OVERVIEW

What is toxic multinodular goiter?

Normally, the thyroid-stimulating hormone (TSH) secreted by the pituitary gland acts on thyroid follicular cells, prompting them to synthesize and secrete thyroid hormones.

However, for certain reasons, thyroid follicular cells may no longer "obey" TSH's commands. They proliferate on their own, forming thyroid nodules and goiter, and autonomously synthesize and secrete excessive thyroid hormones. This leads to hyperthyroidism, causing increased excitability in the nervous, circulatory, and digestive systems, as well as hypermetabolism. This condition is known as toxic multinodular goiter.

Is toxic multinodular goiter common?

This disease is a common cause of hyperthyroidism. In iodine-deficient regions, 48% of hyperthyroidism cases are caused by this condition.

Who is more likely to develop toxic multinodular goiter?

People with iodine deficiency and the elderly are more susceptible to this disease.

SYMPTOMS

What are the common manifestations of toxic multinodular goiter?

The manifestations of this disease are those of hyperthyroidism, and symptoms typically involve multiple organ systems, including:

• Skin: Excessive sweating, warm and smooth skin, itching, brittle nails, etc.;
• Cardiovascular system: Palpitations, increased heart rate, elevated blood pressure, etc.;
• Endocrine and metabolism: Decreased blood lipids, weight loss, elevated blood sugar, thyroid enlargement;
• Respiratory system: Cough, difficulty breathing, especially after activity;
• Digestive system: Increased bowel movements, frequent hunger, increased appetite, liver function impairment, and difficulty swallowing if the thyroid is significantly enlarged;
• Genitourinary system: Frequent urination, increased nocturia, prolonged menstrual cycles, anovulation, amenorrhea in women; gynecomastia, decreased libido, erectile dysfunction, reduced sperm count in men;
• Bones: Osteoporosis, fractures;
• Neuropsychiatric system: Hand tremors, anxiety, irritability, mood swings; elderly patients may exhibit apathy.

Can toxic multinodular goiter lead to serious consequences?

• If left uncontrolled for a long time, the disease can affect the heart, potentially leading to heart failure or even sudden death.
• Severe cases may develop thyroid storm, which is life-threatening.
• Patients with this condition have an increased risk of thyroid cancer compared to the general population.

CAUSES

What causes toxic multinodular goiter?

The exact cause of toxic multinodular goiter is not entirely clear. What is certain is that the disease is directly caused by diffuse hyperplasia of thyroid follicular cells.

The "superior authority," the pituitary gland, uses TSH to "supervise and urge" the thyroid to synthesize and secrete thyroid hormones:

• When thyroid hormone levels are low, TSH increases to promote the synthesis and secretion of thyroid hormones;

• When thyroid hormone levels rise, the "upstream command" TSH decreases, leading to a reduction in the synthesis and secretion of thyroid hormones.

In 20%–80% of patients with toxic nodular goiter, there is a genetic mutation in the TSH receptor within the nodules. This is equivalent to a malfunction in the "messenger" that receives instructions from higher authorities, causing the thyroid follicular cells to behave as if they are constantly under high TSH signaling (even though TSH levels are normal or low). As a result, they proliferate into nodules and uncontrollably secrete excessive thyroid hormones, leading to a series of hyperthyroidism symptoms.

Additionally, under prolonged iodine deficiency, thyroid follicular cells undergo compensatory hyperplasia, forming numerous nodules to "work overtime" and ensure sufficient thyroid hormone production to meet the body's needs. If iodine intake suddenly normalizes or even becomes excessive at this stage, the hyperplastic thyroid nodules may produce an excess of thyroid hormones, triggering a series of hyperthyroidism symptoms.

DIAGNOSIS

What tests are needed to diagnose toxic multinodular goiter?

• Thyroid function: Used to diagnose whether hyperthyroidism is present and its severity.
• Thyrotropin receptor antibody: Used to rule out hyperthyroidism caused by Graves' disease. A positive result usually indicates Graves' disease.
• Thyroid peroxidase antibody and thyroglobulin antibody: Used to assist in diagnosing whether other thyroid diseases, such as Hashimoto's thyroiditis, are present.
• Thyroid ultrasound: Used to evaluate the size, shape, texture, and number of thyroid nodules, providing a preliminary assessment of their nature.
• Thyroid scintigraphy: Used to assist in the diagnosis of toxic multinodular goiter. The scan shows multiple areas of increased uptake of radioactive iodine or technetium in the thyroid.

Which diseases can toxic multinodular goiter be easily confused with?

This condition can be easily confused with hyperthyroidism caused by toxic thyroid adenoma, pituitary thyrotropinoma, or Graves' disease, as well as thyrotoxicosis caused by autoimmune thyroiditis (such as Hashimoto's thyroiditis). The above-mentioned common manifestations and related tests can help differentiate them.

TREATMENT

Which department should I visit for toxic multinodular goiter?

Endocrinology or Thyroid and Breast Surgery. In some hospitals, it may be called Thyroid and Breast Surgery or Two-Gland Surgery.

Does toxic multinodular goiter always require treatment?

If the patient develops "overt hyperthyroidism"—where thyroid function tests show thyroid-stimulating hormone (TSH) below the normal range, and free thyroxine (FT4) and/or triiodothyronine (T3) above the normal range—treatment is necessary.

If the patient only has "subclinical hyperthyroidism"—where TSH is below the normal range but FT4 and T3 are normal—treatment may not always be required. The decision should be made after a doctor’s evaluation. You can search for "subclinical hyperthyroidism" on the Dingxiang Doctor App for more details.

How is toxic multinodular goiter treated?

Treatment options include:

• Symptom control: Beta-blockers (e.g., propranolol, atenolol) can be used to manage symptoms like palpitations and tremors. These can be gradually discontinued once symptoms improve.
• Radioactive ¹³¹I therapy or thyroidectomy: These methods can cure the condition and are preferred. However, hypothyroidism may develop afterward, requiring lifelong medication. Radioactive ¹³¹I is usually the first choice, but surgery is preferred if the goiter compresses the trachea or esophagus or if thyroid cancer is present.
• Antithyroid drugs (ATDs): Such as methimazole and propylthiouracil. ATDs are not suitable for long-term treatment of hyperthyroidism caused by this condition and do not provide a cure. They are only used in special cases, such as during breastfeeding.

What should patients with toxic multinodular goiter pay attention to before and after radioactive ¹³¹I therapy?

Before treatment: Discontinue methimazole for 3 days or propylthiouracil for at least 2 weeks. Stop iodine-containing vitamins 7–10 days prior, avoid iodine-rich foods and medications for 2–3 weeks, and discontinue amiodarone 3–6 months in advance.

After treatment: Since ¹³¹I is radioactive:

• Drink plenty of water and urinate frequently within the first 2 days.
• Stay at home for the first week, maintain a distance of at least 1.8 meters from others, and avoid sharing utensils.
• Minimize close contact with family members, especially children and pregnant women, for 1 month.
• Use a separate bathroom if possible, flush multiple times after use to prevent contamination.
• Avoid pregnancy for 6 months post-treatment.

Is follow-up necessary after treatment for toxic multinodular goiter? How?

Yes.

• For ATD users: Monitor thyroid function every 4–6 weeks, along with liver function and blood tests, until stable.
• For radioactive ¹³¹I therapy: Check thyroid function at 6–8 weeks post-treatment, then every 4–8 weeks. If remission is confirmed, intervals can be extended to at least annually.
• For surgery patients: Monitor thyroid function 4–6 weeks post-surgery. If thyroid hormone replacement begins, check every 6–8 weeks.

What should pregnant women do if they suspect toxic multinodular goiter?

Pregnant women suspected of having this condition should avoid thyroid scintigraphy and radioactive ¹³¹I therapy. Only ATDs are suitable. Propylthiouracil is recommended in the first trimester, with the option to switch to methimazole later. Low-dose beta-blockers may be used short-term for symptom relief.

After breastfeeding ends, thyroid scintigraphy can be performed for definitive diagnosis and treatment adjustment.

Can toxic thyroid adenoma be cured?

Yes, radioactive ¹³¹I therapy and surgery can cure this condition.

DIET & LIFESTYLE

What should patients with toxic multinodular goiter pay attention to in daily life?

• Maintain a comprehensive and balanced diet with adequate intake of protein-rich and vitamin-rich foods.
• Follow an iodine-restricted diet unless pregnant or breastfeeding.
• Avoid alcohol, tea, and coffee consumption.
• Quit smoking.
• Ensure sufficient sleep and maintain an optimistic, relaxed mood.

Can patients with toxic multinodular goiter have normal fertility?

It is recommended that patients conceive only after achieving remission, normal thyroid function, or complete cure. Female patients taking thiourea drugs who urgently wish to become pregnant should switch to propylthiouracil.

Is toxic multinodular goiter hereditary?

The disease has some genetic predisposition, but offspring will not necessarily develop it.

PREVENTION

Can toxic multinodular goiter be prevented?

There is no specific prevention method for this disease, only early detection and early treatment.