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European Thyroid Journal    Follow    
  Full-text available via subscription Subscription journal
     ISSN (Print) 2235-0640 - ISSN (Online) 2235-0802
     Published by Karger Homepage  [103 journals]
  • Persistent Cellular Metabolic Changes after Hemithyroidectomy for Benign
           Euthyroid Goiter
    • Abstract: Background: The significance of perturbations of thyroid-stimulating hormone (TSH) and thyroid hormones within the laboratory reference ranges after hemithyroidectomy is unknown. Our aim was to examine changes in TSH and thyroid hormones after hemithyroidectomy for benign euthyroid goiter, focusing on tissue response by examining the mitochondrial membrane potential (MMP) of peripheral blood mononuclear cells (PBMCs) and basal oxygen consumption (V˙O2). Materials and Methods: In a prospective study on 28 patients and controls, we examined serum TSH and thyroid hormones before hemithyroidectomy and 1, 3, 6 and 12 months after hemithyroidectomy for benign euthyroid goiter. In the hemithyroidectomy group, flow cytometry was used to measure the MMP of tetramethylrhodamine methyl ester (TMRM)- and MitoTracker Green (MTG)-stained PBMCs, and V˙O2 was measured by an Oxycon Pro apparatus. Results: One year after hemithyroidectomy, TSH had increased from a median of 0.97 mIU/l (interquartile range, IQR: 0.69-1.50 mIU/l) to 2.10 mIU/l (IQR: 1.90-3.00 mIU/l; p < 0.001); free thyroxine (fT4) had decreased from a median of 16.0 pmol/l (IQR: 14.9-17.0 pmol/l) to 14.8 pmol/l (IQR: 14.1-16.4 pmol/l; p = 0.009), whereas total triiodothyronine variations did not differ from those in controls. Concomitantly, the MMP of TMRM- and MTG-stained PBMCs was increased by 58% (p < 0.001) and 22% (p = 0.008), respectively. V˙O2 was increased by 14% (p = 0.01). Conclusion: Hemithyroidectomy for benign euthyroid goiter induced persistently increased TSH and decreased fT4, sustained mitochondrial hyperpolarization and increased V˙O2. Our results demonstrate a decrease after hemithyroidectomy of the metabolic state to which the individual is adapted, with persistent cellular metabolic changes in a hemithyroidectomized patient group which is normally considered clinically and biochemically euthyroid. © 2014 European Thyroid Association Published by S. Karger AG, Basel

       
  • Historical Note: Many Steps Led to the ‘Discovery' of
           Thyroid-Stimulating Hormone
    • Abstract: Finding thyroid-stimulating hormone was a process rather than a circumscribed event, and many talented persons participated over many years. Key early participants were Bennet M. Allen and Philip E. Smith who had the misfortune just prior to World War I of independently and simultaneously starting very similar experiments with tadpoles. This led to a series of back and forth publications attempting to establish priority for finding evidence of a thyrotropic factor in the anterior pituitary. Decades of work by others would be required before sophisticated biochemical techniques would bring us to our modern understanding. © 2014 European Thyroid Association Published by S. Karger AG, Basel
      Eur Thyroid J
       
  • Basal Serum Thyroglobulin Measured by a Second-Generation Assay Is
           Equivalent to Stimulated Thyroglobulin in Identifying Metastases in
           Patients with Differentiated Thyroid Cancer with Low or Intermediate Risk
           of Recurrence
    • Abstract: Background: Guidelines for the follow-up of differentiated thyroid cancer (DTC) recommend the measurement of TSH-stimulated thyroglobulin (s-Tg) instead of basal Tg on T4 therapy (b-Tg). However, these guidelines were established using first-generation Tg assays with a functional sensitivity (FS) of 0.5-1.0 ng/ml. Current more sensitive second-generation Tg assays (Tg2G; FS 0.05-0.10 ng/ml) have shown that low-risk DTC patients with undetectable b-Tg rarely have recurrences. Objectives: This study was undertaken to compare b-Tg using a chemiluminescent Tg2G assay (Tg2GICMA; FS 0.1 ng/ml) with s-Tg in DTC patients with an intermediate risk of recurrence. Methods: We evaluated 168 DTC patients with a low (n = 101) and intermediate (n = 67) risk of recurrence treated by total thyroidectomy (147 also treated with radioiodine), with a mean follow-up of 5 years. Results: b-Tg was undetectable with the Tg2GICMA in 142 of 168 patients. s-Tg was 2 ng/ml, 1 had cervical metastases seen after radioiodine. Furthermore, 26 of 168 patients presented detectable b-Tg with the Tg2GICMA; 17 of these 26 patients also presented s-Tg >2 ng/ml. In 10 of these 17 patients, metastases were detected. Cervical US or b-Tg were positive in 14 of 15 patients with recurrent disease. Globally, the sensitivity and negative predictive value of the Tg2GICMA plus US were 93 and 99%, respectively. Conclusion: b-Tg measured with a Tg2GICMA and cervical US, used together, are equivalent to s-Tg in identifying metastases in patients with DTC with a low or intermediate risk of recurrence. © 2014 European Thyroid Association Published by S. Karger AG, Basel

       
  • The European Thyroid Journal in Its Third Year of Publication: A Thriving
           Enterprise
    • Abstract:

       
  • Clinical Consequences of Mutations in Thyroid Hormone Receptor-α1
    • Abstract: Thyroid hormone (TH) exerts its biological activity via the TH receptors TRα1 and TRβ1/2, which are encoded by the THRA and THRB genes. The first patients with mutations in THRB were identified decades ago. These patients had a clinical syndrome of resistance to TH associated with high serum TH and nonsuppressed thyroid-stimulating hormone levels. Until recently, no patients with mutations in THRA had been identified. In an attempt to predict the clinical phenotype of such patients, different TRα1 mutant mouse models have been generated. These mice have a variable phenotype depending on the location and severity of the mutation. Recently, the first humans with mutations in THRA were identified. Their phenotype consists of relatively low serum T4 and high serum T3 levels (and thus an elevated T3/T4 ratio), growth retardation, delayed mental and bone development, and constipation. While, in retrospect, certain features present in humans can also be found in mouse models, the first humans carrying a defect in TRα1 were not suspected of having a THRA gene mutation initially. The current review focuses on the clinical consequences of TRα1 mutations. © 2014 European Thyroid Association Published by S. Karger AG, Basel

       
  • Occurrence of De Quervain's Thyroiditis after Resolution of
           Hypercortisolism following Pasireotide Treatment for Cushing's Disease and
           Surgery for an Adrenocortical Adenoma: Report of Two Cases
    • Abstract: Objective: An increased prevalence of thyroid autoimmunity has been observed after successful treatment of Cushing's syndrome. On the other hand, De Quervain's thyroiditis (DQT), in which autoimmunity is not a pathogenetic contributor, has not been reported during recovery from Cushing's syndrome. We describe 2 female patients with DQT coinciding with the resolution of hypercortisolism after treatment of Cushing's syndrome/disease. Methods: The first patient had been diagnosed with Cushing's disease due to a corticotroph pituitary microadenoma, declined neurosurgery, and was receiving pharmacological treatment with pasireotide. Her hypercortisolism was optimally controlled with a minimum dose. The second patient had undergone unilateral adrenalectomy due to a cortisol-secreting adenoma and was on tapering doses of hydrocortisone due to a suppressed corticotroph axis. Both patients presented with clinical, functional, and imaging features of DQT at a time when their endogenous glucocorticoid levels were very low. Results: Oral glucocorticoid treatment was administered in both cases, resulting in prompt recovery. Conclusions: The incidence of DQT following the resolution of hypercortisolism, either medical or surgical, has not been previously described. The exact pathogenetic mechanism can only be speculated on. Perhaps the relative or absolute glucocorticoid deficiency after effective treatment of hypercortisolism alters immunologic responses and renders patients more vulnerable to thyrolytic processes. © 2014 European Thyroid Association Published by S. Karger AG, Basel

       
  • Classification and Proposed Nomenclature for Inherited Defects of Thyroid
           Hormone Action, Cell Transport, and Metabolism
    • Abstract:
      Eur Thyroid J
       
  • Iodine Status in Europe in 2014
    • Abstract:
      Eur Thyroid J
       
  • Major Haemorrhage during Vitamin K Antagonist Treatment: The Influence of
           Thyroid Hormone Levels
    • Abstract: Background: Annually, approximately 1-3% of patients treated with vitamin K antagonists (VKA) suffer from major haemorrhage. Since high levels of free thyroxine (fT4) are associated with increased thrombosis risk, the aim was to assess whether low levels of fT4 contribute to major haemorrhage in patients under VKA treatment. Methods: The FACTORS (Factors in Oral Anticoagulant Safety) study is a case-control study on patients receiving VKA treatment, including 110 cases with major haemorrhage. Controls were 220 matched participants treated with VKA without major haemorrhage. Odds ratios (OR) and 95% confidence intervals (95% CI) for the association of fT4 levels with major haemorrhage were calculated for different fT4 cutoffs by conditional logistic regression. Results: In patients with an fT4 level below 13 pmol/l, the risk of major haemorrhage was 5-fold increased (OR = 5.1; 95% CI: 0.9-28.6) compared with patients with an fT4 level above 13 pmol/l. At a cutoff of 14 pmol/l, the risk was 3-fold increased (OR = 2.9; 95% CI: 1.0-8.5). High levels of fT4 did not affect bleeding risk. No clear effect of thyroid-stimulating hormone and thyroid peroxidase antibodies was seen on the risk of major haemorrhage. Conclusions: These results indicate that fT4 levels below 14 pmol/l play a role in the aetiology of major haemorrhage in VKA users. © 2014 European Thyroid Association Published by S. Karger AG, Basel
      Eur Thyroid J
       
  • A Rare Case of Dyshormonogenetic Fetal Goiter Responding to Intra-Amniotic
           Thyroxine Injections
    • Abstract: Fetal goiter was detected by routine ultrasound in early pregnancy, gestational week (GW) 18, in a 28-year-old woman with no thyroid history, normal thyroid hormone levels and no TSH receptor or thyroid peroxidase antibodies. An umbilical cord blood sample was drawn in GW 23. The analysis indicated fetal hypothyroidism with TSH >100 mU/l (reference value 6.8 ± 2.9, mean ± SD), fT4 3.8 pmol/l (reference value 16.5 ± 5.3, mean ± SD). Intra-amniotic injections of thyroxine were given in conjunction with ultrasound every 7-10 days, in total nine times during GW 24-33. A dose of 10 µg thyroxine/kg of estimated fetal weight per day was administered on six occasions, and 5 µg/kg/day the last three times. Upon injections of thyroxine further growth of the goiter was reduced. Elevated amniotic TSH levels fell from 13 to 2.5 mU/l (reference range 0.04-0.51). Throughout pregnancy, fetal heart rate and skeletal maturation were within normal limits. In week 34, chorioamnionitis was suspected and the child was delivered by cesarean section. Cord blood revealed TSH 596 mU/l (reference value 8.0 ± 5.12, mean ± SD), fT4 4.4 pmol/l (reference value 19.3 ± 4.3, mean ± SD) and total T3 1.18 nmol/l (reference value 0.5 ± 0.3, mean ± SD); the newborn was put on thyroxine supplementation. Psychomotor development of the child, now 3 years old, has been uneventful. The reported experience of treating dyshormonogenetic fetal goiter is limited but growing, creating a need for guidelines on administration of intra-amniotic thyroxine and monitoring treatment. © 2014 European Thyroid Association Published by S. Karger AG, Basel
      Eur Thyroid J
       
 
 
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