Functional thyroid tissue producing an excess of thyroid hormone occurs in a number of clinical conditions. The major causes in humans are:
High blood levels of thyroid hormones (most accurately termed hyperthyroxinemia) can occur for a number of other reasons:
Neurological manifestations can include tremor, 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") 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). 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 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 is a rare but severe complication of hyperthyrodism, 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, tachycardia, arrhythmia, vomiting, diarrhea, dehydration, coma and death.
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 T4 and/or T3 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 T4 and T3 is still clinically useful.
Measuring specific antibodies, such as anti-TSH-receptor antibodies in Graves' disease, or anti-thyroid-peroxidase in Hashimoto's thyroiditis, 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.
Often hyperthyroidism causes nodules in the thyroid. FNA Biopsy (Fine Needle Aspiration), Ultrasound testing and other radioactive scans can be done to determine whether these nodules are cancerous or not.
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.
A common outcome following radioiodine is a swing to the easily treatable hypothyroidism, and this occurs in 78% of those treated for Graves' thyrotoxicosis and in 40% of those with toxic multinodular goiter or solitary toxic adenoma. Use of higher doses of radioiodine reduces the incidence of treatment failure, with the higher response to treatment consisting mostly of higher rates of hypothyroidism. There is increased sensitivity to radioiodine therapy in thyroids appearing on ultrasound scans as more uniform (hypoechogenic), due to densely packed large cells, with 81% later becoming hypothyroid, compared to just 37% in those with more normal scan appearances (normoechogenic).
However, recent research published in Environmental Science & Technology, a publication of the American Chemical Society, suggests that many cases of feline hyperthyroidism are associated with exposure to environmental contaminants called polybrominated diphenyl ethers (PBDEs), which are present in flame retardants in many household products, particularly furniture and some electronic products.
The study from which the report was based, was conducted jointly by researchers at the EPA's National Health and Environmental Effects Laboratory and Indiana University. In the study, which involved 23 pet cats with feline hyperthyroidism, PDBE blood levels were three times as high as those in younger, non-hyperthyroid cats. Ideally, PBDE and related endocrine disruptors that seriously damage health would not be present in the blood of any animals or humans.
Most recently, mutations of the thyroid stimulating hormone receptor have been discovered which cause a constitutive activation of the thyroid gland cells. Many other factors may play a role in the pathogenesis of the disease such as goitrogens (isoflavones such as genistein, daidzein and quercertin) and iodine and selenium content in the diet.
The most common presenting symptoms are: rapid weight loss, tachycardia (rapid heart rate), vomiting, diarrhea, increased consumption of fluids (polydipsia) and food, and increased urine production (polyuria). Other symptoms include hyperactivity, possible aggression, heart murmurs, a gallop rhythm, an unkempt appearance, and large, thick nails. About 70% of afflicted cats also have enlarged thyroid glands (goiter).
The same three treatments used with humans are also options in treating feline hyperthyroidism (surgery, radioiodine treatment, and anti-thyroid drugs). Drugs must be given to cats for the remainder of their lives, but may be the least expensive option, especially for very old cats. Radioiodine treatment and surgery often cure hyperthyroidism. Some veterinarians prefer radioiodine treatment over surgery because it does not carry the risks associated with anesthesia. Radioiodine treatment, however, is not available in all areas for cats. The reason is that this treatment requires nuclear radiological expertise and facilities, since the animal's urine is radioactive for several days after the treatment, requiring special inpatient handling and facilities usually for a total of 3 weeks (first week in total isolation and the next two weeks in close confinement). Surgery tends to be done only when just one of the thyroid glands is affected (unilateral disease); however following surgery, the remaining gland may become over-active. As in people, one of the most common complications of the surgery is hypothyroidism.
Occasionally dogs will have functional carcinoma in the thyroid; more often (about 90% of the time) this is a very aggressive tumor that is invasive and easily metastasizes or spreads to other tissues (esp. the lungs), making prognosis very poor. While surgery is possible, it is often very difficult due to the invasiveness of the mass in surrounding tissue including the arteries, the esophagus, and windpipe. It may only be possible to reduce the size of the mass, thus relieving symptoms and also allowing time for other treatments to work.
If a dog does have a benign functional carcinoma (appears in 10% of the cases), treatment and prognosis is no different from that of the cat. The only real difference is that dogs tend to appear to be asymptomic, with the exception of having an enlarged thyroid gland appearing as a lump on the neck.