Center for International Health, University of Bergen, Bergen, Norway
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Department of Microbiology, Innlandet Hospital Trust, Lillehammer, Norway
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Department of Clinical Science, University of Bergen, Bergen, Norway
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Department of Research, Innlandet Hospital Trust, Lillehammer, Norway
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caused overdiagnosis of (subclinical) hypothyroidism and subsequent overtreatment ( 4 , 5 , 6 ). However, there is a lack of data that quantify this potential increase in thyroid hormone therapy from a national perspective. Interestingly, the diagnostic
Center for Clinical Metabolic Research, Gentofte Hospital, University of Copenhagen, Hellerup, Denmark
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Department of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark
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Department of Clinical Physiology and Nuclear Medicine, Bispebjerg and Frederiksberg Hospital, University of Copenhagen, Copenhagen, Denmark
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Department of Clinical Pharmacology, Bispebjerg and Frederiksberg Hospital, University of Copenhagen, Copenhagen, Denmark
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Novo Nordisk Foundation Center for Basic Metabolic Research, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark
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Department of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark
Steno Diabetes Center Copenhagen, Herlev, Denmark
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Department of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark
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Department of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark
Department of Biomedical Sciences, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark
Steno Diabetes Center Copenhagen, Herlev, Denmark
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thyroid-stimulating hormone (TSH) (i.e. < 4 mU/L) (visit 2), and after at least 6 months of substitution therapy with TSH < 4 mU/L (visit 3). Levothyroxine therapy was initially evaluated every 4 weeks until the participants were euthyroid and then every 3
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therapy for hypothyroidism ( 17 ). In this context, there is an ongoing discussion on optimal thyroid hormone levels and the best parameter for laboratory surveillance of treatment. Considering the crucial influence of thyroid hormones on cognitive
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Introduction Maternal subclinical hypothyroidism (SCH), which is defined as an increased thyroid-stimulating hormone (TSH) concentration beyond the upper limit of the pregnancy-specific reference range and a normal free-thyroxine (FT4
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Department of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark
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Université Libre de Bruxelles, Bruxelles, Belgium
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School of Medicine, Zagreb, Croatia
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Department of Clinical Nutrition, Landspitali-National University Hospital, Reykjavik, Iceland
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Goldman School of Medicine, Ben Gurion University of the Negev, Beer Sheva, Israel
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Faculty of Medicine, University of Ljubljana, Ljubljana, Slovenia
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Faculty of Medicine, University of Ljubljana, Ljubljana, Slovenia
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Universitat Autònoma de Barcelona, Barcelona, Spain
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Frölunda Specialist Hospital, Västra Frölunda, Sweden
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Department of Internal Medicine, Institute of Medicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden
Wallenberg Centre of Molecular and Translational Medicine, Sahlgrenska University Hospital, Gothenburg, Sweden
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use per 10,000 persons, sex- and age-standardized. Country Country code Thyroid medication Antithyroid medication, users Antithyroid medication, DDD Thyroid hormone therapy, users Thyroid hormone therapy, DDD Belgium
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, and outcomes were analysed. GD is defined as (i) elevated free thyroxine (fT4) (normal range (NR): 10–25 pmol/L), (ii) completely suppressed thyroid-stimulating hormone (TSH) (NR: 0.5–4.5 mU/L), and (iii) elevated thyrotrophin receptor antibodies
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School of Clinical Medicine, Fujian Medical University, Fuzhou, Fujian, China
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Quanzhou Medical College, Quanzhou, Fujian, China
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upon thyroid cells, triggering subsequent cell death ( 3 ). Consequently, there is a reduction in thyroid hormone synthesis and secretion. Some researchers posit that the response of GD patients to RAI therapy correlates with the sensitivity of thyroid
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Introduction Programmed cell death protein-1 (PD-1) blockade therapies are widely used for the treatment of hepatocellular carcinoma (HCC) ( 1 ). In addition to their antitumor effects, anti-PD-1 antibodies have been reported to cause immune
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. TC among male patients tends to be more aggressive at the time of diagnosis and may be associated with a poor prognosis ( 1 , 2 ). This implies a higher TC risk stratification in men. Radioactive iodine therapy (RAI or 131 I therapy) is the main
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hypothyroidism (HT) within 6 months after RAI. Given that patients with post-RAI HT may require lifelong thyroid hormone replacement therapy, it is essential to identify the GD patients with a high risk of early HT before RAI. The pathophysiological mechanisms