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Hyperthyroidism, often called overactive thyroid and sometimes hyperthyreosis, is a condition in which the thyroid gland produces and secretes excessive amounts of the free (not protein bound circulating in the blood) thyroid hormones –triiodothyronine (T3) and/or thyroxine (T4). Graves’ disease is the most common cause of hyperthyroidism. The opposite is hypothyroidism (‘sluggish thyroid’), which is the reduced production and secretion of T3 and/or T4.
Hyperthyroidism is one cause of thyrotoxicosis—the hypermetabolic clinical syndrome which occurs when there are elevated serum levels of T3 and/or T4. Thyrotoxicosis can also occur without hyperthyroidism. Some people develop thyrotoxicosis due to inflammation of the thyroid gland (thyroiditis), which can lead to excessive release of thyroid hormone already stored in the gland (without the accelerated hormone production that characterizes hyperthyroidism). Thyrotoxicosis can also occur after taking too much thyroid hormone in the form of supplements, such as levothyroxine (a phenomenon known as exogenous thyrotoxicosis, alimentary thyrotoxicosis, or occult factitial thyrotoxicosis). Thyroid imaging and radiotracer thyroid uptake measurements, combined with serologic data, enable specific diagnosis and appropriate treatment.
Management differ for thyrotoxicosis caused by hyperthyroidism and thyrotoxicosis caused by other conditions. This often includes: initial temporary use of suppressive thyrostatics medication (antithyroid drugs), and possibly later use of permanent surgical or radioisotope therapy. All approaches may cause underactive thyroid function (hypothyroidism) which is easily managed with levothyroxine or triiodothyronine supplementation. Surgery as an option predates the use of the less invasive radioisotope therapy (radioiodine 131 thyroid ablation), 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.
Thyrotoxicosis or Hyperthyroidism may be asymptomatic, but when it is not, symptoms are due to an excess of thyroid hormone. Thyroid hormone is important at a cellular level, affecting nearly every type of tissue in the body. Thyroid hormone functions as a controller of the pace of all of the processes in the body. This pace is called the metabolic rate (see metabolism).
If there is too much thyroid hormone, every function of the body tends to speed up. Therefore, some of the symptoms of hyperthyroidism may be nervousness, irritability, increased perspiration, heart racing, hand tremors, anxiety, difficulty sleeping, thinning of the skin, fine brittle hair, and muscular weakness—especially in the upper arms and thighs. More frequent bowel movements may occur, but diarrhea is uncommon. Weight loss, sometimes significant, may occur despite a good appetite (though 10% of people with a hyperactive thyroid experience weight gain), vomiting may occur, and, for women, menstrual flow may lighten and menstrual periods may occur less often.
Thyroid hormone is critical to normal function of cells. 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 such as of the hands and anxiety symptoms, digestive system hypermotility, unintended weight loss, and (in “lipid panel” blood tests) a lower and sometimes unusually low serum cholesterol.
Major clinical signs include weight loss (often accompanied by an increased appetite), anxiety, intolerance to heat, hair loss (especially of the outer third of the eyebrows), muscle aches, weakness, fatigue, hyperactivity, irritability, hyperglycemia,polyuria, polydipsia, delirium, tremor, pretibial myxedema (in Graves’ disease), and sweating. Panic attacks, inability to concentrate, and memory problems may also occur. Psychosis and paranoia, common during thyroid storm, are rare with milder hyperthyroidism. Many persons will experience complete remission of symptoms 1 to 2 months after a euthyroid state is obtained, with a marked reduction in anxiety, sense of exhaustion, irritability, and depression. Some individuals may have an increased rate of anxiety or persistence of affective and cognitive symptoms for several months to up to 10 years after a euthyroid state is established. In addition, patients may present with a variety of physical symptoms such as palpitations and arrhythmias (the notable ones being atrial fibrillation), shortness of breath (dyspnea), loss of libido, amenorrhoea, nausea,vomiting, diarrhea, gynaecomastia and feminization.Long term untreated hyperthyroidism can lead to osteoporosis. These classical symptoms may not be present often in the elderly.
Neurological manifestations can include tremors, chorea, myopathy, and in some susceptible individuals (in particular 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.
In Graves’ disease, which is the most common form or cause of hyperthyroidism, the eyes may look enlarged because the eye muscles swell and push the eye forward. This can only be resolved surgically by orbital decompression. Sometimes, one or both eyes may bulge. Some patients have swelling of the front of the neck from an enlarged thyroid gland (a goitre). Because hyperthyroidism, especially Graves’ disease, may run in families, examinations of the members of a family may reveal other individuals with thyroid problems.
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 exophthalmos 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.