Excessive Production Of Thyroid Hormones Research Articles

Exploring the Triad of Thyroid Dysfunction, Chronic Diarrhea and Anemia

Hyperthyroidism, a disorder characterized by excessive thyroid hormone production, typically presents with many symptoms including weight loss, tremors, and heat intolerance. However, in rare instances, it can manifest solely as chronic diarrhea, posing a diagnostic challenge. This case study aims to highlight an unusual presentation of hyperthyroidism and underscore the importance of considering thyroid disease in the differential diagnosis of chronic gastrointestinal symptoms. We present the case of a fifty-year-old woman who, six months prior to her ER visit, had been experiencing severe weight loss and diarrhea along with anemia. Despite her lack of typical hyperthyroidism symptoms, a thorough investigation revealed that hyperthyroidism was the underlying cause of her gastrointestinal issues. This case illustrates that hyperthyroidism can present atypically, solely as chronic diarrhea. The patient's anemia was linked to iron deficiency, worsened by chronic gastrointestinal loss and the hyper metabolic state induced by hyperthyroidism. Treatment of the hyperthyroidism led to significant improvement in her gastrointestinal symptoms and correction of the anemia. This case underscores the critical need to include thyroid disease in the differential diagnosis for patients with chronic diarrhea and weight loss, even in the absence of typical hyperthyroid symptoms. Early recognition and appropriate management of hyperthyroidism can significantly improve patient outcomes by alleviating gastrointestinal manifestations and correcting associated anemia. Clinicians should maintain a high index of suspicion for thyroid dysfunction in patients presenting with unexplained chronic diarrhea and weight loss to ensure timely and accurate diagnosis and treatment.

Patient-centered Management of Hyperthyroidism

ABSTRACT Hyperthyroidism, characterized by excessive thyroid hormone production, demands a patient-centered approach for optimal management. Treatment aims to alleviate symptoms, normalize hormone levels, and prevent complications. It encompasses education and communication of the patients, management of the symptoms of hyperthyroidism, treatment options available, shared decision-making, monitoring, and follow-up, including keeping an eye on adversity, providing psychological support, and nutritional and lifestyle modification. A patient-centered approach to hyperthyroidism management emphasizes shared decision-making, individualized care, and ongoing support to optimize treatment outcomes and enhance patient well-being.

MANAGEMENT OF AORTIC OCCLUSION SYNDROME ASSOCIATED TO GRAVES DISEASE

Background :Leriche syndrome or aortoiliac occlusion disease is caused by atherosclerosis and manifests as a constellation of symptoms that include claudication, erectile dysfunction, and the notable absence of femoral pulses. Graves disease (also known as Basedow) is an autoimmune disorder characterized by excessive thyroid hormone production, leading to hyperthyroidism. It often results in symptoms such as weight loss, rapid heart rate, tremors, and an enlarged thyroid gland (goiter).We present a case study detailing a singular occurrence of Leriche syndrome in a patient concurrently diagnosed with Graves disease, emphasizing the intricate nuances encountered in anesthesia management across both surgical procedures. Case presentation: A 53-year-old North African male with history of smoking presented to the ED with critical limb ischemia. The patient exhibited normal vital signs, except for a sinus tachycardia of 140 beats per minute. Initial blood laboratory tests yielded no abnormalities. However, abdominopelvic computed tomography angiography (CTA) revealed an abdominal aortic aneurysm measuring 46mm in diameter and extending over 107mm. This aneurysm was found to be partially thrombosed above the renal arteries, with complete thrombosis noted at the infrarenal level, extending bilaterally to the iliac arteries. The presence of collateral blood vessels supported the diagnosis of Leriche syndrome. Additionally, further investigation into the sinus tachycardia revealed the patients diagnosis of Graves disease, complicating the vascular surgery. After collegial discussion, a two-stage surgical approach was decided upon. Initially, the patient underwent medical treatment using a rapid thyroid hormone blocking protocol to manage the signs of hyperthyroidism. Following achievement of biochemical and clinical euthyroidism, characterized by stable thyroid hormone levels, the first surgery, total thyroidectomy, was performed. Subsequently, a few days later, the patient underwent a bypass surgery. The postoperative course was marked by successful bypass graft surgery, resulting in improved limb function and absence of further complications. The patient was discharged home 10 days after the second surgery. Conclusion : In this case, the challenge lay in managing both conditions while ensuring controlled heart rate and blood pressure to prevent aneurysm rupture, and concurrently administering anticoagulant therapy to prevent thrombus extension. Our findings suggest that in comparable cases, emphasis on thorough physical examination and medical history is crucial, and interdisciplinary collaboration between different specialties enhances patient survival.

Thyroid psychosis: when your hormones take over your mind: a case report

IntroductionHyperthyroidism, characterized by excessive production of thyroid hormones, is a common endocrine disorder that affects various body systems. While most commonly recognized for its classic symptoms such as weight loss, tremors, and palpitations, it is important to acknowledge that hyperthyroidism can also lead to a rare but significant complication: psychosis. Psychosis in the context of hyperthyroidism refers to the presence of delusions, hallucinations, and disordered thinking, which can significantly impact an individual’s mental health and overall well-being.ObjectivesThis case report aims to describe a rare case of hyperthyroidism-related psychosis in a patient including the clinical presentation, diagnosis, and management. Additionally, we aim to increase awareness of and promote further research into this condition.MethodsWe present a comprehensive case report detailing the clinical course of a 29-year-old male patient with no previous medical or psychiatric history, who sought urgent psychiatric evaluation at the Razi Hospital La Manouba’s emergency department due to escalating symptoms of agitation and paranoia persisting for three days. The patient, identified as Mr. S.O., a Tunisian male, presented with severe agitation and paranoia necessitating the use of restraints upon admission to the psychiatric emergency department. The initial physical examination revealed no notable abnormalities, except for the presence of tachycardia, which was subsequently confirmed on an electrocardiogram, arousing suspicion of a primary psychiatric illness.ResultsWhile the standard blood workup yielded unremarkable findings, the endocrine workup revealed decreased levels of thyroid-stimulating hormone (TSH) and elevated free thyroxine (FT4). Further laboratory investigations demonstrated elevated anti-thyroid-stimulating hormone receptor antibodies, leading to the diagnosis of Graves’ disease. Collaborative consultation with an endocrinologist resulted in the initiation of a treatment regimen consisting of methimazole, propranolol, and risperidone. Notably, within three days of the initiated therapy, the patient exhibited significant improvement in terms of reduced agitation, coherent speech, and the development of self-reflection regarding the episode, ultimately leading to his discharge on the seventh day of hospitalization. This case report serves to highlight the complexity of psychiatric presentations associated with underlying endocrine disorders and underscores the importance of interdisciplinary collaboration in achieving optimal patient outcomes.ConclusionsWhile mental health factors play a significant role in the development of psychosis, it is essential to recognize that underlying medical conditions may also contribute to its onset or exacerbation.Disclosure of InterestNone Declared

Cortical Gray Matter Thickness and Volume Changes and Their Association with Memory Functions in Hyperthyroid Patients

Introduction: Hyperthyroidism, characterized by excessive thyroid hormone production, is a common endocrine disorder that affects various physiological processes, including brain function. Recent advancements in neuroimaging techniques have enabled researchers to investigate structural alterations in the brain associated with hyperthyroidism. This study aimed to examine regional cortical thickness and cortical volume differences across the brain between hyperthyroid patients and control subjects. Methods: We examined localized cortical thicknesses and volumes in 34 hyperthyroid patients and 35 control subjects with high-resolution T1-weighted images using FreeSurfer software and assessed group differences with analysis of covariance (covariates: age, sex, education, and total intracranial volume). Spearman and partial correlations were performed between clinical variables and cortical thicknesses/volumes and between neuropsychological scores and cortical thicknesses/volumes, respectively. Results: Hyperthyroid patients exhibited significantly increased cortical thickness in bilateral superior temporal and superior frontal gyri, along with higher cortical volumes in various regions, including the right superior temporal gyrus, right superior parietal gyrus, right rostral and caudal middle frontal gyrus, and left superior frontal gyrus. Notably, thyroid hormones (fT3, fT4) correlated positively with cortical thicknesses and volumes in the superior temporal gyrus and superior frontal gyrus. Additionally, recognition memory scores negatively correlated with the right superior temporal gyrus and right superior frontal gyrus cortical thickness. Conclusion: The observed cortical thickening and increased cortical volume in specific brain areas provide new insights into the pathophysiological mechanism associated with brain impairment in hyperthyroidism.

FRI538 Discovery And Characterization Of Orally Bioavailable Nonpeptide Thyroid Stimulating Hormone Receptor (TSHR) Antagonists For The Treatment Of Graves’ Disease

Abstract Disclosure: M.A. Fowler: Employee; Self; Crinetics Pharmaceuticals. Stock Owner; Self; Crinetics Pharmaceuticals. C. Regan: Employee; Self; Crinetics Pharmaceuticals. Stock Owner; Self; Crinetics Pharmaceuticals. J. Zhao: Employee; Self; Crinetics Pharmaceuticals. Stock Owner; Self; Crinetics Pharmaceuticals. E. Coutinho: Employee; Self; Crinetics Pharmaceuticals. Stock Owner; Self; Crinetics Pharmaceuticals. B. Fleck: Employee; Self; Crinetics Pharmaceuticals. Stock Owner; Self; Crinetics Pharmaceuticals. A.A. Castellanos: Employee; Self; Crinetics Pharmaceuticals. E. Muller: Employee; Self; Crinetics Pharmaceuticals. M. Johns: Employee; Self; Crinetics Pharmaceuticals. Stock Owner; Self; Crinetics Pharmaceuticals. Y. Tang: Employee; Self; Crinetics Pharmaceuticals. Stock Owner; Self; Crinetics Pharmaceuticals. E. Sturchler: Employee; Self; Crinetics Pharmaceuticals. Stock Owner; Self; Crinetics Pharmaceuticals. M. Chen: Employee; Self; Crinetics Pharmaceuticals. Stock Owner; Self; Crinetics Pharmaceuticals. K. Retting: Employee; Self; Crinetics Pharmaceuticals. Stock Owner; Self; Crinetics Pharmaceuticals. D. Dalvie: Employee; Self; Crinetics Pharmaceuticals. Stock Owner; Self; Crinetics Pharmaceuticals. S.F. Betz: Employee; Self; Crinetics Pharmaceuticals. Stock Owner; Self; Crinetics Pharmaceuticals. S. Markison: Employee; Self; Crinetics Pharmaceuticals. Stock Owner; Self; Crinetics Pharmaceuticals. Graves’ disease is an autoimmune condition that affects approximately 1 in 100 people in the United States and 2-3% of the population worldwide. It is characterized by the production of autoantibodies against TSHR, and the pathology of Graves’ disease is driven by TSHR stimulatory antibodies (TSAb) that result in heightened activation of TSHR. This overstimulation results in hyperthyroidism due to excessive production of thyroid hormones. Approximately 30% of Graves’ disease patients also develop thyroid eye disease (TED or Graves’ orbitopathy) due to overactivation of TSHR in orbital fibroblasts leading to excessive production of hyaluronic acid, adipogenesis, cytokine production, and fibrosis. This can cause a myriad of debilitating symptoms including pain, swelling, blurry vision, diplopia, and proptosis. Several treatments for Graves’ hyperthyroidism are available including anti-thyroid drugs, radioactive iodine (RAI), and surgery. RAI and surgery are definitive treatments for Graves’ hyperthyroidism, but often result in hypothyroidism. In addition, none of the current treatments for Graves’ hyperthyroidism are effective in treating TED and, in some cases, such as with RAI, worsen the condition. Blocking TSHR activation directly via a TSHR antagonist may provide an important new therapeutic mechanism to treat patients with Graves’ disease that would effectively treat both the hyperthyroidism and TED. We have identified several potent and orally bioavailable nonpeptide allosteric antagonists with acceptable drug-like properties. One analog, TSHRant-1, demonstrated potent negative allosteric modulator activity at both the human and rat TSHR. To evaluate the in vivo pharmacodynamics of TSHant-1, we developed a rat model of hyperthyroidism. In this model, subcutaneous administration of the TSAb, M22, to female rats resulted in a robust and long-lasting rise in levels of the thyroid hormone thyroxin (T4). Oral administration of TSHRant-1 dose-dependently suppressed M22-stimulated T4, providing evidence that a nonpeptide allosteric antagonist of TSHR may serve as an effective treatment for Graves’ disease and associated orbitopathy (TED). Presentation: Friday, June 16, 2023

An Explainable Artificial Intelligence Framework for the Predictive Analysis of Hypo and Hyper Thyroidism Using Machine Learning Algorithms

The thyroid gland is the crucial organ in the human body, secreting two hormones that help to regulate the human body’s metabolism. Thyroid disease is a severe medical complaint that could be developed by high Thyroid Stimulating Hormone (TSH) levels or an infection in the thyroid tissues. Hypothyroidism and hyperthyroidism are two critical conditions caused by insufficient thyroid hormone production and excessive thyroid hormone production, respectively. Machine learning models can be used to precisely process the data generated from different medical sectors and to build a model to predict several diseases. In this paper, we use different machine-learning algorithms to predict hypothyroidism and hyperthyroidism. Moreover, we identified the most significant features, which can be used to detect thyroid diseases more precisely. After completing the pre-processing and feature selection steps, we applied our modified and original data to several classification models to predict thyroidism. We found Random Forest (RF) is giving the maximum evaluation score in all sectors in our dataset, and Naive Bayes is performing very poorly. Moreover selecting the feature by using the feature importance method RF provides the best accuracy of 91.42%, precision of 92%, recall of 92% and F1-score of 92%. Further, by analyzing the characteristics and behavior of the dataset, we identified the most important features (TSH, T3, TT4, and FTI) of the dataset. In terms of accuracy and other performance evaluation criteria, this study could advocate the use of effective classifiers and features backed by machine learning algorithms to detect and diagnose thyroid disease. Finally, we did some explainability analysis of our best classifier to understand the internal black-box of our machine learning model and datasets. This study could further pave the way for the researcher as well as healthcare professionals to analyze thyroid disease in real time applications.

Grave’s disease in a case of Goldenhar syndrome

Goldenhar syndrome (GS) is a malformation complex that involves structures arising from the first and second branchial arches. Graves’ disease is an autoimmune disorder resulting in the excessive production of thyroid hormones and is the most common cause of hyperthyroidism in children. We are reporting this case since the clinical association of Graves’ disease in GS has never been reported before and is a rare association of the syndrome. An 11-year-old developmentally normal child presented to us with swelling in front of her neck for the past 6 months associated with loss of weight, increased appetite, increased frequency of defecation, and palpitations. On examination, there was diffuse swelling in the thyroid region that moved with deglutition and did not move with protrusion of the tongue. The child also had an asymmetrical face with bilateral conjunctival dermoid and bilateral preauricular skin tag and pretragal sinus tract on the left side. Hence, a provisional diagnosis of goitre with features of hyperthyroidism in a child with first and second branchial arch syndrome was considered. Technetium 99 scan confirmed diagnosis of Graves’ disease. The child was started on carbimazole and propranolol and gradual improvement in symptoms noted. Propranolol was given for 3 months until symptoms such as palpitations and anxiety subsided and then stopped. Carbimazole was continued.

Antigen-specific immunotherapy to restore antigen-specific tolerance in Type 1 diabetes and Graves' disease.

Type 1 diabetes and Graves' disease are chronic autoimmune conditions, characterized by a dysregulated immune response. In Type 1 diabetes, there is beta cell destruction and subsequent insulin deficiency whereas in Graves' disease, there is unregulated excessive thyroid hormone production. Both diseases result in significant psychosocial, physiological, and emotional burden. There are associated risks of diabetic ketoacidosis and hypoglycaemia in Type 1 diabetes and risks of thyrotoxicosis and orbitopathy in Graves' disease. Advances in the understanding of the immunopathogenesis and response to immunotherapy in Type 1 diabetes and Graves' disease have facilitated the introduction of targeted therapies to induce self-tolerance, and subsequently, the potential to induce long-term remission if effective. We explore current research surrounding the use of antigen-specific immunotherapies, with a focus on human studies, in Type 1 diabetes and Graves' disease including protein-based, peptide-based, dendritic-cell-based, and nanoparticle-based immunotherapies, including discussion of factors to be considered when translating immunotherapies to clinical practice.

Regulation of the cellular redox state and the expression of DNA methyltransferase-1 in peripheral blood mononuclear cells from patients with Graves’ disease

BackgroundGraves’ disease is an autoimmune disorder characterised by excessive production of thyroid hormones, which induces increased cellular metabolism in most tissues and increased production of reactive oxygen species (ROS). The aim of this work was to analyse the effect of ROS on cell viability and the expression of catalase (CAT), glutathione peroxidase-1 (GPx-1), superoxide dismutase (SOD-1) and DNA methyltransferase-1 (DNMT-1) in peripheral blood mononuclear cells (PBMC) from patients with newly diagnosed Graves’ disease or treated with methimazole. Patients and methodsFor this study, women patients with newly diagnosed Graves’ disease (n=18), treated with methimazole (n=6) and healthy subjects (n=15) were recruited. ROS were evaluated by flow cytometry, and the viability/apoptosis of PBMC was analysed by flow cytometry and fluorescence microscopy. Genomic expression of CAT, GPx-1, SOD-1 and DNMT-1 was quantified by real-time PCR. ResultsWe found high levels of ROS and increased expression of CAT, GPx-1, SOD-1 and DNMT-1 in PBMC from patients with newly diagnosed Graves’ disease. Methimazole treatment reversed these parameters. Cell viability was similar in all study groups. ConclusionsROS induces the expression of CAT, GPx-1, and SOD-1. The activity of these enzymes may contribute to the protection of PBMC from the harmful effect of free radicals on cell viability. Increased expression of DNMT-1 may be associated with aberrant methylation patterns in immunoregulatory genes contributing to autoimmunity in Graves’ disease.

Hyperthyroidism in children and adolescents: Experience in a university hospital in Colombia

ResumenIntroducción. El hipertiroidismo es una condición heterogénea caracterizada por la producción excesiva de hormonas tiroideas. Su aparición en la edad pediátrica representa un reto diagnóstico y terapéutico.Objetivo. Describir las características clínicas y paraclínicas, así como la evolución y las diferencias entre las principales causas etiológicas de los pacientes con hipertiroidismo atendidos por el Servicio de Endocrinología Pediátrica del Hospital Universitario San Vicente Fundación en Medellín, Colombia, entre el 1° de julio de 2015 y el 30 de junio de 2020.Materiales y métodos. Se hizo un estudio observacional transversal con recolección retrospectiva de la información.Resultados. Se incluyeron 54 pacientes con una edad media de 11,9 años, 72,2 % de ellos mujeres. El 11,1 % tenía antecedentes familiares de enfermedad de Graves y 29,6 % de otras enfermedades tiroideas. El bocio fue la manifestación clínica más frecuente (83,3 %). El 92,6 % había recibido terapia con metimazol, el 79,6 % requirió betabloqueador y el 11,2 % necesitó una terapia farmacológica adicional. Se presentaron reacciones adversas a la medicación en el 16,7 %. En el 20,4 % de los pacientes hubo resolución del hipertiroidismo (espontánea: 9,3 %; posterior a la ablación con yodo radiactivo: 9,3 %, y después de la cirugía: 1,9 %).Conclusión. El hipertiroidismo es una enfermedad con manifestaciones clínicas diversas. La causa más frecuente es la enfermedad de Graves, seguida por la hashitoxicosis. En este estudio, la hashitoxicosis fue más frecuente que en estudios previos. La duración y los efectos secundarios del tratamiento farmacológico fueron similares a los reportados previamente, pero es de resaltar la mayor frecuencia de agranulocitosis en nuestra población.

Bir Graves Hastasında Primer Hiperparatiroidiye Bağlı Hiperkalsemi

Hyperthyroidism is a hypermetabolic condition associated with excessive production of thyroid hormones by the thyroid gland. Thyroid hormones play an important role in bone and calcium metabolism. Mild to moderate hypercalcemia due to hyperthyroidism has been reported in approximately one in five patients. Hypercalcemia due to hyperthyroidism is associated with decreased or subnormal parathyroid hormone levels. The co-occurrence of hyperthyroidism and primary hyperparathyroidism is rare. However, in patients with hyperthyroidism, it is necessary to evaluate the parathyroid glands if hypercalcemia persists after an euthyroid state is reached.Here, we report the case of a 30-year-old man with hypercalcemia who had Graves' disease and primary hyperparathyroidism and was successfully treated with combined thyroid and parathyroid surgery.

IMPACT OF GRAVES' DISEASE AND ANTITHYROID DRUG THERAPY ON BONE MINERAL DENSITY - PATHOPHYSIOLOGICAL MECHANISMS AND CLINICAL RELEVANCE.

Graves' disease is an autoimmune disease characterized by excessive thyroid hormone production. One of the consequences of that state can be a decrease in bone mineral density (BMD). Graves' disease is often treated with antithyroid drugs (ATD) as first line therapy, which can lead to disease remission. Moreover, recent data show that improvement in BMD can be expected. However, vitamin D deficiency can coexist along with Graves' disease, which is also involved in the process of bone remodeling. It is still not known whether lower values of vitamin D can contribute to onset of Graves' disease and if its supplementation might be helpful in therapy for hyperthyroidism. In the past couple of decades, osteopenia and osteoporosis have become a major health burden not only in post-menopausal women but also as a result of other diseases, leading to extensive research into various pathophysiological mechanisms responsible for bone remodeling. The Wnt (wingless integrated) signaling pathway is a very important factor in bone homeostasis, especially the canonical pathway. Present data indicate that stimulation of the Wnt pathway leads to bone mass increase and, in contrast, its inhibition leads to bone mass decrease. Hence, inhibitors of the canonical Wnt pathway became the focus of interest, in particular sclerostin and dickkopf 1 (DKK1). Hyperthyroidism and osteopenia/osteoporosis are quite common today and can coexist together or as separate entities. In this article, we aimed to give an overview of possible associations and potential mutual pathophysiological mechanisms.

Regulation of the cellular redox state and the expression of DNA methyltransferase-1 in peripheral blood mononuclear cells from patients with Graves’ disease

BackgroundGraves’ disease is an autoimmune disorder characterised by excessive production of thyroid hormones, which induces increased cellular metabolism in most tissues and increased production of reactive oxygen species (ROS). The aim of this work was to analyse the effect of ROS on cell viability and the expression of catalase (CAT), glutathione peroxidase-1 (GPx-1), superoxide dismutase (SOD-1) and DNA methyltransferase-1 (DNMT-1) in peripheral blood mononuclear cells (PBMC) from patients with newly diagnosed Graves’ disease or treated with methimazole. Patients and methodsFor this study, women patients with newly diagnosed Graves’ disease (n=18), treated with methimazole (n=6) and healthy subjects (n=15) were recruited. ROS were evaluated by flow cytometry, and the viability/apoptosis of PBMC was analysed by flow cytometry and fluorescence microscopy. Genomic expression of CAT, GPx-1, SOD-1 and DNMT-1 was quantified by real-time PCR. ResultsWe found high levels of ROS and increased expression of CAT, GPx-1, SOD-1 and DNMT-1 in PBMC from patients with newly diagnosed Graves’ disease. Methimazole treatment reversed these parameters. Cell viability was similar in all study groups. ConclusionsROS induces the expression of CAT, GPx-1, and SOD-1. The activity of these enzymes may contribute to the protection of PBMC from the harmful effect of free radicals on cell viability. Increased expression of DNMT-1 may be associated with aberrant methylation patterns in immunoregulatory genes contributing to autoimmunity in Graves’ disease.

​Comparative Gross Anatomical and Biometrical Studies on Thyroid Gland of Buffalo, Sheep and Goat

Background: The thyroid gland is vital endocrine gland which secretes three hormones i.e. thyroxin (T4), triiodothyronine (T3) and Calcitonin hormones. The thyroxin (T4) and triiodothyronine (T3) hormones are biologically active and are required for maintenance of normal levels of metabolic activity. The thyroid also produces calcitonin from the parafollicular cells which act directly on osteoclast to decrease the bone resorption which lower the blood calcium level. Deficient or excessive production of thyroid hormones may lead to serious pathological states with outward symptoms. Methods: The gross anatomical and biometrical studies were conducted on thyroid gland of buffalo, sheep and goat (n=12) collected immediately after slaughtering from slaughter house and local meat shop. The weight of thyroid gland was measured by weighing balance, volume by water displacement method, length and width of lateral lobes and isthmus by calibrated scale and inelastic thread and thickness of lateral lobes and isthmus was measured by digital vernier calliper. The data was analysed statistically. Result: The lateral lobes were roughly triangular in buffalo and elongated in sheep and oval in goat. The surfaces were granular and rough in buffalo but smooth in sheep and goat. It extended from thyroid cartilage to 2nd tracheal ring in buffalo, 1st to 6th tracheal ring in sheep and 1st to 7th tracheal ring in goat. The left lobe was larger than the right lobe in all the three species studied. The thyroid gland was biggest in buffalo followed by goat and smallest in sheep. The density of isthmus was more than the lobes in sheep and goat but not in buffalo.

Management of Feline Hyperthyroidism and the Need to Prevent Oxidative Stress: What Can We Learn from Human Research?

Feline hyperthyroidism is a clinical syndrome related to an excessive production of thyroid hormones, and it is considered as a spontaneous animal model for human thyrotoxicosis. Many shared features between the feline and the human disease have been identified so far, including pathogenesis, clinical signs, and treatment options. Although methimazole is considered the first-choice drug in both species, several side effects have been described. Furthermore, methimazole could interfere with the oxidative status, already perturbated by the disease. It has been reported in humans that dietary management, mainly through antioxidant supplementation, could mitigate this oxidative burden. The purpose of the review is to describe current therapeutic options in the course of feline hyperthyroidism and to summarize the state of the art relationship between dietary antioxidants administration and the reduction of methimazole side-effects in humans to support the use of this approach also in cats.

The role of oxidative stress in the pathogenesis of Graves’ orbitopathy

Graves' disease (GD) is a chronic autoimmune condition, in which the anti-thyroid stimulating hormone receptor antibodies (TRAb) activate the thyrotropin receptor (TSHR) located on thyrocytes, leading to excessive thyroid hormone production. TSHR is also expressed in extrathyroidal tissues, in particular, within the orbit. The serum levels of TRAb corelate with severity and activity of thyroid orbitopathy (TO). TO is the most common extrathyroidal manifestation of GD. It is an autoimmune inflammation of orbital tissues, that is, extraocular muscles, orbital adipose tissue or a lacrimal gland. Increased orbital fibroblast and adipocyte proliferation, overproduction of glycosaminoglycans, as well as extraocular muscle oedema result in an increased orbital tissue volume and trigger the onset of TO symptoms. The pathophysiology of TO is complex and has not been fully unexplained to date. Orbital fibroblasts show expression of the TSHR, which is the main target of autoimmunity. It has been hypothesised that T-cell activation induced by orbital receptor stimulation by the target antibody results in orbital tissue infiltration, triggering a cascade of events which leads to the production of cytokines, growth factors and reactive oxygen species (ROS). ROS cause damage to many components of the cell: the cell membrane through the peroxidation of lipids and proteins leading to a loss of their function and enzymatic activity. Oxidative stress leads to activation of the antioxidant system which operates through two mechanisms: enzymatic and non-enzymatic. Assessment of the concentration of oxidative stress markers and the concentration or activity of antioxidative system parameters enables evaluation of oxidative stress severity, which in the future may be utilized for assessment of treatment efficacy and prognosis in patients with active OT.

Rola stresu oksydacyjnego w patogenezie orbitopatii Gravesa

Streszczenie Choroba Gravesa-Basedowa (chGB) jest przewlekłą chorobą autoimmunologiczną, której auto-antygenem jest receptor TSH (TSHR) umiejscowiony na tyreocytach, a jego pobudzenie przez przeciwciała przeciwko TSHR (TRAb) powoduje nadmierne wytwarzanie hormonów tarczycy. TSHR wykazuje także ekspresję w tkankach pozatarczycowych, przede wszystkim w tkankach oczodołu, a stężenie TRAb w surowicy krwi dodatnio koreluje z ciężkością oraz aktywnością orbitopatii tarczycowej (OT). OT jest najczęstszym pozatarczycowym objawem chGB. Jest to choroba autoimmunologiczna, w której dochodzi do zmian zapalnych w obrębie tkanek oczodołów, tj.: mięśniach okoruchowych, tkance tłuszczowej oczodołu czy gruczole łzowym. Wzrost proliferacji fibroblastów oczodołowych i adipocytów oraz nadmierne wytwarzanie glikozaminoglikanów, obrzęk mięśni okoruchowych zwiększają objętość tkanek oczodołu i powodują powstanie objawów klinicznych choroby. Patogeneza OT jest złożona i nadal pozostaje niewyjaśniona. Fibroblasty oczodołów wykazują ekspresję TSHR, który jest głównym miejscem ataku autoimmunologicznego. Zgodnie z szeroko akceptowaną hipotezą po pobudzeniu receptorów dochodzi do aktywacji limfocytów T, które naciekając tkanki oczodołu stymulują je do wytwarzania cytokin, czynników wzrostu oraz wolnych rodników tlenowych (WRT). WRT powodują uszkodzenie wielu składowych komórki m.in. błony komórkowej przez peroksydację lipidów oraz białek doprowadzając do utraty ich funkcji i aktywności enzymatycznej. Stres oksydacyjny uaktywnia układ antyoksydacyjny działający poprzez dwa mechanizmy: enzymatyczny oraz nieenzymatyczny. Ocena stężenia markerów stresu oksydacyjnego oraz stężenia lub aktywności parametrów układu antyoksydacyjnego umożliwia ocenę nasilenia stresu oksydacyjnego, co w przyszłości może być wykorzystywane do oceny skuteczności leczenia i rokowania u chorych z aktywną OT.

Diabetes Mellitus and Thyroid Dysfunction, Including Autoimmune Genesis. Mutual Influence of Pathologies

Thyroid disease, including autoimmune genesis, and diabetes mellitus are the two most common endocrine diseases in clinical practice. These pathologies have a mutual influence on each other. On the one hand, thyroid hormones are involved in regulation of carbohydrate metabolism: excessive production of thyroid hormones is associated with hyperglycemia, while hypothyroidism has a decreased level of glucose production by the liver. On the other hand, glucose homeostasis disorder affects the functional state of the thyroid gland: dystrophic, sclerotic and atrophic processes are developing in thyroid gland, what is a manifestation of diabetic microangiopathy. This article demonstrates the need to take into account the mutual influence of pathologies for optimal treatment of this conditions.

Successful intervention with Chinese herbal medicine for hyperthyroidism: Two case reports and a literature review

BackgroundHyperthyroidism, the excessive production of thyroid hormones, is most commonly attributed to autoimmune dysfunction such as Graves’ disease. Western medical treatment of hyperthyroidism includes antithyroid medications, radioiodine, and thyroidectomy, all of which are associated with side effects. We describe the successful treatment of two patients with Graves’ disease who used Chinese herbal medicine (CHM) with or without Western medicine. Case presentationBoth cases (a 50-year-old female [case 1] and a 56-year-old male [case 2]) received the Chinese herbal formula Jia Wei Xiao Yao San (JWXYS) as well as Prunella vulgaris, Fritillaria thunbergii, and Crassostrea gigas. Elevated thyroid hormone levels were restored to normal after 10 months of treatment in case 1 and 8 months in case 2. Neither patient experienced any complications or side effects during CHM treatment. Notably, symptoms and thyroid hormone levels have remained well controlled in both patients over 1 year of follow-up until the time of this report. To explore the possible mechanisms involved in CHM treatment of hyperthyroidism, we searched biomedical literature databases and reviewed the literature up to June 2020. ConclusionsAs for the hyperthyroidism almost was controlled by Western medicine instead of CHM, we report that JWXYS as well as Prunella vulgaris, Fritillaria thunbergii, and Crassostrea gigas was a safe and effective formula and we propose that CHM may be considered as either a first choice or combination therapy to control hyperthyroidism.