The thyroid is a small butterfly-shaped gland that sits at the base of the neck. It releases thyroid hormones that help regulate many organs and essential body functions, including growth, development, and metabolism.
In some people, the thyroid can become overactive and produce too many hormones, negatively affecting the body. This is called hyperthyroidism. There are numerous potential causes of hyperthyroidism, and cases can range from mild to severe.
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Subclinical hyperthyroidism is a mild form of hyperthyroidism. It occurs when a person has low thyroid-stimulating hormone (TSH) levels but has normal triiodothyronine (T3) and thyroxin (T4) thyroid hormone levels.
Typically, the pituitary gland (a tiny hormone-releasing organ at the base of the brain) releases TSH, which acts on the thyroid. In response, the thyroid produces and releases two thyroid hormones, T3 and T4. When these hormones are released, they feed back to the pituitary gland, telling it to down-regulate the release of TSH.
This feedback system is essential because it prevents the excessive production of thyroid hormones and keeps the system in balance. However, this process is impaired in subclinical hyperthyroidism.
There are many potential causes of subclinical hyperthyroidism, including the following:
Graves’ disease is an autoimmune disorder that causes increased thyroid hormone production. This happens because the immune system produces antibodies that attack the thyroid gland.
Thyroiditis is inflammation of the thyroid gland. It can be caused by viruses, bacterial infections, postpartum, and medications, such as amiodarone and interferons.
A toxic multinodular goiter is when lumps (nodules) in the thyroid gland cause increased thyroid hormone production. Goiters are usually benign (not cancerous).
Thyroid hormone replacement is frequently prescribed for people with hypothyroidism. However, over-replacement (generally through levothyroxine) is the most common cause of subclinical hyperthyroidism.
A thyroid adenoma is an overgrowth of normal thyroid tissue, presenting as a benign tumor. This can increase hormone production and lead to subclinical hyperthyroidism.
Pregnancy can cause subclinical hyperthyroidism, particularly during the first trimester.
The thyroid needs iodine to make thyroid hormones. However, excess iodine intake, usually when ingested for medical purposes, such as for contrast for imaging purposes, can cause hyperthyroidism.
Medication that can lower TSH, such as steroids and dopamine, can cause subclinical hyperthyroidism.
The prevalence of subclinical hyperthyroidism varies based on sex, age, and location.
Subclinical hyperthyroidism is a very common disorder and can affect anyone. However, subclinical hyperthyroidism appears to be more common in people taking thyroid hormone replacement, the elderly, and pregnant women.
Despite excessive iodine being a cause of subclinical hyperthyroidism, this condition is significantly prevalent in iodine-deficient regions due to a higher incidence of toxic goiter. In these areas, subclinical hyperthyroidism prevalence can reach up to 15%.¹
Here are some facts about subclinical hyperthyroidism:
About 0.7% of all people in the United States have a mild form of subclinical hyperthyroidism
About 1.8% have a more severe form of subclinical hyperthyroidism
Around 20% of people receiving thyroid hormone replacement develop subclinical hyperthyroidism
Often, people with subclinical hyperthyroidism have no symptoms. They may be unaware they have it until a doctor diagnoses them.
Depending on the cause, subclinical hyperthyroidism can progress very slowly. However, it still has the potential to affect the quality of life.
Subclinical hyperthyroidism symptoms are similar to those of overt hyperthyroidism, including the following:
Rapid heartbeat and heart palpitations
Tremors or feeling shaky
Nervousness and anxiety
Thin, warm, and moist skin
Changes to the menstrual cycle
Reduced feeling of wellbeing
Subclinical hyperthyroidism can either be a temporary or lifelong condition. It can progress to true (overt) hyperthyroidism. However, this only occurs in 5% of people with Grade II (severe) subclinical hyperthyroidism and is even rarer in people with Grade I (mild) subclinical hyperthyroidism.²
Left untreated, complications of subclinical hyperthyroidism can arise. These mainly depend on how long someone has subclinical hyperthyroidism before starting treatment. Fortunately, the potential problems caused by subclinical hyperthyroidism are reversible.
The potential complications of subclinical hyperthyroidism can include the following:
Thyroid hormones influence the electrical activity of the heart. In hyperthyroidism, the heart works harder, and the mass of the left ventricle increases. Someone with subclinical hyperthyroidism is at risk of developing the following:
Reduced exercise tolerance
Irregular heart rate (arrhythmia)
Rapid heart rate (tachycardia)
The risk is higher in people over 65 and those with pre-existing heart problems or other risk factors.
Thyroid hormones increase bone remodeling, which can lead to more bone loss. In subclinical hyperthyroidism, the risk of reduced bone density, fractures, and the development of osteoporosis is higher. This is particularly an issue in women who have been through menopause.
Early research has suggested that subclinical hyperthyroidism is linked to the development of dementia and Alzheimer’s disease.³
Generally, screening is not recommended for asymptomatic people; it’s typically used in populations at greater risk of thyroid disease.
TSH is the best indicator for the initial assessment of thyroid disease. If TSH is abnormal, then T4 and T3 are also tested.
Diagnosis of suspected subclinical hyperthyroidism is based on blood test (laboratory) findings. This includes TSH, T3, and T4.
It’s crucial to differentiate subclinical hyperthyroidism from overt hyperthyroidism. Normal levels of TSH are between 0.4–4.0 mIU/L. When TSH is below this range, it suggests subclinical hyperthyroidism.
In subclinical hyperthyroidism, T4 and T3 levels are within a normal range. T4 should be between the normal range of 4.6–12.0 ug/dL, and T3 should be within the normal range of 80–180 ng/dL. In overt hyperthyroidism, thyroid hormone levels are above the normal range.
There are two categories of subclinical hyperthyroidism:
Grade I subclinical hyperthyroidism: TSH levels are between 0.1–0.4 mIU/L. This is the more common type and is usually the milder form.
Grade II subclinical hyperthyroidism: TSH levels are below 0.1 mIU/L. This is usually the more severe form.
Blood tests may not be enough to confirm a diagnosis of subclinical hyperthyroidism. A physical exam and medical history analysis can help confirm the diagnosis. This can help rule out other causes of low TSH levels, such as pituitary or hypothalamic disease and sick euthyroid syndrome.
TSH may also be below the healthy range in older people, even if they don’t have subclinical hyperthyroidism. Other causes of low TSH levels unrelated to subclinical hyperthyroidism must be ruled out.
Subclinical hyperthyroidism doesn’t always require treatment. Often, patients are advised to “watch and wait” to see whether their thyroid function improves.
Some studies have found that TSH levels spontaneously normalize in almost 50% of people with subclinical hyperthyroidism. Spontaneous remission is more common when the subclinical hyperthyroidism is caused by Graves’ disease rather than a toxic multinodular goiter.
However, treatment is typically recommended for people with severe subclinical hyperthyroidism if they fall into one of the following categories:
They are over the age of 65
They have heart disease, osteoporosis, or symptoms of hyperthyroidism.
They are under age 65 but have been through menopause and are not taking estrogen or bisphosphonate medication.
People with mild subclinical hyperthyroidism may also be offered treatment based on the guidelines above. A doctor may refer their patient with subclinical hyperthyroidism to an endocrinologist (a doctor specializing in hormones) if there is a risk of bone density issues and TSH levels are less than 0.1 mIU/L.
Treatment should be individualized and determined by the cause and severity of the condition. The treatment goal is to restore the thyroid’s normal function and prevents adverse effects.
Treatment options are similar to those offered for overt hyperthyroidism. They may include:
The main antithyroid medications prescribed are methimazole (Tapazole) and propylthiouracil. They can help restore thyroid function by stopping it from producing too many thyroid hormones.
In addition, some studies have found that methimazole can help with bone density and cardiac-related symptoms of subclinical hyperthyroidism (such as a fast heart rate). Antithyroid medications usually are taken for at least six months to reach and maintain normal thyroid function.
Beta-blockers can help manage some of the cardiovascular-related effects of subclinical hyperthyroidism. However, they don’t impact thyroid hormone levels. Thus, they aren’t a direct treatment for subclinical hyperthyroidism.
Using the beta-blocker bisoprolol for six months can improve cardiovascular-related symptoms, reduce the risk of arrhythmias, and reduce the heart rate and left ventricular mass.
Thyroid surgery involves removing part of or the entire thyroid gland. Ablative therapies such as surgery are typically recommended for young people with subclinical hyperthyroidism caused by a toxic multinodular goiter or Graves’ disease.
Radioactive iodine administration is a suitable choice for people with pre-existing heart disease and over the age of 60 with toxic multinodular goiter. This treatment involves ingesting radioactive iodine, which is absorbed by the thyroid gland. It causes the thyroid gland to shrink, preventing the overproduction of hormones.
NSAIDs and steroids can help with symptom management in thyroiditis, a common cause of subclinical hyperthyroidism. Most forms of pain relief, such as ibuprofen and aspirin, are available over the counter, but steroids require a prescription from a doctor.
TSH and thyroid hormone levels should be monitored and reassessed every two to four months. This is particularly important for people who have been recommended to watch and wait rather than undertake treatment.
Not everyone with subclinical hyperthyroidism requires treatment because it’s not known how advantageous it would be. There is limited evidence linking the adverse effects of subclinical hyperthyroidism, such as reduced quality of life, bone density, heart failure, and other heart complications, to the benefits of treatment.⁴
For example, one study found that treating people with Grade I subclinical hyperthyroidism didn’t have a benefit on adverse heart-related problems, such as arrhythmia. In addition, all forms of treatment carry their risks.
Currently, it’s not clear whether the benefits of treating subclinical hyperthyroidism outweigh the risks.⁵ Potential treatment risks include hypothyroidism and relapse of subclinical hyperthyroidism.
If you have concerns about your thyroid function or are experiencing possible symptoms of hyperthyroidism, see your doctor as soon as possible. Your doctor can run tests to determine the cause of your symptoms.
If needed, they can then recommend the best treatment for your circumstances based on your medical history and the cause of your subclinical hyperthyroidism.
Subclinical hyperthyroidism is a condition in which TSH levels are low while thyroid hormone levels are within a normal range.
While subclinical hyperthyroidism can appear harmless and present with no symptoms, it’s indispensable for someone with the condition to regularly monitor their TSH and thyroid hormone levels and undertake any recommended treatment. Subclinical hyperthyroidism can progress to overt hyperthyroidism and can cause several preventable complications.
In subclinical hyperthyroidism, levels of TSH are low, while T3 and T4 levels are within a normal range. In overt hyperthyroidism, TSH levels are low, while T3 and T4 levels are high. Subclinical hyperthyroidism is typically much milder than hyperthyroidism; it often occurs with no symptoms and doesn’t require treatment. Subclinical hyperthyroidism can progress to overt hyperthyroidism.
Subclinical hyperthyroidism is when levels of TSH are low, but T3 and T4 levels are normal. It can be caused by various factors, including Graves’ disease, thyroid medications, tumors, inflammation, and other factors. It is classified as mild or severe based on TSH levels.
Toxic nodule and toxic multinodular goiter | American Thyroid Association
Subclinical hyperthyroidism | Thyroid UK
Thyroid function tests | Endocrine Web
Thyroid disease: challenges in primary care | NPS MedicineWise