Cardiac and Inflammatory Biomarker Signatures in Hyperthyroidism Treated with 35 mg Carbimazole: Influence of Pre-Existing Heart Disease
Downloads
Background: Hyperthyroidism changes cardiovascular, inflammatory, and metabolic pathways. These changes may be aggravated by heart disease. Objective: Both to compare levels of thyroid hormones, proBNP, IL-6, lipid profile, renal function, glucose, and BMI among four groups and to determine whether or not proBNP and IL-6 can detect cardiac disease in hyperthyroid patients. Methods: It was an analytical cross-sectional study, which utilized a dataset of 140 participants (n = 50 healthy controls, n = 30 hyperthyroidism treated with 35 mg carbimazole, n = 30 heart disease, and n = 30 heart disease and hyperthyroidism). ELISA-based measurements were described as thyroid hormones, IL-6 and proBNP. Glucose, lipid profile, and renal functioning were characterized as Cobas c111 chemistry tests. Descriptive statistics, one-way ANOVA, Pearson correlation, Welch t test, and ROC analysis were performed. Results: There was no significant difference in age among groups (p = 0.159). FT4, FT3, TSH, IL-6, proBNP, BMI, triglycerides, glucose, creatinine and urea were found to have strong group effects (all p < .001). The highest level of IL-6 and proBNP was observed in the heart disease with hyperthyroidism. The largest differences were observed in the proBNP (116.00 vs. 847.22 pg/mL, p <.001, d = 4.29) and IL-6 (4.07 vs. 7.62 pg/mL, p <.001, d = 2.41) in the direct comparison between hyperthyroidism with carbimazole proBNP correlated positively with IL-6 (r = .70, p < .001). TSH correlated inversely with FT4 (r = -.79, p < .001). ProBNP had an AUC of 1.000 and IL-6 had an AUC of 0.961 to discriminate heart disease among hyperthyroid patients. Conclusion: Heart disease patients who had hyperthyroidism had a different profile that was characterized by increased cardiac stress, increased inflammatory load, and poor metabolic and renal indices. ProBNP and IL-6 were the best predictors of cardiac involvement in this cohort.
[1] S. Ertek and A. F. Cicero, “Hyperthyroidism and cardiovascular complications: A narrative review on the basis of pathophysiology,” Archives of Medical Science, vol. 9, no. 5, pp. 944–952, 2013, doi: 10.5114/aoms.2013.38685.
[2] A. Abbara et al., “Pharmacodynamic response to anti-thyroid drugs in Graves' hyperthyroidism,” Frontiers in Endocrinology, vol. 11, Art. no. 286, 2020, doi: 10.3389/fendo.2020.00286.
[3] T. Tanaka, M. Narazaki, and T. Kishimoto, “IL-6 in inflammation, immunity, and disease,” Cold Spring Harbor Perspectives in Biology, vol. 6, no. 10, Art. no. a016295, 2014, doi: 10.1101/cshperspect.a016295.
[4] M. Salvi et al., “Increased serum concentrations of interleukin-6 (IL-6) and soluble IL-6 receptor in patients with Graves' disease,” The Journal of Clinical Endocrinology & Metabolism, vol. 81, no. 8, pp. 2976–2979, 1996, doi: 10.1210/jcem.81.8.8768861.
[5] H. Zhang et al., “Effect of thyroid dysfunction on N-terminal pro-B-type natriuretic peptide levels: A systematic review and meta-analysis,” Frontiers in Endocrinology, vol. 14, Art. no. 1083171, 2023, doi: 10.3389/fendo.2023.1083171.
[6] C. V. Rizos, M. S. Elisaf, and E. N. Liberopoulos, “Effects of thyroid dysfunction on lipid profile,” The Open Cardiovascular Medicine Journal, vol. 5, pp. 76–84, 2011, doi: 10.2174/1874192401105010076.
[7] F. Q. Nuttall, “Body mass index: Obesity, BMI, and health: A critical review,” Nutrition Today, vol. 50, no. 3, pp. 117–128, 2015, doi: 10.1097/NT.0000000000000092.
[8] D. S. Ross et al., “2016 American Thyroid Association guidelines for diagnosis and management of hyperthyroidism and other causes of thyrotoxicosis,” Thyroid, vol. 26, no. 10, pp. 1343–1421, 2016, doi: 10.1089/thy.2016.0229.
[9] B. Biondi and D. S. Cooper, “The clinical significance of subclinical thyroid dysfunction,” Endocrine Reviews, vol. 29, no. 1, pp. 76–131, 2008, doi: 10.1210/er.2006-0043.
[10] B. Biondi and D. S. Cooper, “Thyroid hormone excess and the heart,” Circulation, vol. 116, no. 15, pp. 1725–1735, 2007, doi: 10.1161/CIRCULATIONAHA.106.678326.
[11] G. J. Kahaly and L. Bartalena, “Graves’ disease,” New England Journal of Medicine, vol. 376, no. 19, pp. 1842–1853, 2017, doi: 10.1056/NEJMra1510030.
[12] M. Klein and K. Ojamaa, “Thyroid hormone and the cardiovascular system,” New England Journal of Medicine, vol. 344, no. 7, pp. 501–509, 2001, doi: 10.1056/NEJM200102153440707.
[13] M. Antonelli, P. Fallahi, S. M. Ferrari, A. Ragusa, A. Ruffilli, and A. Antonelli, “Cytokines (interleukin-6 and tumor necrosis factor-α) in autoimmune thyroid diseases,” Autoimmunity Reviews, vol. 14, no. 10, pp. 922–930, 2015, doi: 10.1016/j.autrev.2015.06.014.
[14] A. Jabbar, M. Pingitore, A. Pearce, B. Zaman, S. Iervasi, and M. Razvi, “Thyroid hormones and cardiovascular disease,” Nature Reviews Cardiology, vol. 14, no. 1, pp. 39–55, 2017, doi: 10.1038/nrcardio.2016.174.
[15] G. Brent, “Mechanisms of thyroid hormone action,” Journal of Clinical Investigation, vol. 122, no. 9, pp. 3035–3043, 2012, doi: 10.1172/JCI60047.
Copyright (c) 2026 American Journal of Biomedicine and Pharmacy
This work is licensed under a Creative Commons Attribution 4.0 International License.
