Hypothyroidism is an underactive thyroid gland that does not produce enough thyroid hormone to meet the body's needs, causing fatigue, weight gain, cold intolerance, depression, and cognitive sluggishness. Hashimoto's thyroiditis — an autoimmune condition — is the most common cause in iodine-sufficient regions. It is one of the most prevalent chronic diseases worldwide, particularly in women, and is managed with hormone replacement therapy.
What's actually going on in research
Levothyroxine (T4) is the standard treatment and effectively normalizes thyroid-stimulating hormone (TSH) levels in most patients. However, a meaningful subset of patients on levothyroxine continue to experience symptoms despite normal TSH. Trials are studying combination T4/T3 therapy (adding liothyronine), long-acting T3 preparations, and individualized thyroid hormone dosing based on genetics and symptoms rather than TSH alone. Separately, research into preventing progression of Hashimoto's thyroiditis with selenium supplementation and immunomodulation continues.
Combination T4/T3 therapy
Trials are evaluating combination levothyroxine plus liothyronine (T3) for patients with persistent symptoms on T4 alone, with newer long-acting T3 formulations designed to avoid peaks and troughs.
Personalized hormone dosing
Studies using genetic markers including DIO2 polymorphisms are testing whether thyroid hormone dosing guided by genetics and symptom scores improves outcomes beyond TSH-targeted treatment.
Hashimoto's immunomodulation
Selenium supplementation and low-dose naltrexone are in trials for their potential to reduce thyroid autoantibodies and slow gland destruction in autoimmune Hashimoto's thyroiditis.
What to know before you search
Eligibility varies by hypothyroidism etiology, current levothyroxine dose and TSH level, and the presence of persistent symptoms on standard therapy.
What types of trials are currently open
- Combination hormone trials — Testing T4 plus T3 combination regimens and long-acting T3 for symptom relief in treated hypothyroidism.
- Personalized dosing trials — Using genetic and symptom-based algorithms to individualize levothyroxine dosing beyond TSH normalization.
- Hashimoto's immunotherapy trials — Evaluating selenium, low-dose naltrexone, and immune modulators for autoantibody reduction.
- Subclinical hypothyroidism trials — Determining whether treating mildly elevated TSH improves cardiovascular, cognitive, or quality-of-life outcomes.
- Quality-of-life studies — Measuring fatigue, cognition, and mood in hypothyroid patients on different hormone replacement strategies.
Recently added Hypothyroidism trials
Intramuscular Injection of Mashed Parathyroid Tissue Into a Forearm During Thyroid Surgery to Prevent Permanent Postoperative Parathyroid Insufficiency (IMIPAT Study)
Parathyroid insufficiency is a common complication in thyroid surgery and occurs in 6.6 to 24%. Up to 4.4% suffer from permanent hypoparathyroidism requiring life-time substitution of calcium and vitamin D in order to maintain a normal calcium homeostasis. To prevent permanent postoperative parathyroid insufficiency after thyroidectomy, devascularized parathyroid glands are re-implanted intramuscularly by standard. To achieve graft function, meticulous preparation and division of parathyroid tissue is necessary as a prerequisite for tissue nutrition by diffusion until a recapillarization of the parathyroid fragments sets in. There are persistent controversies about the optimal technique for the autotransplantation. The injection of mashed parathyroid tissue into a muscle appears to be a fast, secure and easy tech-nique to provide a sufficient parathyroid hormone (PTH) production in cases of insufficient production of the glands left in-situ. The study is based on the hypothesis that intramuscular injection of mashed parathyroid tissue is a safe procedure that enables graft survival through diffusion and allows for the subsequent production of systemically measurable levels of parathyroid hormone (PTH). The intervention consists of injecting mashed parathyroid tissue into the brachioradialis muscle of the non-dominant arm. The primary objective is to evaluate this technique with respect to both local complications arising from the transplantation procedure and the functional performance of the graft over time. Outcome measures include the PTH gradient between the transplanted and non-transplanted arms, parathyroid hormone levels measured in the antecubital fossa of both arms, and calcium levels. The study population comprises 100 patients, and the trial is designed as a prospective multicentre study. The risk-benefit assessment indicates that the risks associated with participation-particularly local complications and potential graft malfunction-are expected to be low. In patients with familial or renal hyperparathyroidism, autotransplantation of small parathyroid fragments (approximately 1 mm in diameter) has been standard practice for decades. Additionally, the injection of mashed parathyroid tissue into the sternocleidomastoid muscle during surgery has been performed in many centers for years. However, that approach has the limitation that PTH originating from the graft cannot be reliably measured due to anatomical constraints.
SNUH Immune Checkpoint Inhibitor-induced Hypothyroidism Recovery Trial
The goal of this study is to find out whether hypothyroidism caused by immune checkpoint inhibitors (ICIs) can recover after stopping the ICIs. The study also aims to identify factors that can help predict which patients will be able to stop taking thyroid hormone replacement. The main questions the study will answer are: * What percentage of patients recover normal thyroid function and can stop levothyroxine after stopping ICIs? * What clinical or laboratory factors can predict successful withdrawal of levothyroxine? Participants will: * Be adult cancer patients who developed hypothyroidism during ICI treatment and are currently taking levothyroxine * Have already stopped ICI therapy * Gradually reduce their levothyroxine dose every 3 months if their thyroid function remains normal * Stop levothyroxine if thyroid function remains normal at low doses (≤0.025 mg) * Be monitored with thyroid function tests and clinical symptoms at each visit
Find Hypothyroidism trials matched specifically to you
Answer 3 quick questions and we'll show you trials that fit your situation.