Intramuscular injection with plasmid DNA encoding the human thyrotropin receptor (TSHR) has been known to elicit symptoms of Graves disease (GD) in outbred but not inbred mice. In this study, we have examined, firstly, whether intradermal (i.d.) injection of TSHR DNA can induce hyperthyroidism in BALB/c mice and, secondly, whether coinjection of TSHR- and cytokine-producing plasmids can influence the outcome of disease. Animals were i.d. challenged at 0, 3 and 6 weeks with TSHR DNA and the immune response was assessed at the end of the 8th or 10th week. In two experiments, a total of 10 (67%) of 15 mice developed TSHR-specific antibodies as assessed by flow cytometry. Of these, 4 (27%) mice had elevated thyroxine (TT4) levels and goitrous thyroids with activated follicular epithelial cells but no evidence of lymphocytic infiltration. At 10 weeks, thyroid-stimulating antibodies (TSAb) were detected in two out of the four hyperthyroid animals. Interestingly, in mice that received a coinjection of TSHR-
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Objective: Biallelic TSHR mutations cause congenital hypothyroidism (CH). Serum TSH levels of monoallelic TSHR mutation carriers range from normal to mildly elevated, and thus the size of its effect remains unclear. The objectives were to examine the association between monoallelic TSHR mutations and positivity at newborn screening (NBS) for CH, and to test whether the association was modified by another genetic factor. Subjects and methods: We enrolled 395 patients that had a positive result in NBS, and sequenced TSHR Monoallelic TSHR mutation carriers were further sequenced for DUOX2 Molecular functions of the mutations were verified in vitro The frequency of the mutations in the study subjects was compared with a theoretical value in the Japanese general population ...
Atıf İçin Kopyala Baş V. N. , Cangul H., Agladioglu S., Kendall M., Cetinkaya S., Maher E., et al. Journal of pediatric endocrinology & metabolism : JPEM, cilt.25, ss.1153-6, 2012 (SCI Expanded İndekslerine Giren Dergi) ...
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Pearce S.H., Foster D.J., Imrie H., et al. Thyroid, 1997. 7(6): p.923-7. The characterization of a spontaneous animal model equivalent to a human form of
This anti-TSH receptor (TRAb) ELISA kit is a reliable quantitative procedure for measuring TSH (thyrotropin) receptor autoantibodies (TRAb) in human serum.
There is increasing evidence that the TSHR is present in orbital tissue. TSHR mRNA has been found in tissue homogenates by polymerase chain reaction (PCR),6 and immunohistochemistry has shown that orbital fibroblasts express TSHR at certain stages of their maturation.12 As recently shown, 20% of mice immunised with TSHR developed GD and orbital pathology,13-15 suggesting that an autoimmune reaction against TSHR is the first event in TAO.. The morphological alterations that we observed in the human EOM biopsies were very similar to those described in the animal models but changed as the disease progressed. The active stage was characterised by infiltration of polymorphonuclear cells and lymphocytes, proliferation of fibroblasts, and oedema. The chronic stage was marked by fibrosis and adipogenesis and the infiltrating cells are mainly lymphocytes and mast cells. Mast cells have been previously reported in human TAO biopsies16 and this was confirmed in our study. Their close proximity to ...
Graves disease, which is the most common cause of hyperthyroidism worldwide, is an autoimmune disorder characterized by thyroid-stimulating hormone receptor antibody production. A shared antigenicity between the thyroid receptors and the orbital tissue is believed to be responsible for the ophthalmopathy, which is clinically observed in 50% of the patients. The ocular manifestations of Graves disease vary in severity from mild corneal exposure to vision loss and are a function of the degree of inflammatory infiltration. Sequelae include proptosis, lid retraction with subsequent exposure keratitis and restriction of extraocular movements resulting in diplopia. In some patients (5%), the optic nerve becomes compressed in the orbital apex, which results in impaired visual acuity and visual field defects. In the early inflammatory phase, an appropriate treatment includes systemic corticosteroids and external beam irradiation. The orbital manifestations during the stable phase are generally ...
CONTEXT: Graves disease (GD) is caused by persistent, unregulated stimulation of thyrocytes by thyroid-stimulating antibodies (TSAbs) that activate the TSH receptor (TSHR). We previously reported the first small-molecule antagonist of human TSHR and showed that it inhibited receptor signaling stimulated by sera from four patients with GD. OBJECTIVE: Our objective was to develop a better TSHR antagonist and use it to determine whether inhibition of TSAb activation of TSHR is a general phenomenon. DESIGN: We aimed to chemically modify a previously reported small-molecule TSHR ligand to develop a better antagonist and determine whether it inhibits TSHR signaling by 30 GD sera. TSHR signaling was measured in two in vitro systems: model HEK-EM293 cells stably overexpressing human TSHRs and primary cultures of human thyrocytes. TSHR signaling was measured as cAMP production and by effects on thyroid peroxidase mRNA. RESULTS: We tested analogs of a previously reported small-molecule TSHR inverse ...
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The hyperthyroidism of Graves disease is caused by thyrotropin receptor autoantibodies. These antibodies mimic the TSH that normally binds to the receptor and stimulate the thyroid to produce thyroid hormone. These antibodies are generally detected by two types of assays. One type of assay measures the ability of IgG to inhibit binding of TSH to solubilized TSH receptor in an enzyme immunoassay format (TRAb or TBII). The other type of assay is more of a bioassay in that it measures the ability of the patients IgG (or serum) to stimulate cAMP production in tissue cultures of various kinds. It is clear from the literature that the solublized receptor binding assays are not clinically interchangable with the functional bioassays because the populations of antibodies measured by each assay are not completely concordant. This results, in part, due to the fact that not all TSH receptor binding immunoglobulins are stimulatory. Some of the receptor binding antibodies are inhibitory and have been ...
Public Release: 8-Jan-2016 Researchers determine mechanism that triggers normal and abnormal hormone production American Society for Biochemistry and Molecular Biology IMAGE: Model of a glycoprotein hormone receptor (white backbone ribbon) with bound hormone and the activating antibody visualizes a potential arrangement and the principle mechanism of glycoprotein hormone receptor activation. view more Credit: Journal…
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Special note about Community Feature Content. Any content and/or opinions uploaded, expressed or submitted through any Community Feature or any other publicly available section of the Web Site (including password-protected areas), and all articles and responses to questions, other than the content explicitly authorized by the Company, are solely the opinions and responsibility of the person or entity submitting them and do not necessarily reflect the opinions of the Company. By way of example, any recommended or suggested use of products or services available from the Company that is posted through a Community Feature is not a sign of approval or recommendation by the Company. If you choose to follow any such recommendation you do so at your own risk.. Links to Third Party Sites. The Web Site may contain links to other websites on the internet. The Company is not responsible for the content, products, services or practices of any third party websites, including without limitation sites linked to ...
TSHレセプターは分子量約100kDaの糖蛋白で,この蛋白にTSHが結合すると活性化され刺激が伝達される。このレセプターに対する自己抗体が自己免疫性甲状腺疾患(バセドウ病,及び甲状腺機能低下症の一部)の患者血中に認められる。 ...
DI-fusion, le Dépôt institutionnel numérique de lULB, est loutil de référencementde la production scientifique de lULB.Linterface de recherche DI-fusion permet de consulter les publications des chercheurs de lULB et les thèses qui y ont été défendues.
Human thyrotropin (TSH), luteotropin (LH), follitropin (FSH), and chorionic gonadotropin are members of the heterodimeric glycoprotein hormone family. The common α subunit forms noncovalent heterodimers with different β subunits. Two novel human glycoprotein hormonelike genes, α2 (A2) and β5 (B5), recently have been identified. Using a yeast two-hybrid assay, the two subunits were found as potential heterodimerization partners. Immunological analyses confirmed the heterodimerization of A2 and B5 in transfected cells and their colocalization in the anterior pituitary. Recombinant A2/B5 heterodimeric glycoproteins, purified using cation exchange and size fractionation chromatography, activated human TSH receptors, but not LH and FSH receptors, and showed high affinity to TSH receptors in a radioligand receptor assay. The heterodimer also stimulated cAMP production and thymidine incorporation by cultured thyroid cells and increased serum thyroxine levels in TSH-suppressed rats in vivo. This new ...
The importance of thyrotropin receptor (TSHR) agonist antibodies in the manifestations of Graves disease (GD) is recognized. There are, however, no convincing reports of TSHR-specific T cells. We have previously cloned T cells specific for thyroglobulin and thyroid peroxidase (TPO) from GD lymphoid infiltrates and used autologous EBV-transformed B cell lines (EBVL) transfected with an expression vector encoding TPO to efficiently detect TPO-specific T cells. Here we used EBVL transfected with TSHR to seek TSHR-specific T cells in the GD infiltrates, after cloning the in vivo activated T cells without antigen. 3 out of 30 clones responded vigorously and reproducibly to EBVL-TSHR, with a mean stimulation index | 7. Their release of IL-2, IL-4, and IL-10 after stimulation with soluble anti-CD3 and phorbol ester was indistinguishable from the other clones from this thyroid. However, they produced relatively little IFN gamma (median IL-4/IFN gamma ratio of 0.80) compared with the other clones (median IL-4
Graves disease, the most common form of hyperthyroidism in children, is caused by Thyrotropin (TSH) Receptor Antibodies (TRAbs) that mimic the action of TSH. The disease leads to significant morbidity in children both due to the prolonged course of antithyroid medication often required for sustained immunological remission and the high risk of relapse when medication is withdrawn. The ability to predict which patients are most likely to fail medical management would greatly improve the choice of therapy. In the past, large goiter size, age at diagnosis, increased biochemical severity, and decreased body mass index have all been associated with a poorer prognosis, but these clinical indicators lack sensitivity and specificity. Preliminary data suggest that the new TRAb assays are both sensitive and specific for the measurement of TRAbs in children with Graves disease. In addition, variation in these antibodies over time is not the same in all patients. The goal of this proposal will be to ...
The aim was to examine the impact of lipopolysaccharide-induced systemic inflammation on expression of mRNA for cocaine- and amphetamine-regulated transcript (CART) and the thyrotropin receptor (TSHR) and its ligands in CNS areas of relevance for feeding controls and metabolism. Lipopolysaccharide effects on plasma levels of TSH and CART peptides were also examined.Lipopolysaccharide (150-200 μg/mouse) was injected in C57BL/6J mice and tissue and plasma samples taken after 24 h. To establish if plasma increase in CART peptide levels were prostanoid dependent, indomethacin was given via the drinking water beginning 48 h prior to LPS. We evaluated mRNA expression for CART, TSHR, TSHβ, and thyrostimulin in brain and pituitary extracts. Plasma levels of TSH, CARTp, and serum amyloid P component were analyzed by ELISA.Lipopolysaccharide suppressed TSHR mRNA expression in the arcuate nucleus and the pituitary. CART mRNA expression was reduced in the arcuate nucleus but elevated in the pituitary of ...
Gregorio D. Chazenbalk, Pavel Pichurin, Chun-Rong Chen, Francesco Latrofa, Alan P. Johnstone, Sandra M. McLachlan, Basil Rapoport. ...
TRH/Thyrotropin Releasing Hormone 2mg for Anti-Aging Thyrotropin Releasing factor (TRF), Thyroliberin or Protirelin Sequence: (pyro)Glu-His-Pro-NH2 Molecular formula: C16H22N6O4 Molecular Weight: 362.38367 CAS Number: 24305-27-9 Standard: Medical...
The TSH test measures the thyroid-stimulating hormone blood level. Get a TSH blood test near you at a local lab to check your TSH levels at a reasonable cost - Accesa Labs
The TSH test measures the thyroid-stimulating hormone blood level. Get a TSH blood test near you at a local lab to check your TSH levels at a reasonable cost - Accesa Labs
Aims: To investigate whether levels of thyroid-stimulating hormone (TSH) within the normal range are associated with an increased risk of new vascular events and mortality in patients with clinical manifest vascular diseases and whether this relation
Thyrotropin suppression and disease progression in patients with differentiated thyroid cancer: results from the National Thyroid Cancer Treatment Cooperative R
DI-fusion, le Dépôt institutionnel numérique de lULB, est loutil de référencementde la production scientifique de lULB.Linterface de recherche DI-fusion permet de consulter les publications des chercheurs de lULB et les thèses qui y ont été défendues.
tsh3 - MedHelps tsh3 Center for Information, Symptoms, Resources, Treatments and Tools for tsh3. Find tsh3 information, treatments for tsh3 and tsh3 symptoms.
குணக்குறித் தோன்றா தைராய்டு சுரப்புக் குறையானது, தைரோட்ரோபின் (TSH) அளவு அதிகரித்து, ஆனால் தைராக்ஸின் (T4) மற்றும் ட்ரியோடோதைரோனைன் (T3) அளவுகள் இயல்பாக இருக்கும்பட்சத்தில் ஏற்படுகிறது.[1] முதல்நிலை தைராய்டு சுரப்புக் குறையில், TSH அளவுகள் அதிகமாகவும் T4 மற்றும் T3 அளவுகள் குறைவாகவும் உள்ளன. வழக்கமாக T4 மற்றும் T3 அளவு அதிகரிக்கும் போது TSH அளவு குறைய வேண்டும் என்பதால், நாளமில்லாச் ...
Graves disease is the most prevalent disorder of the thyroid. Graves disease is an autoimmune disorder in which the thyroid produces more thyroid hormone than the body needs. Thyroid hormone controls the metabolism and increases the metabolic rate causing weight loss, trembling, excessive sweating, and heart pounding. The pituitary gland found within the skull usually regulates thyroid hormones by the production of thyroid-stimulating hormone; it tells the thyroid to produce the thyroid hormone. Graves disease is an autoimmune disorder that causes a malfunction that releases antibodies that mimic thyroid-stimulating hormone. The abnormal antibodies present within the body notify the thyroid to keep producing thyroid hormone by stimulating thyroid-stimulating hormone receptors [Bram 2005]. Hyperthyroidism is when too much thyroid hormone is produced within the body leading to metabolic rate increase. Some symptoms include increased sweating, shakiness, heat intolerance, hair loss, and fatigue [Bram
Subjects who are heterozygous for thyroid stimulating hormone receptor (TSHR) gene mutations present various phenotypes that range from euthyroid to hyperthyrotropinemia. Similarly, heterozygous dual oxidase 2 (DUOX2) gene mutations result in variable phenotypes, such as transient congenital hypothyroidism, subclinical hyperthyrotropinemia, and euthyroid in children. Here, we describe an 8-year-old boy who had normal newborn screening results, but who developed nonautoimmune hypothyroidism at the age of 1 year and 8 months of age. He was heterozygous for previously reported R450H-TSHR mutation and heterozygous for a novel double mutant allele A1323T-DUOX2 and L1343F-DUOX2. He needed levothyroxine (l-T4) replacement therapy to keep serum TSH levels within normal limits; l-T4 dose of 2.01-2.65 μg/kg/day corresponded to the dose taken by children homozygous for R450H-TSHR and by children with permanent congenital hypothyroidism. Therefore, the coexistence of a heterozygous TSHR mutation and a ...
TY - JOUR. T1 - TSH receptor and thyroid-specific gene expression in human skin. AU - Cianfarani, Francesca. AU - Baldini, Enke. AU - Cavalli, Antonella. AU - Marchioni, Enrico. AU - Lembo, Luigi. AU - Teson, Massimo. AU - Persechino, Severino. AU - Zambruno, Giovanna. AU - Ulisse, Salvatore. AU - Odorisio, Teresa. AU - DArmiento, Massimino. PY - 2010/1. Y1 - 2010/1. N2 - Experimental evidence suggests that in autoimmune thyroid diseases (AITDs) the skin is a target of autoantibodies against thyroid-specific antigens; however, the role of these autoantibodies in skin alterations remains unclear. To gain insight into the function of nominally thyroid-specific genes in skin, we analyzed the expression of thyroid-stimulating hormone-receptor (TSH-R), thyroglobulin (Tg), sodium iodide symporter (NIS), and thyroperoxidase (TPO) genes in normal human skin biopsies and cultured primary keratinocytes and dermal fibroblasts. The results revealed the presence of all the transcripts in skin biopsies. ...
The aim was to examine the impact of lipopolysaccharide-induced systemic inflammation on expression of mRNA for cocaine- and amphetamine-regulated transcript (CART) and the thyrotropin receptor (TSHR) and its ligands in CNS areas of relevance for feeding controls and metabolism. Lipopolysaccharide effects on plasma levels of TSH and CART peptides were also examined. Lipopolysaccharide (150-200 μg/mouse) was injected in C57BL/6J mice and tissue and plasma samples taken after 24 h. To establish if plasma increase in CART peptide levels were prostanoid dependent, indomethacin was given via the drinking water beginning 48 h prior to LPS. We evaluated mRNA expression for CART, TSHR, TSHβ, and thyrostimulin in brain and pituitary extracts. Plasma levels of TSH, CARTp, and serum amyloid P component were analyzed by ELISA. Lipopolysaccharide suppressed TSHR mRNA expression in the arcuate nucleus and the pituitary. CART mRNA expression was reduced in the arcuate nucleus but elevated in the pituitary of mice
Background : Its been widely accepted that this epitope (s) and/or functional characteristics of thyrotropin receptor antibodies (TSHRAb) from Graves patients are heterogenous among patients. of blocking TSHRAb in most patients, albeit the other characteristics were the same as those in Group 1. 3) Group 3 (n=19) patients had low TSAb activities both in CHO-hTSHR cells and in FRTL-5 cells, seldom had blocking TSHRAb, but they had high TBII activities. 4) Group 4 (n = 30) could be categorized as moderate disease group, as they had low activities in all kinds of TSHRAb assay and had low antimicrosomal antibody activities. 5) Group 5 (n=14) was characterized by moderate TSAb activities with atypical epitope (s), rare blocking TSHRAb and moderate TBII activities. 6) Group 6 (n=10) sufferers got high TSAb actions with regular epitopes, preventing AUY922 TSHRAb and low TBII activities seldom. 7) Group 7 (n = 6) was seen as a high TSAb actions with atypical epitopes and high TBII actions. Pretreatment ...
To investigate the possible participation of immunoglobulin E (IgE) in the autoimmune process of Graves disease, incidence of elevation of serum IgE level, TSH receptor antibody (TRAb), and thyroid status were studied in 66 patients with hyperthyroi
Aim of the study: The paper presents some clinical and laboratory parameters reflecting activity and severity of Graves ophtalmopathy (GO) and discusses the correlation between them.. Subjects and methods: The study included 25 GO cases, with mean age 47.7±11.2 years and a female/male ratio of 21/4. The patients were evaluated clinically, by assessment of thyroid status (TSH, FT3, FT4, thyrotropin receptor autoantibodies (TRAb)) and by orbital imagistic means (CT or MRI scan). The mean duration of GO was 19.7 months (3 96 months). The patients were under treatment with antithyroid drugs.. Results: Based on EUGOGO activity and severity criteria, the cases were divided in two subgroups: 16 cases with active ophtalmopathy (4 mild and 12 moderate/severe forms) and 9 cases with inactive disease (5 mild and 4 moderate/severe forms).. The severity of GO was quantified, using EUGOGO recommendations, allotting points for each parameter. Active GO cases showed higher severity scores (right eye: ...
TRAb was measured by a 2° generation method. The Fig. 4 shows the results of TRAb measurements in patients with various newly diagnosed thyroid disorders and in healthy controls. The horizontal dotted line indicates the distinction between the values of TRAb positive and negative (cut-off 1.0 IU / L). It can be seen as patients with Graves disease have almost all of a value above the cut-off while the healthy controls, as well as patients with non-toxic goitre, are all negative TRAb (except one). In patients with autoimmune hypothyroidism, characterized by the presence of thyroglobulin autoantibody (TgAb) and thyroperoxidase autoantibody (TPOAb), there is a low percentage of TRAb (probably type blockers). In summary this study shows an excellent specificity of the method with the ability to discriminate between patients with GD from healthy ones ...
This was a meta-analysis of individual patient data in 14 cohort studies included in the Thyroid Studies Collaboration consortium. The authors used a common thyrotropin reference range of 0.45-4.49 mIU/L for all cohorts except for the Whickham Survey (in which authors used a reference range of 0.5-5.9 mIU/L because the first-generation thyrotropin assay used in that study yields consistently higher levels than measurements of current assays). The authors determined hazard ratios (HRs) of CHD mortality and CHD events according to thyrotropin levels after adjustment for age, sex, and smoking status.. ...
Expression Plasmids. A sequence-verified human TSHR cDNA cloned into pSVL (courtesy of Dr. G. Vassart, Brussels, Belgium) was used. Respectively, for lectin binding ELISA, we used a TSHR-GFP fusion protein (courtesy of Dr R. Latif, New York) in which the human TSHR sequence lacking the stop codon was ligated into the mammalian expression vector pEGFP-N1 (BD Biosciences Clontech, Palo Alto, CA). For SIAT8a, we used the pcDNA3.1 GeneStorm Expression-Ready Clone RG001497 (Invitrogen, Carlsbad, CA). The full-length cDNAs encoding the human SIAT1 and SIAT4a were subcloned into the eukaryotic expression vector pcDNA3.1/V5-His C (Invitrogen, Paisley, UK).. Tissue Samples. All AFTNs were identified by ultrasound and scintigraphy. All preoperatively identified nodules were also identified at surgery and postoperatively characterized by histology according to the World Health Organization criteria (Hedinger, 1988). Somatic TSH receptor mutations in the hot nodules were determined previously by denaturing ...
Definition of thyroid-stimulating hormone stimulation test. Provided by Stedmans medical dictionary and Drugs.com. Includes medical terms and definitions.
Microbiome modification (beneficial modification of the gut microbioma relates to a reduction at the end of treatment of at least 5% of the Firmicutes:Bacteroides ratio and 30% of the anti-TSHr antibody titer and of total IgG and IgA concentrations ...
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CHO-Anti-Human TSHR F(ab) stable cell line is clonally-derived from a CHO cell line, which has been transfected with an anti-human TSHR F(ab) gene to allow expression of the F(ab). It is an example of a cell line transfected using our proprietary CBTGS gene screening and amplification system.
Downs syndrom (DS) är en vanlig kromosomavvikelse. Kortvuxenhet och psykomotorisk utvecklingsstörning är kardinaltecken vid DS. Endokrina avvikelser är också frekvent förekommande.. Tillväxt är en bra indikator på barns hälsa. Nyfödda barn med DS är kortare än andra nyfödda, och skillnaden i längd ökar under barndomen. Sjukdomar som påverkar tillväxten upptäcks ofta via ett förändrat tillväxtmönster. Detta kan lätt förbises vid DS eftersom tillväxten redan är avvikande. Användning av syndromspecifika tillväxtkurvor ökar möjligheterna till diagnostik av sjukdomar som stör längdtillväxten. Vi har framställt tillväxtkurvor för barn med DS, vilka finns tillgängliga inom svensk barnsjukvård och barnhälsovård.. Längdtillväxt styrs av nedärvda faktorer från föräldrarna liksom av nutrition, hälsa och hormoner. Genetiska faktorer, kopplade till kromosom 21, kan påverka tillväxten vid DS, men tillväxtstörningens exakta bakgrund är inte känd. I vuxen ...
Question - Suffering from polyanthrolgia, TSH. Taking Thyroine sodium, Calgel, Saaz-DS. Permanent cure?. Ask a Doctor about Thyroid-stimulating hormone, Ask an Orthopaedic Surgeon
The hyt/hyt mouse (BALB/cBY-hyt, C.hytRF) provides a useful model for exploring the effect of inherited severe primary hypothyroidism. Studies were undertaken to try to define the basis of the primary hypothyroidism in mice homozygous for the autosomal recessive gene, hyt. These mice had congenital hypothyroidism of fetal onset after 15 days post conception. Through their lifetime, the hyt/hyt mice had reduced serum thyroxine (T4), triiodothyronine (T3), reduced thyroid gland intralumenal colloid on electron microscopy and a 100-fold elevation of TSH-like activity compared to hyt/+ littermates. Thyroglobulin made in hyt/hyt animals was similar in size to normal thyroglobulin which was inconsistent with a major structural thyroglobulin gene defect. The thyroglobulin was iodinated. Marked, erratic dilation of rough endoplasmic reticulum (RER) was noted in hyt/hyt mouse follicular cells. Despite these ultrastructural findings, pulse chase and immunoprecipitation studies with isolated hyt/hyt and normal
Graves disease is associated with tachydysrythmia, cardiac ischaemia and cardiomyopathy - all uncommon in young adults without previous cardiac disease. We present three young individuals who developed cardiac complications after periods of uncontrolled Graves disease. Subject 1: A 34-year-old female had severe thyrotoxic symptoms for weeks. Investigations showed fT4: 98.4 (11-25 pmol/L), fT3: 46.9 (3.1-6.8 pmol/L), TSH ,0.01 (0.27-4.2 mU/L) and thyrotrophin receptor antibody (TRAb): 34.8 (,0.9 U//l). She had appropriate treatment but several weeks later she became breathless despite improving thyroid function. Echocardiography showed a pericardial effusion of 2.9 cm. She responded well to steroids and NSAIDs but developed active severe Graves orbitopathy after early total thyroidectomy. Subject 2: A 28-year-old male developed thyrotoxic symptoms (fT4: 38 pmol/L, fT3: 13.9 pmol/L, TSH ,0.01 (for over 6 months) and TRAb: 9.3 U/L). One month after starting carbimazole, he developed acute heart ...
The response to treatment in Graves hyperthyroidism is unpredictable, and factors postulated to predict outcome have not generally proved clinically useful or been widely adopted in clinical practice. We audited outcome in 536 patients with Graves hyperthyroidism presenting consecutively to determine whether simple clinical features predict disease presentation and response to treatment. At presentation males had slightly more severe biochemical hyperthyroidism [free T4: males, 64.3 +/- 3.0 pmol/L (mean +/- SE); females, 61.3 +/- 1.7 (P = 0.45); free T3: males, 24.3 +/- 1.5 pmol/L; females, 21.0 +/- 0.6, (P = 0.04)]. Patients less than 40 yr at diagnosis had more severe hyperthyroidism than patients more than 40 yr old [free T4: |40 yr, 64.3 +/- 2.0; |40 yr, 56.7 +/- 2.3 (P = 0.02); free T3: |40 yr, 22.8 +/- 0.8; |40 yr, 19.0 +/- 0.9 (P = 0.003)]. Males had a lower remission rate than females after a course of antithyroid medication [19.6% vs. 40%; odds ratio, 0.37; 95% confidence interval (CI), 0.17
Methods In a cross-sectional study we compared skin severity modifiedRodnan total skin scores (TSS) to circulating TSH levels in 43 patients with scleroderma (18 with diffuse form, 25 with limited form). SSc patients with hypothyroidism necessitating thyroid hormonal replacement therapy and patients with positive TSH receptor antibodies were not enrolled. We also concurrently measured free triiodothyronine (FT3), free thyroxine (FT4), TSH receptor antibodies (TRAb), anti-thyroid peroxidise (TPOAb) and anti-thyroglobulin (TgAb), all by chemiluminescence immunoassay.. ...