At the time of diagnosis, children and adolescent with HT may be asymptomatic, and the main reasons for referral are goiter, hypothyroid symptoms, and findings which occur while working on unrelated problems or for high-risk groups[
11]. Thyroid function at presentation may significantly vary in the different pediatric reports[
12‐
16], ranging from euthyroidism to overt hypothyroidism or, occasionally, hyperthyroidism[
12]. Further complaints of thyroid function reported in children and adolescent at HT presentation include either subclinical hypothyroidism[
13‐
15], or more rarely, subclinical hyperthyroidism[
16]. In a very recent study, we respectively evaluated clinical and laboratory characteristics at HT diagnosis in 608 children and adolescent from three pediatric endocrinology centers in Northern and Southern Italy. The aims of our investigation were to assess the frequency of thyroid function patterns at HT diagnosis and to analyze the factors that may affect the status of thyroid at time of diagnosis[
17]. Our test results at presentation showed euthyroidism in 52.1% of patients, overt or subclinical hypothyroidism in 41.4%, and overt or subclinical hyperthyroidism in 6.5%. The mean age of patients with thyroid dysfunctions was significantly lower than that found in euthyroid children. Other variables related to thyroid function patterns were prepubertal status, association with either Down or Turner syndromes, which correlated with increased risk of thyroid dysfunctions, and association with other autoimmune disease, which correlated with decreased risk of thyroid dysfunctions[
17]. On overall, thyroid function patterns at HT presentation seem to be mainly conditioned by children age, with an increased risk of severe gland dysfunctions in the cases with early HT presentation[
17]. Other factors that may also be involved are the association with either chromosomopathies or other autoimmune disease[
17] and environmental factors[
18].
The transient hyperthyroid phase of HT is known as hashitoxicosis (Htx), and is believed to result from unregulated release of stored thyroid hormones during inflammatory-mediated destruction of the thyroid gland[
19]. Htx has been reported as the second commonest cause of thyrotoxicosis in childhood, after GD[
20]. Presenting signs and symptoms of Htx can be very similar to those generally observed in GD, as previously reported in a retrospective study on clinical presentation of Htx in children[
21]. Therefore, differential diagnosis of Htx from GD can be particularly challenging when the diagnosis is only based on clinical and biochemical features[
22].