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Thyrotoxicosis

Thyrotoxicosis is a metabolic imbalance that results from thyroid hormone overproduction or thyroid hormone over-release from the gland. The most common form of thyrotoxicosis is Graves' disease, which increases thyroxine production, enlarges the thyroid gland (goiter), and causes multiple system changes.

Incidence of Graves' disease is highest between ages 30 and 40, especially in people with family histories of thyroid abnormalities; only 5% of patients with thyrotoxicosis are younger than age 15

With treatment, most patients can lead normal lives. However, thyroid storm - an acute, severe exacerbation of thyrotoxicosis - is a medical emergency that may lead to life-threatening cardiac, hepatic, or renal consequences.

Causes

Thyrotoxicosis may result from genetic and immunologic factors.

• An increased incidence of this disorder in monozygotic twins points to an inherited factor, probably an autosomal recessive gene.
• This disease occasionally coexists with other endocrine abnormalities, such as diabetes mellitus, thyroiditis, and hyperparathyroidism.
• Thyrotoxicosis may also be caused by the production of autoantibodies (thyroid-stimulating immunoglobulin and thyroid-stimulating hormone [TSH]­binding inhibitory immunoglobulin), possibly because of a defect in suppressor- T-lymphocyte function that allows the formation of autoantibodies.
• In latent thyrotoxicosis, excessive dietary intake of iodine and, possibly, stress can precipitate clinical thyrotoxicosis.
• In a person with inadequately treated thyrotoxicosis, stress - including surgery, infection, toxemia of pregnancy, and diabetic ketoacidosis - can precipitate thyroid storm.

Signs and symptoms

The thyroid gland, which is in the front of the neck, controls the rate of at which the body's cells work (the metabolic rate). In thyrotoxicosis, the rate of metabolism is increased, and this results in most of the symptoms:

• weight loss in spite of increased appetite
• rapid heart rate
• a fine tremor
• increased nervousness and emotional instability
• intolerance of heat, and excessive sweating
• staring, bulging eyes
• enlargement of the thyroid gland, which is at the front of the neck, at the level of the voice box.

Diagnosis

The diagnosis of thyrotoxicosis usually is straightforward and depends on a careful clinical history and physical examination, a high index of suspicion, and routine hormone determinations. The following tests confirm the disorder:

• Radioimmunoassay shows increased serum thyroxine (T4 ) and triiodothyronine (T3 ) concentrations.
• Thyroid scan reveals increased uptake of radioactive iodine 131 in Graves' disease, and usually in toxic multinodular goiter and toxic adenoma. Radioactive uptake is low in thyroiditis and thyrotoxic factitia. This test is contraindicated if the patient is pregnant.
• TSH levels are decreased.
• Thyroid-releasing hormone (TRH) stimulation test indicates thyrotoxicosis if the TSH level fails to rise within 30 minutes after the administration of TRH. TRH testing is rarely necessary and is currently done to highly sensitive TSH assays.
• Ultrasonography confirms subclinical ophthalmopathy.

Treatment

Treatment varies depending on the cause of the condition and the severity of symptoms. Hyperthyroidism is usually treated with antithyroid medications, radioactive iodine (which destroys the thyroid and thus stops the excess production of hormones), or surgery to remove the thyroid.

If the thyroid must be removed with radiation or surgery, replacement thyroid hormones must be taken for the rest of the person's life.

Beta-blockers like propranolol are used to treat some of the symptoms including rapid heart rate, sweating, and anxiety until the hyperthyroidism

Another treatment that is sometimes used is the injection of radioactive iodine ( ¹³¹I, a longer lasting isotope than is used for scanning) which is concentrated in the thyroid gland and results in damage to and destruction of some of the cells of the thyroid. can be controlled.

Prevention

There are no general prevention measures to prevent hyperthyroidism.