A decade of hospitalizations for hyperthyroidism in the US

Salim, Michael; DeHart, Luke; El-Amir, Zain; Wani, Farah; Kichloo, Asim

doi:10.1080/08998280.2022.2106452

Cited by 1 publication

(1 citation statement)

References 22 publications

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“…The prevalence of hyperthyroidism-related cardiac problems appears to be higher in older individuals with Graves’ disease or toxic untreated hyperthyroidism [ 40 ]. Hyperthyroidism may affect functional parameters of the left ventricle, including the ejection fraction [ 67 ]. About 6% of hyperthyroid patients appear to have heart failure as their most common clinical presentation, with roughly half of them having left ventricular systolic dysfunction.…”

Section: Introductionmentioning

confidence: 99%

SGLT2 inhibitor as a potential therapeutic approach in hyperthyroidism-induced cardiopulmonary injury in rats

Bastawy,

El-Mosallamy,

Aljuaydi

et al. 2024

Pflugers Arch - Eur J Physiol

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Hyperthyroidism-induced cardiac disease is an evolving health, economic, and social problem affecting well-being. Sodium-glucose cotransporter protein 2 inhibitors (SGLT2-I) have been proven to be cardio-protective when administered in cases of heart failure. This study intended to investigate the potential therapeutic effect of SGLT2-I on hyperthyroidism-related cardiopulmonary injury, targeting the possible underlying mechanisms. The impact of the SGLT2-I, dapagliflozin (DAPA), (1 mg/kg/day, p.o) on LT4 (0.3 mg/kg/day, i.p)-induced cardiopulmonary injury was investigated in rats. The body weight, ECG, and serum hormones were evaluated. Also, redox balance, DNA fragmentation, inflammatory cytokines, and PCR quantification in heart and lung tissues were employed to investigate the effect of DAPA in experimentally induced hyperthyroid rats along with histological and immunohistochemical examination. Coadministration of DAPA with LT4 effectively restored all serum biomarkers to nearly average levels, improved ECG findings, and reinstated the redox balance. Also, DAPA could improve DNA fragmentation, elevate mtTFA, and lessen TNF-α and IGF-1 gene expression in both organs of treated animals. Furthermore, DAPA markedly improved the necro-inflammatory and fibrotic cardiopulmonary histological alterations and reduced the tissue immunohistochemical expression of TNF-α and caspase-3. Although further clinical and deep molecular studies are required before transposing to humans, our study emphasized DAPA’s potential to relieve hyperthyroidism-induced cardiopulmonary injury in rats through its antioxidant, anti-inflammatory, and anti-apoptotic effects, as well as via antagonizing the sympathetic over activity.

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Section: Introductionmentioning

confidence: 99%