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Endocrine Disease
Published in John S. Axford, Chris A. O'Callaghan, Medicine for Finals and Beyond, 2023
FBC: Check FBC before starting treatment as there is a risk of drug-induced agranulocytosis. fT3/fT4 are raised, TSH suppressed. Thyrotropin receptor (TSHR) and thyroid-stimulating antibodies (TsAB) are raised in GD.
Hyperthyroidism
Published in Vincenzo Berghella, Maternal-Fetal Evidence Based Guidelines, 2022
See also hypothyroid guidelines (see Chap. 6). Ninety-five percent of cases are due to TSIs [8] stimulating excess thyroid hormone production from the thyroid gland (Graves’ disease). These IgG antibodies bind to and activate the G-protein-coupled thyrotropin receptor, which then stimulates follicular hypertrophy and hyperplasia, as well as increases thyroid hormones production, T3 more than T4 [2]. Women with Graves’ disease have 40–50% remission of the disease in 12–18 months [9].
Thyroid emergencies: Myxedema coma and thyroid storm
Published in Nadia Barghouthi, Jessica Perini, Endocrine Diseases in Pregnancy and the Postpartum Period, 2021
Dushyanthy Arasaratnam, Nadia Barghouthi, Jessica Perini, Robert Weingold
Thyrotoxicosis (presence of excess thyroid hormone) in pregnancy, as indicated by low TSH and elevated T4 and T3, can arise from various sources (see Chapter 3b).Graves’ disease: Endogenous active overproduction of thyroid hormone (hyperthyroidism), identified during pregnancy by elevated thyrotropin receptor antibodies (TRAb) or thyroid-stimulating immunoglobulins (TSI)Toxic adenoma or multinodular goiter: Endogenous overproduction of thyroid hormone from nodule(s)Acute thyroiditis: Sudden release of preformed thyroid hormone
Discovery and design of G protein-coupled receptor targeting antibodies
Published in Expert Opinion on Drug Discovery, 2023
Sean M. Peterson, Catherine J. Hutchings, Cameron F. Hu, Melina Mathur, Janelle W. Salameh, Fumiko Axelrod, Aaron K. Sato
Like GLP-1 R, GIPR and PTHR1, many GPCRs can have large, extended extracellular domains, typically at their N-terminus (Figure 1). One GPCR, called thyrotropin receptor or thyroid stimulating hormone receptor (TSHR), has a large leucine-rich repeat extracellular N-terminal domain and autoantibodies have been discovered that activate TSHR by binding to this extracellular domain leading to Graves’ disease [20–22]. Like TSHR, Class C metabotropic glutamate receptors (mGluR) have a large N-terminal domain with a Venus flytrap structure at the distal end, and camelid single-domain antibodies (nanobodies), DN10 and DN13, have been developed that activate mGluRs [23]. The mGluR family of receptors require dimerization of the extracellular domains, and DN10 and DN13 both recognize unique epitopes that bridge the two dimerized extracellular domains. Interestingly, DN10 recognizes mGluR2 homodimers, while DN13 cross reacts with mGluR2 homodimers and mGluR2/mGluR4 heterodimers. This unique pharmacology was shown to be effective at enhancing the inhibitory action of mGluR2 agonists in neurons and DN13 impaired fear conditioning in mice. DN10 and DN13 were also recently used to detect mGluR2 homodimers and mGluR2/mGluR4 heterodimers in vivo using time-resolved FRET sensors labeling the nanobodies [24]. In addition, a biased agonist antibody has been described which binds to the related receptor, mGluR7 [25].
The Role of TPOAb in Thyroid-Associated Orbitopathy: A Systematic Review
Published in Ocular Immunology and Inflammation, 2022
Georgios Kyriakos, Alexandros Patsouras, Errika Voutyritsa, Christos Gravvanis, Eirini Papadimitriou, Paraskevi Farmaki, Lourdes Victoria Quiles-Sánchez, Vasiliki E. Georgakopoulou, Christos Damaskos, Antonio Ríos-Vergara, Luis Marín-Martínez, Evangelos Diamantis
Considering the association between TAO and thyroid dysfunction, the presence of anti-thyroid antibodies is believed to play a role in the pathogenesis and clinical status of TAO patients. The most commonly reported thyroidal antibodies are antithyroid peroxidase (TPOAb), antithyroglobulin (TgAb), and anti-thyrotropin receptor antibodies (TRAb).8 Specifically, TRAb levels showed the greatest association with TAO.9 The thyrotropin receptor is expressed not only in the thyroid follicular cells but also in the orbital fibroblasts.10 The autoimmunity directed against the receptor on orbital tissues induces infiltration of inflammatory cells, hyaluronic acid accumulation, and the orbital adipose tissue expansion, which eventually leads to the remodeling of orbital connective tissues and fibrosis in its final stage.11 However, there are still some limitations regarding its clinical use, as these antibodies are not present in all cases.12
A unique presentation of Graves’ disease in a pregnant woman with severe hypothyroidism
Published in Gynecological Endocrinology, 2022
Mario Rotondi, Giulia Bendotti, Laura Croce, Martina Molteni, Andrea Carbone, Flavia Magri, Elizabeth N. Pearce, Luca Chiovato
Graves’ disease is the most prevalent form of hyperthyroidism in women of childbearing age, although its incidence is only 0.2–0.4% in unselected pregnant women [2]. In early pregnancy, Graves’ disease must be differentiated from transient gestational thyrotoxicosis, a self-limited disorder that may occur due to elevated β-hCG concentrations [3]. Graves’ hyperthyroidism results from TSH-receptor activation by antibodies (Abs) to the thyrotropin (TSH) receptor (TRAb). Thyrotropin receptor (TSH-R) antibodies can have different functional properties, mimicking or blocking the action of TSH, or they can be functionally neutral [4]. Thus, thyroid function can fluctuate from hyper- to hypothyroidism and vice versa, according to changes in the ratio between circulating Thyroid-blocking antibodies (TBAb) and Thyroid Stimulation antibodies (TSAb) [5–8]. However, shifting from one thyroid function status to the other is infrequently observed [9–11]. According to recent studies, shifts in the ratio of circulating TBAb and TSAb may be more frequent in patients with chromosomal abnormalities such as Turner syndrome and Down syndrome or in those patients in whom other autoimmune conditions are concomitantly associated with Graves’ disease [12].