China
Africa
Explore chapters and articles related to this topic
Biochemistry
Published in Burkhard Madea, Asphyxiation, Suffocation,and Neck Pressure Deaths, 2020
T3 and T4 synthesis and release are controlled and regulated by a classical ‘negative feedback system’. This involves reciprocal interactions between the thyroid gland and higher levels of control using information conveyed by circulating hormones. In this system, referred to as the hypothalamic−pituitary−thyroid axis, thyrotropin-releasing hormone (TRH) is secreted by the hypothalamic paraventricular nucleus into portal circulation, acting on the anterior pituitary thyrotropes to stimulate thyrothropin (thyroid-stimulating hormone, TSH) release. This subsequently acts via TSH receptors (TSHR) on thyroid follicular cells to stimulate cell proliferation as well as T4 and T3 synthesis and secretion [6,22,60,76].
Regulation of the Pituitary Gland by Dopamine
Published in Nira Ben-Jonathan, Dopamine, 2020
The main target of TSH, whose expression is restricted to the pituitary thyrotrophs, is the follicular cells of the thyroid gland. The actions of TSH on thyroid cells are mediated by TSHR, a G protein–adenylyl cyclase–coupled receptor and include changes in thyroid cell morphology and growth, iodine metabolism, and stimulation of the production and release of T3 and T4. TSH is a glycoprotein consisting of alpha and beta subunits. The alpha-subunit, composed of 92 amino acids is thought to be the effector unit responsible for the stimulation of adenylate cyclase. The β subunit, composed of 118 amino acids, is unique to TSH, and determines its receptor specificity [77]. The rat and human TSH gene consists of three exons, whereas the mouse gene has five exons. The α-subunit is produced in excess of the beta-subunit and is rate limiting in the production of the non-covalent α-β dimer. Expression of the TSHβ gene is stimulated by the transcription factors Pit-1 and Gata2, whereas TSHβ gene expression is suppressed by thyroid hormones. TRH plays a dominant role in the stimulation of TSH synthesis.
Organ-specific autoimmune diseases
Published in Gabriel Virella, Medical Immunology, 2019
Gabriel Virella, George C. Tsokos
Graves’ disease, also known as thyrotoxicosis, diffuse toxic goiter, and exophthalmic goiter, is the result of the production of antibodies against the thyroid-stimulating hormone receptor (TSHR), usually of the IgG1 isotype. Three functional types of TSHR antibodies can be detected in patients with Graves’ disease. In 80%–90% of the patients with Graves’ disease, the antibodies stimulate the production of thyroid hormones by activating the adenylate cyclase system after binding to the TSH receptor the activity of the thyroid gland. For that reason they have been known by a variety of descriptive terms, including long-acting thyroid stimulator (LATS). A second type of TSHR antibodies induces apoptosis of the cells expressing it, contributing to the development of thyroid inflammation. Finally, a third type of TSHR antibodies blocks the receptor and does not stimulate the production of thyroid hormones. These antibodies are detected in about 4% of patients with Graves’ disease, and when their activity predominates (in about 50% of the cases in which they are detected), cause hypothyroidism, while the remaining patients may be euthyroid or hyperthyroid depending on the ratio of blocking versus stimulating antibodies. These blocking antibodies can also be detected in about 10% of patients with Hashimoto's thyroiditis.
First case report of papillary thyroid carcinoma arising within a functional teratoma in Graves’ disease patient
Published in Gynecological Endocrinology, 2021
Chih-Chien Cheng, Wen-Ping Yang
PTC may arise within mature ovarian teratomas[4], excessive production of thyroid hormones by PTC had ever been reported [9]. Our case was diagnosed GD in preoperative 4 years by presence of thyrotoxicosis and high plasma TRAb level, and was been treated with antithyroid drugs periodically. Two months after the oophorectomy of the teratoma, her anti-thyroid drug was discontinued because of euthyroid status and low TRAb. No specific sonographic finding of thyroid scan and the plasma levels of TSH, free T4, TRAb are subsequently within normal range in the 2 years follow up. We suspected her previous thyrotoxicosis depending on two possible conditions: (1) the ovarian tumor can autonomously produce hyperfunction (because of the tissue strong staining of thyroglobulin) and (2) GD. The diagnosis of functioning teratoma is challenging. The evidence for the presence of a functioning struma ovarii could be based on increase radioiodine uptake by the ovary. But radioiodine scanning was not performed preoperatively to our case. After resection of the ovarian lesion, thyroid function was closely monitored, the laboratory signs of hyperthyroidism remitted. These results demonstrate the possible contribution from the PTC in teratoma to hyperthyroidism in our patient. Recently, TSHR mutations may be associated with the malignant phenotype in hyperfunctioning [10]. But gene survey was not performed to our case.
Single-stage Orbital Decompression, Strabismus and Eyelid Surgery in Moderate to Severe Thyroid Associated Orbitopathy
Published in Orbit, 2022
Francesco M. Quaranta-Leoni, Matteo Di Marino, Antonella Leonardi, Sara Verrilli, Raffaello Romeo
Twenty patients (34 eyes) of group 1 (12 females, 8 males; mean age, 49.6 ± 9.2 years) were operated on from January 2016 to December 2018; demographic and surgical features of patients of this group are summarized in Table 1. Four patients had prior thyroidectomy, three had prior radioactive iodine treatment, three patients were active smokers at the time of surgery; all patients had stable thyroid levels, but seven patients had raised TSHR antibodies. Mean clinical activity score was 4 ± 1.1. Twenty-five patients of groups 2 and 3 (32 eyes) were operated on from January 2012 to October 2015. All cases had a complete preoperative and postoperative examination including visual acuity, Hertel exophthalmometry, margin reflex distance from upper and lower eyelid (MRD1 and MRD2), complete orthoptic evaluation, color vision, pupillary exam, measurement of intraocular pressure in primary position and in upgaze, visual fields, orbital and maxillo-facial CT scan and nasal endoscopy. MRD1 and MRD2 of the affected eyelid were controlled by means of both clinical and photographic determination to exclude the influence of a chin-up head posture that could modify the measurements and photographic determinations were used for data analysis. MRD1, MRD2 and Hertel exophthalmometry measurements were recorded, and postoperatively photographs were taken for all patients at every follow-up consultation. Nasal endoscopy was performed to exclude the presence of nasal septal deviation, sinus pathology, middle turbinate pneumatization or nasal polyps. All cases had at least a 1-year follow-up with a range from 1 to 5 years and a mean follow-up of 2.9 ± 1.8 years.
No detection of TSH or TSHR in oral lichen planus lesions in patients with or without hypothyroidism
Published in Acta Odontologica Scandinavica, 2020
Mari Vehviläinen, Abdelhakim Salem, Muhammad Yasir Asghar, Tuula Salo, Maria Siponen
Thyroid-stimulating hormone receptor (TSHR) on the thyroid follicular cells is a member of the family of G protein-coupled receptors and is the primary regulator of thyroid hormone synthesis and secretion [15]. The expression of TSHR is not restricted to the thyroid gland. Active TSHR has been detected in a variety of human and animal tissues, including osteoblasts, osteoclasts, bone marrow cells, cardiomyocytes, adipocytes, fibroblasts and skin keratinocytes [16,17].