HYPERTHYROIDISM

HYPERTHYROIDISM

 

Mauro Czepielewski, MD., Ph.D. in Endocrinology – São Paulo State University School of Medicine (UNIFESP). Vice-Director of the State University Rio Grande do Sul School of Medicine (UFRGS). Associate Professor – Internal Medicine Department/UFRGS.

 

What is it?

A number of signs and symptoms arising from the excess of hormones from the thyroid gland.

How does it develop?

Symptoms appear as a result from excessive functional activity of the thyroid gland or intake of thyroid hormones.

Among the several causes for an increased functional activity of the thyroid, the most important are:
 

	toxic diffuse goiter (Basedow-Graves’ disease),
	toxic multinodular goiter,
	toxic uninodular goiter (toxic adenoma).

Toxic diffuse goiter is an autoimmune disorder in which the organism produces antibodies that stimulate the production and release of hormones by the thyroid, and can be associated to other autoimmune disorders.

Toxic multinodular goiter is usually a condition of slow progression, in which there’s a proliferation of several follicles of the gland, forming several nodules, which are bulky and visible sometimes.

Adenomas are single nodules, in general more than 3 cm in diameter, which overproduce thyroid hormones.

What does one experience?

Patients have:
 

	excessive hunger,
	increased bowel movements,
	nervousness, insomnia, emotional weakness,
	tremble,
	heat intolerance,
	palpitations,
	weight loss,
	vivid, staring glaze
	warm, moist skin,
	brittle fingernails, and dry, brittle, curly hair.

In women, menstrual alterations and infertility occur. For most people, this clinical condition is associated with a visible enlargement in the lower part of the neck, forming the so-called goiter. In patients with diffuse goiter, eye signs of inflammatory response may occur, characterized by eyelid retraction, protusion of the eye globes (bulging eyes) and palsy of the muscles controlling eye movements. This set of eye alterations is called exophthalmy.

How does the doctor diagnose it?

The diagnosis is established from the clinical observation of the symptoms described above in a patient, or when the cause of arrhythmia or abdominal pain coupled with weight loss (mainly in old patients) is investigated. Laboratory diagnosis is established through TSH and T4 levels in the blood. If T4 values increase and TSH values drop, the patient is a hyperthyroidism carrier. So we have to investigate the cause, which may be autoimmune, uninodular or multi-nodular. This diagnosis is established by the presence of antireceptor antibodies to TSH by iodine uptake and thyroid scintillography, and by thyroid ultrasound.

In patients with large goiters and compressive manifestations in the neck region, such as difficulty swallowing food and shortage of air, it may be necessary to take radiographs of the chest, or mediastinum and/or neck. For old or intensely ill patients, general tests and electrocardiogram must also be performed.

How is it treated?

The treatment targets the hormonal excess and/or its underlying cause.

In patients with toxic diffuse goiter, iodine uptake can be assessed, followed by the administration of a calculated dose of radioactive iodine (iodine 131) which will destroy the thyroid tissue with excessive functional activity. This effect will take place in a few weeks. In the period while the normalization of thyroid functioning is not achieved, the patient can take a medication that blocks the action of these hormones (ß-blocker: propanolol), and a significant improvement in the symptoms takes place. Should this fail to occur, or in the presence of severe hyperthyroidism, the patient will be initially treated with antithyroidal drugs (methimazole or propanolol) until the control of the disease is achieved.

In patients with multinodular goiter, if the goiter is sizeable and shows compressive signs, the treatment of choice is thyroid surgery (thyroidectomy), which only will be performed after clinical management of the hyperthyroidal state. The control of hyperthyroidism can be achieved with methimazole (Tapazol) or propylthiouracil, which must be taken for several weeks.

For smaller nodular goiters, or those for which no surgical contraindication exists, the patient may also receive radioactive iodine, following the control of the condition with methymazole or propylthiouracil.

In patients with toxic uninodular goiter, hyperthyroidism must be compensated with methymazole/propylthiouracil, and, subsequently, the patient will be subjected to subtotal thyroidectomy. In patients with small nodules or surgical contraindications, radioactive iodine may be employed as well.

After the condition is resolved, either by using radioactive iodine or by surgery, the patient must be monitored periodically so as to detect eventual hypothyroidism that may occur as a complication from these treatments.

How is it prevented?

There are no prevention mechanisms for several diseases. On the other hand, earlier detection of the disease can be performed especially if we properly investigate every patient presenting with uninodular or multinodular goiter. With this respect, the performance of routine thyroid palpation whenever the patient is examined can be very helpful.