SAT-345 - T3 Dependance in A Pediatric Patient with Autoimmune Hypothyroidism Refractory to Levothyroxine Monotherapy

Autoimmune hypothyroidism is the most common autoimmune condition in pediatrics. The gold standard treatment is levothyroxine, which provides safe and effective therapy for most patients. In some cases, however, patients continue to experience clinical symptoms despite normalization of thyroid function tests (TFTs). With inconsistencies, this has been attributed to the low T3/T4 ratio exhibited by levothyroxine-treated patients in combination with genetic or immunological susceptibilities (1). In clinical practice, these patients may benefit from T3 supplementation, even when TSH and free T4 remain normal. However, reports of cases requiring T3 to achieve normalization of TFTs, as in our case, remain limited.

We present the case of a 12-year-old female with autoimmune hypothyroidism requiring T3 supplementation to achieve near-normal TFTs. The patient had recently emigrated from Cuba and had discontinued treatment for 2 years at presentation. Initial examination revealed a visible goiter and bradycardia. Laboratory evaluation demonstrated an elevated TSH of 900 uiU/ml, which down trended to 570 uiU/ml with an undetectable free T4 after Levothyroxine 50 mcg daily for one month. Subsequently, Levothyroxine was increased to 88 mcg for two weeks, then 125 mcg, and finally 200 mcg with only mild biochemical improvement, with a TSH of 467 uiU/ml and free T4 of 0.2 ng/dl after two months of treatment. This prompted the addition of liothyronine 5 mcg BID. However, the patient then discontinued treatment due to social reasons, leading to a rise in TSH to 998 uiU/ml and free T4 again becoming undetectable. Once combined therapy was finally started, TSH decreased to 34 uiU/ml within four days, with normalization of free T4. Repeat labs two weeks later showed elevated free T4 with normalization of TSH, and T3 was discontinued. One month later, laboratories again demonstrated low free T4 of 0.55 ng/dl and an elevated TSH of 11.5 uiU/ml, indicating T3 dependence, and combination therapy was therefore resumed. The family denied soy or iodine excess exposure and vowed adherence to the administration of levothyroxine, and later to levothyroxine and T3.

This case highlights a rare presentation of autoimmune hypothyroidism with dependance on T3 supplementation to achieve biochemical euthyroid status. While Levothyroxine monotherapy is effective in most cases, this case suggests an individual factor, such as altered thyroid hormone metabolism or underlying genetic susceptibility, contributed to the absence of response to levothyroxine. Recognizing this uncommon presentation will aid in implementing an individualized treatment plan when standard therapy fails.

1. Ettleson, M. D., & Bianco, A. C. (2020). Individualized therapy for hypothyroidism: Is T4 enough for everyone? The Journal of Clinical Endocrinology & Metabolism, 105(9), e3090–e3104. https://doi.org/10.1210/clinem/dgaa430

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