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Graves Disease

Graves Disease is an autoimmune disorder causing excessive thyroid hormone production (hyperthyroidism) due to stimulation of the thyroid gland by antibodies that activate the thyroid-stimulating hormone (TSH) receptor

Also called

Autoimmune hyperthyroidism

ICD-10

E05.0

Specialty

Endocrine

Onset

Chronic

Reviewed

August 2026

On This Page

Overview

–Graves Disease is the most common cause of hyperthyroidism.

-It occurs when autoantibodies stimulate the TSH receptor on thyroid follicular cells, causing increased production of thyroid hormones (T3 and T4).

-It commonly presents with weight loss, heat intolerance, palpitations, tremor, and anxiety. It may also cause Graves ophthalmopathy and pretibial myxedema

Etiology & Risk Factors

-Etiology

•Graves Disease is caused by an autoimmune response in which antibodies bind to and activate the TSH receptor on thyroid follicular cells.


-These antibodies include:
• Thyroid-stimulating immunoglobulins (TSI)
• TSH receptor antibodies (TRAb)


-Activation of the TSH receptor causes:

• Increased thyroid hormone synthesis
• Increased thyroid gland growth
• Diffuse thyroid enlargement

 

-Risk Factors:

• Female sex
• Family history of Graves Disease or autoimmune thyroid disease
• Personal history of autoimmune disease
• Young to middle adulthood
• Pregnancy and postpartum period
• Smoking (strong risk factor for Graves ophthalmopathy)
• Excess iodine exposure

Pathophysiology

-Genetic susceptibility + environmental triggers
→ Loss of immune tolerance
→ Activation of autoreactive B and T lymphocytes
→ Production of TSH receptor antibodies (TSI/TRAb)
→ Antibodies stimulate TSH receptors on thyroid follicular cells
→ ↑ Thyroid hormone synthesis and release (↑ T3 and ↑ T4)
→ Negative feedback suppression of pituitary TSH
→ Low TSH + high thyroid hormones → Hypermetabolic state → symptoms of thyrotoxicosis


-Autoimmune inflammation of orbital tissues → Activation of fibroblasts and increased glycosaminoglycan deposition → Orbital tissue swelling → Graves ophthalmopathy

Clinical Presentation

-Symptoms:

• Weight loss despite increased appetite
• Heat intolerance
• Excessive sweating
• Palpitations
• Anxiety
• Irritability
• Tremor
• Fatigue
• Insomnia
• Increased bowel frequency
• Menstrual irregularities

 

-Signs:

• Tachycardia
• Fine tremor
• Warm, moist skin
• Weight loss
• Hyperactive reflexes
• Goiter
• Thyroid bruit due to increased vascularity

 

-Graves Ophthalmopathy
• Proptosis (exophthalmos)
• Periorbital swelling
• Eye irritation
• Diplopia
• Reduced eye movement in severe cases

History Taking

-Ask about:

• Weight loss
• Appetite changes
• Heat intolerance
• Sweating
• Palpitations
• Tremor
• Anxiety and irritability
• Sleep disturbance
• Bowel habit changes

Physical Examination

-General Examination:

• Assess weight and BMI
• Measure pulse and blood pressure
• Assess temperature
• Look for anxiety or agitation
• Observe for tremor
• Assess hydration status

 

-Thyroid Examination:


• Diffuse thyroid enlargement
• Soft, smooth goiter
• Thyroid bruit due to increased blood flow

 

-Cardiovascular:


• Tachycardia
• Irregular rhythm if atrial fibrillation occurs
• Signs of heart failure in severe disease

Investigations

-Biochemistry / Specific Tests


-Thyroid Function Tests:


-Typical findings:


Primary hyperthyroidism:
• ↓ TSH
• ↑ Free T4
• ↑ Free T3


-Thyroid-Stimulating Immunoglobulin (TSI)


• Positive in many patients.
• Supports the diagnosis of Graves Disease.
TSH Receptor Antibodies (TRAb)
• Useful for confirming Graves Disease.
• Helpful in pregnancy to assess fetal risk.


-Thyroid Peroxidase Antibodies (TPO Antibodies):
• May be positive.
• Less specific than TSI/TRAb.

 

-Imaging
Radioactive Iodine Uptake Scan


Shows:
• Diffuse increased uptake throughout the thyroid gland 

-Useful for distinguishing Graves Disease from other causes of thyrotoxicosis.


-Thyroid Ultrasound
May show:
• Enlarged thyroid
• Increased blood flow on Doppler ultrasound

Diagnosis

-Graves Disease is diagnosed by:


• Clinical features of hyperthyroidism
• Thyroid function tests showing:
• Low TSH
• High free T4 and/or free T3
• Positive TSH receptor antibodies (TRAb/TSI)

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Management

1. First-Line / Emergency Management

Stable Hyperthyroidism

  • Beta-blocker for symptom control.

  • Start antithyroid medication when indicated.

Thyroid Storm

  • Beta-blocker

  • Antithyroid drug

  • Iodine after antithyroid drug

  • Corticosteroids

  • Supportive care and treatment of the trigger

 

2. Definitive Treatment

  • Radioactive iodine: destroys thyroid tissue.

  • Thyroidectomy: preferred for large goiter, suspicious nodules/cancer, compressive symptoms, selected pregnancy cases, or severe ophthalmopathy.

 

3. Medical Treatment

  • Methimazole (MMI): First-line antithyroid drug in most patients.

  • Carbimazole: Prodrug of methimazole; commonly used outside the United States.

  • Propylthiouracil (PTU): Preferred during the first trimester of pregnancy and in thyroid storm.

  • Propranolol: Beta-blocker used for palpitations, tremor, and anxiety.

  • Atenolol: Beta-blocker used for symptomatic control.

 

4. Surgical / Procedural Treatment

Thyroidectomy for:

  • Large goiter
  • Suspected cancer
  • Compressive symptoms
  • Need for rapid definitive control

Complications

• Thyroid storm
• Atrial fibrillation
• Heart failure
• Osteoporosis
• Muscle weakness
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• Infertility
• Pregnancy complications

Prognosis

–Graves Disease has a good prognosis with appropriate treatment.


–Many patients achieve remission after antithyroid therapy, while others require definitive treatment.


-Prognosis depends on:
• Disease severity
• Goiter size
• Smoking status
• Presence of ophthalmopathy

Key Points / Clinical Pearls

• Graves Disease is the most common cause of hyperthyroidism.
• It is an autoimmune disease caused by TSH receptor stimulation.
• TSH receptor antibodies (TRAb) are the key diagnostic antibodies.
• Typical thyroid function pattern: ↓ TSH + ↑ Free T4/T3.
• Common symptoms include weight loss, heat intolerance, tremor, and palpitations.
• Graves Disease causes a diffuse, hyperfunctioning goiter.
• Graves ophthalmopathy is a characteristic extrathyroid manifestation.
• Smoking worsens Graves eye disease.
• Beta-blockers help control symptoms but do not treat the underlying cause.

  • Ross DS, Burch HB, Cooper DS, et al. 2016 American Thyroid Association Guidelines for Diagnosis and Management of Hyperthyroidism and Other Causes of Thyrotoxicosis. Thyroid. 2016;26(10):1343-1421. Thyroid .
  • Kahaly GJ, Bartalena L, Hegedüs L, Leenhardt L, Poppe K, Pearce SH. 2018 European Thyroid Association Guideline for the Management of Graves' Hyperthyroidism. Eur Thyroid J. 2018;7(4):167-186. European Thyroid Journal .
  • Smith TJ, Hegedüs L. Graves' Disease. N Engl J Med. 2016;375(16):1552-1565. New England Journal of Medicine .
  • Bartalena L, Kahaly GJ, Baldeschi L, et al. The 2021 European Group on Graves' Orbitopathy (EUGOGO) Clinical Practice Guidelines for the Medical Management of Graves' Orbitopathy. Eur J Endocrinol. 2021;185(4):G43-G67. European Journal of Endocrinology .
  • National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK). Graves' Disease . National Institutes of Health.
  • National Library of Medicine (NIH). Graves Disease . StatPearls.