# De Novo Graves’ Disease in a 10-Year-Old Girl Receiving Gonadotropin-Releasing Hormone Agonist Therapy for Idiopathic Central Precocious Puberty: A Case Report

## TL;DR

A 10-year-old girl developed Graves' disease while undergoing GnRH agonist therapy for early puberty, suggesting a possible link between the treatment and thyroid issues.

## Contribution

This case report highlights a potential connection between GnRH agonist therapy and the onset of Graves' disease in children.

## Key findings

- The patient showed suppressed TSH and elevated FT3/FT4 levels with positive TRAb, consistent with Graves' disease.
- Discontinuation of GnRH agonist and thiamazole treatment normalized thyroid function.
- GnRH agonists may contribute to autoimmune thyroid disorders through hypoestrogenism and lymphocyte activation.

## Abstract

We present a case of Graves' disease in a 10-year-old girl with a family history of thyroid disease, which may represent a significant risk factor. The patient developed this condition while receiving gonadotropin-releasing hormone (GnRH) agonist therapy for idiopathic central precocious puberty. The patient presented with headache and vomiting during leuprorelin acetate treatment. Thyroid function tests revealed suppressed thyroid-stimulating hormone (TSH) levels accompanied by elevated free triiodothyronine (FT3) and free thyroxine (FT4) concentrations and positive TSH receptor antibodies (TRAb). Thyroid ultrasonography demonstrated diffuse glandular enlargement with increased vascularity, consistent with Graves' disease. Subsequently, GnRH agonist therapy was discontinued, and thiamazole treatment resulted in normalized thyroid function. Given the rarity of Graves' disease in the pediatric population, this case suggests a potential contributory role of GnRH agonist therapy in its onset. Current evidence suggests that GnRH agonists precipitate autoimmune thyroid disorders predominantly through two pathways: (i) a sustained hypoestrogenism-driven immune rebound state and (ii) direct GnRH-mediated lymphocyte activation. These mechanisms, combined with our patient's family history, highlight the potential importance of thyroid function monitoring in children receiving long-term GnRH agonist therapy, particularly those with a similar genetic predisposition.