TSH Receptor Blocking Antibodies Research Articles

FRI569 A Therapeutic Dilemma: Spontaneous Oscillating Graves' Disease And Hypothyroidism

Abstract Disclosure: D. Suravajjala: None. J. Case: None. S. Kolli: None. V. Eranki: None. Spontaneous recurrent conversions between hyperthyroidism and hypothyroidism in Graves’ disease (GD) is very rare. We present a case of GD with spontaneous oscillation since diagnosis. From our review, less than 10 cases have been reported in the literature with alternating hyper and hypothyroidism. The patient is a 68-year-old female diagnosed with GD 4 years back with TSH <0.01 (0.4 - 4.5 uIU/mL) and TSI 25.70 (0.00-0.5 IU/L). She denied viral illness, radiation exposure, Lithium or Amiodarone use. Ultrasound thyroid was consistent with GD. Thyroid uptake scan was also consistent with GD. Eventually, Methimazole (MMI) 10 mg daily was initiated. About five months after MMI treatment, she was found to be hypothyroid with TSH 9.030 (0.4-4.5 uIU/mL) and FT4 0.99 (0.9-2.2 ng/dl) which led to discontinuation of MMI. 2 months later, she was clinically hyperthyroid with TSH 0.026, FT4 2.93 (0.9-2.2 ng/dl), TSI 9.59 (0-0.55 IU/L). MMI 5 mg daily was resumed, and as she preferred medical management, other treatment options for GD were not considered. Six months after low dose MMI, patient again reverted to hypothyroidism with TSH 21.420, FT4 0.82. MMI 5 mg was changed to every other day. After 8 months, she was found to be clinically and biochemically hypothyroid with TSH 147, FT4 0.41 (0.9-2.2 ng/dl), TSI 7.98 (0-0.55 IU/L). With the suspicion that she had burnt out GD, she was started on Levothyroxine (LT4) 100 mcg daily. Two months after LT4 initiation, she became clinically hyperthyroid with TSH 0.010 (0.4-4.5 uIU/mL) and FT4 1.91 (0.9-2.2 ng/dl). When trial of LT4 dose reduction failed to alleviate patient hyperthyroid symptoms, it was discontinued and MMI was resumed at 2.5 mg qd. Within 3 months she reverted to hypothyroidism. HAMA interference was as well ruled out. Although the patient's thyroid function ranged spontaneously from hyperthyroidism to hypothyroidism, she was still reluctant for definitive treatment options for GD, including RAI ablation and total thyroidectomy. As GD patients may have definitive treatment early, spontaneous conversion between hyperthyroidism and hypothyroidism is usually not seen in GD and most episodes usually occur several years after discontinuation of antithyroid drugs. It is known that both TSH receptor stimulating antibodies (TSAb) and TSH receptor blocking antibodies (TBAb) can be produced at the same time. The presence of hyper or hypothyroidism may depend on the equilibrium between stimulating and blocking antibodies. Switching of TSH receptor antibodies between stimulation and blockage is uncommon. Diagnosis demands careful clinical and biochemical assessments. Alternatively, the case may be easily mistaken for excessive thyroid suppression or replacement. This condition is difficult to manage, and definitive treatment options could be considered with I-131 ablation, thyroidectomy, or pharmacological treatment (block and replace). Presentation: Friday, June 16, 2023

FRI565 Spontaneous Conversion Of Long-standing Hypothyroidism To Grave’s Disease: A Case Report

Abstract Disclosure: M. Dominic: None. M. Shakir: None. A. Kakkar: None. O.Z. Syed: None. A. Sood: None. D.A. Alvarez: None. Introduction: Autoimmune thyroid diseases associated with IgG4 include Hashimoto’s thyroiditis (HT) and Graves’ disease (GD). HT involves a combination of antibody-mediated thyroid gland destruction and inhibition of thyroid hormone production through a predominance of TSH receptor-blocking antibodies (TBAb). GD is due to increased thyroid hormone production in response to thyroid-stimulating antibodies (TSAb). Although transition to hypothyroidism in patients with GD is commonly encountered in clinical practice, conversion of primary hypothyroidism to GD is a rare event and is described here. Clinical Case: We describe the case of an 81-year-old female with primary hypothyroidism diagnosed more than 10 years ago. She was briefly treated with desiccated thyroid which was later changed to levothyroxine, and she remained euthyroid for several years on Levothyroxine 88 mcg daily. In 05/2021 her routine blood test showed suppressed TSH of less than 0.01uIU/mL for the first time, and it remained consistently low with elevated free T4 & T3 levels despite gradually reducing levothyroxine dose. Patient also started to have tremors, weight loss and anxiety during this period. She was found to have a hypermetabolic thyroid nodule during a PET-CT for evaluation of newly diagnosed Gastrointestinal Stromal Tumor in 09/2022. Levothyroxine was stopped shortly thereafter, but the hyperthyroid labs persisted, following which TSAb levels were obtained and found positive. She was started on methimazole 10 mg twice daily, which resulted in symptomatic improvement and marked reduction of T3 & T4 levels in one month. Clinical lessons: Over-replacement is the most common cause of hyperthyroid symptoms in patients receiving thyroid hormone replacement. Primary hypothyroidism is usually a permanent condition requiring lifelong therapy. Conversion of this condition to GD is a rare entity and can be missed in clinical practice by being mistaken for levothyroxine over-replacement. Proposed mechanisms for conversion of long-standing hypothyroidism to hyperthyroidism include fluctuating levels of TBAbs and TSAbs, spontaneous development of autoimmunity and rarely, production of TSAbs in patients with established Hashimoto’s thyroiditis. Another proposed theory is initial hypothyroidism due to extensive autoimmune gland damage in patients with GD who later develop hyperthyroidism after tissue recovery. It should be noted that this transition to GD has been reported to occur even 30 years after the diagnosis of hypothyroidism. Thus in patients with well-established hypothyroidism requiring lower thyroid replacement doses than before, and labs showing persistent hyperthyroid picture with no evident cause, a careful evaluation is required to check for conversion to GD in order to start appropriate treatment at the earliest. Presentation: Friday, June 16, 2023

Abstract #1382972: Between a Rock and a Hard Place: A Case of Amiodarone Induced Thyrotoxicosis Presenting with Methimazole Induced Agranulocytosis

Amiodarone is a frequently used anti-arrhythmic drug which may often cause thyroid dysfunction. Management of amiodarone induced thyrotoxicosis (AIT) often hinges on distinguishing between type I and II AIT which is not often possible. When antithyroid drugs (ATD) are used, higher than average doses are often needed, increasing risk for complications. We report a case of a 67-year-old man who presented with palpitations, tremors, hyperdefecation and weight loss, consistent with thyrotoxicosis. He had been treated with amiodarone for paroxysmal atrial fibrillation (a-fib) for several years. Admission labs showed TSH < 0.01 uIU/ml (0.36-3.74 uIU/ml), free T4 3.32 ng/dL (0.76-1.46), total T3 237 ng/dL (86-192), negative thyrotropin receptor blocking antibodies < 1.10 IU/L (0.0-1.75), thyroglobulin antibodies < 20 IU/mL (0.0-40.0) and thyroid peroxidase antibodies < 10.0 IU/mL (0.0-35.0). Thyroid ultrasound showed a mildly enlarged, heterogeneous thyroid without discrete nodules and normal vascularity. He was treated empirically for both type I and type II AIT with methimazole 40 mg and prednisone 40 mg. Despite treatment, he returned with similar complaints one month later. EKG showed a-fib with a heart rate of 120 bpm. Repeat labs showed TSH < 0.01 uIU/ml, free T4 4.01 ng/dL and total T3 146 ng/dL. His overall evaluation was consistent with impending thyroid storm. CBC was notable for a WBC and ANC of 4.0 10ˆ3 cells/μL and 520 cells/μL respectively, which decreased further to a nadir of 2.6 10ˆ3 cells/μL and 62 cells/μL the following day. The inability to use ATDs in the setting of severe agranulocytosis made thyroidectomy an attractive option. His WBC improved with discontinuation of methimazole and resolved completely a day after administration of G-CSF. He was treated with potassium Iodide, prednisone, cholestyramine and metoprolol in preparation for surgery. He did well after surgery and was discharged home in stable condition on postoperative day two. AIT types I and II are distinct clinical entities. First line treatment consists of ATDs for AIT type I, and steroids for AIT type II. In the acute setting it may be difficult to distinguish between both types and some patients may have features of both. Importantly, a 10-fold increased risk for ATD associated agranulocytosis has been reported in patients with AIT compared to thyrotoxicosis due to other etiologies. Higher doses of ATDs are often required in AIT and the risk for agranulocytosis from ATDs is likely dose dependent. Although neutropenia resolves in most patient in 1-3 weeks after cessation of ATDs, use of G-CSF may shorten recovery times, decrease risk for infections and shorten hospital stays.

Abstract #1311147: Spontaneous Persistent Hypothyroidism After Medical Treatment for Graves’ Disease: A Series of 4 Cases

Spontaneous hypothyroidism following medical treatment of Graves’ disease may occur in 5% to 20% of cases. Mechanisms include autoimmune thyroiditis or the development of thyrotropin receptor blocking antibodies. This report presents a case series of 4 patients with such infrequent phenomenon.

Characterization of Apparently Paradoxical Thyrotropin Binding Inhibitory Immunoglobulins With Neutral Bioactivity.

ContextThe thyrotropin (TSH) receptor (TSH-R) autoantibody activity is clinically measured by inhibition of labeled ligand (TSH or M22) binding to the TSH-R (TSH-binding inhibitory immunoglobulin [TBII]) or by stimulation (TSH-R stimulating antibody [TSAb]) or inhibition (TSH-R blocking antibody [TSBAb]) of 3′,5′-cyclic adenosine 5′-monophosphate (cAMP) production in isolated cells.ObjectiveWe experienced a patient with hypothyroid Graves disease (GD) having strong positive TBII but with almost neutral bioactivities on the TSH-R. The aim of this study is the characterization of this apparently paradoxical TBII (serum sample S).MethodsWe first compared the TBII, TSAb, and TSBAb activities of serum sample S with mixtures of stimulating (S-mAb) and blocking monoclonal Ab (B-mAb). Next, we serially measured cAMPs stimulated by various serum samples in the presence or absence of TSH.ResultsMixtures of S-mAb and B-mAb did not reproduce the characteristics of serum sample S. Instead, serum sample S had a unique feature that blocked the TSH-stimulated cAMP initially but disappeared the blocking activity thereafter to reach the control level.ConclusionWe present here the TBIIs with neutral bioactivities found in the patient with autoimmune thyroid disease, which strongly inhibit TSH binding to the TSH-R but exerts neither TSAb nor TSBAb activity. Differences in the methods of detecting TRAb between TBII in vitro and bioassay may cause the discrepancy. Although serum sample S may be an extreme example, a variety of TRAb that not only stimulates or blocks but also interferes with TSH-R binding for only a short time may exist in the serum samples of GD patients.

Thyroid Disorders.

Thyroid Disorders.

A Grave Turn on Hashimoto’s Thyroiditis - A Case Series on Four Patients With Autoimmune Hypothyroidism that Converted to Grave’s Disease

Disclaimer: The view(s) expressed herein are those of the author(s) and do not reflect the official policy or position of Brooke Army Medical Center, the U.S. Army Medical Department, the U.S. Army Office of the Surgeon General, the Department of the Army, the Department of the Air Force, or the Department of Defense or the U.S. Government. Introduction: The most common cause of hypothyroidism is Hashimoto’s thyroiditis, a destructive autoimmune injury to the thyroid gland. Rarely, autoimmune hypothyroidism can be caused by thyroid-stimulating hormone (TSH) receptor blocking antibodies (TSHRab), and can be difficult to differentiate clinically from Hashimoto’s. Grave’s disease is the most common etiology of hyperthyroidism, and is typically caused by activation from TSHRab acting as an agonist for the TSH receptor. Patients with autoimmune thyroiditis, whether from TSHRab or Hashimoto’s, have been infrequently reported to convert to Grave’s disease1–3. Presentation: We present four cases whom initially presented with typical symptoms of hypothyroidism, were diagnosed with autoimmune hypothyroidism and started on levothyroxine. All four cases were later found to be hyperthyroid and ultimately diagnosed and treated for Grave’s disease. Conclusion: Primary hypothyroidism can rarely transition to a hyperthyroid state, although these cases may be underreported. The mechanism isn’t well understood, but is hypothesized to be from a switch of a predominance of TSH receptor blocking antibodies (TBAb) to that of thyroid stimulating antibodies (TSAb)1. Assays using competitive binding for TSH receptor antibodies will not differentiate between blocking and stimulating antibodies4. A high index of suspicion is needed to diagnose these individuals.

Investigation of TSH receptor blocking antibodies in childhood-onset atrophic autoimmune thyroiditis.

.Atrophic autoimmune thyroiditis (AAT) is a type of autoimmune hypothyroidism without goiter. TSH receptor-blocking antibodies (TSBAb) are involved in its etiology in adults. Reportedly, this disease is extremely rare in children. In this study, we aimed to investigate the prevalence of TSBAb during AAT onset in children using a commercially available cell-based bioassay TSAb kit. We conducted a multicenter retrospective observational study. We collected data of patients with AAT who were < 15 yr old, enrolled in a collaborative research group, and diagnosed since July 2003. AAT was defined as acquired autoimmune hypothyroidism without thyroid enlargement. Eighteen patients (including 15 females) whose TSH receptor antibody (TRAb) or TSBAb levels were measured within a year from the initial visit were included. The median age at diagnosis was 9.3 years, and the estimated time between onset and diagnosis was 2.6 yr. The positive rate for either TSBAb or TRAb was 38.8% (95% confidence interval: 18.3–59.5%). There were no significant differences in age, the estimated time between onset and diagnosis, and FT4 levels at diagnosis between the TSBAb-positive and -negative groups. Unlike previous reports, we showed that the prevalence of TSBAb-positivity in childhood-onset AATs is not rare, as in adults.

SUN-566 Sspontaneous Oscillating Hypothyroidism and Hyperthyroidism: A Rare Autoimmune Entity

Graves disease is autoimmune thyroid disorder with overproduction of thyroid hormones secondary to production of TSH receptor antibodies (TSAB). Many of patients diagnosed with graves disease in end stage or after treatment with ablation therapy develop hypothyroidism need life long treatment with thyroxin replacement therapy its very common for Graves disease to covert to Hypothyroid, we describe here rare phenomenon “Oscillating hypothyroidism and hyperthyroidism” in this rare entity of endocrine disorder patients with hypothyroidism spontaneously convert to Graves disease. Pathophysiology behind this rare phenomenon is production of antibodies TSH receptor stimulating (TSAb) and TSH receptor blocking antibodies (TBAb) most likely accounts for presentations of alternating hyperthyroidism and hypothyroidism. To achieve stability of thyroid function, definitive therapy is recommended to remove the pathological thyroid either with surgery of via radioactive iodine ablation. We present her case of 37-year-old female with the PMH of type 1 Diabetes and Hoshimoto thyroiditis being treated with subcutaneous insulin and Levothyroxine, patients thyroid disorder has been controlled with levothyxine for 2 decades, She presented to ED with the complaint of thyroid storm, patient had all symptoms of thyrotoxicosis along with thyroid opthalamopathy (exophthalmos), thyromegaly, thyroid bruit, pretibial myxedema, labs works showed high free T3, high free T4 and very low TSH and Positive TSAb and increase Iodine uptake ( previous labs showed : very high TSh , FT4, FT3 and Positive TBAb , Patient was diagnosed with Graves disease and treated with radioactive thyroid ablation and life long thyroid replacement therapy. This is one of rare disorder in which patients condition keeps switching between hypo to hyper thyroid and vice versa , definite therapy for this treatment is surgical ablation of affected gland.

Graves' Disease: Can It Be Cured?

Whether or not Graves' hyperthyroidism can be really cured, depends on the definition of “cure.” If eradication of thyroid hormone excess suffices for the label “cure,” then all patients can be cured because total thyroidectomy or high doses of 131I will abolish hyperthyroidism albeit at the expense of creating another disease (hypothyroidism) requiring lifelong medication with levothyroxine. I would not call this a “cure,” which I would like to define as a state with stable thyroid stimulating hormone (TSH), free thyroxine, and triiodothyronine serum concentrations in the normal range in the absence of any thyroid medication. Surgery and radioiodine are unlikely to result in so-defined cures, as their preferable aim as stated in guidelines is to cause permanent hypothyroidism. Discontinuation of antithyroid drugs is followed by 50% recurrences within 4 years; before starting therapy the risk of recurrences can be estimated with the Graves' Recurrent Events After Therapy (GREAT) score. At 20-year follow-up about 62% had developed recurrent hyperthyroidism, 8% had subclinical hypothyroidism, and 3% overt hypothyroidism related to TSH receptor blocking antibodies and thyroid peroxidase antibodies. Only 27% was in remission, and might be considered cured. If the definition of “cure” would also include the disappearance of thyroid antibodies in serum, the proportion of cured patients would become even lower.

TSH-receptor-blocking antibody (TBAb) positive hypothyroidism presenting with myopathy

TSH-receptor-blocking antibody (TBAb) positive hypothyroidism presenting with myopathy

Conversion to Graves disease from Hashimoto thyroiditis: a study of 24 patients.

The conversion of Hashimoto's thyroiditis (HT) to hyperthyroidism due to thyrotropin receptor antibodies is intriguing and considered rare. The contribution of TSH receptor blocking antibodies (TRAb), which may be stimulators (TSAb) or blockers (TBAb), is suspected. We describe clinical and biological variables in a series of patients switching from Hashimoto's thyroiditis to Grave's disease. Retrospective case study of 24 patients with Hashimoto's thyroiditis followed during 48 ± 36 months that developed later Graves' disease (GD). These variables were analysed in the hypo and hyperthyroid phase: age, sex, initial TSH, free triiodothyronine (fT3), free thyroxine (fT4), anti-TPO, TBII antibodies, parietal cell autoantibodies, time between hypo and hyperthyroidism, thyroid volume and levothyroxine doses (LT). In HT, mean TSH was 9.4 ± 26.1 UI/L and levothyroxine treatment was 66.2 ± 30.8 µg/day. The switch to GD was observed 38 ± 45 months after HT diagnosis. As expected, we found significant differences on TSH, FT3, FT4 and TBAb levels. Three out of 14 patients had parietal cell autoantibodies. In two of these three cases there was an Helicobacter pylori infection. There were no significant differences between HT and GD groups with respect to thyroid volume. To our knowledge, large series documenting the conversion of HT to GD are scarce. Although rare, this phenomenon should not be misdiagnosed. Suspicion should be raised whenever thyroxine posology must be tapered down during the follow-up of HT patients. Further immunological and genetic studies are needed to explain this unusual autoimmune change.

Transient hypothyroidism in the newborn: to treat or not to treat.

Transient congenital hypothyroidism (CH) refers to a temporary deficiency of thyroid hormone identified after birth, with low thyroxine (T4) and elevated thyrotropin (TSH), which later recovers to improved thyroxine production, typically in first few months of infancy. Approximately 17% to 40% of children diagnosed with CH by newborn screening (NBS) programs were later determined to have transient hypothyroidism. Causes of transient CH are prematurity, iodine deficiency, maternal thyrotropin receptor blocking antibodies, maternal intake of anti-thyroid drugs, maternal or neonatal iodine exposure, loss of function mutations and hepatic hemangiomas. The classic clinical symptoms and signs of CH are usually absent immediately after birth in vast majority of infants due to temporary protection from maternal thyroxine. NBS has been largely successful in preventing intellectual disability by early detection of CH by performing thyroid function tests in infants with abnormal screening results. In this review we present the evidence for decision making regarding treatment vs. withholding treatment in infants with transient CH and present a rational approach to identifying transient CH based on American Academy of Pediatrics (AAP) recommendation.

Thyroid stimulating hormone exhibits the impact on LDLR/LDL-c via up-regulating hepatic PCSK9 expression

ContextThyroid stimulating hormone (TSH) has received increasing attention as being closely associated with increased low-density lipoprotein cholesterol (LDL-c) level and higher atherosclerotic risks. Proprotein convertase subtilisin/kexin type 9 (PCSK9) is known for increasing circulating LDL-c level by inducing LDL receptor degradation. However, whether TSH influences hepatic PCSK9 expression and LDL-c metabolism remains unclear. MethodsFirst, the correlation between TSH and lipid profiles were investigated in euthyroid population and in subclinical hypothyroidism patients. Then, an in vitro study was conducted to validate the effects of TSH on hepatic PCSK9 expression in HepG2 cells. ResultsSerum TSH concentrations positively correlated with LDL-c levels in euthyroid subjects. Subclinical hypothyroidism patients with higher serum TSH levels showed significantly increased serum PCSK9 levels than the matched euthyroid participants (151.29 (89.51–293.03) vs. 84.70 (34.98–141.72) ng/ml, P<0.001), along with increased LDL-c concentrations. In HepG2 cells, LDLR expression on the plasma membrane was decreased, and PCSK9 mRNA and protein levels were synchronously upregulated after recombinant human TSH (rhTSH) treatment, while the effects could be blocked by TSH receptor blocking antibody K1-70. Sterol regulatory element binding protein (SREBP) 1c and SREBP2 mRNA expressions were enhanced after rhTSH treatment, and specific siRNAs significantly inhibited the effects of rhTSH. Furthermore, there was a noticeable induction of PCSK9 expression by rhTSH even though HMGCR gene expression was silenced. ConclusionWe conclude a regulating role of TSH on hepatic PCSK9 expression, which further contributing to a higher LDL-c level.

Prevalence and clinical relevance of thyroid stimulating hormone receptor-blocking antibodies in autoimmune thyroid disease.

The prevalence and clinical relevance of thyroid stimulating hormone (TSH) receptor (TSHR) blocking antibodies (TBAb) in patients with autoimmune thyroid disease (AITD) was investigated. Serum TBAb were measured with a reporter gene bioassay using Chinese hamster ovary cells. Blocking activity was defined as percentage inhibition of luciferase expression relative to induction with bovine TSH alone (cut-off 40% inhibition). All samples were measured for TSHR stimulatory antibody (TSAb) and TSHR binding inhibiting immunoglobulins (TBII). A total of 1079 unselected, consecutive patients with AITD and 302 healthy controls were included. All unselected controls were negative for TBAb and TSAb. In contrast, the prevalence of TBAb-positive patients with Hashimoto's thyroiditis and Graves' disease was 67 of 722 (9·3%) and 15 of 357 (4·2%). Of the 82 TBAb-positive patients, thirty-nine (48%), 33 (40%) and 10 (12%) were hypothyroid, euthyroid and hyperthyroid, respectively. Ten patients were both TBAb- and TSAb-positive (four hypothyroid, two euthyroid and four hyperthyroid). Thyroid-associated orbitopathy was present in four of 82 (4·9%) TBAb-positive patients, with dual TSHR antibody positivity being observed in three. TBAb correlated positively with TBII (r=0·67, P<0·001) and negatively with TSAb (r=-0·86, P<0·05). The percentage of TBII-positive patients was higher the higher the level of inhibition in the TBAb assay. Of the TBAb-positive samples with >70% inhibition, 87% were TBII-positive. Functional TSHR antibodies impact thyroid status. TBAb determination is helpful in the evaluation and management of patients with AITD. The TBAb assay is a relevant and important tool to identify potentially reversible hypothyroidism.

A case of neonatal graves' Disease in a premature infant with negative thyrotropin stimulating antibodies

Neonatal hyperthyroidism is a disorder usually caused by the passage of maternal thyrotropin receptor antibodies. Thyrotropin receptor antibodies can be stimulatory, neutral, or inhibitory. We present a case of neonatal hyperthyroidism in a preterm infant born to a mother with Graves' disease that was thyrotropin receptor stimulating antibody negative. Thyrotropin receptor blocking antibody levels were elevated. Anti-thyroid medication could only be weaned once thyrotropin blocking antibody levels significantly declined. We presume the clinical symptoms of hyperthyroidism in the infant were secondary to the interaction of thyrotropin blocking antibodies with the TSH receptor.

Patients with TSH-Receptor Blocking Antibodies Give a “Positive” Result for Stimulating Activity in Several Commercial Assays

Clinical ThyroidologyVol. 28, No. 7 SummariesPatients with TSH-Receptor Blocking Antibodies Give a “Positive” Result for Stimulating Activity in Several Commercial AssaysStephen W. SpauldingStephen W. SpauldingSearch for more papers by this authorPublished Online:7 Jul 2016https://doi.org/10.1089/ct.2016;28.206-207AboutSectionsView articleView Full TextPDF/EPUB Permissions & CitationsPermissionsDownload CitationsTrack CitationsAdd to favorites Back To Publication ShareShare onFacebookTwitterLinked InRedditEmail View article"Patients with TSH-Receptor Blocking Antibodies Give a “Positive” Result for Stimulating Activity in Several Commercial Assays." Clinical Thyroidology, 28(7), pp. 206–207FiguresReferencesRelatedDetailsCited byFunctional TSH receptor antibodies in children with autoimmune thyroid diseases26 January 2018 | Autoimmunity, Vol. 51, No. 2Performance and Specificity of 6 Immunoassays for TSH Receptor Antibodies: A Multicenter Study8 August 2017 | European Thyroid Journal, Vol. 6, No. 5 Volume 28Issue 7Jul 2016 InformationCopyright 2016 American Thyroid Association, Inc.To cite this article:Stephen W. Spaulding.Patients with TSH-Receptor Blocking Antibodies Give a “Positive” Result for Stimulating Activity in Several Commercial Assays.Clinical Thyroidology.Jul 2016.206-207.http://doi.org/10.1089/ct.2016;28.206-207Published in Volume: 28 Issue 7: July 7, 2016PDF download

Hipertiroidismo: Experiência de uma Consulta de Endocrinologia Pediátrica

Introduction: Hyperthyroidism may have multiple etiologies, including Graves disease, toxic multinodular goiter and toxic adenoma. Although there is still some controversy, the first-line therapeutic option in Graves disease should be the one that best suit the characteristics of the patient and, when possible, adapted to their values and preferences.Objective: To characterize pediatric patients with hyperthyroidism followed in a Pediatric Endocrinology Center.Methods: Retrospective study with review of medical records of patients followed for hyperthyroidism between 2001 and 2013. Variables analyzed included demographic data, personal and family history, clinical and analytic presentation, diagnostic tests, treatment and follow-up.Results: The study comprised 13 patients, the median age at diagnosis was 14 years and 85% were female. Regarding to etiology, 77% had Graves disease, 8% autoimmune hyperthyroidism with negative titer of thyrotropin receptor-blocking antibodies (TRAb), 8% multinodular goiter and 8% neonatal transient hyperthyroidism. In clinical presentation, we highlight the following symptoms: anxiety/irritability (46%), sudoresis (31%), palpitations (31%) and weakness/fatigue (31%) and the following signals: goiter (77%), weight loss (62%) and tachycardia (54%). 92% of patients had elevated antithyroid antibodies titers; 85% had an elevated TRAb titer. The first therapeutic option was mainly the methimazole (92%). One patient relapsed after discontinuing antithyroid medication and underwent radioiodine ablation. The patient with multinodular goiter underwent total thyroidectomy because of follicular tumor suspicion.Conclusion: Data obtained are consistent with the literature. Therapy with methimazole presents a reduced risk of adverse reactions but low probability of remission so, in selected cases, definitive treatment should be considered.

A study of the etiology of transient congenital hypothyroidism in Niigata Prefecture, Japan

Background Several conditions have been known to causetransient congenital hypothyroidism (TCH), including transplacental passage of TSH receptor blocking antibody (TSBAb), maternal antithyroid drug usage, iodine deficiency, iodine excess, fetal prematurity and inactivatingDUOX2mutations. However, the underlying etiology of TCH is not determined in some cases. In this study, we conducted the first systematic investigation on the etiology of TCH, using screening population-based cohort in Niigata Prefecture, Japan.

Congenital Hypothyroidism

Congenital Hypothyroidism