Hyperthyroidism is a syndrome that expresses excessive secretion of thyroid hormone from the thyroid gland. Hyperthyroidism and thyrotoxicosis are not the same. Thyrotoxicosis is a condition in which the body is affected by these excess thyroid hormones. This effect may not be present in every case of hyperthyroidism. That is, hyperthyroidism can lead to thyrotoxicosis.

The thyroid gland is an endocrine organ in the neck, in the anterior lower region of the trachea, close to the breastbone. It is the largest endocrine gland in our body. It weighs 20-30 grams. It has two lobes. It has two symmetrical lobes on the right and left. It produces thyroid hormones and calcitonin hormone.

Hyperthyroidism is a syndrome that expresses excessive secretion of thyroid hormone from the thyroid gland. Hyperthyroidism and thyrotoxicosis are not the same. Thyrotoxicosis is a condition in which the body is affected by these excess thyroid hormones. This effect may not be present in every case of hyperthyroidism. That is, hyperthyroidism can lead to thyrotoxicosis.

Thyroid hormones are produced in the follicles of the thyroid gland as a result of the conversion of iodides in the colloid structure called thyroglobulin into thyroid hormones by the thyroid peroxidase enzyme and secreted into the blood. In order for thyroid hormones to be secreted into the blood, stimulation is expected from the pituitary gland with the hormone TSH. Depending on the diurnal rhythm of the body, this warning usually peaks between midnight and 04:00 in the morning, and thyroid hormone secretion is increased.

The majority of thyroid hormones are secreted as T4, which is inactive thyroid hormone, and a small amount as T3, which is active thyroid hormone. The T4 hormone is then activated by converting to T3 in the circulation.

The most common causes of hyperthyroidism are:

  • Graves’ disease (autoimmune, more common in young people)
  • Toxic multinodular goiter (more common in the elderly)
  • Exogenous iodine-induced hyperthyroidism (Jod-Basedow phenomenon)
  • Thyroid adenomas (Plummer’s disease)
  • De Quervain’s thyroiditis (subacute thyroiditis)
  • Postpartum thyroiditis
  • Thyroiditis due to inappropriate intake of thyroid medication (excessive use of thyroxine in the diet)
  • Ectopic thyroid tissues (especially ovaries)
  • Medicines (amiadaron or iodine-containing medicines)
  • Thyroid cancers
  • Hydatiform mole
  • TSH-secreting pituitary tumors
  • Insensitivity of the pituitary to thyroid hormones

Hyperthyroidism is a picture affected by iodine intake. It is more common in areas with high dietary iodine intake.

Depending on the cause of hyperthyroidism, the pathology in the thyroid gland may vary. Symptoms and clinical picture in patients may vary accordingly. Detailed information about each cause of hyperthyroidism is given in our other articles.

Symptoms of hyperthyroidism:

An increase in appetite is frequently seen in patients with hyperthyroidism. At the same time, these patients may develop irritability, palpitations, tremors, shortness of breath, fatigue, diarrhea or increased intestinal motility due to the effect of thyroid metabolism. The body’s metabolism is accelerated. Weight loss may occur despite muscle weakness, heat intolerance, and sweating. Menstrual irregularities can also be added to the table.

As hyperthyroidism increases the body’s metabolism, energy production is increased. The patient may complain that he has lost weight despite not dieting.

In the case of hyperthyroidism, it is not necessary to have an enlargement or tenderness in the thyroid gland. It varies depending on the underlying cause.

Diagnosis of hyperthyroidism:

The first thing to do in all patients with suspected thyroid disease is to examine the thyroid hormone profile. TSH, T3 and T4 hormones are examined. TSH is a hormone secreted from the pituitary and provides the balance of thyroid hormones (T3 and T4). If thyroid hormones are low, TSH secretion from the pituitary gland increases during the hours that need to be increased. TSH secretion is also stimulated by the hormone TRH from the hypothalamus in the brain. This cycle continues according to the diurnal rhythm of our body.

When T3 and T4 are insufficient, TSh is secreted, increasing the secretion of these hormones from the thyroid. When TSH is secreted in excess, T3 and T4 hormones can also increase excessively. This indicates an abnormal condition. When TSH is insufficient, T3 and T4 hormones can be secreted insufficiently. If the thyroid gland secretes T3 and T4 hormones independently of TSH hormone, TSH hormone levels are reduced in order not to worsen the situation. This reduction occurs when the pituitary detects the T3 level in the blood and suppresses TSH secretion.

Since hyperthyroidism can cause atrial fibrillation in the heart, one of the first tests that may come to mind in patients with atrial fibrillation or palpitation may be to evaluate thyroid hormone levels.

Thyroid ultrasonography can be applied in patients with hyperthyroidism. Thyroid nodules, if present, may be seen.

Since most causes of hyperthyroidism are Graves’ disease or toxic multinodular goiter, the thyroid gland may be enlarged enough to be palpable on examination. In some patients, iodine activity of the thyroid can be evaluated with a radioactive iodine uptake test. Radoactive iodine is taken up more by the active thyroid gland.

Although there is hyperthyroidism, low radioactive thyroid uptake may suggest De Quervain’s thyroiditis (subacute thyroiditis), painless thyroiditis, oral iodine-induced hyperthyroidism, and drug-induced hyperthyroidism. Since thyroid follicles are disrupted in thyroiditis patients, they send their thyroid hormones to the blood and hyperthyroidism occurs in the blood. Therefore, the uptake of radioactive iodine remains low, as the active thyroid secretion process works poorly.

Thyroid antibodies can also be evaluated while investigating the causes of hyperthyroidism. Thyroid antibodies can be examined, especially in cases with suspected Graves’ disease.

Radioisotope thyroid screening using technetium-99m pertechnetate in combination with radioactive iodine may be required in some patients to evaluate the activity of the thoriodi gland. With this scan, hyperactive, normal or hypoactive regions of the thyroid are detected. The hypoactive areas detected in this scan are the main problem areas. Thyroid functions do not work in hypoactive areas and there is a possibility of thyroid cancers that cause functional changes in the thyroid tissue.

Treatment of hyperthyroidism:

Treatment of hyperthyroidism depends on the cause of the hyperthyroidism. First, the active symptoms of the patient should be treated, and then the cause of the hyperthyroidism should be treated.

Beta blockers can be used for palpitations and anxiety symptoms, which are the most disturbing symptoms of hyperthyroidism. Agents such as verapamil can be used in patients who cannot use beta-blockers. This condition of the patient needs to be evaluated in detail.

The definitive treatments for hyperthyroidism are treatment for the underlying cause. For this, radioactive iodine treatment (RAI), thionamide treatment or surgical treatment are applied. Which one will be preferred will vary according to the cause of the disease and the exact diagnosis. Close follow-up is important because patients receiving these treatments will develop a predisposition to hypothyroidism.

Antithyroid drugs such as thionamide (methimazole or propylthiouracil) can be used. Antithyroid drugs suppress the synthesis of thyroid hormone and prevent tissues from being exposed to excess thyroid hormone. It is not a permanent treatment. Hyperthyroidism occurs again when the drug is discontinued. It may take a few months for the thyroid hormone level to return to normal. If a choice between methimazole or propylthiouracil is required, it is not used because it may cause congenital defects in pregnant women, although methimazole is safer. Propylthiouracil is preferred in pregnant women. Side effects such as agranulocytosis, hepatitis, vasculitis and drug-induced lupus may rarely be seen in patients treated with antithyroid drugs. In case of sudden onset of fever, chills, sore throat or signs of infection, it is recommended that patients discontinue the drug and be checked.

Radioactive iodine therapy is another definitive treatment method. It is applied with iodine-131. Radioactive iodine uptake test is applied with iodine-124. With a single dose application of iodine-131, it destroys the thyroid tissue in the thyroid gland and suppresses thyroid hormone production. It should be checked that the patient receiving iodine-131 treatment is not pregnant. It may take several months for thyroid hormones to return to normal after iodine-131 treatment. In some patients, if there is no normalization, radioactive iodine-131 treatment may be required again. Thyroid hormone support may be required if hypothyroidism develops when there is excessive suppression after treatment.

Surgical treatment is one of the other definitive treatment methods of hyperthyroidism. Depending on the underlying cause, total or partial surgery may vary. Preparation with antithyroid drugs may be required before surgical treatment. Hypothyroidism may develop after surgical treatment. There may also be risks and complications arising from the surgery itself. Post-surgical hypothyroidism can be improved with thyroid hormone supplementation.

When hyperthyroidism is treated, it is usually a benign picture. However, if left untreated, it can cause serious negative consequences such as thyrotoxicosis and thyroid storm.

Excessive suppression due to antithyroid drugs used for the improvement of hyperthyroidism in pregnant women should be carefully monitored as it may cause hypothyroidism in the baby.

On the other hand, neonatal hyperthyroidism, which is the reflection of hyperthyroidism in pregnant women to the baby, can also develop. This condition is usually temporary. It occurs as a result of TSH receptor stimulating antibodies coming from the mother and passing through the placenta, stimulating the thyroid of the baby. It usually resolves spontaneously 5-6 months after birth. However, in some genetic abnormalities, it can be permanent or long-term.