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[ 3 ]. In Europe women are 1.7- to 6.8-fold more frequently affected by hypothyroidism than men [ 1 , 2 ]. The liver is an important site of TH metabolism and, therefore, thyroid dysfunction is associated with many hepatic alterations, such as a
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dissect mechanisms of TH action. In this study, we aimed to investigate whether age may result in alterations of proposed TH transporters in liver as a classical TH target organ. To this aim, young (4 months) versus aged (20 months) C57BL/6NTac male mice
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activities in cell cycle, DNA repair, and apoptosis [ 11 ]. Our knowledge on PTU-induced changes in the status of proteins associated with DNA methylation and genome stabilization in rat liver during development is very poor. This has prompted us to
Amsterdam Gastroenterology Endocrinology Metabolism, Amsterdam, the Netherlands
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Amsterdam Gastroenterology Endocrinology Metabolism, Amsterdam, the Netherlands
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Department of Laboratory Medicine, Endocrine Laboratory, Amsterdam UMC, University of Amsterdam, Amsterdam, the Netherlands
Amsterdam Reproduction & Development Research Institute, Amsterdam, the Netherlands
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Introduction Deiodinases The thyroid produces the thyroid hormone, mainly thyroxine (T4) and to a lesser extent tri-iodothyronine (T3). Within the liver, thyroid hormones are transported across the cell membrane by thyroid hormone
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Association (ATA) guidelines, after surgery, serum calcitonin (Ct) and carcino-embryonic antigen (CEA) must be periodically tested in order to assess disease status, particularly when serum Ct is >150 pg/mL ( 2 ). MTC metastasizes most commonly to the liver
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Princess Máxima Center for Pediatric Oncology, Utrecht, The Netherlands
Oncode Institute, Utrecht, The Netherlands
Institute for Genome Stability in Ageing and Disease, CECAD Research Centre, Cologne, Germany
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Oncode Institute, Utrecht, The Netherlands
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/TCR ( 24 ). These results indicated that DNA damage may attenuate thyroid hormone signaling during aging through modulation of deiodinase activity. The hypothyroid state in livers of normal and accelerated aging was associated with decreased activity of
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IFB Adiposity Diseases, Leipzig University Medical Centre, Leipzig, Germany
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IFB Adiposity Diseases, Leipzig University Medical Centre, Leipzig, Germany
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established that TH stimulate both a lipogenesis/lipolysis ‘futile cycle' and that elevated TH concentrations lead to fat loss [ 6 ]. This is in particular regulated by the liver-specific crosstalk of the active TH 3,5,3′-triiodo- L -thyronine (T 3 ) by
Department of Medicine, King Chulalongkorn Memorial Hospital, Bangkok, Thailand
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Department of Preventive and Social Medicine, Faculty of Medicine Siriraj Hospital, Mahidol University, Bangkok, Thailand
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Department of Preventive and Social Medicine, Faculty of Medicine Siriraj Hospital, Mahidol University, Bangkok, Thailand
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Introduction Nonalcoholic fatty liver disease (NAFLD) is a major health problem. It is one of the most common causes of chronic liver disease with a global prevalence of 25% [ 1 ]. The presentation of NAFLD ranges from simple steatosis to
Department of Medicine, Thyroid Outpatient Clinic, Division of Endocrinology, Escola Paulista de Medicina, Universidade Federal de São Paulo, Sao Paulo, Brazil
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Lipid Clinic Heart Institute (InCor), University of Sao Paulo Medical School Hospital, Sao Paulo, Brazil
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School of Medicine, Faculdade Israelita de Ciências da Saúde Albert Einstein, Sao Paulo, Brazil
Center for Clinical and Epidemiological Research, University Hospital, University of São Paulo School of Medicine, Sao Paulo, Brazil
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secondary to a decrease in LDL receptor’s activity and clearance of triglyceride-rich lipoproteins [ 7 - 9 ]. Excessive triglyceride accumulation in the liver is manifested through the diagnosis of steatosis, a component of non-alcoholic fatty liver
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Background: The levothyroxine absorption test for evaluation of pseudomalabsorption in patients with primary hypothyroid is not standardised. An individual in whom a workup for malabsorption is warranted remains undefined. Methods: Twenty-five euthyroid, 25 newly diagnosed hypothyroid, 25 treated hypothyroid with normalised TSH, and 25 hypothyroid subjects with elevated TSH despite adequate dose of levothyroxine for more than 6 months, and 10 euthyroid subjects with true malabsorption were administered levothyroxine (10 μg/kg or maximum 600 μg) to study its absorption profile by measuring free T4 level at hourly intervals for 5 h. Results : Free T4 peaked at 3 h with marginal insignificant decline at 4 h in all groups. The increments of free T4 (between baseline and 3 h) of the four groups (except malabsorption) were not statistically different. The mean increment of free T4 in true malabsorption was 0.39 ng/dL (95% CI: 0.29–0.52) and it was 0.78 ng/dL (95% CI: 0.73–0.85) (10.4 pmol/L) for other groups combined together. The cut off of free T4 increment at 3 h from baseline above 0.40 ng/dL had a sensitivity of 97% and specificity of 80% (AUC 0.904, p < 0.001) to exclude true malabsorption. Conclusion: Subjects with elevated TSH on adequate dose of LT4 can be reliably diagnosed to be non-adherent to treatment with levothyroxine absorption test. The incremental value above 0.40 ng/dL (5.14 pmol/L) at 3 h may be useful to identify individuals where workup of malabsorption is unwarranted.
