Hyperthyroidism

Treatment for Hyperthyroidism

Hyperthyroidism develops when the body is exposed to excessive amounts of thyroid hormone. This disorder occurs in almost one percent of all Americans and affects women five to ten times more often than men. In its mildest form, hyperthyroidism may not cause recognizable symptoms. More often, however, the symptoms are discomforting, disabling, or even life-threatening.

WHAT ARE THE FEATURES OF HYPERTHYROIDISM?
When hyperthyroidism develops, a goiter (enlargement of the thyroid) is usually present and may be associated with some or many of the following features:
• Fast heart rate, often more than 100 beats per minute
• Becoming anxious, irritable, argumentative
• Trembling hands
• Weight loss, despite eating the same amount or even more than usual
• Intolerance of warm temperatures and increased likelihood to
perspire
• Loss of scalp hair
• Tendency of fingernails to separate from the nail bed
• Muscle weakness, especially of the upper arms and thighs
• Loose and frequent bowel movements
• Smooth skin
• Change in menstrual pattern
• Increased likelihood for miscarriage
• Prominent “stare” of the eyes
• Protrusion of the eyes, with or without double vision (in patients with Graves’ disease)
• Irregular heart rhythm, especially in patients older than 60 years of age
• Accelerated loss of calcium from bones, which increases the risk of osteoporosis and fractures

CAUSES
Graves’ disease
Graves’ disease (named after Irish physician Robert Graves) is an autoimmune disorder that frequently results in thyroid enlargement and hyperthyroidism. In some patients, swelling of the muscles and other tissues around the eyes may develop, causing eye prominence, discomfort or double vision. Like other autoimmune diseases, this condition tends to affect multiple family members. It is much more common in women than in men and tends to occur in younger patients.

Toxic multinodular goiter
Multiple nodules in the thyroid can produce excessive thyroid hormone, causing hyperthyroidism. Typically diagnosed in patients over the age of 50, this disorder is more likely to affect heart rhythm. In many cases, the person has had the goiter for many years before it becomes overactive.

Toxic nodule
A single nodule or lump in the thyroid can also produce more thyroid hormone than the body requires and lead to hyperthyroidism. This disorder is not familial.

Subacute thyroiditis
This condition may follow a viral infection and is characterized by painful thyroid gland enlargement and inflammation, which results in the release of large amounts of thyroid hormones into the blood.
Fortunately, this condition usually resolves spontaneously. The thyroid usually heals itself over several months, but often not before a temporary period of low thyroid hormone production (hypothyroidism) occurs.

Postpartum thyroiditis
Five to ten percent of women develop mild to moderate hyperthyroidism within several months of giving birth. Hyperthyroidism in this condition usually lasts for approximately one to two months.
It is often followed by several months of hypothyroidism, but most women will eventually recover normal thyroid function. In some cases, however, the thyroid gland does not heal, so the hypothyroidism becomes permanent and requires lifelong thyroid hormone replacement. This condition may occur again with subsequent pregnancies.

Silent thyroiditis
Transient (temporary) hyperthyroidism can be caused by silent thyroiditis, a condition which appears to be the same as postpartum thyroiditis but not related to pregnancy. It is not accompanied by a painful thyroid gland.

Excessive iodine ingestion
Various sources of high iodine concentrations, such as kelp tablets, some expectorants, amiodarone (Cordarone, Pacerone — a medication used to treat certain problems with heart rhythms) and x-ray dyes may occasionally cause hyperthyroidism in patients who are prone to it.

Overmedication with thyroid hormone
Patients who receive excessive thyroxine replacement treatment can develop hyperthyroidism. They should have their thyroid hormone dosage evaluated by a physician at least once each year and should NEVER give themselves “extra” doses.

DIAGNOSIS
Characteristic symptoms and physical signs of hyperthyroidism can be detected by a physician. In addition, tests can be used to confirm the diagnosis and to determine the cause.
TSH (thyroid – stimulating hormone or thyrotropin) test
A low TSH level in the blood is the most accurate indicator of hyperthyroidism. The body shuts off production of this pituitary hormone when the thyroid gland even slightly overproduces thyroid hormone.
If the TSH level is low, it is very important to also check thyroid hormone levels to confirm the diagnosis of hyperthyroidism.
Other tests
Estimates of free thyroxine and free triiodothyronine – the active thyroid hormones in the blood. When hyperthyroidism develops, free thyroxine and free triiodothyronine levels rise above previous values in that specific patient (although they may still fall within the normal range for the generalpopulation), and are often considerably elevated.
TSI (thyroid-stimulating immunoglobulin) – a substance often found in the blood when Graves’ disease is the cause of hyperthyroidism. This test is not routinely ordered since it does not usually affect treatment decisions or help in the diagnosis.
Radioactive iodine uptake (RAIU – a measurement of how much iodine the thyroid gland can collect) and thyroid scan (a thyroid scan shows how the iodine is distributed throughout the thyroid gland). This information can be useful in determining the cause of hyperthyroidism and ultimately its treatment.
Sometimes a general physician can diagnose and treat the cause of hyperthyroidism, but assistance is often needed from an endocrinologist, a physician who specializes in managing thyroid disease.

TREATMENT FOR HYPERTHYROIDISM
Before the development of current treatment options, the death rate from severe hyperthyroidism was as high as 50 percent. Now several effective treatments are available and, with proper management, death from hyperthyroidism is rare. Deciding which treatment is best depends on what caused the hyperthyroidism, its severity, and other conditions present. A physician who is experienced in the management of thyroid diseases can confidently diagnose the cause of hyperthyroidism and prescribe and manage the best treatment program for each patient.
Antithyroid drugs
In the United States, two drugs are available for treating hyperthyroidism: propylthiouracil (PTU) and methimazole (MMI). In general, AACE and the ATA recommend prescribing MMI over PTU. There are a few situations however where PTU should be used over MMI: during the first trimester of pregnancy to avoid an increased risk of a rare birth defect; if the patient is allergic to or intolerant of MMI; or when life-threatening thyrotoxicosis occurs. Some patients with hyperthyroidism caused by Graves’ disease experience a spontaneous or natural remission of hyperthyroidism after a 12- to 18-month course of treatment with these drugs, and may sometimes avoid permanent underactivity of the thyroid (hypothyroidism), which often occurs as a result of using the other methods of treating hyperthyroidism. Unfortunately, the remission is frequently only temporary, with the hyperthyroidism recurring after several months or years off medication and requiring additional treatment, so relatively few patients are treated solely with antithyroid medication in the United States.
Antithyroid drugs may cause an allergic reaction in about five percent of patients who use them. This usually occurs during the first six weeks of drug treatment. Such a reaction may include rash or hives; but after discontinuing use of the drug, the symptoms resolve within one to two weeks and there is no permanent damage. A more serious effect, but occurring in only about one in 250-500 patients during the first four to eight weeks of treatment, is a rapid decrease of white blood cells in the bloodstream. This could increase susceptibility to serious infection. Symptoms such as a sore throat, infection, or fever should be reported promptly to your physician, and a blood cell count should be done immediately. In nearly every case, when a person stops using the medication, the white blood cell count returns to normal.
Very rarely, antithyroid drugs may cause severe liver problems, which can be detected by blood tests or joint problems characterized by joint pain and/or swelling. Your physician should be contacted if there is yellowing of the skin (“jaundice”), fever, loss of appetite, or abdominal pain.
Radioactive iodine treatment
Iodine is an essential ingredient in the production of thyroid hormone. Each molecule of thyroid hormone contains either four (T4) or three (T3) molecules of iodine. Since most overactive thyroid glands are quite hungry for iodine, it was discovered in the 1940′s that the thyroid could be “tricked” into destroying itself by simply feeding it radioactive iodine. The radioactive iodine is given by mouth, usually in capsule form, and is quickly absorbed from the bowel. It then enters the thyroid cells from the bloodstream and gradually destroys them. Maximal benefit is usually noted within three to six months.
It is not possible to eliminate “just the right amount” of the diseased thyroid gland, since radioiodine eventually damages all thyroid cells. Therefore, most endocrinologists usually strive to completely destroy the diseased thyroid gland with a single dose of radioiodine. This results in the intentional development of an underactive thyroid state (hypothyroidism), which is easily, predictably and inexpensively corrected by lifelong daily use of oral thyroid hormone replacement therapy.
Although every effort is made to calculate the correct dose of radioiodine for each patient, not every treatment will successfully correct the hyperthyroidism, particularly if the goiter is quite large and a second dose of radioactive iodine is occasionally needed.
Thousands of patients have received radioiodine treatment, including former President of the United States George Bush and his wife, Barbara. The treatment appears to be a very safe, simple, and reliably effective one. Because of this, it is considered by most thyroid specialists in the United States to be the treatment of choice for hyperthyroidism cases caused by overproduction of thyroid hormone.
Radioactive iodine treatment should never be given to a pregnant woman! Small amounts of radioactive iodine will also be excreted in breast milk. Since radioiodine could permanently damage the infant’s thyroid, breast-feeding is not allowed. If radioiodine is inadvertently administered to a woman who is subsequently discovered to be pregnant, the advisability of terminating the pregnancy should be discussed with the patient’s obstetrician and endocrinologist. Therefore, prior to administering diagnostic or therapeutic radioiodine treatment, pregnancy testing is mandatory whenever pregnancy is possible.
Surgical removal of the thyroid
Although seldom used now as the preferred treatment for hyperthyroidism, operating to remove most of the thyroid gland may occasionally be recommended in certain situations, such as a pregnant woman with severe uncontrolled disease in whom radioiodine would not be safe for the baby. Surgery usually leads to permanent hypothyroidism and lifelong thyroid hormone replacement therapy.
Other treatments
A drug from the class of beta-adrenergic blocking agents (which decrease the effects of excess thyroid hormone) may be used temporarily to control hyperthyroid symptoms until other therapies take effect. In cases where hyperthyroidism is caused by thyroiditis or excessive ingestion of either iodine or thyroid hormone, this may be the only type of treatment required.
Appropriate management of hyperthyroidism requires careful evaluation and ongoing care by a physician experienced in the treatment of this complex condition.

he Ethics of Neural Prosthetics

A family of new medical devices designed to return sight to the blind, movement to the paralyzed, and hearing to the deaf are poised to enter the physician’s arsenal of weapons. Known collectively as neural prostheses, these implantable devices interact directly with the nervous system and allow for the amelioration of conditions that heretofore have been beyond the pale of medical ministrations.

Neural prostheses include retinal implants, auditory brainstem implants, functional electrical stimulation systems to activate paralyzed muscles, and brain-computer interface systems to enable locked-in patients to manipulate a computer via their thoughts. Cochlear implants, which have already returned hearing to thousands of deaf individuals, also fall into this category. Eventually, electrodes implanted in the brain – currently used for a brain-computer interface – could conceivably be used to enhance the memory, learning ability, concentration, and visual and auditory capabilities of able-bodied individuals as well.

Along with the potential to do great good, neural prostheses also present a minefield of ethical questions that must be dealt with as the technology approaches clinical utilization. Having learned from the missteps of some earlier medical researchers, it is now difficult, if not impossible, to find a neural prosthetic investigator who has not, to one extent or another, considered the ethical ramifications of his or her work. This fact became evident to me as I researched my recently released book about neural prostheses, Shattered Nerves: How Science Is Solving Modern Medicine’s Most Perplexing Problem.

Because many neural prosthetic devices are at or near the human testing stage, the ethical questions of most immediate concern revolve around determining when an implant is ready for human testing and how researchers can ensure that volunteers fully appreciate what they are getting into. As for when to test these implants in humans, physicians – who by nature and training are oriented toward taking quick action – are generally prone to come down on the side of  implanting sooner rather than later, whereas engineers tend to be a more cautious lot who favor waiting until every conceivable facet of animal testing is exhausted.

Indicative of the lack of census on this issue are the stances taken by Philip Troyk, a professor of bioengineering at the Illinois Institute of Technology in Chicago, who heads a visual cortex project, and Terry Hambrecht, a physician who is also an electrical engineer and the former head of the National Institutes of Health’s Neural Prosthesis Program. Hambrecht had experimentally implanted penetrating microelectrodes in the visual cortices of several humans following years of safety testing in monkeys. The work demonstrated that an individual who was totally blind could experience spots of light at precise locations in the visual field. Troyk, however, is not convinced that the brain will be able to create coherent images out of spots of light, and feels that before further human testing is conducted, his team needs to understand more about how the brain breaks the signals received from the million nerve fibers in the optic nerve into their constituent parts and then processes them to create vision.

“We feel we are obligated to try, to the best we scientifically can, to understand that we can manipulate the visual system at the fundamental level. Then we will have something to offer the human volunteer. . . . It’s a much more sophisticated argument than just saying, ‘Put it in, try it, and see what you get,’” said Troyk. Hambrecht takes exception. He feels that Troyk’s further experimentation in monkeys could “seriously delay the development of a visual prosthesis for blind humans. I feel that our NIH group’s human experimentation answered essentially all the significant questions that might have been asked in monkeys and raised pattern recognition, stimulation interaction, and cognitive adaptation questions that can only be answered with more sophisticated implants in blind humans,” he said.

When it comes to the related question of informed consent, however, there is universal acceptance of the need to ensure that potential test subjects are made fully aware of the risks involved and are not swayed by desperation. The numerous interviews I conducted with recipients of various neural prostheses indicate that investigators are doing a good job of informing volunteers of the pros and cons of their participation. All of the patients said they had been made fully aware of the fact that the devices they were receiving were experimental in nature and held little if any promise of benefiting them directly. While they obviously hoped to realize at least some improvement in their conditions, the patients had realistic views of the potential outcomes. In fact, I did not speak to one person who voiced regret over having volunteered to receive an implant, even though in some cases the benefit was small and in others there were setbacks. And surprisingly, none of them was greatly concerned about having an unproven foreign object implanted in their bodies.

While the physical risks of receiving experimental neural prosthetic implants are given careful scrutiny, academic discussions of informed consent tend to overlook the psychological impact of participation in test programs, which in the vast majority of cases is positive and substantial. Some test subjects draw considerable satisfaction from feeling that they are full-fledged members of the research teams developing their implants, a feeling that is reciprocated by the researchers themselves. The volunteers also derive satisfaction from knowing that they may be helping future generations of people with similar maladies. It seems to give their deprivations purpose. As Harold Churchey, an experimental retinal implant recipient blinded by retinitis pigmentosa, put it, “Even though I might be over the hill, if I can help some young person, I’m for it, so long as the good Lord gives me strength.”

As for the physical improvements realized by the volunteers, however small, it was uncanny that even though each of the patients I spoke with was interviewed individually, they virtually all used essentially the same language to describe their response, namely that “something is better than nothing.”

As Connie Schoeman who can now see small spots of light generated by the 16-electrode array that sits on her right retina told me, “With something like retinitis pigmentosa, where there has never been anything that could be done to help people, this is going to offer an opportunity, maybe not to get complete vision back, but something. And something, I tell you, sure beats nothing.” Ditto for Marilyn Davidson, who was the first person to be implanted with an auditory brainstem implant. The original device had to be removed due to complications, and though the hearing it afforded her was quite limited, she clamored for another system saying, “I had the ABI long enough to know it helped me, and anything is better than nothing.”

Then there is Jim Jatich, a quadriplegic who wears two hand manipulation implants, who asked, “How do you repay someone for giving you the use of your hands back?” And Jennifer French, paralyzed in a snowboarding accident yet able to walk down the aisle at her wedding with an experimental standing implant, who said, “There is nothing better than looking back at an empty wheelchair.”

The potential for neural prostheses to do good must be tempered with the understanding that the road to realization is pitted with potholes that remain to be negotiated. Yet the promise is stimulating indeed.



Read more: http://www.thehastingscenter.org/Bioethicsforum/Post.aspx?id=346&blogid=140#ixzz1IHbB2yh1

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