Decreased serum levels of IL-27and IL-35 in patients with Graves disease

ABSTRACT Objectives Graves' disease (GD) is an autoimmune disease causing the overproduction of the thyroid hormone from thyroid gland. This disease is mainly the result of the production of antibodies against TSH receptors. Cytokines play an important role in orchestrating the pathophysiology in autoimmune thyroid disease. The regulatory role of IL-12 on TH1 cells has been proven. IL-27 and IL-35, members of IL-12 cytokine family, are two cytokines that have been newly discovered. IL-35 has been identified as a novel immunosuppressive and anti-inflammatory cytokine while IL-27 has both inflammatory and anti-inflammatory functions. The objective of the current study was to examine the changes in the serum level of the foregoing cytokines in GD patients in comparison to healthy controls. Materials and methods In this study, serum levels of IL-27 and IL-35 were determined by an ELISA method; anti TPO and anti Tg were measured by an RIA method in 40 new cases of Graves's disease. The findings were compared with 40 healthy controls. Results The results showed a significant difference between IL-27 and IL-35 regarding their serum levels with P values of 0.0001 and 0.024, respectively; anti TPO and anti Tg levels of the cases were also significantly different from controls (p < 0.001). Conclusion The reduction in the serum levels of IL-27 and IL-35 in GD patients compared to normal subjects suggests the possible anti-inflammatory role of these cytokines in GD.

Changes in Thyroid Peroxidase and Thyroglobulin Antibodies Might Be Associated with Graves' Disease Relapse after Antithyroid Drug Therapy

BACKGROUND: Graves' disease (GD) is an autoimmune thyroid disorder caused by antibodies stimulating the thyrotropin (TSH) receptor. TSH receptor antibody (TRAb) measurement is useful for predicting GD relapse after antithyroid drug (ATD) treatment. However, the association of other thyroid autoantibodies with GD relapse remains obscure. METHODS: This retrospective study enrolled patients with GD who were initially treated with ATD. TRAb, thyroid peroxidase antibody (TPOAb), and thyroglobulin antibody (TgAb) were measured at the initial diagnosis and at the time of ATD discontinuation. RESULTS: A total of 55 patients were enrolled. The mean age was 49.7 years, and 39 patients (70.9%) were female. Antibody positivity at diagnosis was 90.9%, 69.1%, and 61.9% for TRAb, TPOAb, TgAb, respectively. Median ATD treatment period was 15.1 months. At the time of ATD withdrawal, TRAb titers decreased uniformly overall. Conversely, TPOAb and TgAb showed various changes. After withdrawal of ATD, 19 patients (34.5%) experienced relapse. No clinical features or laboratory results were significantly related to relapse in the overall patient group. However, in the TPOAb positive group at diagnosis, increasing titer of TPOAb or TgAb after ATD treatment was significantly and independently related to relapse free survival (TPOAb: hazard ratio [HR], 17.99; 95% confidence interval [CI], 1.66 to 195.43; P=0.02) (TgAb: HR, 5.73; 95% CI, 1.21 to 27.26; P=0.03). CONCLUSION: Changes in TPOAb or TgAb titers during treatment might be useful for predicting relapse after ATD treatment in patients with positive TPOAb at diagnosis.

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 1¹³¹I 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.

Laboratory Testing in Thyroid Conditions - Pitfalls and Clinical Utility

Thyroid disorders are common, affecting more than 10% of people in the US, and laboratory tests are integral in the management of these conditions. The repertoire of thyroid tests includes blood tests for thyroid-stimulating hormone (TSH), free thyroxine, free triiodothyronine, thyroglobulin (Tg), thyroglobulin antibodies (Tg-Ab), thyroid peroxidase antibodies (TPO-Ab), TSH receptor antibodies (TRAb), and calcitonin. TSH and free thyroid hormone tests are frequently used to assess the functional status of the thyroid. TPO-Ab and TRAb tests are used to diagnose Hashimoto's thyroiditis and Graves' disease, respectively. Tg and calcitonin are important tumor markers used in the management of differentiated thyroid carcinoma and medullary thyroid carcinoma (MTC), respectively. Procalcitonin may replace calcitonin as a biomarker for MTC. Apart from understanding normal thyroid physiology, it is important to be familiar with the possible pitfalls and caveats in the use of these tests so that they can be interpreted properly and accurately. When results are discordant, clinicians and laboratorians should be mindful of possible assay interferences and/or the effects of concurrent medications. In addition, thyroid function may appear abnormal in the absence of actual thyroid dysfunction during pregnancy and in critical illness. Hence, it is important to consider the clinical context when interpreting results. This review aims to describe the above-mentioned blood tests used in the diagnosis and management of thyroid disorders, as well as the pitfalls in their interpretation. With due knowledge and care, clinicians and laboratorians will be able to fully appreciate the clinical utility of these important laboratory tests.

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

ABSTRACT Objective: 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. Subjects and methods: 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). Results: 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. Conclusions: 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.

Mutation screening in the genes PAX-8, NKX2-5, TSH-R, HES-1 in cohort of 63 Brazilian children with thyroid dysgenesis

ABSTRACT Objective: To evaluate the candidate genes PAX-8, NKX2-5, TSH-R and HES-1 in 63 confirmed cases of thyroid dysgenesis. Subjects and methods: Characterization of patients with congenital hypothyroidism into specific subtypes of thyroid dysgenesis with hormone levels (TT4 and TSH), thyroid ultrasound and scintigraphy. DNA was extracted from peripheral blood leukocytes and the genetic analysis was realized by investigating the presence of mutations in the transcription factor genes involved in thyroid development. Results: No mutations were detected in any of the candidate genes. In situ thyroid gland represented 71.1% of all cases of permanent primary congenital hypothyroidism, followed by hypoplasia (9.6%), ectopia (78%), hemiagenesis (6.0%) and agenesis (5.5%). The highest neonatal screening TSH levels were in the agenesis group (p < 0.001). Conclusions: Thyroid dysgenesis is possibly a polygenic disorder and epigenetic factors could to be implicated in these pathogeneses.

Advances in genetic research of congenital hypothyroidism in China / 中国当代儿科杂志

Congenital hypothyroidism (CH), which results from insufficient thyroid hormone biosynthesis, is one of the most common neonatal endocrine disorders. Thyroid dysgenesis and thyroid dyshormonogenesis are the two causes of CH and either one will lead to deficiencies of enzymes during thyroid hormone biosynthesis and insufficient thyroid hormone biosynthesis. Recently, researchers have performed extensive studies on genetics of CH. This paper reviews genes reported to be associated with CH in China.

Nonautoimmune congenital hyperthyroidism due to p.Asp633Glu mutation in the TSHR gene

Most cases of congenital hyperthyroidism are autoimmune forms caused by maternal thyroid stimulating antibodies. Nonautoimmune forms of congenital hyperthyroidism caused by activating mutations of the thyrotropin receptor (TSHR) gene are rare. A woman gave birth to a boy during an emergency cesarean section at 33 weeks of gestation due to fetal tachycardia. On the 24th day of life, thyroid function tests were performed due to persistent tachycardia, and hyperthyroidism was confirmed. Auto-antibodies to TSHR, thyroid peroxidase, and thyroglobulin were not found. The patient was treated with propylthiouracil and propranolol, but hyperthyroidism was not well controlled. At 3 months of age, the patient had craniosynostosis and hydrocephalus, and underwent a ventriculoperitoneal shunt operation. Direct sequencing of the TSHR gene showed a heterozygous mutation of c.1899C>A (p.Asp633Glu) in exon 10. No mutations were discovered in any of the parents in a familial genetic study. We have reported a case of sporadic nonautoimmune congenital hyperthyroidism, by a missense mutation of the TSHR gene, for the first time in South Korea.

Pretibial Myxedema Presenting as Severe Elephantiasis

Elephantiasis is a symptom characterized by the thickening of the skin and underlying tissues in the legs. Pretibial myxedema (PTM) is a non-frequent manifestation of autoimmune thyroiditis, particularly Graves' disease. Lesions of myxedema occur most commonly on the pretibial surfaces, also develop at sites of previous injury or scars and other areas. A 49-year-old male presented with severe elephantiasis on the both pretibial areas, dorsum of the feet, ankles and toes. Twenty years previously, he had received radioactive iodine treatment for thyrotoxicosis. Laboratory tests showed that the patient's thyroid function was normal, but the level of thyroid stimulating hormone (TSH) receptor antibodies was very high (>40 IU/L). The biopsy confirmed PTM. Interestingly, the connective tissue was stained with the TSH receptor antibodies in the deep dermis. Elephantiasic PTM is a severe form of the myxedema and there is few reported case. We report a rare case of PTM with appearance of severe elephantiasis.

Relación entre linfocitos T reguladores (T regs) y anticuerpos anti-receptores de TSH (TRab) y el riesgo de cáncer de tiroides en enfermedad de Graves / Relationship between T regulatory lymphocytes (Tregs) and TSH receptor antibodies (TRab) on risk of thyroid cancer in Graves disease

Durante los últimos años se ha estudiado la relación entre enfermedad de Graves (EG), TSH, TRAb y cáncer de tiroides, existiendo estudios que demuestran mayor prevalencia y agresividad del cáncer de tiroides en pacientes con EG, mientras otros refutan estos hallazgos sugiriendo que serían producto del sesgo de selección. Aquellos estudios que plantean una relación causal entre EG y el desarrollo de cáncer de tiroides, la atribuyen a la presencia de autoanticuerpos TSI, que estimularían el foco de malignidad. Se cree que las citoquinas producidas localmente en pacientes con EG trabajarían en conjunto con los TRAb para determinar la agresividad del cáncer papilar de tiroides en estos pacientes. Dentro de las células reclutadas por el tumor para evadir la respuesta inmune se encuentran los linfocitos Treg, que estarían elevados en paciente con EG, llevando a la disminución de la respuesta inmune y creando un ambiente permisivo para la proliferación celular. Por tratarse de una línea de investigación reciente, no existe consenso sobre el tema y sus implicancias en el tratamiento de los pacientes con EG. La finalidad de este artículo es realizar una revisión de la literatura que exponga y contraste la información disponible a la fecha.

In recent years the relationship between Graves’ disease (GD), TSH, TRAb and thyroid carcinoma has been studied. Research studies show a higher prevalence and aggressiveness of thyroid carcinoma in patients with GD, however other researchers refute these findings suggesting it’s due to selection bias. Increasing evidence suggests a causal relationship between GD and the development of thyroid carcinoma, mainly because of the existence of TSI autoantibodies that could stimulate the focus of malignancy. It is believed that cytokines produced locally in patients with GD work alongside with TRAb regulating the aggressiveness of papillary thyroid carcinoma in these patients. Within the cells recruited by the tumor to elude the immune system we find Treg lymphocytes, which have been found to be increased in patients with GD, leading to a diminished immune response, creating a permissive environment for cell proliferation. Since this is a relatively new line of research, there is no consensus on the subject and its relevance for the treatment of patients with GD. The aim of this article is to show recent literature available on the subject.

Enhancement of Osteogenic Differentiation by Combination Treatment with 5-azacytidine and Thyroid-Stimulating Hormone in Human Osteoblast Cells

BACKGROUND AND OBJECTIVES: The role of thyroid-stimulating hormone (TSH) signaling on osteoblastic differentiation is still undetermined. The aim of this study was to investigate the effects of 5-aza-2′-deoxycytidine (5-azacytidine) on TSH-mediated regulations of osteoblasts. MATERIALS AND METHODS: MG63, a human osteoblastic cell-line, was treated with 5-azacytidine before inducing osteogenic differentiation using osteogenic medium (OM) containing L-ascorbic acid and β-glyceophosphate. Bovine TSH or monoclonal TSH receptor stimulating antibody (TSAb) was treated. Quantitative real-time PCR analyses or measurement of alkaline phosphatase activities were performed for evaluating osteoblastic differentiation. RESULTS: Studies for osteogenic-related genes or alkaline phosphatase activity demonstrated that treatment of TSH or TSAb alone had no effects on osteoblastic differentiation in MG63 cells. However, treatment of 5-azacytidine, per se, significantly increased osteoblastic differentiation and combination treatment of 5-azacytidine and TSH or TSAb in the condition of OM showed further significant increase of osteoblastic differentiation. CONCLUSION: Stimulating TSH signaling has little effects on osteoblastic differentiation in vitro. However, in the condition of epigenetic modification using inhibitor of DNA methylation, TSH signaling positively affects osteoblastic differentiation in human osteoblasts.

A Case of Acute Cerebral Infarction and Thyroid Storm Associated with Moyamoya Disease

Coexistence of moyamoya disease and Graves' disease is rare. A 41-year-old woman presented with symptoms of left-sided hemiparesis and dysarthria. Magnetic resonance imaging and angiography revealed acute infarction of the right thalamus and occipital lobe with complete obstruction of the distal internal carotid arteries and obstruction of the right P2. Free thyroxine, thyroid-stimulating hormone (TSH), and TSH receptor antibody levels were 79.33 pmol/L, 0.007 uIU/mL, and 151.5 u/L, respectively. She received antiplatelet therapy and standard antithyroid drug dose. After admission, seizure and unexplained fever occurred. The thyroid storm score (Burch and Wartofsky scale) was 90 points. After intensive treatment, mental status and thyrotoxicosis-related symptoms ameliorated and vital signs stabilized. We describe a case of thyroid storm following cerebrovascular ischemic events in a Korean woman with moyamoya disease and Graves' disease. Thyroid storm combined with cerebrovascular events can lead to severe morbidity and mortality. Prompt recognition and strict management are crucial.

Association of polymorphisms of rs179247 and rs12101255 in thyroid stimulating hormone receptor intron 1 with an increased risk of Graves' disease: A meta-analysis / 华中科技大学学报（医学）（英德文版）

The polymorphisms of thyroid stimulating hormone receptor (TSHR) intron 1 rs179247 and rs12101255 have been found to be associated with Graves' disease (GD) in genetic studies. In the present study, we conducted a meta-analysis to examine this association. Two reviewers systematically searched eligible studies in PubMed, Web of Science, Embase and China Biomedical Literature Database (CBM). A meta-analysis on the association between GD and TSHR intron 1 rs179247 or rs12101255 was performed. The odd ratios (OR) were estimated with 95% confidence interval (CI). Meta package in R was used for the analyses. Seven articles (13 studies) published between 2009 and 2014, involving 5754 GD patients and 5768 controls, were analyzed. The polymorphism of rs179247 was found to be associated with an increased GD risk in the allele analysis (A vs. G: OR=1.40, 95% CI=1.33-1.48) and all genetic models (AA vs. GG: OR=1.94, 95% CI=1.73-2.19; AA+AG vs. GG: OR=1.57, 95% CI=1.41-1.74; AA vs. AG+GG: OR=1.54, 95% CI=1.43-1.66). The site rs12101255 also conferred a risk of GD in the allele analysis (T vs. C: OR=1.50, 95% CI=1.40-1.60) and all genetic models (TT vs. CC: OR=2.22, 95% CI=1.92-2.57; TT+TC vs. CC: OR=1.66, 95% CI=1.50-1.83; TT vs. TC+CC: OR=1.74, 95% CI=1.53-1.98). Analysis of the relationship between rs179247 and Graves' ophthalmopathy (GO) showed no statistically significant correlation (A vs. G: OR=1.02, 95% CI=0.97-1.07). Publication bias was not significant. In conclusion, GD is associated with polymorphisms of TSHR intron 1 rs179247 and rs12101255. There is no association between rs179247 SNPs and GO.

Changes in bone mineral density and trabecular bone score in Graves' disease patients after anti-thyroid therapy

OBJECTIVE: The purpose of this study was to evaluate changes in bone quantity based on bone mineral density (BMD) and bone quality based on trabecular bone score (TBS) in Graves' disease patients after anti-thyroid therapy. RESEARCH DESIGN AND METHOD: This retrospective study included premenopausal female and male patients with Graves' disease who received BMD measurement more than two times during treatment. BMD and thyroid function tests with free thyroxine (FT4), total triiodothyronine (T3), thyroid stimulating hormone (TSH), and TSH receptor antibody (TRAb) levels were collected two times during follow-up. TBS was calculated using TBS insight® software (version 2.1) from dual-energy X-ray absorptiometry images. RESULTS: Thirty Graves' disease patients (17 males, 56%; 13 premenopausal females, 44%) with a mean age of 35.3 ± 9.9 years were included. The mean follow-up period was 20.7 ± 8.5 months. The median levels of FT4, TSH and TRAb improved at follow-up [2.55 ng/dL (Interquartile range (IQR) 2.07-3.78) to 1.28 ng/dL (IQR 1.23-1.39), 0.015 mIU/L (IQR 0.01-0.04) to 0.89 mIU/L (IQR 0.35-1.55), 17.0 IU/L (IQR 5.0-40.3) to 5.0 IU/L (5.0-6.0), respectively; p < 0.001]. Median BMD (lumbar spine) values also improved from 1.118 g/cm² (IQR 1.000-1.119) to 1.167 g/cm² (IQR 1.050-1.219) ( p = 0.001) at follow-up. TBS increased from 1.377 (IQR 1.299-1.422) to 1.390 (IQR 1.327-1.430) after treatment ( p = 0.038). CONCLUSIONS: Both bone quality and density improved after anti-thyroid treatment in premenopausal female and male Graves' disease patients.

Graves' Patient with Thymic Expression of Thyrotropin Receptors and Dynamic Changes in Thymic Hyperplasia Proportional to Graves' Disease Activity

Thymic hyperplasia is frequently observed in Graves' disease. However, detectable massive enlargement of the thymus is rare, and the mechanism of its formation has remained elusive. This case showed dynamic changes in thymic hyperplasia on serial computed tomography images consistent with changes in serum thyrotropin receptor (TSH-R) antibodies and thyroid hormone levels. Furthermore, the patient's thymic tissues underwent immunohistochemical staining for TSH-R, which demonstrated the presence of thymic TSH-R. The correlation between serum TSH-R antibody levels and thymic hyperplasia sizes and the presence of TSH-R in her thymus suggest that TSH-R antibodies could have a pathogenic role in thymic hyperplasia.

Usefulness of Measuring Thyroid Stimulating Antibody at the Time of Antithyroid Drug Withdrawal for Predicting Relapse of Graves Disease

BACKGROUND: Hyperthyroidism relapse in Graves disease after antithyroid drug (ATD) withdrawal is common; however, measuring the thyrotropin receptor antibody (TRAb) at ATD withdrawal in order to predict outcomes is controversial. This study compared measurement of thyroid stimulatory antibody (TSAb) and thyrotropin-binding inhibitory immunoglobulin (TBII) at ATD withdrawal to predict relapse. METHODS: This retrospective study enrolled patients with Graves disease who were treated with ATDs and whose serum thyroid-stimulating hormone levels were normal after receiving low-dose ATDs. ATD therapy was stopped irrespective of TRAb positivity after an additional 6 months of receiving the minimum dose of ATD therapy. Patients were followed using thyroid function tests and TSAb (TSAb group; n=35) or TBII (TBII group; n=39) every 3 to 6 months for 2 years after ATD withdrawal. RESULTS: Twenty-eight patients (38%) relapsed for a median follow-up of 21 months, and there were no differences in baseline clinical characteristics between groups. In the TSAb group, relapse was more common in patients with positive TSAb at ATD withdrawal (67%) than patients with negative TSAb (17%; P=0.007). Relapse-free survival was shorter in TSAb-positive patients. In the TBII group, there were no differences in the relapse rate and relapse-free survivals according to TBII positivity. For predicting Graves disease relapse, the sensitivity and specificity of TSAb were 63% and 83%, respectively, whereas those of TBII were 28% and 65%. CONCLUSION: TSAb at ATD withdrawal can predict the relapse of Graves hyperthyroidism, but TBII cannot. Measuring TSAb at ATD withdrawal can assist with clinical decisions making for patients with Graves disease.

Clinical Implication of TSH Receptor Antibody Measurement

Autoantibodies directed against the thyrotropin receptor have been well known to be an important pathogenesis of Graves' disease. However, the diagnosis and management of Graves' disease are still mainly dependent on thyroid function itself and clinical manifestation of thyrotoxic patients. That is mainly due to the low sensitivity of early generation of thyrotropin receptor assay methods. The development of sensitive thyrotropin receptor measuring tools through third generation immunometric assay made the diagnosis of Graves' disease with mild hyperthyroidism accurate and convenient for patients. Bioassay to detect thyroid stimulating immunoglobulin is also commercially available nowadays, which theoretically discriminate thyroid stimulating antibodies from thyrotropin receptor-blocking antibodies. Although the use of these serologic markers plays an informative role in accurately diagnosing Graves' disease and predicting the prognosis of disease, consideration of the heterogeneous nature of autoimmunity of Graves' disease and the limitation of indirect antibody assay is also required for proper management of Graves' disease patients. In this review, the clinical usefulness of thyrotropin receptor antibody in various clinical situations of Graves' disease was overviewed.

Dilated cardiomyopathy with Graves disease in a young child

Graves disease (GD) can lead to complications such as cardiac arrhythmia and heart failure. Although dilated cardiomyopathy (DCMP) has been occasionally reported in adults with GD, it is rare in children. We present the case of a 32-month-old boy with DCMP due to GD. He presented with irritability, vomiting, and diarrhea. He also had a history of weight loss over the past few months. On physical examination, he had tachycardia without fever, a mild diffuse goiter, and hepatomegaly. The chest radiograph showed cardiomegaly with pulmonary edema, while the echocardiography revealed a dilated left ventricle with an ejection fraction (EF) of 28%. The thyroid function test (TFT) showed elevated serum T3 and decreased thyroid stimulating hormone (TSH) levels. The TSH receptor autoantibody titer was elevated. He was diagnosed with DCMP with GD; treatment with methylprednisolone, diuretics, inotropics, and methimazole was initiated. The EF improved after the TFT normalized. At follow-up several months later, although the TFT results again showed evidence of hyperthyroidism, his EF had not deteriorated. His cardiac function continues to remain normal 1.5 months after treatment was started, although he still has elevated T3 and high TSH receptor antibody titer levels due to poor compliance with drug therapy. To summarize, we report a young child with GD-induced DCMP who recovered completely with medical therapy and, even though the hyperthyroidism recurred several months later, there was no relapse of the DCMP.

Dilated cardiomyopathy with Graves disease in a young child

Graves disease (GD) can lead to complications such as cardiac arrhythmia and heart failure. Although dilated cardiomyopathy (DCMP) has been occasionally reported in adults with GD, it is rare in children. We present the case of a 32-month-old boy with DCMP due to GD. He presented with irritability, vomiting, and diarrhea. He also had a history of weight loss over the past few months. On physical examination, he had tachycardia without fever, a mild diffuse goiter, and hepatomegaly. The chest radiograph showed cardiomegaly with pulmonary edema, while the echocardiography revealed a dilated left ventricle with an ejection fraction (EF) of 28%. The thyroid function test (TFT) showed elevated serum T3 and decreased thyroid stimulating hormone (TSH) levels. The TSH receptor autoantibody titer was elevated. He was diagnosed with DCMP with GD; treatment with methylprednisolone, diuretics, inotropics, and methimazole was initiated. The EF improved after the TFT normalized. At follow-up several months later, although the TFT results again showed evidence of hyperthyroidism, his EF had not deteriorated. His cardiac function continues to remain normal 1.5 months after treatment was started, although he still has elevated T3 and high TSH receptor antibody titer levels due to poor compliance with drug therapy. To summarize, we report a young child with GD-induced DCMP who recovered completely with medical therapy and, even though the hyperthyroidism recurred several months later, there was no relapse of the DCMP.