Subclinical Hypothyroidism - Symptoms and Treatment

Hypothyroidism is the name of the disease caused by the poor functioning of the thyroid gland, responsible for the production of hormones that control our metabolism. Subclinical hypothyroidism, the focus of this article, is a mild form of hypothyroidism, usually without symptoms but already detectable through laboratory tests.



The thyroid is an organ located at the base of the neck, whose function is to produce the hormones responsible for controlling the speed of our metabolism. Thyroid hormones are called triiodothyronine (T3) and thyroxine (T4). An increase in the blood concentration of these hormones speeds up our metabolism; already a reduction causes a contrary effect, by making it legitimate.

Hypothyroidism is the disease caused by the lack of T3 and T4, whereas hyperthyroidism is the disease caused by its excess.

The functioning of the thyroid and consequently the production of T3 and T4 are controlled by another hormone, called TSH, produced in the pituitary gland of the brain. Therefore, in a very simplified way, when the body needs to accelerate its metabolism, the brain increases the release of TSH, which in turn stimulates the thyroid to produce T3 and T4. On the other hand, if the body needs to decelerate metabolism, the TSH release drops and the thyroid will produce less T3 and T4. The release of TSH is done in a well controlled way, in order to maintain the thyroid producing only the amount of T3 and T4 required, without causing excess or lack of these hormones.

In classical hypothyroidism the patient usually has low levels of T3 and T4 and elevated levels of TSH. This is because patients have a diseased thyroid gland, unable to produce more hormones, even if stimulated by elevated levels of TSH. As much as the pituitary increases the release of TSH, the thyroid is unable to respond to this hormone.

In a large part of these patients, the disease is progressive, with increasing levels of TSH being required over time to keep the thyroid functioning properly.

The disease progresses to the point where the gland is so diseased that it is no longer able to produce minimal amounts of hormones, even when stimulated by very high levels of TSH. At this time, the patient no longer presents subclinical hypothyroidism, but frank hypothyroidism.

Subclinical hypothyroidism is a type of "prehypothyroidism", a phase prior to the onset of frank hypothyroidism. The thyroid is ill but is still able to produce thyroid hormones if stimulated by elevated levels of TSH. So we have a situation where the patient has TSH levels above normal, but their levels of T4 and T3 are still normal (in clinical practice, we only need to measure the blood levels of free T4, as I will explain later).

About 5 to 10% of the population has subclinical hypothyroidism, most of them are unaware of this situation. Subclinical hypothyroidism is more common in women than in men. The incidence is also higher in whites and the elderly. The causes are basically the same as frank hypothyroidism, with Hashimoto's thyroiditis being the main cause.

Subclinical hypothyroidism is a laboratory diagnosis because once the patient still has normal levels of thyroid hormones, he or she does not have any (or almost no) symptoms.

As previously mentioned, the patient with subclinical hypothyroidism has normal levels of free T4 and elevated TSH levels, usually between 5 and 10 mU/L (some sites use 4.5 and 15 mU/L as limits). Typically, when TSH is already well above 10 mU/L, the patient no longer has subclinical hypothyroidism, since free T4 is usually low and the patient already has symptoms of hypothyroidism. Therefore, subclinical hypothyroidism usually has elevated TSH, but never much higher than 10 or 15 mU/L.

It is important to note that to be considered subclinical hypothyroidism, the patient can not have frank symptoms of hypothyroidism.

In subclinical hypothyroidism, free T4 levels are normal and the patient presents at most only mild and nonspecific symptoms, such as mild fatigue, mild discomfort to perform tasks or a small intolerance to cold. All these symptoms are common and can occur at any given time in life, especially in periods of stress, overwork, onset of viruses, etc.

Therefore, in subclinical hypothyroidism there are no relevant clinical symptoms that aid in diagnosis. The diagnosis can only be made with laboratory tests.

A large proportion of patients with subclinical hypothyroidism will eventually develop candid hypothyroidism. Studies show that after 10 to 20 years up to 55% of patients with subclinical hypothyroidism will have already progressed to the full form of the disease.

The risk of progression is related to the initial TSH concentration (patients with higher TSH levels between 12 and 15 mU/L are at higher risk) and the presence of thyroid antibodies, such as anti-TPO. The underlying disease also has a high influence on the risk of progression to free hypothyroidism. Patients with thyroid autoimmune disease, such as Hashimoto's thyroiditis, or who have received radioiodine or high-dose radiation therapy tend to develop into hypothyroidism.

Spontaneous recovery has also been described in patients with subclinical hypothyroidism, although the actual frequency of this phenomenon has not yet been fully elucidated. There are patients with criteria for subclinical hypothyroidism who, after a few years, have standardized laboratory tests without any treatment being established. In general, patients with TSH persistently less than 10 mU / L and negative for thyroid antibodies.

Since many patients with subclinical hypothyroidism are asymptomatic, many of them may develop the problem, not take notice, and after a few years heal spontaneously, again without being aware of the situation. These cases, of course, did not see statistics, which makes it difficult to determine the true incidence of spontaneous cure of subclinical hypothyroidism.

Although not causing symptoms and in some cases disappearing spontaneously, subclinical hypothyroidism does not appear to be a totally innocuous problem. There are several studies that suggest a relationship between subclinical hypothyroidism and an increased risk of cardiovascular diseases, such as angina and heart attacks, especially in patients with TSH greater than 10 mU/L. Patients with subclinical hypothyroidism also tend to have higher cholesterol levels than the general population.

In addition to cardiovascular problems, patients with subclinical hypothyroidism, especially those with higher TSH, also have a higher risk of hepatic steatosis.

The major question we have when diagnosing subclinical hypothyroidism is whether or not to start treatment with levothyroxine, the synthetic form of the hormone T4.

Currently, no work has shown relevant benefits of levothyroxine use in asymptomatic patients with TSH between 4.5 and 10 mU/L. The treatment of subclinical hypothyroidism in these cases is very controversial. Those who advocate the use of levothyroxine argue that there is no evidence that there is damage with hormone replacement, as well as the possibility of improving previously unrecognized symptoms, such as fatigue and mild mood changes. The current consensus, however, only recommends monitoring TSH levels every 6 to 12 months in this group of patients, unless the patient has symptoms that can be easily attributed to hypothyroidism.

In some situations, the decision not to treat is not so simple. This includes patients with high cholesterol, high risk of cardiovascular disease, or antibodies to the thyroid. Women who want to become pregnant and are unable to get pregnant may also have fertility improvement if they are treated with levothyroxine.

In patients with subclinical hypothyroidism and TSH above 10 mU/L the controversy is much lower. Most international endocrinology societies recommend the use of levothyroxine in these cases because treatment helps prevent progression to frank hypothyroidism.

The dose of levothyroxine should always be as low as possible to maintain TSH between 0.5 and 2.5 mU/L in young patients and 3 to 5 mU/L in elderly patients.

During pregnancy, the physiology of thyroid hormones changes completely, making normal TSH values different in this group. During the first trimester of pregnancy, subclinical hypothyroidism is defined as normal free T4 values associated with a TSH above 2.5 mU/L. In the second and third trimester we considered subclinical hypothyroidism values of TSH above 3 mU/L.

Because thyroid hormones are essential for the neurological development of the fetus, the current consensus is to treat all pregnant women who have criteria for subclinical hypothyroidism.