ISSN 2415-3060 (print), ISSN 2522-4972 (online)
  • 12 of 42
JMBS 2017, 2(4): 68–74
Clinical Medicine

Serum Chemerin and Nesfatin-1 Levels and Peculiarities of Clinical Characteristics in Patients with Hypertension and Obesity

Ivanchenko S. V.

The Framingham study has played a decisive role in creating the concept of risk factors. It studied the features of the clinical course of hypertension associated with comorbid pathology the relationship between obesity, incidence of hypertension and the risk of adverse cardiovascular events for the first time. However, in recent years, there have been published a number of studies where the association of increased cardiovascular risk with obesity has been questioned, known as the "paradox of obesity" or "reverse epidemiology." Considering the high rate of comorbidities in hypertension as well as high prevalence of overweight and obesity as a global problem, the search for new biomarkers that would most accurately assess cardiovascular risk in patients of this cohort remains of high relevance. The purpose of the research is to investigate the relationship between serum levels of chemerin and nesfatin-1 and the peculiarities of the clinical characteristics in observed hypertensive patients, depending on the presence and grade of obesity. Materials and methods. According to the standard protocol, 82 hypertensive patients with an average age of 60 (55; 66) years were examined (including 26 overweight and 39 obese patients). The serum levels of chemerin and nesfatin-1 were determined by ELISA using Human Chemerin and Human Nesfatin-1 ELISA Kits (Kono Biotech Co., Ltd., PRC). Statistical processing was performed using Mann-Whitney's criteria, cluster analysis. Quantitative signs are given as the median (Me), the upper (UQ) and lower (LQ) quartiles. Results and discussion. The most favorable course of hypertension was observed in patients from the closest to control group cluster by the levels of both cytokines and from the cluster with relatively low chemerin and high nesfatin-1 levels. The highest rate of patients (100,0%) with complicated hypertension, 50,0% of whom previously had an adverse cardovascular event, was found in the cluster with high serum chemerin and relatively low nesfatin-1. In clusters with high serum levels of both cytokines or high serum chemerin and low nesfatin-1, a significantly higher rate of patients with complicated hypertension as well as higher grade of hypertension were found. Patients who were referred to high-chemerin clusters with relatively low of nesfatin-1 or high values of both cytokines had significantly higher heart rate on admission vs patients with cytokine levels close to control and with relatively low serum cemerin / high nesfatin-1 content. We have found no clear differences in the distribution of the clinical stages of CHF as well as NYHA classes depending on the cluster of chemerin and nesfatin-1 serum levels. Conclusions. Clarification of chemerin and nesfatin-1 values as the new markers of metabolic disorders and clinical course in hypertensive patients with obesity is relevant for further research, being potentially helpful for optimizing early diagnostics and prediction of the outcomes in such patients.

Keywords: cytokines, metabolic syndrome, cardiovascular risk, comorbidity

Full text: PDF (Ukr) 273K

  1. Fadeenko GD. Gridnev AE. Ozhirenie i risk serdechno-sosudistykh zabolevaniy. Liki Ukraini. 2009; 7 (133): 55-64. [Russian].
  2. Angerаs O, Albertsson P, Karason K, Råmunddal T, Matejka G, James S, Lagerqvist B, Rosengren A, Omerovic E. Evidence for obesity paradox in patients with acute coronary syndromes: a report from the Swedish Coronary Angiography and Angioplasty Registry. Eur Heart J. 2013; 34 (5): 345–53.
  3. Boban M, Persic V, Jovanovic Z, Brozina A, Miletic B, Rotim A, Drinkovic N Jr, Manola S, Laskarin G, Boban L. Obesity dilemma in the global burden of cardiovascular diseases. Int J Clin Pract. 2014; 68 (2): 173–9.
  4. Carnethon MR, De Chavez PJD, Biggs ML, Lewis CE, Pankow JS, Bertoni AG, Golden SH, et al. Association of weight status with mortality in adults with incident diabetes. JAMA. 2012; 308 (6): 581–90.
  5. Clark AL, Fonarow GC, Horwich TB. Obesity and the Obesity Paradox in Heart Failure. Prog Cardiovasc Dis. 2014; 56 (4): 409–14.
  6. Clearfield M, Pearce M, Nibbe Y, Crotty D, Wagner A The "New Deadly Quartet" for cardiovascular disease in the 21st century: obesity, metabolic syndrome, inflammation and climate change: how does statin therapy fit into this equation? Curr Atheroscler Rep. 2014; 16 (1): 380-9.
  7. Dalamaga M. Obesity, insulin resistance, adipocytokines and breast cancer: New biomarkers and attractive therapeutic targets. World J Exp Med. 2013; 3 (3): 34–42.
  8. De Schutter A, Lavie CJ, Milani RV. The impact of obesity on risk factors and prevalence and prognosis of coronary heart disease-the obesity paradox. Prog Cardiovasc Dis. 2014; 56 (4): 401–8.
  9. Lavie CJ, Milani RV, Ventura HO, et al. Obesity and cardiovascular disease: risk factor, paradox and impact of weight loss. J Am Coll Cardiol. 2009; 53 (21): 1925–32.
  10. Rydén L, Grant PJ, Anker SD, Berne C, Cosentino F, Danchin N, Deaton C, Escaned J, et al. ESC Guidelines on diabetes, pre-diabetes, and cardiovascular diseases developed in collaboration with the EASD. Eur Heart J. 2013; 34 (39): 3035-87.
  11. Schols AMWJ, Broekhuizen R, Weling-Scheepers CA, Wouters EF. Body composition and mortality in chronic obstructive pulmonary disease. Am J Clin Nutr. 2005; 82 (1): 53–9.
  12. Surya M, Artham MD, Lavie CJ, et al. Obesity and Hypertension, Heart Failure, and Coronary Heart Disease-Risk Factor, Paradox, and Recommendations for Weight Loss. Ochsner J. 2009; 9 (3): 124-32.