.: ORİJİNAL ARAŞTIRMA
Evaluation of Epicardial Adipose Tissue Thickness and Proinflammatory Cytokines in Subclinical Hypothyroidism: A Case Control Study
Subklinik Hipotiroidide Epikardiyal Yağ Doku Kalınlığı ve Proinflamatuar Sitokinlerin Değerlendirilmesi: Bir Vaka Kontrol Çalışması
Turkiye Klinikleri J Intern Med. 2022;7(2/3):45-50
doi: 10.5336/intermed.2022-89994
Makale Dili: EN
Tam Metin
Ücretsiz Erişim
ABSTRACT
Objective: Epicardial adipose tissue (EAT) is an adipose tissue located between the myocardial surface and the visceral layer of the pericardium. Epicardial adipose tissue thickness (EATT) is a sign of atherosclerosis. It has been reported that EATT is increased in patients with subclinical hypothyroidism (SCH). It is suggested that EAT may cause coronary atherosclerosis through paracrine and vasocrine pathways mediated by adipokines / cytokines. In this study, it was aimed to evaluate the relationship of EATT in SCH with proinflammatory cytokines (interleukin-6 (IL-6), highly sensitive C-reactive protein (hsCRP), monocyte chemo attractant protein-1 (MCP-1) and tumor necrosis factor-alpha (TNF-alpha)). Material and Methods: A total of 32 cases of SCH and 27 healthy volunteers were prospectively included in the study. EATT were measured by echocardiography. IL-6, hsCRP, MCP-1 and TNF-alpha were measured through simultaneously taken serum samples. Results: EATT was significantly higher in SCH compared to the control group (p=0.05). Groups were similar in terms of age, BMI, totalcholesterol, LDL-cholesterol levels; but only HDL-cholesterol was found to be significantly higher in SCH group (p=0.034). There was no significant difference between the SCH and the control group in terms of IL-6, hsCRP, MCP-1 and TNF-alpha. Conclusion: EATT was found to be increased in SCH. But, serum levels of proinflammatory cytokines were similar between groups. In the SCH group, there was no relationship between EATT and proinflammatory cytokines. Although EATT is an indicator of atherosclerosis, it may have different control mechanisms in SCH in terms of proinflammatory bioactive molecule synthesis and secretion.
Keywords: Subclinical hypothyroidism; epicardial adipose tissue; monocyte chemo attractant protein-1; tumor necrosis factor-alpha
Objective: Epicardial adipose tissue (EAT) is an adipose tissue located between the myocardial surface and the visceral layer of the pericardium. Epicardial adipose tissue thickness (EATT) is a sign of atherosclerosis. It has been reported that EATT is increased in patients with subclinical hypothyroidism (SCH). It is suggested that EAT may cause coronary atherosclerosis through paracrine and vasocrine pathways mediated by adipokines / cytokines. In this study, it was aimed to evaluate the relationship of EATT in SCH with proinflammatory cytokines (interleukin-6 (IL-6), highly sensitive C-reactive protein (hsCRP), monocyte chemo attractant protein-1 (MCP-1) and tumor necrosis factor-alpha (TNF-alpha)). Material and Methods: A total of 32 cases of SCH and 27 healthy volunteers were prospectively included in the study. EATT were measured by echocardiography. IL-6, hsCRP, MCP-1 and TNF-alpha were measured through simultaneously taken serum samples. Results: EATT was significantly higher in SCH compared to the control group (p=0.05). Groups were similar in terms of age, BMI, totalcholesterol, LDL-cholesterol levels; but only HDL-cholesterol was found to be significantly higher in SCH group (p=0.034). There was no significant difference between the SCH and the control group in terms of IL-6, hsCRP, MCP-1 and TNF-alpha. Conclusion: EATT was found to be increased in SCH. But, serum levels of proinflammatory cytokines were similar between groups. In the SCH group, there was no relationship between EATT and proinflammatory cytokines. Although EATT is an indicator of atherosclerosis, it may have different control mechanisms in SCH in terms of proinflammatory bioactive molecule synthesis and secretion.
Keywords: Subclinical hypothyroidism; epicardial adipose tissue; monocyte chemo attractant protein-1; tumor necrosis factor-alpha
ÖZET
Amaç: Epikardiyal yağ dokusu (EYD), miyokardiyal yüzey ileperikardın visseral tabakası arasında yer alan bir yağ dokusudur. Epikardiyal yağ doku kalınlığı (EYDK) aterosklerozun belirteçlerinden biridir. Subklinik hipotiroidili (SKH) hastalarda, EYDK'nin arttığı bildirilmektedir. EYD'nin adipokin/ sitokin aracılı parakrin ve vazokrin yolaklar ile koroner ateroskleroza neden olabileceği öne sürülmektedir. Ancak SKH'de proinflamatuar sitokinler ile EYDK'nin ilişkisi net değildir. Bu çalışmada, SKH'de EYDK'nin proinflamatuar sitokinler [interlökin (IL-6), yüksek hassasiyetli C-reaktif protein (high sensitivity C-reactive protein 'hs-CRP'), monosit kemoatraktan protein-1 (monocyte chemo attractant protein-1 'MCP-1') ve tümö rnekrozis faktöralfa (TNF-α)] ile ilişkisinin değerlendirilmesi amaçlandı. Gereç ve Yöntemler: SKH tanılı 32 olgu ve 27 sağlıklı gönüllü prospektif olarak çalışmaya dâhil edildi. Olguların EYDK'lari ekokardiyografiile ölçüldü. Eş zamanlı alınan serum örneklerinde IL-6, hs- CRP, MCP-1 ve TNF-α düzeyleri ölçüldü. Bulgular: SKH'li olgularda, EYDK kontrol grubuna göre anlamlı yüksekti (p=0,05). Gruplar yaş, beden kitle indeksi, total kolesterol, düşük yoğunluklu lipoprotein kolesterol düzeyleri açısından benzerdi; ancak yüksek yoğunluklu lipoprotein kolesterol SKH grubunda anlamlı olarak yüksek bulundu (p=0,034). Hasta grubu ve kontrol grubu arasında IL-6, hs-CRP, MCP-1 ve TNF-α açısından anlamlı farklılık saptanmadı. Sonuç: SKH olgularında, EYDK artmış olarak saptandı. Karşıt olarak serum proinflamatuar sitokinlerin düzeyleri kontrol grubundan farklı değildi. Proinflamatuar sitokinlerle EYDK arasında anlamlı ilişki bulunamadı. EYDK, aterosklerozun bir göstergesi olmasına rağmen proinflamatuar biyoaktif molekül sentezi ve salgılanması açısından SKH durumunda farklı kontrol mekanizmalarına sahip olabilir.
Anahtar Kelimeler: Subklinik hipotiroidi; epikardiyal adipoz doku; monosit kemoatraktan protein-1; tümör nekrozis faktör-alfa
Amaç: Epikardiyal yağ dokusu (EYD), miyokardiyal yüzey ileperikardın visseral tabakası arasında yer alan bir yağ dokusudur. Epikardiyal yağ doku kalınlığı (EYDK) aterosklerozun belirteçlerinden biridir. Subklinik hipotiroidili (SKH) hastalarda, EYDK'nin arttığı bildirilmektedir. EYD'nin adipokin/ sitokin aracılı parakrin ve vazokrin yolaklar ile koroner ateroskleroza neden olabileceği öne sürülmektedir. Ancak SKH'de proinflamatuar sitokinler ile EYDK'nin ilişkisi net değildir. Bu çalışmada, SKH'de EYDK'nin proinflamatuar sitokinler [interlökin (IL-6), yüksek hassasiyetli C-reaktif protein (high sensitivity C-reactive protein 'hs-CRP'), monosit kemoatraktan protein-1 (monocyte chemo attractant protein-1 'MCP-1') ve tümö rnekrozis faktöralfa (TNF-α)] ile ilişkisinin değerlendirilmesi amaçlandı. Gereç ve Yöntemler: SKH tanılı 32 olgu ve 27 sağlıklı gönüllü prospektif olarak çalışmaya dâhil edildi. Olguların EYDK'lari ekokardiyografiile ölçüldü. Eş zamanlı alınan serum örneklerinde IL-6, hs- CRP, MCP-1 ve TNF-α düzeyleri ölçüldü. Bulgular: SKH'li olgularda, EYDK kontrol grubuna göre anlamlı yüksekti (p=0,05). Gruplar yaş, beden kitle indeksi, total kolesterol, düşük yoğunluklu lipoprotein kolesterol düzeyleri açısından benzerdi; ancak yüksek yoğunluklu lipoprotein kolesterol SKH grubunda anlamlı olarak yüksek bulundu (p=0,034). Hasta grubu ve kontrol grubu arasında IL-6, hs-CRP, MCP-1 ve TNF-α açısından anlamlı farklılık saptanmadı. Sonuç: SKH olgularında, EYDK artmış olarak saptandı. Karşıt olarak serum proinflamatuar sitokinlerin düzeyleri kontrol grubundan farklı değildi. Proinflamatuar sitokinlerle EYDK arasında anlamlı ilişki bulunamadı. EYDK, aterosklerozun bir göstergesi olmasına rağmen proinflamatuar biyoaktif molekül sentezi ve salgılanması açısından SKH durumunda farklı kontrol mekanizmalarına sahip olabilir.
Anahtar Kelimeler: Subklinik hipotiroidi; epikardiyal adipoz doku; monosit kemoatraktan protein-1; tümör nekrozis faktör-alfa
REFERANSLAR:
- Cooper DS. Clinical practice. Subclinical hypothyroidism. N Engl J Med. 2001;345(4):260-5. [Crossref] [PubMed]
- Moon S, Kong SH, Choi HS, Hwangbo Y, Lee MK, Moon JH, et al. Relation of subclinical hypothyroidism is associated with cardiovascular events and all-cause mortality in adults with high cardiovascular risk. Am J Cardiol. 2018;122(4):571-7. [Crossref] [PubMed]
- Moon S, Kim MJ, Yu JM, Yoo HJ, Park YJ. Subclinical hypothyroidism and the risk of cardiovascular disease and all-cause mortality: a meta-analysis of prospective cohort studies. Thyroid. 2018;28(9):1101-10. [Crossref] [PubMed]
- Sun J, Yao L, Fang Y, Yang R, Chen Y, Yang K, et al. Relationship between subclinical thyroid dysfunction and the risk of cardiovascular outcomes: a systematic review and meta-analysis of prospective cohort studies. Int J Endocrinol. 2017;2017:8130796. [Crossref] [PubMed] [PMC]
- Kang YE, Kim JM, Joung KH, Lee JH, You BR, Choi MJ, et al. The roles of adipokines, proinflammatory cytokines, and adipose tissue macrophages in obesity-associated ınsulin resistance in modest obesity and early metabolic dysfunction. PLoS One. 2016;11(4):e0154003. [Crossref] [PubMed] [PMC]
- Iozzo P. Myocardial, perivascular, and epicardial fat. Diabetes Care. 2011;34 Suppl 2(Suppl 2):S371-9. [Crossref] [PubMed] [PMC]
- Sacks HS, Fain JN. Human epicardial adipose tissue: a review. Am Heart J. 2007;153(6):907-17. [Crossref] [PubMed]
- Nagy E, Jermendy AL, Merkely B, Maurovich-Horvat P. Clinical importance of epicardial adipose tissue. Arch Med Sci. 2017;13(4):864-74. [Crossref] [PubMed] [PMC]
- Korkmaz L, Sahin S, Akyuz AR, Ziyrek M, Anaforoglu I, Kose M, et al. Epicardial adipose tissue increased in patients with newly diagnosed subclinical hypothyroidism. Med Princ Pract. 2013;22(1):42-6. [Crossref] [PubMed] [PMC]
- Unubol M, Eryilmaz U, Guney E, Akgullu C, Kurt Omurlu I. Epicardial adipose tissue in patients with subclinical hypothyroidism. Minerva Endocrinol. 2014;39(2):135-40. [PubMed]
- Balta S, Demırkol S, Kucuk U, Arslan Z, Unlu M, Yesil FG. Epicardial adipose tissue should be evaluated with other inflammatory markers in patients with subclinical hypothyroidism. Med Princ Pract. 2013;22(6):603. [Crossref] [PubMed] [PMC]
- Serter R, Demirbas B, Korukluoglu B, Culha C, Cakal E, Aral Y. The effect of L-thyroxine replacement therapy on lipid based cardiovascular risk in subclinical hypothyroidism. J Endocrinol Invest. 2004;27(10):897-903. [Crossref] [PubMed]
- Aydogdu A, Karakas EY, Erkus E, Altıparmak İH, Savık E, Ulas T, et al. Epicardial fat thickness and oxidative stress parameters in patients with subclinical hypothyroidism. Arch Med Sci. 2017;13(2):383-9. [Crossref] [PubMed] [PMC]
- Mattace-Raso FU, van der Cammen TJ, Hofman A, van Popele NM, Bos ML, Schalekamp MA, et al. Arterial stiffness and risk of coronary heart disease and stroke: the Rotterdam Study. Circulation. 2006;113(5):657-63. [Crossref] [PubMed]
- Yao K, Zhao T, Zeng L, Yang J, Liu Y, He Q, et al. Non-invasive markers of cardiovascular risk in patients with subclinical hypothyroidism: A systematic review and meta-analysis of 27 case control studies. Sci Rep. 2018;8(1):4579. [Crossref] [PubMed] [PMC]
- Rodondi N, den Elzen WP, Bauer DC, Cappola AR, Razvi S, Walsh JP, et al; Thyroid Studies Collaboration. Subclinical hypothyroidism and the risk of coronary heart disease and mortality. JAMA. 2010;304(12):1365-74. [Crossref] [PubMed] [PMC]
- Collet TH, Bauer DC, Cappola AR, Asvold BO, Weiler S, Vittinghoff E, et al; Thyroid Studies Collaboration. Thyroid antibody status, subclinical hypothyroidism, and the risk of coronary heart disease: an individual participant data analysis. J Clin Endocrinol Metab. 2014;99(9):3353-62. [Crossref] [PubMed] [PMC]
- Lee Y, Lim YH, Shin JH, Park J, Shin J. Impact of subclinical hypothyroidism on clinical outcomes following percutaneous coronary intervention. Int J Cardiol. 2018;253:155-60. [Crossref] [PubMed]
- Blum MR, Gencer B, Adam L, Feller M, Collet TH, da Costa BR, et al. Impact of thyroid hormone therapy on atherosclerosis in the elderly with subclinical hypothyroidism: a randomized trial. J Clin Endocrinol Metab. 2018;103(8):2988-97. [Crossref] [PubMed]
- Seo C, Kim S, Lee M, Cha MU, Kim H, Park S, et al. Thyroid hormone replacement reduces the risk of cardiovascular diseases in diabetic nephropathy patients with subclinical hypothyroidism. Endocr Pract. 2018;24(3):265-72. [Crossref] [PubMed]
- Kanaya AM, Harris F, Volpato S, Pérez-Stable EJ, Harris T, Bauer DC. Association between thyroid dysfunction and total cholesterol level in an older biracial population: the health, aging and body composition study. Arch Intern Med. 2002;162(7):773-9. [Crossref] [PubMed]
- Bauer DC, Ettinger B, Browner WS. Thyroid functions and serum lipids in older women: a population-based study. Am J Med. 1998;104(6):546-51. [Crossref] [PubMed]
- Imaizumi M, Akahoshi M, Ichimaru S, Nakashima E, Hida A, Soda M, et al. Risk for ischemic heart disease and all-cause mortality in subclinical hypothyroidism. J Clin Endocrinol Metab. 2004;89(7):3365-70. [Crossref] [PubMed]
- Iacobellis G, Bianco AC. Epicardial adipose tissue: emerging physiological, pathophysiological and clinical features. Trends Endocrinol Metab. 2011;22(11):450-7. [Crossref] [PubMed] [PMC]
- Xu Y, Cheng X, Hong K, Huang C, Wan L. How to interpret epicardial adipose tissue as a cause of coronary artery disease: a meta-analysis. Coron Artery Dis. 2012;23(4):227-33. [Crossref] [PubMed]
- Silaghi A, Piercecchi-Marti MD, Grino M, Leonetti G, Alessi MC, Clement K, et al. Epicardial adipose tissue extent: relationship with age, body fat distribution, and coronaropathy. Obesity (Silver Spring). 2008;16(11):2424-30. [Crossref] [PubMed]
- Eiras S, Teijeira-Fernández E, Salgado-Somoza A, Couso E, García-Caballero T, Sierra J, et al. Relationship between epicardial adipose tissue adipocyte size and MCP-1 expression. Cytokine. 2010;51(2):207-12. [Crossref] [PubMed]
- Kokkotou E, Marafelia P, Mantzos EI, Tritos NA. Serum monocyte chemoattractant protein-1 is increased in chronic autoimmune thyroiditis. Metabolism. 2002;51(11):1489-93. [Crossref] [PubMed]
.: İşlem Listesi