Introduction

Thyrotoxicosis refers to a clinical syndrome caused by excess circulating thyroid hormones, leading to a hypermetabolic state. While the most common cause is primary hyperthyroidism, such as Graves’ disease or toxic multinodular goitre, thyroiditis is another important but transient cause of thyrotoxicosis.¹

Thyroiditis refers to inflammation of the thyroid gland, which leads to destruction of thyroid follicles and the release of preformed thyroid hormones into the bloodstream. This differs from primary hyperthyroidism, where excessive hormone production is due to increased glandular function. The thyrotoxic phase of thyroiditis is self-limited, often followed by a hypothyroid phase before returning to normal function.

Understanding the types of thyroiditis, their causes, clinical presentation, and appropriate management is essential for differentiating thyroiditis-related thyrotoxicosis from other hyperthyroid conditions and ensuring proper treatment.

Types of thyroiditis leading to thyrotoxicosis

Thyroiditis encompasses several types of thyroid inflammation that can cause transient thyrotoxicosis due to the release of stored thyroid hormones. Unlike primary hyperthyroidism, thyroiditis-related thyrotoxicosis is not due to increased hormone production and is usually self-limited. The main types include:

Subacute de quervain's thyroiditis

• Cause: viral infection or post-viral inflammatory response²
• Symptoms
  • Painful, tender thyroid with swelling
  • Fever, sore throat, fatigue
  • Hyperthyroid symptoms (palpitations, weight loss, heat intolerance)
• Pathophysiology
  • Viral infection triggers an inflammatory response, leading to thyroid follicular destruction and hormone leakage
  • Progresses through thyrotoxic, hypothyroid, and recovery phases over weeks to months
• Diagnosis
  • Low TSH (thyroid-stimulating hormone), high T3/T4
  • Elevated ESR, CRP (markers of inflammation)
  • Low radioactive iodine uptake (RAIU) due to hormone release rather than increased synthesis
• Treatment
  • NSAIDs or corticosteroids for pain and inflammation
  • Beta-blockers for symptom relief

Painless (silent) thyroiditis

• Cause: autoimmune-mediated destruction of the thyroid³
• Symptoms
  • Mild thyrotoxicosis, often asymptomatic
  • Non-tender, slightly enlarged thyroid
  • This may be associated with Hashimoto’s thyroiditis
• Pathophysiology
  • Lymphocytic infiltration damages thyroid follicles, causing hormone release
  • Typically self-limited, progressing to a hypothyroid phase before recovery
• Diagnosis
  • Low TSH, high T3/T4
  • Positive thyroid peroxidase (TPO) antibodies
  • Low RAIU uptake
• Treatment
  • Supportive care with beta-blockers for symptoms
  • Monitoring for potential progression to hypothyroidism

Postpartum thyroiditis

• Cause: autoimmune process triggered by postpartum immune rebound⁴ 
• Symptoms
  • Occurs within 12 months after delivery
  • Hyperthyroid phase (thyrotoxicosis) followed by a hypothyroid phase
• Pathophysiology
  • Pregnancy suppresses the immune system, and its reactivation postpartum can attack thyroid cells
• Diagnosis
  • Similar to painless thyroiditis (low TSH, high T3/T4, positive TPO antibodies, low RAIU)
• Treatment
  • Symptomatic management with beta-blockers
  • Some cases may lead to permanent hypothyroidism, requiring thyroid hormone replacement

Drug-induced thyroiditis

• Causes include medications like:^5,8
  • Amiodarone ( leading to type 2 thyrotoxicosis)
  • Immune checkpoint inhibitors (used in cancer treatment)
  • Lithium (affects thyroid hormone metabolism)
• Symptoms:
  • Thyrotoxicosis followed by hypothyroidism
  • Variable thyroid tenderness
• Diagnosis:
  • History of drug use
  • Low RAIU uptake
• Treatment:
  • Discontinuation of the causative drug, if possible
  • Corticosteroids are used in severe cases

Each type of thyroiditis follows a triphasic course (thyrotoxic → hypothyroid → recovery), and differentiation from Graves’ disease or toxic nodular goitre is critical to avoid unnecessary antithyroid treatments.

Differentiating thyroiditis from other causes of thyrotoxicosis

Since thyroiditis-related thyrotoxicosis is caused by inflammation-induced release of preformed thyroid hormones, rather than increased synthesis, it is important to differentiate it from primary hyperthyroidism (such as Graves’ disease or toxic nodular goitre). Proper diagnosis prevents unnecessary use of antithyroid drugs, which are ineffective for thyroiditis.^6,7

Key diagnostic differences

Additional diagnostic tests

• Erythrocyte sedimentation rate (ESR) / C-reactive protein (CRP)
  • Elevated in subacute thyroiditis (inflammatory response)
  • Normal in Graves’ disease and toxic nodular goitre
• Neck ultrasound
  • Thyroiditis – heterogeneous, hypoechoic gland
  • Graves’ disease – increased vascularity (thyroid inferno on Doppler)
  • Toxic nodules – presence of single or multiple nodules

Key takeaways for differentiation

1. RAIU scan is the most important test – low uptake confirms thyroiditis, while high uptake suggests Graves’ or toxic nodular goitre
2. The presence of thyroid pain suggests subacute thyroiditis
3. Thyroid autoantibodies (TSI vs. TPO) help differentiate autoimmune thyroid diseases
4. Clinical course is transient in thyroiditis but persistent in primary hyperthyroidism

Correct diagnosis ensures thyroiditis is managed with supportive care (not antithyroid drugs), while Graves’ disease and toxic nodular goitre receive definitive hyperthyroidism treatment.

Summary

Thyroiditis is an important but often transient cause of thyrotoxicosis, resulting from inflammatory destruction of thyroid follicles rather than excessive hormone production. It presents in different forms, including subacute, painless, postpartum, and drug-induced thyroiditis, each with distinct causes and clinical courses. Unlike Graves’ disease or toxic nodular goitre, thyroiditis-related thyrotoxicosis is self-limited and typically follows a triphasic pattern: an initial thyrotoxic phase, followed by a hypothyroid phase, and eventual recovery.

Accurate diagnosis is crucial to avoid unnecessary antithyroid medications, which are ineffective for thyroiditis. Key diagnostic tools include radioactive iodine uptake (RAIU) scanning, inflammatory markers (ESR/CRP), and thyroid autoantibody testing. Management is supportive, focusing on symptom relief through the use of beta-blockers and anti-inflammatory medications, such as NSAIDs or corticosteroids, as needed.

Ultimately, recognising thyroiditis as a distinct cause of thyrotoxicosis ensures appropriate treatment and monitoring, reducing complications and preventing long-term thyroid dysfunction.