- 1 General information
- 2 What is Subclinical Hypothyroidism
- 3 Causes
- 4 Symptoms and Complications
- 5 Diagnosis
- 6 Treatment
- 7 Prevention
Subclinical hypothyroidism is a disorder of the thyroid gland characterized by an increase in steric levels of the thyrostimulating hormone (TSH) associated with thyroid hormone values (thyroxine and triiodothyronine) in the norm.
In this condition, the typical symptoms of established hypothyroidism are scarce or absent: the increase in TSH levels manages to maintain the values of thyroid hormones in the normal range.
Thyroid: key points
Before defining the characteristics of subclinical hypothyroidism, it is necessary to briefly remember some notions related to the thyroid gland:
- The thyroid is a small endocrine gland, located in the anterior region of the neck, in front and sideways to the larynx and trachea. The main hormones it produces – thyroxine (T4)and triiodothyronine (T3) – control metabolic activities and are responsible for the proper functioning of most of the body’s cells.
- More specifically, thyroid hormones signal how fast the body must work and how it should use food and chemicals, to produce energy and perform its functions properly. Not only that: the thyroid intervenes in the processes of growth and development of many tissues and stimulates cellular activities, optimizing, in particular, the functions of the cardiovascular system and the nervous system.
- Hormone production is activated and deactivated via a feed-back system. Among the various factors involved in this mechanism, the thyroid-stimulating hormone (TSH) is responsible for maintaining the concentration of stable thyroid hormones in the bloodstream.
What is Subclinical Hypothyroidism
Subclinical hypothyroidism is a thyroid dysfunction in which:
- Seeric concentrations of the thyreostimolant hormone increase beyond the normality threshold (high TSH);
- The levels of thyroxine (T4) and triiodothyronine (T3) remain in the reference range.
Subclinical hypothyroidism can be caused by multiple causes.
In most cases, this condition occurs as a result of a tyropathy caused by an autoimmune process that recognizes the thyroid gland as a target.
- Hashimoto’s thyroiditis (the main cause of subclinical hypothyroidism);
- Basedow-Graves disease.
Other causes of subclinical hypothyroidism may be:
- Previous acute flogosi;
- Iodic deficiency (diet: iodine-poor or food-rich diet, called “gozzigens,” which hinder its assimilation; endemic: long stay in iodocareent geographical areas, especially mountainous and far from the sea);
- Iatrogene, in particular:
- Previous ablative therapy with radioactive iodine;
- Thyroid removal surgery(thyroidectomy);
- Medications(amiodarone, lithium,radiological contrast means containing iodine etc.);
- Insufficient replacement therapy;
- External radiotherapy of the head and neck (administered, for example, in the case of larynx carcinoma, Hodgkin’s lymphoma, leukemia, intracranial malignancies, etc.).
Subclinical hypothyroidism can also occur in the idiopathic form (i.e. for unidentifiable causes).
Who is most at risk
Subclinical hypothyroidism is relatively frequent (prevalence is estimated at between 4 and 10% in the general population).
The condition mainly affects with advancing age and in the female sex (critical periods for thyroid function are pregnancy and menopause).
Subclinical hypothyroidism is particularly prevalent in those with Hashimoto thyroiditis.
Those most likely to develop subclinical hypothyroidism are:
- Patients with Down’s Syndrome;
- Women in the postpartum period (within 6 months);
- Women in menopause;
- Elderly patients;
- Patients with type 1 diabetes mellitus;
- Patients with heart failure;
- Patients familiar with tauopathies;
- Patients with other autoimmune diseases.
Symptoms and Complications
By its very definition, subclinical hypothyroidism is asymptomatic: the increase in TSH levels manages to maintain the values of thyroid hormones in the normal range. However, some patients report a non-specific symptomatic, which may be associated with thyroid hypofunctionality.
It should be remembered that subclinical hypothyroidism is a condition in which the alteration of thyroid function is of mild-to-moderate degree. If neglected, however, dysfunction can progress to established hypothyroidism (circulating levels of TSH are high and the values of thyroid hormones are below the normal limits, so they are insufficient to maintain a state of heutiroidism).
Subclinical hypothyroidism: main symptoms
The manifestations of subclinical hypothyroidism can be nuanced or mild.
Symptomology usually occurs after a long subclinical course and can include:
- Muscle weakness;
- Daytime sleepiness;
- Intolerance to cold;
- Difficulty concentrating;
- Dry and rough skin;
- Eyelid edema;
- Memory loss;
In most cases, subclinical hypothyroidism remains stable for several years and can sometimes regress.
The risk of subclinical hypothyroidism from progressing towards the established form is greater in elderly patients and those with high values of anti-thyroid antibodies (indicative parameter of the presence of autoimmune diseases).
Problems associated with subclinical hypothyroidism
In recent years, several scientific studies have associated subclinical hypothyroidism with various clinical conditions.
In addition to the possible progression of dysfunction to established hypothyroidism,:
- Increased level of low-density lipoproteins;
- Increased cardiovascular risk;
- Cognitive decline (in older patients);
- Anxiety and depression.
In addition, patients with subclinical hypothyroidism are more likely to develop:
- Hypercholesterolemia (increase in the level of total cholesterol);
- Coronary heart disease;
- Peripheral artery disease.
Subclinical hypothyroidism is often discovered accidentally, following the level of thyroid hormones and TSH or during examinations to ascertain the causes of non-specific symptoms (such as drowsiness, fatigue or alterations in the menstrual cycle).
Diagnosis of subclinical hypothyroidism can be formulated based on:
- Accurate patient history;
- Presence of symptoms and signs of mild hypofunction of the thyroid gland;
- Dosing of the syric concentrations of TSH, T4 Free (FT4) and free T3 (FT3) after a simple blood draw.
Subclinical hypothyroidism is characterized by high seetic levels of TSH (tireostimolant hormone) associated with normal levels of free thyroid hormones (FT3 and FT4) on two occasions at least 2-3 months apart.
The feedback of anti-Tireoglobulin antibodies (Ab anti-TG) and anti-Tireoperossidas (Ab anti-TPO) antibodies in the blood establishes the autoimmune etiology of subclinical hypothyroidism and the opportunity to begin L-Tiroxine replacement therapy (L-T4).
Thyroid ultrasound, scintigraphy, and agoaspirato are a useful supplementary for the evaluation of the clinical case, as they provide information on the morphology and functional abilities of the thyroid.
What tests are used for subclinical hypothyroidism?
The blood tests useful for the diagnosis of subclinical hypothyroidism are:
- Dosing of TSH, FT3 and FT4 (free form of T4);
- Stimulation test with TRH (tireotropin release hormone);
- Dosing of anti-tireoperossidas (Ab anti-TPO) and anti-tireoglobulin (Ab anti-TG) antibodies;
- Total cholesterol dosage, HDL, LDL and triglycerides.
In subclinical hypothyroidism, levels of circulating thyroid hormones are typically found within normal limits, associated with a high seeric TSH value. The dosage of anti-thyroid antibodies indicates the presence of antibodies responsible for the most common form of hypothyroidism, that is, autoimmune.
What to do when you encounter high TSH?
The first thing to do is to repeat the dosage of TSH, after 2 or 12 weeks to exclude a transient anomaly. The evaluation of FT4 is useful in defining the condition of subclinical hypothyroidism and allows to assess the degree of severity.
Subclinical Hypothyroidism vs Transitional Increase of TSH
The dosage of TSH is the most sensitive laboratory data for the diagnosis of subclinical hypothyroidism. It should be considered, however, that some physiological or pathological situations can increase the secretion of TSH transiently.
Causes of this phenomenon include sleep disorders, circadian rhythm abnormalities (e.g. night work), exposure to toxic substances (pesticides, industrial chemicals, etc.), some forms of thyroiditis (subacute or postpartum), antithyroid drugs or inhibiting the secretion of TSH (glucocorticoids, dopamine etc.), major surgery, severe trauma, infections and malnutrition.
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Subclinical hypothyroidism therapy involves the administration of thyroid hormone-based drugs (replacement therapy with L-thyroxine, L-T4; eg. levothyroxine), initially at low doses. The purpose of the treatment is to restore a condition of heutiroidism.
Before adhering to any replacement therapy with L-thyroxine, however, the doctor should monitor the dysfunction in a short period of time (approximately 3-6 months) and confirm the increase in TSH (it may be due to a transient anomaly).
If L-tiroxine is not taken (due to a lack of adherence to the therapeutic protocol by the patient) or is not sufficient, a condition of hypothyroidism is created. For this reason, during taking the drug, the patient with subclinical hypothyroidism must undergo regular follow-ups, to control the effects of treatment.
Subclinical hypothyroidism: scheme for monitoring
- After the first feedback of high TSH and thyroid hormones in the norm, dosing TSH, FT4 and anti-Tireoperoxides (Ab anti-TPO) antibodies in the blood after 2-3 months.
- If TSH is in the norm do not perform further examinations;
- If TSH is high (i.e. subclinical hypothyroidism is persistent):
- Perform an ultrasound examination of the thyroid gland;
- Evaluate thyroid function (TSH and FT4) every 6 months; after 2 years, this control can become annual.
In general, thyroid function should be evaluated in pregnant women, those who develop symptoms of hypothyroidism or during other hematochemical examinations.
Treatment of subclinical hypothyroidism: yes or no?
Even today, the treatment or otherwise of subclinical hypothyroidism is controversial in the various guidelines.
In general, thyroid hormone replacement therapy begins when TSH values are greater than 10 thU/ml. With regard to concentrations below 10 U/ml, however, the increased stimulation of TSH on the thyroid gland tends to be used to ensure a normal production of thyroid hormones. Therapy can be initiated for TSH values of between 4 and 10 thU/ml in the case of chronic autoimmune thyroiditis or nodular thyroid pathology.
The only condition in which the treatment of subclinical hypothyroidism is always indicated in the adult is pregnancy, to avoid the effects of dysfunction on gestation and fetal development. The onset of therapy can be considered by your doctor in the presence of clinical symptoms or in the case of co-existing hyperlipidemia and heart failure.
Unfortunately, there is no prevention for subclinical hypothyroidism.
The best strategy to avoid the consequences associated with loss of thyroid gland function is to diagnose the condition as soon as possible.
Measuring seetric TSH and free T4 levels on a regular basis (approximately, every 6-12 months) allows you to assess the progression of the clinical picture (if not treated) or adjust the dosage of L-tiroxine to restore a condition of heutiroidism.
Follow-up also allows to monitor the possible evolution of subclinical hypothyroidism in the established form.