No coração, doses elevadas de hormônio tireoideano (T3) por tempo prolongado promove hipertrofia cardíaca. Os mecanismos envolvidos neste processo necessitam de maior esclarecimento. Analisou-se dados de um ensaio de microarray de tecido cardíaco de ratos submetidos a hipertireoidismo experimental. O algoritmo MAS5 foi mais eficiente para processamento dos dados. Identificou-se os filamentos grossos, banda M e discos intercalares como hotspots de atuação do T3. A T-Caderina apresentou aumento transitório nos níveis de mRNA e proteicos sob efeito do T3. Estudo de imunofluorescência evidenciou marcação para T-Caderina próxima à membrana plasmática de cardiomiócitos. Com 24 horas de tratamento com T3, observamos aumento global e difuso de marcação para T-Caderina. Obeservou-se marcação nuclear para T-Caderina. Portanto, é possível que a T-caderina possa estar envolvida no processo de hipertrofia cardíaca. Todavia, para verificar essa possibilidade, são necessários mais estudos. / Cardiac hypertrophy is observed in response to long-term hyperthyroidism. The molecular basis of cardiac hypertrophy induced by hyperthyroidism remains to be determined. Using microarray approach, the gene expression profile of heart tissue from rats submitted to hyperthyroidism were analysed. MAS5 were found to be the best for our low-level analysis. Sarcomeric hotspots such as thick-filaments, M-band and intercalated disks under thyroid hormone (T3) treatment were identified. T3 induced transient mRNA and protein levels of T-Cadherin, a interecalated disks member. T-Cadherin were observed next to plasmatic membrane on immunofluorescence analysis. On 24 hours group, diffuse cytoplasmic T-Cadherin staining were evident. Another interesting aspect was T-Cadherin nuclear staining in all groups. Moreover, T-Cadherin possibly play role in T3-induced cardiac hypertrophy. However further studies are needed to verify this possibility.

Hypertyreos kännetecknas av en förhöjd funktion i tyreoidea vilket bidrar till en ökad frisättning av tyreoideahormonerna thyroxin och trijodtyronin som påverkar ämnesomsättningen i kroppen. Graves’ sjukdom, toxisk nodös struma och autonomt adenom är olika varianter av hypertyreos som behandlas med radiojodbehandling respektive tyreostatikabehandling eller med kirurgi. Vid radiojodbehandling är det viktigt att massan av tyreoidea bestäms korrekt för att undvika över- respektive underbehandling. För närvarande är planar scintigrafi (PS) den mätmetod som används på isotopterapiavdelningen vid Skånes universitetssjukhus i Lund. Vid PS erhålls tvådimensionella bilder som används för uppskattning av massan. De tvådimensionella bilderna ger ingen djupinformation vilket kan leda till att tjockleken av tyreoidea feluppskattas. Tjockleken behövs för att erhålla en korrekt tyreoideamassa, och för att minimera denna feluppskattning kan en SPECT/CT-mätning (Single-Photon Emission Computed Tomography/Computed Tomography) utföras där tredimensionella bilder erhålls. Syftet med denna studie är att utvärdera hur uppskattningen av tyreoideamassan skiljer sig mellan de två mätmetoderna samt hur radiojodbehandlingen kan påverkas av detta. Studien omfattade fantommätningar samt bildtagning på 19 deltagare med hypertyreos. Resultaten visade att massuppskattningen av tyreoidea skiljer sig mellan PS- och SPECT/CT-mätningar. SPECT/CT-mätningarna förväntades ge en bättre massuppskattning vilket ger att skillnaderna mellan mätmetoderna påvisade över respektive underbehandlingar av tyreoidea jämfört med standarddoserna somanvänds på kliniken. / Hyperthyroidism is characterized by an overactive thyroid which contributes to anexcessive production of the thyroid hormones triiodothyronine and thyroxine which are responsible for regulation of the metabolism. Graves’ disease, multinodular goiter and toxic adenoma are different disorders that are treated with antithyroid medications, radioiodine treatment or surgery. For radioiodine treatment the thyroid mass is an important parameter that needs to be determined correctly to avoid an incorrect treatment. The thyroid mass is currently estimated by planar scintigraphy (PS) at the department of radionuclide therapy at Skånes University Hospital in Lund. PS provides two-dimensional imaging of the thyroid, which is used to determine the mass of the thyroid. Two-dimensional images do not give any information about the depth information which can cause errors in estimation of the thyroid thickness. The thickness of the thyroid is essential to obtain a correct thyroid mass, to minimize the errors a three-dimensional imaging can be made with a SPECT/CT (Single-Photon Emission Computed Tomography-/Computed Tomography). The aim of this study is to evaluate how the estimation of the thyroid mass differs between the two measurement methods and also how that can affect the radioiodine treatment. The study included phantom measurements and 19 participants with hyperthyroidism. The results of this study showed that the estimation of the thyroid mass differ between the PS- and SPECT/CT-measurements. The SPECT/CT-measurements is assumed to give more accurate mass estimations and given this, the differences of estimated mass showed both over- and undertreated thyroid compared with the standard doses that are used in the clinic.

Hyperthyroidism causes secondary osteoporosis through favoring bone resorption over bone formation, leading to bone loss with elevated bone fragility. Osteocytes that reside within lacunae inside the mineralized bone matrix orchestrate the process of bone remodeling and can themselves actively resorb bone upon certain stimuli. Nevertheless, the interaction between thyroid hormones and osteocytes and the impact of hyperthyroidism on osteocyte cell function are still unknown. In a preliminary study, we analyzed bones from male C57BL/6 mice with drug-induced hyperthyroidism, which led to mild osteocytic osteolysis with 1.14-fold larger osteocyte lacunae and by 108.33% higher tartrate-resistant acid phosphatase (TRAP) activity in osteocytes of hyperthyroid mice compared to euthyroid mice. To test whether hyperthyroidism-induced bone changes are reversible, we rendered male mice hyperthyroid by adding levothyroxine into their drinking water for 4 weeks, followed by a weaning period of 4 weeks with access to normal drinking water. Hyperthyroid mice displayed cortical and trabecular bone loss due to high bone turnover, which recovered with weaning. Although canalicular number and osteocyte lacunar area were similar in euthyroid, hyperthyroid and weaned mice, the number of terminal deoxynucleotidyl transferase–mediated deoxyuridine triphosphate nick end labeling (TUNEL)-positive osteocytes was 100% lower in the weaning group compared to euthyroid mice and the osteocytic TRAP activity was eightfold higher in hyperthyroid animals. The latter, along with a 3.75% lower average mineralization around the osteocyte lacunae in trabecular bone, suggests osteocytic osteolysis activity that, however, did not result in significantly enlarged osteocyte lacunae. In conclusion, we show a recovery of bone microarchitecture and turnover after reversal of hyperthyroidism to a euthyroid state. In contrast, osteocytic osteolysis was initiated in hyperthyroidism, but its effects were not reversed after 4 weeks of weaning. Due to the vast number of osteocytes in bone, we speculate that even minor individual cell functions might contribute to altered bone quality and mineral homeostasis in the setting of hyperthyroidism-induced bone disease. © 2022 The Authors. Journal of Bone and Mineral Research published by Wiley Periodicals LLC on behalf of American Society for Bone and Mineral Research (ASBMR).

L’hyperthyroïdie représente la maladie endocrinienne la plus commune chez les chats gériatriques. Ses répercussions systémiques sont similaires chez l’espèce féline et l’humain. L’hypertension pulmonaire se développe chez plus du deux tiers des humains hyperthyroïdiens. L’objectif de cette étude est d’évaluer si l’hyperthyroïdie féline affecte les paramètres hémodynamiques pulmonaires mesurés à l’échocardiographie (volet rétrospectif) ainsi que leur évolution dans le temps (volet prospectif). L’étude rétrospective a été réalisée à partir des examens échocardiographiques révisés de 26 chats hyperthyroïdiens non traités. Pour l’étude prospective, 7 chats hyperthyroïdiens non traités ont été recrutés et des échocardiographies ont été réalisées au moment du diagnostic, puis un mois et six mois suivant le retour à l’état euthyroïdien. Les groupes hyperthyroïdiens de chacun des volets ont été comparés à un groupe de chats sains (n = 15). Les chats hyperthyroïdiens présentent 1) une hyperdynamie ventriculaire droite, 2) un ratio du temps d’accélération sur le temps d’éjection du flux pulmonaire et une vitesse pulmonaire maximale augmentés et 3) un débit ou une fréquence cardiaque augmentés. L’évolution de ces changements dans le temps n’a montré aucune différence significative. Cette étude montre pour la première fois la présence d’altérations hémodynamiques pulmonaires à l’échocardiographie chez les chats hyperthyroïdiens. Les changements observés sont en partie différents de ceux décrits chez les humains hyperthyroïdiens, suggérant des mécanismes d’adaptation particuliers à l’espèce féline. Une importante variation à même la population féline dans la réponse métabolique aux hormones thyroïdiennes est soupçonnée. Des études supplémentaires sont nécessaires pour corréler les changements échocardiographiques observés au développement d’hypertension pulmonaire chez les chats hyperthyroïdiens. / Hyperthyroidism represents the most common endocrine disease in cats >10-years-old. Several of its multisystemic repercussions are similar between feline species and humans, including an increased basal metabolic rate and an activation of the sympathetic nervous system. Pulmonary hypertension has been reported in more than two third of humans with hyperthyroidism. This study aims to determine whether feline hyperthyroidism affects pulmonary arterial hemodynamics (retrospective study) and their progression in time (prospective study) with echocardiography. A bi-center retrospective study was realized from reviewed echocardiographic examinations of 26 untreated hyperthyroid cats. For the prospective study, 7 untreated hyperthyroid cats were recruited, and echocardiographic examinations were performed initially, followed by one and six months after treatment of hyperthyroidism. Hyperthyroid groups of each study were compared to a group of healthy cats (n = 15). Hyperthyroid cats presented 1) an hyperdynamic right ventricle, 2) elevated acceleration to ejection time ratio of the pulmonary flow and maximal pulmonary velocity and 3) a higher cardiac output or heart rate than healthy cats. The magnitude of these changes did not vary significantly over time. This study shows for the first time the presence of pulmonary hemodynamic alterations in hyperthyroid cats using echocardiography. These changes are partially different from those described in hyperthyroid humans, suggesting adaptation mechanisms specific to the feline species. Significant variation within the feline population in the metabolic response to thyroid hormones is suspected. Further studies are needed to correlate echocardiographic changes with the development of pulmonary hypertension in hyperthyroid cats.

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