Autoimmune Thyroid Disease in T1DM and Hashitoxicosis

These 2 articles discussed various aspects of autoimmune thyroid disease (AITD) in children. Kordonouri et al documented the high incidence of AITD in children and adolescents with type 1 diabetes mellitus (T1DM) in Berlin and its increasing frequency with advancing age and duration of disease. These investigators prospectively assessed thyroid function and determined the presence of antibodies to thyroid peroxidase (TPO) and thyroglobulin (TG) beginning approximately 1.2 years after the diagnosis of T1DM and yearly thereafter in 659 patients (358 boys). Fifteen percent of subjects had positive thyroid antibody titers when first tested (20% females, 12% males). (The incidence of positive TPO antibodies in apparently normal children in Berlin is 3.4%.) By 18 years of age, 19% of females and 9% of males with T1DM had clinical (thyromegaly) and/or laboratory (hyperthyrotropinemia, TPO, and TG antibody titers >100 U/mL) evidence of AITD. In 9% of T1DM patients, treatment with thyroxine was required because of an elevated TSH concentration and/or thyromegaly. In a subset of 126 children and adolescents (80 boys), thyroid function and the presence of thyroid antibodies were ascertained at the time of diagnosis of T1DM and yearly for the next 5 years. In this subgroup, 18% of patients (n=23) had positive titers of anti-TPO and/or anti-TG at diagnosis of T1DM and 7 more patients developed antibodies over the next five years (cumulative incidence 24%); 19 of these subjects required treatment. The investigators concluded that the incidence of AITD was high in patients with T1DM and increased with age and duration of disease. They urged prospective assessment of thyroid function in all children and adolescents with T1DM in order to ameliorate any adverse impact that even subclinical hypothyroidism might have on glycemic control in these patients.

Nabhan and colleagues reported a retrospective chart review of 104 children whose coded diagnosis was Hashimoto thyroiditis in an attempt to describe the clinical features and natural history of Hashitoxicosis (Htx). The authors defined Htx as biochemical hyperthyroidism in the presence of thyroid autoimmunity. In this study 35 cases (34%) were excluded because of miscoding; of these, 25 had other forms of acquired hypothyroidism and 10 had congenital hypothyroidism. The remaining 69 cases with documented Hashimoto’s thyroiditis were examined for demographic and clinical information; 8 cases (11.6%) were initially biochemically hyperthyroid. There were no demographic differences (age of diagnosis, sex, family history) between the children with Htx and the other 61 children who were euthyroid or hypothyroid. Thyroid stimulating immunoglobulin (TSI) was measured in 7 of the 8 children and was elevated in only 3 subjects. Thyroid uptake ¹²³I scans were performed in 4 of 8 children and showed increased uptake in 2 patients. No subject had both an elevated TSI titer and increased ¹²³I uptake. Three of 8 children were clinically hyperthyroid with tremors, palpitations, and tongue fasciculations. Two children were treated; one with a beta-blocker alone for 1 month and the other with methimazole for 3 months. The hyperthyroidism lasted from 31 to 168 days. Three children became hypothyroid and 5 became euthyroid. Subjects received follow-up for 3 to 33 months.

The authors noted that the variable autoimmune and biochemical findings in the children with Htx made the diagnosis confusing. They also suggested that the actual incidence of Htx may be greater than their data show since many of the children were asymptomatic and the duration of the disorder varied.

First Editor’s Comment: Autoimmune thyroid disease represents a broad spectrum of clinical disorders that vary from virulent hyperthyroidism (Graves’ disease) at one end of its spectrum to atrophic hypothyroidism at the opposite extremity. It is well known that AITD is extremely common in children and adolescents with T1DM. The report by Kordonouri et al clearly documents its increased frequency in this disorder and offers supportive data for the practice of prospective and annual assessment of thyroid function and the measurement of antibodies to TPO and TG. The “hyperthyroidism” of AITD that occurs early in its course most likely reflects the extrusion of thyroid hormones from their intrafollicular storage sites into the circulation as the thyroid acini are destroyed by the invading inflammatory cells. As well recorded by Nabhan et al, this transient state is extremely common by historical review but not frequently encountered clinically because of its relatively brief duration. Htx may at times exhibit features not only of Graves’ disease (to which it is pathogenetically related) but of subacute (viral) thyroiditis as well which is also self limited, remitting spontaneously, and has suppressed radioiodine uptake, but an elevated sedimentation rate.

Second Editor’s Comment: The authors stated in their discussion they have “characterized the frequency and natural history of Htx in children with autoimmune thyroiditis”. Unfortunately they did not. While the information presented is interesting, the sample size was very small; too small to draw significant conclusions. Some intriguing information was left out. Did the children with Htx present with weight loss? Did they have a goiter? Did the authors have any suggestions as to when to consider Htx and when to diagnosis hyperthyroidism? It would be very important to examine the same data for children whose medical records were coded for hyperthyroidism over the time span. The obvious question is how did they differ from the children who were coded as Hashimoto's thyroiditis. Perhaps looking at a different data set may help answer these questions and the authors should be encouraged to do so.

Cumulative incidence (probability) of autoimmune thyroiditis according to the duration of type 1 diabetes in 659 children and adolescents: (A) in the total group, (B) stratified to gender of patients.


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