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Year : 2015  |  Volume : 12  |  Issue : 1  |  Page : 35-38

Hyperthyroidism in children: A report of 6 cases with follow-up

1 Department of Pediatrics, Manipal Hospital, Bengaluru, Karnataka, India
2 Department of Endocrinology, Manipal Hospital, Bengaluru, Karnataka, India

Date of Web Publication18-Dec-2014

Correspondence Address:
Dr. Jeevarathnam Dhivyalakshmi
C/o Dr. A. Karunagaran, M.S., (ENT), 60/39, Model Hutment Road, CIT Nagar, Nandanam, Chennai - 600 035, Tamil Nadu
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0973-0354.147292

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Hyperthyroidism in children is rare. The purpose of this study is to present a case series enlightening various symptoms of hyperthyroidism along with review recommendations in the literature concerning hyperthyroidism in children. We report 6 children aged (2 years to 14 years) presented to us with various manifestations of hyperthyroidism ranging from acute encephalopathy to exopthalmos and diarrhea. Among them 4 were female and 2 were male. 4 children (2 male and 2 female) had Graves's disease, 1 had toxic nodule on left lobe of thyroid and the other child had transient hyperthyroidism due to thyroiditis. Case 1 presented with thyroid encephalopathy. The adolescent girl mentioned in case 3 presented with menstrual irregularity. All children were started on antithyroid drugs and beta blockers. Case 3 had undergone radioactive iodine ablative therapy twice for uncontrollable symptoms.

Keywords: Graves disease, hyperthyroidism in children, thyrotoxicosis in children, thyroiditis, toxic adenoma

How to cite this article:
Dhivyalakshmi J, Bhattacharyya SS, Bhat N K. Hyperthyroidism in children: A report of 6 cases with follow-up. Thyroid Res Pract 2015;12:35-8

How to cite this URL:
Dhivyalakshmi J, Bhattacharyya SS, Bhat N K. Hyperthyroidism in children: A report of 6 cases with follow-up. Thyroid Res Pract [serial online] 2015 [cited 2022 Aug 14];12:35-8. Available from: https://www.thetrp.net/text.asp?2015/12/1/35/147292

  Introduction Top

Hyperthyroidism can be overt or subclinical. Clinical features vary from acute encephalopathy to chronic symptoms. The current study describes 6 children who presented with hyperthyroidism and their follow up, along with review of recent recommendations in the literature.

  Patient and Methods Top

All children in our study are born to non consanguineous parents at full term and appropriate for gestational age. All had normal developmental milestones. There was no history of thyroidal illness in the family except for cases 4 and 5. The child mentioned in case 2 was referred to us after 6 months of carbimazole therapy in view of uncontrolled symptoms. CDC 2000 charts were used for anthropometric assessment. Clinical presentation, anthropometry, physical examination details, and investigations are mentioned in [Table 1]. Except for case 3, all children are prepubertal.
Table 1: Clinical profile

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  Discussion Top

Thyrotoxicosis is a clinical state caused by inappropriately high thyroid hormone action due to raised thyroid hormone levels by any etiology. Hyperthyroidism is inappropriate high synthesis and secretion of thyroid hormones by the thyroid gland. The prevalence of hyperthyroidism is approximately 1.2% (0.5% overt and 0.7% subclinical). The most common cause is Graves' disease (GD), followed by toxic adenoma and transient hyperthyroidism following thyroiditis. [1]

The usual symptoms in children are due to increased adrenergic stimulation (palpitations, tremors) and behavioral changes (restlessness, poor sleep, declining academic performance). Symptoms are more pronounced in younger patients. The other symptoms less commonly seen are anxiety, proptosis, excess appetite, weight loss, and heat intolerance. Goiter is present in up to 95% of cases. Eye signs present in about 50% of children with GD. [2]

Serum TSH and FT4 levels are the commonly performed investigations. Free T3 level is required only if FT4 level is normal. The usual findings are elevated serum FT4 and FT3 and undectable TSH. In subclinical hyperthyroidism, FT4 can be normal, serum T3 may be elevated, and serum TSH will be < 0.01 mU/L. Radioactive iodine uptake scan of thyroid (RAIU) should be performed if the clinical presentation is not diagnostic of GD or if thyroid nodularity is present. Diffuse and high uptake is seen in GD. Toxic nodular goiter will have focal uptake in the adenoma and suppressed uptake in the surrounding and contralateral thyroid tissue. RAIU will be near zero in subacute thyroiditis and factitious causes. I 123 has a short half life and gets organified in thyroid; hence, it is preferred over Tc 99 or 131 I. Ultrasonography does not have diagnostic advantage compared to RAIU. Low serum thyroglobulin level with near-zero RAIU indicates factitious hyperthyroidism. Thyrotropin receptor antibodies (TRAb) and 2 nd generation thyrotropinbinding inhibitor immunoglobulin (TBII) assays are specific for GD compared to thyroid-stimulating immunoglobulins (TSI) and 1 st generation TBII assays. [3],[4],[5],[6]

Antithyroid drugs (ATDs) namely Thionamides-methimazole (MMI) and propylthiouracil (PTU)-are the preferred initial treatment for GD. Prior to initiation of ATD, baseline complete blood count and liver function test has to be done. Due to higher incidence of fulminant hepatotoxicity, PTU is not used in children. [7]

MMI is not available in India; hence, carbimazole (converted to MMI in vivo) is used at 0.1-1 mg/kg/day in 2-3 divided doses. T3, FT4, and TSH levels should be monitored monthly at first and then every 2-4 months. T4 levels normalize first, followed by T3, and lastly TSH. Therefore, drug dosage should be adjusted according to T3 levels. It may take several months for thyroid hormones to normalize; carbimazole dosage can then be reduced to 50% (titration method). The block and replace method is not recommended due to higher prevalence of adverse effects. [1],[8] Allergic reaction, myalgia, arthralgia, and hypothyroidism from overt treatment are the common adverse effects of carbimazole. Agranulocytosis is very rare in children and usually occurs within the first 100 days of ATD. Hence, white cell counts have to be monitored during febrile illness. Withheld ATD till adverse effects resolves; change of ATD is not recommended, hence changing to therapy with radioactive iodine or surgery is advised. [1],[9]

Beta adrenergic blockade is recommended for children with heart rates >100 beats per min. Chances of remission after 2 years of ATD therapy are less with large thyroid gland (>2.5 times the normal size for age), non-Caucasian, prepubertal children (younger age), FT4 >4 ng/dl at diagnosis, and high TRAb while on treatment. Only about 25% of children with GD go into remission with every 2 years of continued treatment. [10]

For GD not in remission, recommended treatment options are radio iodine therapy ( 131 I therapy) or thyroidectomy. 131 I therapy requires pretreatment with MMI and beta blockers so that total T4 and FT4 are normalized 3-4 days before treatment. At that time, patients are placed only on beta blockers. Thyroid hormone levels will start falling by 1 week of radioiodine therapy. Limitations of 131 I therapy are tenderness over thyroid, radiation sialadenitis, risk of thyroid cancer and nodule formation, hypothyroidism (develops 2-3 months post treatment). Hence, 131 I therapy should be avoided in children younger than 5 years of age and goiter more than 80 g in size; hence surgery is preferred (total or near total thyroidectomy). Preoperative preparation with MMI and iodides are necessary to render the child euthyroid. Complications are hemorrhage, recurrent laryngeal nerve palsy, transient hypoparathyroidism, and permanent hypothyroidism. [11],[12]

For the single toxic thyroid nodule, surgical removal (partial thyroidectomy) is the preferred treatment. The incidence of persistent and recurrent hyperthyroidism and complications are less in surgery compared to 131 I therapy. Transient hyperthyroidism due to thyroiditis (autoimmune or subacute) usually does not require any therapy other than symptomatic management (β-blockers and analgesics). The duration of thyrotoxic phase usually ranges from 31 to 168 days. [13],[14]

  Conclusion Top

The current study aims to bring awareness regarding various clinical presentation of hyperthyroidism in children along with review of recent recommendations from the literature. Children in our report had various symptoms (from acute encephalopathy to chronic diarrhea) and various causes of hyperthyroidism. TSH and FT4 are all that required for diagnosis. RAIU scan is recommended for differentiating various causes. Anti thyroid drugs (MMI) are the first line agents for treatment for GD. Radioactive iodine ablation is not advised for children younger than 5 years and huge goiter. Surgery is preferred for autonomous single toxic nodule. Transient hyperthyroidism due to thyroiditis requires only symptomatic management. A high degree of suspicion for hyperthyroidism is required for earlier detection and management.

  References Top

Bahn RS, Burch HB, Cooper DS, Garber JR, Greenlee MC, Klein I et al. Hyperthyroidism and other causes of thyrotoxicosis: Management guidelines of the American Thyroid Association and American Association of Clinical Endocrinologists. Endocr Pract 2011;17:456-520.  Back to cited text no. 1
Clayton GW. Thyrotoxicosis in children. In: Kaplan SA, editors. Clinical Pediatric and Adolescent Endocrinology. Philadelphia: WB Saunders Co, 1982:110-7.  Back to cited text no. 2
Dufour DR. Laboratory tests of thyroid function: Uses and limitations. Endocr Metab Clin North Am 2007;36:155-69.  Back to cited text no. 3
Latrofa F, Vitti P, Pinchera A. Causes and laboratory investigations in thyrotoxicosis. In: Wass JAH, Stewart PM, editors. Oxford Textbook of Endocrinology and Diabetes. 2 nd ed. Newyork: Oxford University Press; 2011. p. 466.  Back to cited text no. 4
Bogazzi F, Vitti P. Could improved ultrasound and power Doppler replace thyroidal radioiodine uptake to assess thyroid disease? Nat Clin Pract Endocrinol Metab 2008;4:70-1.  Back to cited text no. 5
Giuliani C, Cerrone D, Harii N, Thornton M, Kohn LD, Dagia NM, et al. A TSHr-LH/CGr chimera that measures functional TSAb in Graves' disease. J Clin Endocrinol Metab 2012;897:E1106-15.  Back to cited text no. 6
Rivkees SA, Mattison DR. Propylthiouracil (PTU) hepatoxicity in children and recommendations for discontinuation of use. Int J Pediatr Endocrinol 2009:132-41.  Back to cited text no. 7
Razvi S, Vaidya B, Perros P, Pearce SH. What is the evidence behind the evidence-base? The premature death of block-replace antithyroid drug regimens for Graves' disease. Eur J Endocrinol 2006;154:783-6.  Back to cited text no. 8
Rivkees SA, Stephenson K, Dinauer C. Adverse events associated with methimazole therapy of graves' disease in children. Int J Pediatr Endocrinol 2010;2010:176970.  Back to cited text no. 9
Glaser NS, Styne DM. Organization of pediatric endocrinologists of northern California collaborative graves' disease study group 2008 predicting the likelihood of remission in children with Graves' disease: A prospective, multicenter study. Pediatrics 2008;121:e481-8.  Back to cited text no. 10
Rivkees SA, Dinauer C. An optimal treatment for pediatric Graves' disease is radioiodine. J Clin Endocrinol Metab 2007;92:797-800.  Back to cited text no. 11
Sherman J, Thompson GB, Lteif A, Schwenk WF 2 nd , van Heerden J, Farley DR, et al. Surgical management of Graves disease in childhood and adolescence: An institutional experience. Surgery 2006;140:1056-62.  Back to cited text no. 12
Vidal-Trecan GM, Stahl JE, Eckman MH. Radioiodine or surgery for toxic thyroid adenoma: Dissecting an important decision. A cost-effectiveness analysis. Thyroid 2004;14:933-45.  Back to cited text no. 13
Nabhan ZM, Kreher NC, Eugster EA. Hashitoxicosis in children: Clinical features and natural history. J Pediatr 2005;146:533-6.  Back to cited text no. 14


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