# Medical Treatment of Hyperthyroidism; Efficacy and Safety Considerations

**Authors:** Fereidoun Azizi, Hengameh Abdi, Seyed Alireza Ebadi, Ladan Mehran, Atieh Amouzegar

PMC · DOI: 10.34172/aim.33502 · 2025-12-01

## TL;DR

This paper reviews the effectiveness and safety of antithyroid drugs for treating hyperthyroidism, emphasizing their role in long-term management.

## Contribution

The paper provides a comprehensive review of clinical evidence on antithyroid drug efficacy and safety for hyperthyroidism management.

## Key findings

- Antithyroid drugs are effective for controlling hyperthyroidism and preventing relapse.
- Long-term ATD treatment is a safe option for many patients with hyperthyroidism.
- More research is needed to determine optimal treatment duration and patient suitability.

## Abstract

Antithyroid drugs (ATDs) are often the first treatment option for hyperthyroidism due to their efficacy and safety profile. Long-term ATD treatment can effectively control hyperthyroidism and prevent relapse. In this review, we summarize the findings of clinical trials and clinical experiences on the use of ATD treatment for hyperthyroidism. We discuss the efficacy and safety of ATD treatment, as well as the optimal duration of treatment. The evidence suggests that ATD therapy is selected as initial therapy, treatment of relapse of hyperthyroidism and in patients with persistent elevation of TSH receptor antibodies after 18 months of ATD therapy. Long-term ATD treatment can be an effective and safe option for management of many patients with hyperthyroidism. However, additional studies are needed to establish the most efficacious treatment duration and to identify patients who are most likely to benefit from long-term ATD treatment.

## Linked entities

- **Diseases:** hyperthyroidism (MONDO:0004425)

## Full-text entities

- **Genes:** TSHR (thyroid stimulating hormone receptor) [NCBI Gene 7253] {aka CHNG1, LGR3, hTSHR-I}
- **Diseases:** pruritus (MESH:D011537), ATD (MESH:D000081015), pituitary adenoma (MESH:D010911), Graves' orbitopathy (MESH:D049970), liver damage and dysfunction (MESH:D008107), overactive thyroid gland (MESH:D053201), trophoblastic disease (MESH:D014328), hyperparathyroidism (MESH:D006961), ATD (MESH:D001260), cardiovascular complication (MESH:D002318), nodular (multinodular) toxic goiter (MESH:C564546), autoimmune disorder (MESH:D001327), Agranulocytosis (MESH:D000380), infections (MESH:D007239), goiter (MESH:D006042), hyperactivity of thyroid gland (MESH:D013966), hepatitis (MESH:D056486), adenoma (MESH:D000236), endocrine disease (MESH:D004700), metastasis (MESH:D009362), resistance to thyroid hormone (MESH:D018382), nodular toxic disease (MESH:D004194), struma ovarii (MESH:D013330), thyroid malignancy (MESH:D009369), Graves' Hyperthyroidism (MESH:D006980), thyrotoxicosis (MESH:C566386), follicular thyroid cancer (MESH:C572845), vasculitis (MESH:D014657), Graves' Disease (MESH:D006111), hypothyroid (MESH:D007037), glomerulonephritis (MESH:D005921), ANCA-associated (MESH:D056648), allergic reactions (MESH:D004342)
- **Chemicals:** Iodine (MESH:D007455), TSH (MESH:D013972), T3 (MESH:D014284), levothyroxine (MESH:D013974), Thionamide (-), radioiodine (MESH:C000614965), propylthiouracil (MESH:D011441), lipid (MESH:D008055), methimazole (MESH:D008713)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Figures

2 figures with captions in the complete paper: https://tomesphere.com/paper/PMC13000336/full.md

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Source: https://tomesphere.com/paper/PMC13000336