Hyperthyroidism is the term for overactive tissue within the thyroid gland, resulting in overproduction and thus an excess of circulating free thyroid hormones: thyroxine (T 4 ), triiodothyronine (T 3 ), or both. Thyroid hormone is important at a cellular level, affecting nearly every type of tissue in the body.
Thyroid hormone functions as a stimulus to metabolism and is critical to normal function of the cell. In excess, it both overstimulates metabolism and exacerbates the effect of the sympathetic nervous system, causing "speeding up" of various body systems and symptoms resembling an overdose of epinephrine (adrenaline). These include fast heart beat and symptoms of palpitations, nervous system tremor and anxiety symptoms, digestive system hypermotility (diarrhea), and weight loss.
On the other hand, a lack of functioning thyroid tissue results in a symptomatic lack of thyroid hormone, termed hypothyroidism.
Signs and symptoms
Major clinical signs include weight loss (often accompanied by an increased appetite), anxiety, intolerance to heat, hair loss, weakness, hyperactivity, irritability, apathy, depression, polyuria, polydipsia, delirium, tremor, pretibial myxedema, and sweating. Additionally, patients may present with a variety of symptoms such as palpitations and arrhythmias (notably atrial fibrillation), shortness of breath (dyspnea), loss of libido, nausea, vomiting, and diarrhea. Long term untreated hyperthyroidism can lead to osteoporosis. In the elderly, these classical symptoms may not be present.
Neurological manifestations can include tremors, chorea, myopathy, and in some susceptible individuals (particularly of Asian descent) periodic paralysis. An association between thyroid disease and myasthenia gravis has been recognized. The thyroid disease, in this condition, is autoimmune in nature and approximately 5% of patients with myasthenia gravis also have hyperthyroidism. Myasthenia gravis rarely improves after thyroid treatment and the relationship between the two entities is not well understood. Some very rare neurological manifestations that are dubiously associated with thyrotoxicosis are pseudotumor cerebri, amyotrophic lateral sclerosis and a Guillain-Barré-like syndrome.
Minor ocular (eye) signs, which may be present in any type of hyperthyroidism, are eyelid retraction ("stare"), extra-ocular muscle weakness, and lid-lag. In hyperthyroid stare (Dalrymple sign) the eyelids are retracted upward more than normal (the normal position is at the superior corneoscleral limbus, where the "white" of the eye begins at the upper border of the iris). Extra-ocular muscle weakness may present with double vision. In lid-lag (von Graefe's sign), when the patient tracks an object downward with their eyes, the eyelid fails to follow the downward moving iris, and the same type of upper globe exposure which is seen with lid retraction occurs, temporarily. These signs disappear with treatment of the hyperthyroidism.
Neither of these ocular signs should be confused with exophthalmos (protrusion of the eyeball) which occurs specifically and uniquely in hyperthyroidism caused by Graves' disease (Note that not all exopthalmos is caused by Graves' disease, but when present with hyperthyroidism is diagnostic of Graves disease). This forward protrusion of the eyes is due to immune mediated inflammation in the retro-orbital (eye socket) fat. Exophthalmos, when present, may exacerbate hyperthyroid lid-lag and stare.
Thyrotoxic crisis (or thyroid storm) is a rare but severe complication of hyperthyroidism, which may occur when a thyrotoxic patient becomes very sick or physically stressed. Its symptoms can include: an increase in body temperature to over 40 degrees Celsius (104 degrees Fahrenheit), tachycardia, arrhythmia, vomiting, diarrhea, dehydration, coma and death.
Causes
Functional thyroid tissue producing an excess of thyroid hormone occurs in a number of clinical conditions.
The major causes in humans are:
- Graves' disease (the most common etiology with 70-80%)
- Toxic thyroid adenoma
- Toxic multinodular goitre
High blood levels of thyroid hormones (most accurately termed hyperthyroxinemia ) can occur for a number of other reasons:
- Inflammation of the thyroid is called thyroiditis. There are a number of different kinds of thyroiditis including Hashimoto's thyroiditis (immune mediated), and subacute thyroiditis (DeQuervain's). These may be initially associated with secretion of excess thyroid hormone, but usually progress to gland dysfunction and thus, to hormone deficiency and hypothyroidism.
- Oral consumption of excess thyroid hormone tablets is possible, as is the rare event of consumption of ground beef contaminated with thyroid tissue, and thus thyroid hormone (termed "hamburger hyperthyroidism").
- Amiodarone, an anti-arrhythmic drug is structurally similar to thyroxine and may cause either under- or overactivity of the thyroid.
- Postpartum thyroiditis (PPT) occurs in about 7% of women during the year after they give birth. PPT typically has several phases, the first of which is hyperthyroidism. This form of hyperthyroidism usually corrects itself within weeks or months without the need for treatment.
Diagnosis
A diagnosis may be suspected on history and physical examination, and is confirmed with blood tests.
Measuring the level of thyroid-stimulating hormone (TSH) in the blood is usually all that is required. A low TSH indicates that the pituitary gland is being inhibited by increased levels of T 4 and/or T 3 in the blood, and is therefore a reliable marker of hyperthyroidism. Rarely, a low TSH indicates primary failure of the pituitary, or temporary inhibition of the pituitary due to another illness (euthyroid sick syndrome) and so checking the T 4 and T 3 is still clinically useful.
Measuring specific antibodies, such as anti-TSH-receptor antibodies in Graves' disease, or anti-thyroid-peroxidase in Hashimoto's thyroiditis—a common cause of HYPOthyroidism—may also contribute to the diagnosis.
Thyroid scintigraphy is a useful test to distinguish between causes of hyperthyroidism, and this entity from thyroiditis.
In addition to testing the TSH levels, many doctors test for T3, Free T3, T4 and/or Free T4 for more detailed results.
The diagnosis of hyperthyroidism is confirmed by blood tests that show a decreased thyroid stimulating hormone (TSH) level and elevated T4 and T3 levels. TSH is a hormone made by the pituitary gland in the brain that tells the thyroid gland how much hormone to make. When there is too much thyroid hormone, the TSH will be low. A radioactive iodine scan (a test that uses injected radioactive iodine to examine the activity of the thyroid gland) will show an enlarged thyroid gland that is over-functioning.
Treatment
The major and generally accepted modalities for treatment of hyperthyroidism in humans involve initial temporary use of suppressive thyrostatics medication, and possibly later use of permanent surgical or radioisotope therapy. All approaches may cause under active thyroid function (hypothyroidism) which is easily managed with levothyroxine supplementation.
Temporary medical therapy
Thyrostatics
Thyrostatics are drugs that inhibit the production of thyroid hormones, such as carbimazole (used in UK) and methimazole (used in US), and propylthiouracil. Thyrostatics are believed to work by inhibiting the iodination of thyroglobulin by thyroperoxidase, and thus, the formation of tetra-iodothyronine (T 4 ). Propylthiouracil also works outside the thyroid gland, preventing conversion of (mostly inactive) T 4 to the active form T 3 . Because thyroid tissue usually contains a substantial reserve of thyroid hormone, thyrostatics can take weeks to become effective, and the dose often needs to be carefully titrated over a period of months.
A very high dose is often needed early in treatment, but if too high a dose is used persistently, patients can develop symptoms of hypothyroidism.
Beta-blockers
Many of the common symptoms of hyperthyroidism such as palpitations, trembling, and anxiety are mediated by increases in beta adrenergic receptors on cell surfaces. Beta blockers are a class of drug which offset this effect, reducing rapid pulse associated with the sensation of palpitations, and decreasing tremor and anxiety. This doesn't help the underlying problem of excess thyroid hormone, but makes the symptoms much more manageable, particularly as definitive treatment with thryostatic drugs can take a number of months to work. Propranolol in the US, and Metoprolol in the UK, are most frequently used to augment treatment for hyperthyroid patients.
Permanent treatments
Surgery as an option predates the use of the less invasive radioisotope therapy, but is still required in cases where the thyroid gland is enlarged and causing compression to the neck structures, or the underlying cause of the hyperthyroidism may be cancerous in origin.
Surgery
Surgery (to remove the whole thyroid or a part of it) is not extensively used because most common forms of hyperthyroidism are quite effectively treated by the radioactive iodine method, and because there is a risk of also removing the parathyroid glands, and of cutting the recurrent laryngeal nerve, making swallowing difficult. Howev
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