to islet Pathophysiology. Biochim Biophys Acta, 1537, 3, 179-203. [PubMed: 11731221].
47. Kajimoto, Y. & Kaneto, H. (2004). Role of oxidative stress in pancreatic β-cell dysfunction. Annal of the New York Acad Sci, 1011, 168-176.
48. Eizirik, D. L., Cardozo, A. K. & Cnop, M. (2008). The role for endoplasmic reticulum stress in diabetes mellitus. Endocrine Reviews, 29, 1, 42-61.
49. Cai, D. & Liu, T. (2012). Inflammatory cause of metabolic syndrome via brain stress and NF-kB. Aging, 4, 2, 98-115.
50. Gurzov, E. N. & Eizirik, D. L. (2011). Bcl-2 proteins in diabetes: mitochondrial pathways of beta-cell death and dysfunction. Trends in Cell Biology, 21, 7, 424-431.
51. Russo, I. (2012). The prothrombotic tendency in metabolic syndrome: focus on the potential mechanisms involved in impaired haemostasis and fibrinolytic balance. Scientifica, 1-17.
52. De Pergola, G., Pannacciulli, N., Coviello, P., et al. (2008). P-selectin plasma levels in obesity: association witj insulin resistance and related metabolic and prothrombotic factors. Nutrition, Metabolism and Cardiovascular Diseases, 18, 3, 227-232.
53. Fuentes, E., Fuentes, F., Vilahur, G., Badimon, L. & Palomo, I. (2013). Mechanism of chronic state of inflammation as mediators that link obese adipose tissue and metabolic syndrome. Mediators of inflammation, 1-11.
54. Sur, G., Floca, E., Kudor-Szabadi, K., Sur, M. L., Sur, D. & Samasca, G. (2014). The relevance of inflammatory markers in metabolic syndrome. MAEDICA, 9, 1, 15-18.
55. Ridker, P. M., Hennekens, C. H., Buring, J. E. & Rifai, N. (2000). C-reactive protein and other markers of inflammation in the prediction of cardiovascular dosease in women. N Engl J Med, 342, 836-843.
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Publicado
2020-11-12
Cómo citar
Carvajal Carvajal, C. (2020). SINDROME METABÓLICO: DEFINICIONES, EPIDEMIOLOGÍA, ETIOLOGÍA, COMPONENTES Y TRATAMIENTO. Medicina Legal De Costa Rica, 34(1). Recuperado a partir de //www.binasss.sa.cr/ojssalud/index.php/mlcr/article/view/42
Sección
Revisiones de literatura
La propiedad intelectual de los trabajos aceptados es de sus autores, no obstante el acceso a ellos es totalmente abierto y gratuito, por lo que podrán ser reproducidos total o parcialmente con la única limitación de reconocer la autoría y la fuente de publicación ( Revista Medicina Legal de Costa Rica), siempre y cuando dicha explotación no tenga carácter comercial.
