Why the study?
It was hypothesized that mechanisms of 131I-induced cardiotoxicity differ between differentiated thyroid cancer patients with and without T2DM, with metformin potentially conferring cardioprotection.
Does metformin reduce radiation-induced cardiac injury biomarkers (cTn I, NT-proBNP, NT-proANP, ST2/IL-33R) and inflammation in female differentiated thyroid cancer patients with type 2 diabetes mellitus receiving high cumulative doses of 131I compared to those without diabetes?
Does metformin reduce radiation-induced cardiac injury biomarkers (cTn I, NT-proBNP, NT-proANP, ST2/IL-33R) and inflammation in female differentiated thyroid cancer patients with type 2 diabetes mellitus receiving high cumulative doses of 131I compared to those without diabetes?
Answers are grounded in this paper and cite their sources.
In female thyroid cancer patients receiving high cumulative doses of 131I, mechanisms of subclinical cardiotoxicity differ by diabetes status, with metformin demonstrating a dose-dependent cardioprotective reduction in inflammation and troponin I release among patients with T2DM.
Starting from the metabolic profile of type 2 diabetes mellitus (T2DM), we hypothesized that the mechanisms of ¹³¹I-induced cardiotoxicity differ between patients diagnosed with differentiated thyroid cancer (DTC) with/without T2DM, with metformin potentially acting as a cardioprotective agent by mitigating inflammation in patients with T2DM. To address this hypothesis, we quantified, using ELISA, the serum concentration of several key biomarkers that reflect cardiac injury (NT-proBNP, NT-proANP, ST2/IL-33R, and cTn I) in 74 female patients with DTC/−T2DM and 25 with DTC/+T2DM treated with metformin. All patients received a cumulative oral dose of 131I exceeding 150 mCi (5.55 GBq) over approximately 53 months. Our results showed the following: (i) In DTC/−T2DM patients, high-cumulative 131I doses promote a pro-inflammatory state that accelerates the development of cardiotoxicity. Monitoring NT-proBNP, ST2/IL-33R, and cTn I in these patients may help identify those at risk of developing cardiac complications. (ii) In patients with DTC/+T2DM, high-cumulative 131I doses lead to the release of NT-proANP (r = 0.63), which signals that the atria are under significant stress. (iii) In patients with DTC/+T2DM, metformin suppresses inflammation, leading to a dose-dependent reduction in cTn I (r = −0.59). Monitoring cTn I and NT-proANP, and considering the use of metformin as part of the therapeutic strategy, could help manage cardiotoxicity in T2DM patients undergoing 131I therapy.
No takes yet. Share an insight, caveat, or question.
Stanciu et al. (2024) studied this question.
Synapse has enriched 10 related papers. Consider them for comparative context: