Purpose: To study pathological changes in the thyroid gland of patients with Graves' disease (GD) treated with thyroid arterial embolization.
Methods: Thirty-seven patients with GD were treated through transcatheter thyroid arterial embolization. Of these patients, twenty-two had biopsy of the thyroid gland at different time points before and after the embolization for the study of pathology. Serum thyroid hormones, TSH and TRAb were also studied at these time points. Thyroid size was evaluated in all patients using color Doppler ultrasound or CT scan.
Results: Thyroid size decreased immediately or several days following embolization. Pathological study demonstrated mainly acute infarction and necrosis at 7 days post embolization. At 6 months, chronic inflammation and fibrous hyperplasia were the primary findings in the gland, and at 3 years following embolization, mesenchyma hyperplasia and follicle atrophy were primarily present in the embolized thyroid tissue. The thyroid hormones and TSH gradually resumed to normal range after embolization while TRAb decreased significantly.
Conclusion: Thyroid arterial embolization can cause GD thyroid gland a series of pathological changes of acute ischemia and necrosis and later, chronic inflammation, fibroplasia and atrophy to decrease secretion of thyroid. The pathological changes within the thyroid gland after embolization form the basis of thyroid arterial embolization in treating GD hyperthyroidism.
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http://dx.doi.org/10.25011/cim.v32i2.6034 | DOI Listing |
Pflugers Arch
January 2025
Gangarosa Department of Environmental Health, Rollins School of Public Health, Emory University, Atlanta, GA, 30322, USA.
Plasma thyroid hormone (TH) binding proteins (THBPs), including thyroxine-binding globulin (TBG), transthyretin (TTR), and albumin (ALB), carry THs to extrathyroidal sites, where THs are unloaded locally and then taken up via membrane transporters into the tissue proper. The respective roles of THBPs in supplying THs for tissue uptake are not completely understood. To investigate this, we developed a spatial human physiologically based kinetic (PBK) model of THs, which produces several novel findings.
View Article and Find Full Text PDFNat Genet
January 2025
Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, MA, USA.
Complex diseases often have distinct mechanisms spanning multiple tissues. We propose tissue-gene fine-mapping (TGFM), which infers the posterior inclusion probability (PIP) for each gene-tissue pair to mediate a disease locus by analyzing summary statistics and expression quantitative trait loci (eQTL) data; TGFM also assigns PIPs to non-mediated variants. TGFM accounts for co-regulation across genes and tissues and models uncertainty in cis-predicted expression models, enabling correct calibration.
View Article and Find Full Text PDFRev Cardiovasc Med
December 2024
Department of Cardiothoracic Surgery, The First Affiliated Hospital of Chongqing Medical University, 400016 Chongqing, China.
Introduction: Coronary atherosclerosis serves as the primary pathological etiology underlying coronary artery disease (CAD). Thyroid hormones show potential as risk factors, aside from the main standard modifiable cardiovascular risk factors (SMuRFs). This research seeks to elucidate the link between thyroid activity and coronary atherosclerosis.
View Article and Find Full Text PDFAACE Clin Case Rep
August 2024
Section of Endocrinology, Diabetes, Nutrition & Weight Management, Boston University Chobanian & Avedisian School of Medicine, Boston, Massachusetts.
Background/objective: Medullary thyroid cancer often results in elevated calcitonin levels, which can cause localized formation of calcitonin amyloid, though rarely complications of systemic calcitonin amyloidosis have been reported. The objective of this report is to encourage awareness of calcitonin amyloid causing nephrotic syndrome in patients with metastatic medullary thyroid cancer.
Case Report: A 65-year-old woman with weakness, fatigue, anasarca, anemia, thrombocytopenia, venous and arterial thrombi, and a cavitary right lung lesion was transferred for care.
Endocr Pract
December 2024
Department of Cardiovascular Medicine, the Second Affiliated Hospital, Xi'an Jiaotong University, Xi'an, Shaanxi, P.R. China.
Objective: Thyroid-stimulating hormone (TSH) is related to increased atrial fibrillation (AF) inducibility and plays an important role in a variety of cardiovascular diseases. However, the association of baseline TSH with in-hospital outcomes in patients with AF and coronary artery disease (CAD) is unknown. This study aimed to investigate the distribution of baseline TSH and its association with in-hospital outcomes (major adverse cardiovascular events [MACE], all-cause death, or heart failure [HF]) in AF patients combined with CAD.
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