Subclinical hypothyroidism occurs when the thyroid gland is stressed but still producing sufficient thyroid hormone. It is detected when the levels of Thyroid Stimulating Hormone or TSH is elevated. This indicates that increased stimulation is required for the thyroid gland to function normally.
TSH is produced by the pituitary gland which controls the production of thyroid hormones from the thyroid gland. An increase in TSH occurs when there is disease of the pituitary or when the thyroid gland is not producing enough thyroid hormones. The control of thyroid hormone secretion is regulated via a feedback loop whereby the pituitary senses the level of circulating hormone and adjusts its level of TSH production. Thus when the T3 and T4 levels are low the pituitary increases its production of TSH to try and compensate. Rarely the pituitary may secrete excess amounts of TSH due to a tumour of its TSH-secreting cells (a TSH-oma). However in this instance the T3 and T4 are high and the person’s symptoms are of an overactive thyroid.
In order for diagnosis to be made, the levels of thyroid hormones T3 (triiodothyronine) and T4 (thyroxine) must also be measured. Only when these are normal in the face of raised TSH is subclinical hypothyroidism present. There may or may not be symptoms.
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The commonest cause of subclinical hypothyroidism is chronic autoimmune thyroiditis, also known as Hashimoto’s thyroiditis. In this condition a person’s immune system attacks the thyroid gland, producing antibodies against it. It occurs in up to 10% of the population, being more common in women and increasing with age.
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As with any disease, it is important that you watch for the early warning signs of hyperthyroidism. However, only your doctor can tell for sure whether or not you have the disease. Your doctor may examine:
- your history and physical appearance
- the amount of thyroid hormones, thyroid stimulating hormone (TSH), and thyroid stimulating antibodies in your blood
- the structure and function of your thyroid gland, using thyroid imaging, which takes a picture of the gland after you have been given a small amount of radioactive iodine
What do antithyroid drugs do?
Antithyroid drugs block pathways leading to thyroid hormone production.
Antithyroid drugs used in this country are Propylthiouracil (PTU) and Tapazole®. Some physicians will recommend antithyroid medication as a first line of treatment to see if the patient is one of the lucky 30% of patients who go into a remission after taking antithyroid medication for one to two years. (Patients are said to be in remission if their hyperthyroidism does not recur after discontinuing the antithyroid drugs.) If antithyroid drugs do not work for the patient, then physicians usually recommend radioactive iodine.
Antithyroid drugs are also used to treat very young children, older patients with heart conditions, and pregnant women. For severe or complicated cases of hyperthyroidism, especially in older patients, PTU or Tapazole® can be given for four to six weeks to bring the hyperthyroidism under better control prior to administering radioactive iodine treatment.
In cases when women are diagnosed with Graves’ disease while they are pregnant, PTU is prescribed. The smallest dose possible is given because the medication does cross over to the fetus. The mother should be checked every three to four weeks during the pregnancy so that the lowest possible dose can be given. Too much PTU can cause fetal goiter, hypothyroidism, and mental retardation.
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Are there any side effects?
Antithyroid drugs cause side effects in about 10% of patients. Reactions can include:
- skin rash
- swollen, stiff, painful joints
- sore throat and fever
- low white blood count, which can lead to serious infections
- jaundice (yellow coloring of the skin) and, rarely, liver failure.
Most side effects clear up once the drugs are stopped. If you think you are having a reaction to anti-thyroid drugs, call your doctor immediately.
What can be expected with antithyroid drug treatment?
- Several pills are taken from one to four times a day, every day for six to 24 months.
- Some patients complain that the pills have an unpleasant smell and taste.
- There is usually some symptom relief within one to two weeks. In some cases, it can take several months to relieve symptoms.
- Antithyroid drugs have a relatively low success rate. While PTU or Tapazole® may correct the problem temporarily or for a few years, the chances of a permanent remission are about 30% once the drugs are stopped.
- The likelihood of achieving a permanent remission is increased if the patient takes the medication for one to two years.
- There are side effects in 10% of the people treated with Tapazole® or PTU. These are:
- skin rash over most of the body swollen, stiff, painful joints
- sore throat and fever — if this happens, the antithyroid drugs should be stopped immediately and the physician contacted
- jaundice
- liver damage, which is fatal in rare cases
- Because antithyroid drugs pass into breast milk, only PTU in a dosage less than 200 mg a day is advised if the baby is not weaned.
- Within 15 years, the thyroid gland may burn out, resulting in hypothyroidism, and the patient will need thyroid hormone replacement.
As with any disease, it is important that you watch for the early warning signs of hypothyroidism. However, only your doctor can tell for sure whether or not you have the disease. Your doctor may examine:
- your history and physical appearance
- the amount of thyroid hormones, thyroid stimulating hormone (TSH), and antithyroid antibodies in your blood.
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Subclinical hypothyroidism is also more common in those who have had previous radioactive iodine treatment for overactive thyroid conditions. Other causes of hypothyroidism are subacute thyroiditis and postpartum thyroiditis which are transient and usually reversible. Autoimmune hypothyroidism in children and adolescents is reversible in up to 20%. Elevated TSH can also occur with recovery from non-thyroidal illness, certain drugs (such as dopamine antagonists and amiodarone) and adrenal insufficiency.
Progression from subclinical hypothyroidism to overt hypothyroidism is said to be about 2-5% per annum. It is more likely to occur with higher TSH values and when there are positive antibodies. Progression is also more likely in men with the condition. Treatment is controversial. Some advocate treatment as the condition has been associated with coronary heart disease.
If the TSH is high, a repeat test in 3 months should always be done to exclude transient, reversible causes of hypothyroidism. Additional tests to determine the presence of thyroid antibodies would be also be recommended. Treatment then depends on the absolute value of TSH and the presence of symptoms. Treatment may also be considered in the presence of goitre (an enlargement of the thyroid gland) or during pregnancy.
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Treatment of symptomatic patients with subclinical hypothyroidism should be continued for 3-6 months before deciding whether or not there is improvement. The risks of thyroxine replacement are few if the TSH levels are kept in the normal range. If the TSH falls below normal there is then a risk of heart palpitations. Response to treatment should be monitored by blood tests, checking it every 6-8 weeks initially, at 3 months and 6 months after stabilisation, and then once a year. Starting doses are in the range of 50 – 100 µg, although 25 µg may be sufficient. Dose adjustment is by increments of 25 – 50 µg. In those above 60 or where there is ischaemic heart disease the 25 µg starting dose and dose adjustment is preferred. The T4 and TSH levels should be within the normal ranges. Low TSH and high-normal or raised T4 are suggestive of overtreatment.
Subclinical hypothyroidism is a common condition occurring in about 10% of the population. Treatment with thyroxine may be commenced in the presence of persistently high TSH levels and the presence of anti-thyroid antibodies. TSH levels of 5 – 10 mU/L without antibodies may be observed.
