Anti-thyroid Receptor Antibodies Research Articles

The Causes of Thyrotoxicosis, Clinical Features, and Treatment Strategies in a Former Iodine Deficient Area

Thyrotoxicosis is a hypermetabolic condition caused by excess thyroid hormones in the circulation with/without increased production from the thyroid gland. In this prospective study, we aimed to investigate the causes of thyrotoxicosis, clinical features, and treatment strategies in a former iodine-deficient area. Thyroid function tests, antithyroid and antithyroid receptor antibodies, and routine thyroid ultrasonography was obtained, and a thyroid scintigraphy/radioactive iodine uptake test was performed on need. A statistically significant difference was found between toxic multinodular goiter (TMNG) and Graves’ disease (GD) groups when mean corpuscular volume (MCV), mean corpuscular hemoglobin (MCH), alanine aminotransferase (ALT), and aspartate aminotransferase (AST) values were analyzed. TSH levels were significantly lower in GD patients compared to those in TMNG and TNG patients, but free triiodothyronine (FT3) and free thyroxine (FT4) values were higher. A high level of TSH receptor antibody (TRAb) was observed in patients with normal antithyroid peroxidase (Anti-TPO). TRAb levels were found to be high. Anti-TPO and anti-thyroglobulin (Anti-Tg) levels were observed to be positively correlated with sT3 and sT4 levels. TMNG is the leading cause of thyrotoxicosis; despite sufficient iodide intake in our former iodine-deficient region, TMNG is characteristically seen in older patients with much lower thyroid hormone levels than GD. According to the study results, the diagnosis of patients with thyrotoxicosis, their clinical presentation, the treatment they will receive, early detection of postoperative complications were predicted

A patient-specific treatment model for Graves\u2019 hyperthyroidism

BackgroundGraves’ is disease an autoimmune disorder of the thyroid gland causedby circulating anti-thyroid receptor antibodies (TRAb) in the serum. TRAb mimics the action of thyroid stimulating hormone (TSH) and stimulates the thyroid hormone receptor (TSHR), which results in hyperthyroidism (overactive thyroid gland) and goiter. Methimazole (MMI) is used for hyperthyroidism treatment for patients with Graves’ disease.MethodsWe have developed a model using a system of ordinary differential equations for hyperthyroidism treatment with MMI. The model has four state variables, namely concentration of MMI (in mg/L), concentration of free thyroxine - FT4 (in pg/mL), and concentration of TRAb (in U/mL) and the functional size of the thyroid gland (in mL) with thirteen parameters. With a treatment parameter, we simulate the time-course of patients’ progression from hyperthyroidism to euthyroidism (normal condition). We validated the model predictions with data from four patients.ResultsWhen there is no MMI treatment, there is a unique asymptotically stable hyperthyroid state. After the initiation of MMI treatment, the hyperthyroid state moves towards subclinical hyperthyroidism and then euthyroidism.ConclusionWe can use the model to describe or test and predict patient treatment schedules. More specifically, we can fit the model to individual patients’ data including loading and maintenance doses and describe the mechanism, hyperthyroidism→euthyroidism. The model can be used to predict when to discontinue the treatment based on FT4 levels within the physiological range, which in turn help maintain the remittance of euthyroidism and avoid relapses of hyperthyroidism. Basically, the model can guide with decision-making on oral intake of MMI based on FT4 levels.

A Rare Presentation of Euthyroid Orbitopathy in Papillary Thyroid Carcinoma

ABSTRACTOphthalmopathy is one of the known presenting features of Grave's disease. Its due to development of antithyroid receptor antib odies. Rarely it may b e asso ciated with th yroid malignancies developing in the Grave's nodule. There are few case reports of patients with coexisting thyroid associated orbitopathy (TAO) and thyroid carcinoma. Sometimes it may be the presenting symptom of an occult thyroid malignancy. Its still rarer if the patient is euthyroid on presentation. It is associated with low titers of antithyroid receptor antibodies. Here we present a very rare case of symmetrical nonmetastatic orbitopathy in a euthyroid papillary carcinoma of thyroid.Key messageIts important to rule out coexisting thyroid cancer in patient presenting with orbitopathy even if euthyroid. Orbitopathy may regress after thyroidectomy. Association of thyroid cancer, autoimmunity and orbitopathy is still to be proven due to lack of large case series.How to cite this articleChaturvedi P, Vaidya A, Tamhankar AS. A Rare Presentation of Euthyroid Orbitopathy in Papillary Thyroid Carcinoma. Int J Head Neck Surg 2013;4(3):145-147.

Unilateral pitting edema of the leg as a manifestation of Graves’ disease: a case report

IntroductionGraves’ hyperthyroidism has a number of well-recognized but relatively rare extrathyroid manifestations such as thyroid acropachy, pretibial myxedema, and congestive heart failure.Case presentationA 38-year-old Caucasian woman presented to the out-patient clinic with symptoms of hyperthyroidism lasting for approximately five months. Remarkably, she had developed pitting edema of her left leg four months before. She had gone through a conventional assessment, but the reason for the edema was not revealed. At presentation to the endocrinology clinic, the skin of both legs was of normal color and pitting edema on her left leg was of a diffuse nature and spread from her toes to two thirds of her leg. The skin surface of her left leg was smooth and had no elevations or discoloration, whereas her right leg appeared normal. Based on signs and symptoms of thyrotoxicosis and suppressed thyroid-stimulating hormone level (less than 0.001mIU/L, local reference of 0.4 to 4), treatment of 10mg of thiamazole three times a day was started. Additional blood tests revealed marked Graves’ hyperthyroidism with elevated free T4 and anti-thyroid receptor antibodies. Within a month, the free T4 level was normalized and the edema was completely cleared and never reappeared during the treatment course of 12 months.ConclusionsTo the best of our knowledge, this is the first description of unilateral treatment-responsive leg edema as a manifestation of Graves’ hyperthyroidism. However, the pathophysiological mechanism underlying this case of edema remains unclear.

Thyroid hormones in human follicular fluid and thyroid hormone receptors in human granulosa cells

To demonstrate the presence of thyroid hormone in human follicular fluid (FF) and the binding of antithyroid hormone antibodies in human granulosa cells (GCs). Follicular fluids and GCs collected from women undergoing oocyte retrieval after superovulation. In Vitro Fertilization-America/Allegheny General Hospital and Reproductive Sciences Research Laboratories, the Department of Obstetrics and Gynecology, The Medical College of Pennsylvania/Allegheny Campus. Follicular fluid levels of triiodothyronine (T3) determined by a microparticle enzyme immunoassay and FF levels of thyroxine (T4) determined by a fluorescence polarization immunoassay. Three anti-thyroid receptor antibodies were used to determine the presence of thyroid receptor. The binding of these antibodies in GCs was assessed by fluorescent microscopy and flow cytometry. Both T3 and T4 were present in the FF of eight patients studied. A large majority of the samples of individual fluids fell within the normal range for serum. There was a positive correlation between serum T4 values and FF T4 values. The three antithyroid receptor antibodies showed positive nuclear staining of GCs by fluorescent microscopy. The antibody to all thyroid hormone receptors yielded 35% positive cells by flow cytometry, and the site specific antibody for either the alpha-1 or beta-1 receptors yielded 78% and 44% positive cells, respectively. These data demonstrated, for the first time, the presence of T3 and T4 in human FF and the presence of T3 binding sites in human GCs and suggest a role for thyroid hormone in the regulation of human GCs.