Graves’ disease in a patient with Down syndrome: a shift from hyperthyroidism to hypothyroidism

2021 ◽  
Vol 14 (9) ◽  
pp. e242612
Author(s):  
Sara Todo Bom Costa ◽  
Vanessa Albino ◽  
Ana Peres ◽  
Patrícia Ferreira

Down syndrome (DS) is associated with an increased risk of multisystemic dysfunction, namely endocrine abnormalities. Thyroid dysfunction is the most common endocrinological disorder, and it can manifest as either hypothyroidism or hyperthyroidism. A 16-year-old patient with DS developed hyperthyroidism after a lifetime of alternating between subclinical hypothyroidism and euthyroidism. He presented new onset weight loss, agitation and diarrhoea. Laboratory studies were compatible with hyperthyroidism. Thyroid receptor antibodies (TRAbs) were positive, antithyroid peroxidase antibodies and thyroglobulin antibodies were negative. Antithyroid medication (methimazole) was prescribed and, despite therapy adjustments, laboratory evaluation revealed new onset hypothyroidism with persistently positive TRAbs. He experienced weight gain and remained in a hypothyroid state even with withdrawal of methimazole and administration of levothyroxine. This case illustrates an example of Graves’ disease with coexisting stimulating and inhibiting TRAbs that led to a shift from hyperthyroidism to hypothyroidism, a rare condition in patients with DS.

2019 ◽  
Vol 2019 ◽  
pp. 1-3
Author(s):  
Nurin Chatur ◽  
Marina Castro ◽  
Kin Fan Young Tai

Neonatal hyperthyroidism is usually caused by the passage of maternal thyroid receptor antibodies. This relatively rare condition has various manifestations including cholestasis, prematurity, and cardiomegaly. We present a case of a preterm infant with neonatal Graves’ disease who presented with cholestasis, cardiomegaly, and a macularpapular rash that was thought to be suspicious for congenital infection. This case has been reported to illustrate lessons learnt for early identification of a neonate with Graves’ disease in order to expedite treatment.


1993 ◽  
Vol 128 (2) ◽  
pp. 156-160 ◽  
Author(s):  
Brita Winsa ◽  
Agneta Mandahl ◽  
F Anders Karlsson

We have evaluated the association between smoking, Graves' disease and endocrine ophthalmopathy in a case-control study of 208 patients with newly diagnosed Graves' disease and carried out a retrospective survey of 72 patients treated for Graves' disease and admitted to our ward because of endocrine ophthalmopathy. In the prospective study, patients with Graves' disease smoked significantly more than their healthy controls (41% vs 30%, p<0.01 for current smokers, odds ratio 1.6, 95% confidence interval 1.1-2.3, and p<0.05 for patients with a history of smoking, odds ratio: 1.4, 95% confidence interval 1.0-1.9). Among the patients with endocrine ophthalmopathy at diagnosis, there were slightly more patients with a history of smoking (p <0.05, odds ratio 2.1, 95% confidence interval 1.1-3.9), but not more current smokers when compared with the remaining group. The patients with eye problems tended to have a more active disease with higher levels of thyroxine and TSH-receptor antibodies, but no difference was seen in thyrogastric autoantibodies. No effect of smoking on thyroid hormone and autoantibody levels could be detected. In the retrospective survey we found 64%, 71% and 87% smokers among patients with moderate, severe and malignant eye disease, respectively. In summary, the results show that smoking is associated with an increased risk of contracting Graves' disease and that it enhances the severity of the eye disease in cases that develop endocrine ophthalmopathy during the course of treatment.


2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A958-A958
Author(s):  
Esther H Fantin ◽  
Iuri Martin Goemann

Abstract Introduction: Antithyroid drug (ATD) therapy is the first-line treatment of Graves’ hyperthyroidism. Agranulocytosis, although rare, is a life-threatening condition associated with ATD therapy. For patients who recovered from ATD-induced agranulocytosis, surgery or radioiodine (RAI) therapy are adequate options to restore the patient’s euthyroid state. Here we report a case of ATD-related agranulocytosis where lithium therapy was used before RAI to control thyrotoxicosis and prevent worsening of hyperthyroidism. Case Report: A 74-year-old female with a previous history of hypertension presented with a 2-month history of weight loss (12 lbs), palpitations and shortness of breath. She was afebrile with a heart rate of 110, a blood pressure of 149/80, a fine tremor and a moderate diffuse goiter. She had a normal eye exam. Laboratory evaluation demonstrated TSH &lt;0.01 uIU/mL (0.35-5.5), FT4 3.11 ng/dL (0.51-1.65) and TSH receptor antibody (TRAb) 40 (&lt;1,0 U/L), consistent with thyrotoxicosis due to Graves’ disease. She was started on methimazole (MMI) 15mg and metoprolol. After four weeks, symptoms resolved and thyroid function tests (TFT) improved. However, after two months of treatment, she was hospitalized for fever, diarrhea and abdominal pain. White blood cell count (WBC) was 650/μL, and neutrophil count was 90/μL. A diagnosis of gastroenteritis and agranulocytosis was made and MMI was stopped. After seven days, symptoms resolved, the neutrophil count was 2200/ul and TFT were acceptable (FT4 1.25, ng/dL TT3 1.67 ng/ml, TSH &lt; 0.02 uIU/mL). She was discharged without ATDs and a RAI dose of 20 mCi was scheduled. However, RAI therapy had to be postponed due to COVID-19 pandemic restrictions. After 3 weeks, TFT worsened and therapy with lithium carbonate 300 mg TID was started as the patient refused thyroidectomy. Lithium was initiated 12 days before RAI therapy and was maintained 7 days after the procedure. No side effects associated with lithium treatment were reported. TFT 7 days after RAI were FT4 1.43, ng/dL TT3 2.05 ng/ml and TSH &lt; 0.02 uIU/mL. One month later, the patient was euthyroid without need for thyroid medication and remains on follow up. Discussion: Serum thyroid hormone (TH) concentrations usually increase after RAI therapy for Graves’ disease, a worrisome fact in patients with increased risk for cardiovascular complications. Previous studies report that pre-RAI treatment with lithium prevents changes in serum TH concentrations and enhances RAI therapy’s effectiveness. Here, treatment with lithium was used to control thyrotoxicosis and prevent further increase in TH levels associated with RAI therapy. Lithium is particularly suitable for patients with ATD-related side effects before definitive therapy (radioiodine or thyroidectomy). The antithyroid effect of lithium in this setting should be further studied.


1973 ◽  
Vol 73 (3) ◽  
pp. 483-488 ◽  
Author(s):  
F. Adlkofer ◽  
H. Schleusener ◽  
L. Uher ◽  
A. Ananos ◽  
C. Brammeier

ABSTRACT Crude IgG of sera from 3 patients with Graves' disease, which contained LATS-activity and/or thyroid antibodies, was fractionated by isoelectric focusing in a pH-range between 6.0 to 10.0. LATS-activity was found in IgG-subfractions from pH 7.5 to 9.5, thyroglobulin antibodies and thyroid microsomal antibodies from pH 6.0 to 10.0. It was not possible to separate LATS-activity from the thyroid antibodies by this technique. The results indicate that LATS and the thyroid antibodies are heterogeneous and of polyclonal origin.


1983 ◽  
Vol 102 (1) ◽  
pp. 49-56 ◽  
Author(s):  
Tjerk W. A de Bruin ◽  
Daan van der Heide ◽  
Maria C. Krol

Abstract. An immunoprecipitation assay was developed to determine the presence of antibodies against human TSH1 receptors. With this assay we were able to demonstrate that in comparison with sera from normal controls, 24 out of 30 (80%) sera from patients with untreated Graves' disease could immunoprecipitate more [125I]TSH-TSH receptor complexes. In 9 assays, an average of 14.1 ± 3.7% (sd) of the [125I]TSH-TSH receptor complexes was immunoprecipitated by the 30 Graves' sera vs 9.8 ± 3.0% by the normal pool serum (n = 23) (P < 0.001) and 7.7 ± 2.8% by the 22 normal sera (P < 0.001). One serum of the 24 positive Graves' sera was studied in detail. The results suggest that this serum contained an anti-TSH receptor auto-antibody directed towards a different determinant on the TSH receptor than the TSH binding site.


2019 ◽  
Author(s):  
Keziban Demir ◽  
Hakan Kursat ◽  
Sevde Yazici ◽  
Hamide Pişkinpaşa ◽  
Evin Bozkir ◽  
...  

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