home Audience 2 Subclinical hyperthyroidism (thyrotoxicosis): clinical picture, symptoms and treatment. Subclinical thyrotoxicosis: causes, symptoms, treatment Subclinical thyrotoxicosis how it affects appearance

Subclinical hyperthyroidism (thyrotoxicosis): clinical picture, symptoms and treatment. Subclinical thyrotoxicosis: causes, symptoms, treatment Subclinical thyrotoxicosis how it affects appearance

Thiereotoxicosis is less common than hypothyroidism, and can also occur in a subclinical form. The prevalence of clinically overt thyrotoxicosis in the United States is 0.5%, and subclinical thyrotoxicosis is 0.7%.

What is thyrotoxicosis of the thyroid gland

Thyrotoxicosis is an excess of thyroid hormones. Like hypothyroidism, it is not a stand-alone diagnosis. We are talking about thyrotoxicosis syndrome, i.e. about the complex of symptoms characteristic of excess thyroid hormones.

The terms "hyperthyroidism" and "thyrotoxicosis" are similar, but not identical. When we talk about hyperthyroidism, we mean overactive thyroid gland. When we talk about thyrotoxicosis, we mean any situation where there is an excess of thyroid hormones in the blood. Hyperthyroidism is the most common, but not the only cause of thyrotoxicosis.

Too difficult? Only at first glance. We'll deal with it in order.

Thyrotoxicosis can lead to dysfunction of other endocrine glands, primarily the adrenal cortex. Hypocortisolism in the acute stage can lead to the death of the patient even with dental intervention.

Cause of thyrotoxicosis of the thyroid gland

All causes of thyrotoxicosis can be divided into three groups:

Increased thyroid function, hyperproduction of thyroid hormones (Graves-Bazedow disease, functional autonomy of the thyroid gland).
Damage (destruction) of the thyroid follicles with the release of their contents into the bloodstream.
Overdose of thyroid hormone drugs.

In all cases, the level of T4 and T3 increases in the bloodstream, which leads to the same clinical picture - thyrotoxicosis syndrome.

Diffuse toxic goiter

The cause of thyrotoxicosis is diffuse toxic goiter. Patients develop thyroid-stimulating antibodies. In addition to an enlarged thyroid gland and hypersecretion of T4 and T3, ophthalmopathy is observed, and less commonly, skin lesions. There is a hereditary predisposition to the disease. Diffuse toxic goiter can occur after childbirth, infection, or as a result of mental trauma, although the exact cause of the disease is not known.

Using radiation diagnostic methods (ultrasound, MRI), ophthalmopathy can be detected in 50% of patients, but upon examination this sign is noticeable much less frequently. The staring gaze and wide open (bulging) eyes characteristic of thyrotoxicosis are caused by an increase in sympathetic tone. Exophthalmos and periorbital edema are specific for diffuse toxic goiter. They arise due to an increase in the volume of connective tissue and retrobulbar fat, which can lead to diplopia. Periorbital connective tissue and eye muscles are subject to lymphocytic infiltration. A direct toxic effect of TSH on the tissues of the orbit is assumed, since receptors for TSH are found in them. Due to significant eye damage, consultation with an ophthalmologist is necessary.

Pretibial myxedema is characterized by swelling of the anterior surface of the leg and hyperpigmented papules or plaques raised above the surface of the skin. This symptom occurs in 1-2% of patients and is combined with severe Graves' ophthalmopathy. Histological examination reveals lymphocytic infiltration of the dermis and local accumulation of glycosaminoglycans. In the early stages, topical corticosteroids are effective.

Multinodular toxic goiter and toxic thyroid adenoma

Most patients have a somatic activating mutation of the gene encoding the TSH receptor. Detection of a toxic adenoma of the thyroid gland makes it possible to exclude cancer of this localization.

Thyrotoxicosis caused by iodine preparations

Iodine-induced thyrotoxicosis usually occurs in patients with treated nodular toxic goiter who take large amounts of iodine-containing drugs. The disease occurs mainly in areas with iodine deficiency, but it is also possible where the intake of this microelement is sufficient. Iodine enhances the secretion of thyroid hormones, leading to thyrotoxicosis. Iodine thyrotoxicosis can also be a consequence of the use of radiocontrast agents, amiodarone, or large quantities of iodine-containing nutritional supplements.

Secondary thyrotoxicosis

A rare cause of thyrotoxicosis is thyrotropinoma (a pituitary adenoma that secretes TSH). It is characterized by a clinical picture of thyrotoxicosis, including goiter.

Symptoms and signs of thyrotoxicosis of the thyroid gland

Symptoms of thyrotoxicosis (hyperthyroidism): enlargement of the thyroid gland, exophthalmos, the so-called “angry gaze” (eye slits wide open, eyes shining, rare blinking), increased heart rate, tearfulness, nervousness, insomnia, weight loss despite a good appetite, fatigue, poor tolerance to high ambient temperatures. If a patient is suspected of having this disease (state of subcompensation), consultation with an endocrinologist is recommended to resolve the issue of the safety of outpatient dental treatment. If the patient refuses to consult with the attending physician, the refusal is issued in accordance with modern legislation.

Symptoms of thyrotoxic crisis (decompensation): severe muscle weakness, increased body temperature, profuse sweating, headache, increased blood pressure, nausea, vomiting, diarrhea, the appearance of heart rhythm disturbances (usually atrial fibrillation). If these symptoms occur, routine dental treatment should be postponed. Emergency dental care - only in a hospital setting.
Medication preparation is carried out with sedatives. For the purpose of pain relief, anesthetics that do not contain epinephrine (Mepivastezin) or contain it in a minimum dosage of 1:200,000 (Ubistezin) are used.

Diagnosis and diagnosis of thyrotoxicosis of the thyroid gland

Thyrotoxicosis can be classified as a so-called “tram diagnosis”. What does it mean? The external manifestations of the disease are so vivid that, having accidentally seen a patient in a crowd (on public transport), the doctor accurately makes a diagnosis at first sight.

Thyrotoxicosis syndrome is the complete opposite of hypothyroidism syndrome. These are two opposite states that can be compared according to the principles of “cold - hot”, “dry - wet”, “slow - fast”.

Like hypothyroidism, thyrotoxicosis can be subclinical and manifest.

Subclinical thyrotoxicosis characterized by low TSH and normal T4 free levels. and T 3 free. There are no clear signs of thyrotoxicosis in this condition. This is not a “tram diagnosis”.

manifest thyrotoxicosis has a pronounced clinical picture, while TSH is very low and T 4 is free. and/or T 3 free. increased. It is in this case that we can talk about a “tram diagnosis”.

Usually, after such a start to the conversation, a trusting contact arises between the doctor and the patient, which is especially important in case of thyrotoxicosis, because with this syndrome the character becomes nasty, capricious and absurd.

Irritability, tearfulness, increased excitability, fussiness are common companions of thyrotoxicosis. This is not the patient's fault, it is the disease.

Like hypothyroidism, thyrotoxicosis affects all organs and systems. You already understand that the pathological symptoms of thyrotoxicosis are radically opposite to the symptoms of hypothyroidism.

Diagnosis is based on symptoms as well as laboratory results. Laboratory studies typically include serum levels of TSH, free T4, and total or free T3 (the 2011 American Endocrine Association guidelines note that there is a lack of standardization in measuring free T3 as opposed to T4). The degree to which T3 and T4 levels increase depends on the disease. In diffuse toxic goiter and toxic adenoma, the T3 level is usually higher than the T4 level due to stimulation of the conversion of T4 to T3 in the thyroid gland.

Diagnosis of thyrotoxicosis only on the basis of reduced TSH levels.

Detection of a low TSH level in itself cannot be a basis for making a diagnosis of thyrotoxicosis and, especially, for prescribing thyreostatics. If a low TSH level is detected, the doctor should prescribe a further examination - determination of free fractions of T4 and T3. After this, it becomes clear whether we are dealing with overt thyrotoxicosis (including T3 thyrotoxicosis) or with subclinical thyrotoxicosis. If, when obvious thyrotoxicosis is detected, the next step is to search for its cause, then subclinical thyrotoxicosis does not always require active action from the doctor.

In addition, in patients in serious condition, who for some reason are excluded from thyrotoxicosis, low TSH levels are often associated with the so-called euthyroid pathology syndrome (see below). When determining the level of free T4 in such patients, it turns out to be normal or low.

A widespread mistake is to establish a diagnosis of diffuse toxic goiter in all patients with thyrotoxicosis without nodular formations in the gland, while the terms “thyrotoxicosis” and “DTG” are considered synonymous. Despite the fact that thyrotoxicosis is indeed the most common cause of thyrotoxicosis, in the absence of endocrine ophthalmopathy (EOP, which makes it possible to establish the diagnosis of thyrotoxicosis without additional examinations), it is necessary to exclude other causes.

Let us recall that the algorithm for examining a patient with thyrotoxicosis involves making a differential diagnosis in a patient without an image intensifier using scintigraphy and/or determining the level of antibodies (AT) to the TSH receptor. Ignorance of this algorithm or failure to follow it leads to the unreasonable prescription of thyreostatics for destructive thyrotoxicosis. The exception is cases of clinically and laboratory-expressed thyrotoxicosis, lasting more than three months, or recurrent after discontinuation of thyreostatics. This course is typical for DTZ.

Lack of differential diagnosis for iodine-induced and cytokine-induced thyroiditis.

When identifying thyrotoxicosis, it is important to collect a history of concomitant diseases and therapy received. The number of patients receiving antiarrhythmic therapy with amiodarone or treatment with cytokines (primarily due to antiviral therapy for hepatitis B and C), as well as the number of procedures using iodinated radiocontrast agents, is growing. All these patients have an increased risk of dysfunction of the thyroid gland, including the development of thyrotoxicosis, however, such thyrotoxicosis can be both destructive and autoimmune. Since the tactics for these conditions are fundamentally different, for differential diagnosis one should use scintigraphy of the thyroid gland, and if this is impossible, determination of the level of AT to rTSH.

Determination of the level of antibodies to thyroid peroxidase and thyroglobulin in thyrotoxicosis and erroneous diagnosis of autoimmune thyroiditis when they are elevated.

The indications for determining AT levels to thyroid peroxidase (TPO) and thyroglobulin (TG) are quite narrow. It is not advisable to determine them in a patient with thyrotoxicosis, since the result does not represent any clinical significance. An increase in the level of AT to TPO is not a specific sign of autoimmune thyroiditis (AIT). The level of AT to TPO and TG can be high in any autoimmune lesion of the gland (Graves disease, postpartum/silent thyroiditis, subacute thyroiditis, AIT). An erroneous diagnosis of AIT in Graves' disease leads to inadequate treatment of the latter (short courses of thyreostatics, watchful waiting, refusal of radical treatment).

Screening for hypothyroidism in pregnant women is becoming widespread in our country. Unfortunately, TSH and free T4 are often determined too late (in the second and even third trimesters), when correction of hypothyroidism is no longer so important. When determining TSH and free T4 in a timely manner (with a gestational age of 8-12 weeks), it is important to correctly interpret the results obtained. Let us remember that the cut-off points for hypothyroidism in pregnant women during this period are different, and the lower limit of the norm does not exist, since quite often in healthy pregnant women TSH is below the reference limits for non-pregnant women, and free T4 may slightly exceed these limits. Ignorance of these features leads to overdiagnosis of DTG in pregnant women, erroneous prescription of thyreostatics, and even recommendations for termination of pregnancy.

Late diagnosis/no diagnosis in elderly patients.

As is known, the clinical picture of thyrotoxicosis in elderly patients is not so bright and is often limited to cardiac manifestations, unmotivated weight loss and mood changes. Because heart failure and cardiac arrhythmias, cognitive impairment, and weight changes due to other causes are common in older adults, the diagnosis of thyrotoxicosis may be delayed for years. It is especially important to remember to exclude thyrotoxicosis in elderly patients with atrial fibrillation.

Subclinical thyrotoxicosis

Subclinical (latent) thyrotoxicosis is a condition in which TSH levels are reduced, T4 and T3 levels remain within normal limits, and clinical signs of thyrotoxicosis are mild or absent. Treatment is indicated if there is a risk of developing clinically significant thyrotoxicosis, atrial tachyarrhythmias are observed (or the risk of their development is increased), weight loss and other manifestations of thyrotoxicosis, as well as decreased bone density. It has been shown that with subclinical thyrotoxicosis the risk of atrial fibrillation increases.

In postmenopausal women not receiving menopausal hormone therapy, subclinical thyrotoxicosis contributes to the development of osteoporosis and fractures. Treatment is indicated in the presence of atrial tachyarrhythmias, osteoporosis or osteopenia, unexplained weight loss and other symptoms of thyrotoxicosis. To normalize TSH levels, antithyroid drugs are prescribed. If the treatment has a good effect, radioactive iodine therapy is recommended. The probability of remission is about 30%, but with a milder course of the disease it may be higher.

Treatment of thyrotoxicosis of the thyroid gland

Prescription of thyreostatics for destructive thyrotoxicosis.

Usually this error is caused by incorrect diagnosis, when all patients with thyrotoxicosis syndrome are diagnosed with thyrotoxicosis. However, there is an erroneous practice of prescribing small doses of thyreostatics even for destructive thyrotoxicosis. Let us recall that with the destruction of thyrocytes, thyrotoxicosis is never long-lasting, resolves on its own and does not require the administration of thyreostatics, since hyperfunction of thyrocytes is not accompanied and does not pose any serious risks to the patient. The maximum that may be required in the thyrotoxic phase of various thyroiditis is the administration of β-blockers for a short period of time to relieve symptoms (palpitations, tremor); for subacute thyroiditis and amiodarone-induced thyrotoxicosis type 2, glucocorticoids are indicated.

Prescription of thyreostatics when only decreased TSH is detected.

Low TSH with normal levels of peripheral thyroid hormones can occur with subclinical thyrotoxicosis (onset of thyrotoxicosis, destructive thyroiditis, subcompensated functional autonomy). Detection of reduced TSH involves the determination of free T4 and T3; if their level is normal, a repeat determination of thyroid function is required after 2-3 months. In women of reproductive age, one should not forget about a possible pregnancy, which the woman may not yet know about. If subclinical thyrotoxicosis persists, then it is possible to search for its cause, primarily the subclinical stage of thyrotoxicosis and subcompensated functional autonomy. For this purpose, thyroid scintigraphy is prescribed; It is also possible to determine the level of AT to rTSH. There is currently no convincing evidence that treatment of subclinical thyrotoxicosis provides any benefit, but cardiovascular morbidity is significantly increased in patients with subclinical hyperthyroidism. Therefore, observational tactics are not recommended in every case; the prescription of thyreostatics is recommended in patients with persistently reduced TSH levels under the following conditions: age over 65 years, high risk of osteoporosis, clinically pronounced symptoms of thyrotoxicosis. Assessment of thyroid function in seriously ill patients should be carried out according to strict indications; if possible, TSH determination is recommended to be postponed until recovery or compensation of the underlying disease.

Persistent prescription of conservative therapy for recurrent immunogenic thyrotoxicosis.

Relapse of DTG serves as an indication for radical treatment.

Intermittent prescription of thyreostatics for many years and then their withdrawal “until the next relapse” is quite common in our country and sooner or later leads to visceral complications of thyrotoxicosis and disability of the patient.

Unfortunately, RIT remains a difficult to access treatment method in our country. There are few specialized centers, and the cost of treatment is high. Most patients with DTD do not even receive information about the existence of this possibility. However, many patients, being adequately informed, prefer RIT to surgical treatment.

There are often cases when the patient himself finds information about this method of therapy, but the attending physician misinforms him about the risks of treatment, saying that RIT is contraindicated at a young age, with a large size of the gland, and sometimes even frightening the patient with the development of oncopathology.

Currently, pregnancy and breastfeeding are considered an absolute contraindication to the treatment of thyrotoxicosis using the RIT method. There are no age restrictions for adult patients; in children with DTG, it is also possible to prescribe radioiodine therapy for recurrent thyrotoxicosis.

Since the coexistence of thyrotoxicosis and colloid nodules is possible, when thyrotoxicosis is detected in persons with nodular formations in the thyroid gland, the diagnosis should be confirmed by scintigraphy of the gland. The choice of lifelong conservative therapy can be justified only in elderly people with high anesthetic risks, in case of refusal or impossibility of performing RIT.

There are three known treatment methods. The choice of a specific method depends on the clinical situation, plans and preferences of the patient. In Russia and, to a lesser extent, in European countries, conservative treatment is traditionally considered first-line therapy. However, if there are predictors of ineffectiveness of such therapy, this tactic is erroneous and harms the patient.

It is advisable to consider radical treatment as the method of choice in the following cases:

gland volume more than 30-40 ml;
severe thyrotoxicosis with high levels of AT to rTSH;
intolerance to thyreostatics (primarily allergic reactions, agranulocytosis);
increased level of AT to rTSH after 6 months. conservative therapy.

In addition, when explaining the low effectiveness of conservative treatment (under initially favorable clinical conditions, its effectiveness does not exceed 30-40%), the need to take medications for a year.

Lack of alertness regarding possible agranulocytosis and drug-induced hepatitis when prescribing thyreostatics.

In our country, the usual practice when prescribing thyreostatics is more or less regular monitoring of a general blood test; transaminase levels are much less often monitored. However, the most serious side effects of methimazole and propylthiouracil can develop at any time, regardless of the duration of therapy, and require immediate withdrawal of the antithyroid drug, and sometimes urgent medical intervention. Therefore, when prescribing thyreostatic therapy, the patient should always be warned that if suspicious symptoms develop (itching rash, jaundice, discolored stool or dark urine, joint pain, abdominal pain, anorexia, nausea, severe weakness, fever, sore throat ) you should immediately stop taking the thyreostat and consult a doctor. Routine determination of white blood cell levels and/or liver tests in asymptomatic patients is not recommended. If symptoms suspicious for liver damage or agranulocytosis develop, appropriate laboratory testing should be performed immediately.

Use of a “block and replace” regimen with inappropriately small doses of thyreostatics and thyroxine.

The “block and replace” regimen has some advantages over the “block” regimen, namely better maintenance of euthyroidism and no need for monthly monitoring of hormonal levels. However, when using small doses of thyrostatic and thyroxine (for example, the prescription of 5 mg of thiamazole and 25 mcg of thyroxine is quite common), these advantages are completely neutralized. The “block and replace” regimen involves prescribing a dose of thyrostatic agent that will cause drug-induced hypothyroidism. Accordingly, this deficiency of thyroxine must be adequately compensated. For example, European experts recommend that doctors use 30 mg of thiamazole and a full replacement dose of thyroxine.

Monitoring the effectiveness of treatment based on TSH levels.

TSH during the treatment of DTG can remain reduced for a long time (up to six months) after drug compensation has been achieved. It is not uncommon for TSH to remain low for some time even after drug-induced hypothyroidism has been achieved.

If the patient is taking medications to treat hyperthyroidism, make sure that the patient takes the medications on time and that their therapeutic effect peaks during the period of dental care.

Diffuse toxic goiter

Antithyroid drugs, radioactive iodine and surgical treatment are used. In patients under 50 years of age without cardiovascular disease, treatment begins with antithyroid drugs. Thionamides have an immunosuppressive effect by inhibiting the synthesis of thyroid-stimulating antibodies. When the titer of thyroid-stimulating antibodies decreases, remission may occur. Approximately one third of patients achieve long-term remission after 6-12 months of treatment with thionamides. Treatment for longer than 18 months does not increase the frequency of remissions; at this point, by the joint decision of the doctor and the patient, therapy with antithyroid drugs can be continued or switched to another treatment. The most dangerous side effect of thionamides, which occurs with a frequency of 3:1000, is agranulocytosis. Other rare side effects are rash, cholestasis and hepatitis.

Elderly and sick people in whom antithyroid drugs do not have an effect are prescribed radioactive iodine. Pregnant and breastfeeding women are not prescribed radioactive iodine due to the risk of hypothyroidism in the child. In adults who are not pregnant, treatment with radioactive iodine is safe and effective. Treatment with radioactive iodine may worsen the symptoms of Graves' ophthalmopathy. The use of prednisone can reduce the incidence of this complication. With more severe thyrotoxicosis, 3-5 days after the administration of radioactive iodine, you can resume taking anti-thyroid drugs, but the effectiveness of treatment must be assessed every 2-3 weeks.

Thyroidectomy is indicated for patients who refuse other types of treatment, pregnant women who require significant antithyroid drugs, as well as patients who, in addition to diffuse toxic goiter, have a node suspicious for a malignant tumor. Thyroidectomy is preferred over subtotal thyroid resection due to lower complication rates (0% and 8%, respectively). Before surgery, antithyroid drugs and iodine preparations are prescribed to reduce the risk of complications.

To relieve the adrenergic symptoms of thyrotoxicosis, a short course of β-blockers is used, which eliminate tremor, anxiety and tachycardia faster than antithyroid drugs. Beta blockers should only be prescribed in combination with antithyroid drugs.

Other antithyroid drugs include potassium iodide and sodium iodide, which suppress the secretion of thyroid hormones. The action of iodides begins faster than that of antithyroid drugs, but lasts only a few days. These drugs are used for thyrotoxic crisis.

Subclinical thyrotoxicosis is a type of endocrine pathology that develops long before the appearance of its symptoms. Patients remain in good health for a long time, but as the level of TSH (thyrotropin) decreases and the thyroid hormones T4 (thyroxine) and T3 (triiodothyronine) are normal, dangerous complications often arise.

Subclinical thyrotoxicosis is a type of endocrine pathology that develops long before the appearance of its symptoms.

Symptoms

The course of the disease is often characterized by a complete absence of pathological signs. In those cases when they do occur, due to their mild severity, many people mistakenly take them for manifestations of accumulated fatigue and stress. However, there are a number of characteristic symptoms, when they appear, a subclinical variant of thyrotoxicosis can be suspected.

The list of such signs includes:

increased sweating;
attacks of tachycardia, when the number of heart contractions, even at rest, is 100-120 beats per minute;
persistent feeling of hunger;
digestive disorders;
sudden mood swings, excessive nervousness;
sleep disturbance;
decreased performance.

Causes

Most often, the disease develops in women over 40-50 years of age, although it can also occur in young people.

Thyrotoxicosis is sometimes identified with hyperthyroidism, since they have many similar manifestations, including crises and coma. However, in domestic endocrinology, these pathologies are classified as independent diseases.

The development of subclinical thyrotoxicosis is most often caused by the following reasons:

deficiency of natural iodine in foods, water, air;
long-term use of hormonal medications;
significant hormonal imbalances;
diseases of the heart and blood vessels;
damage to the nervous system;
surgical treatment of the thyroid gland;
use of radioactive iodine;
hereditary predisposition.

Diagnostics

The following can be used to identify a subclinical type of thyrotoxicosis:

Blood test.
Ultrasound of the thyroid gland.

Since this disease is characterized by a sharp reduction in the production of thyrotropin with normal synthesis of thyroxine and triiodothyronine, such an imbalance is detected using hormonal blood tests.

Electrocardiography instrumentally confirms the presence of heart rhythm disturbances, which in most patients manifest themselves in the form of tachycardia.

Ultrasound allows a final diagnosis to be made. Using ultrasound, the doctor receives complete information about the volume, structure and lesions of the gland. In difficult cases, especially if an oncological process is suspected, organ puncture is prescribed, followed by histological analysis, computed tomography or magnetic resonance imaging.

Treatment

The main objectives of the treatment of subclinical thyrotoxicosis:

Restoring hormonal balance in the body.
Improving blood composition (normalization of hemoglobin and glucose levels).
Strengthening the heart, blood vessels, nervous system.

In complex drug treatment, preparations containing microdoses of iodine compounds are of paramount importance. With their help, endocrinologists achieve improved functioning of the thyroid gland. Doctors often prescribe glucocorticosteroids. Antiarrhythmic drugs help normalize contractions of the heart muscle.

Therapy using radioactive iodine is considered effective. In this case, it is extremely important to accurately select a treatment regimen. An overdose has a detrimental effect on the functioning of the gland. If an excess amount of iodine accumulates in the tissues of the organ, the production of the hormones T4 and T3 will decrease, and hypothyroidism may develop.

Treatment must take into account the causes of subclinical thyrotoxicosis:

in case of primary disruption of the gland, iodine preparations are not prescribed immediately, but a wait-and-see approach with monitoring is chosen;
if the disease is caused by improper use of medications, they are limited to adjusting drug therapy;
with the development of thyrotoxicosis due to concomitant diseases, especially in older people, the primary goal of treatment is to eliminate the root cause.

When choosing a wait-and-see approach, doctors often advise using traditional methods that have a mild healing effect on the thyroid gland. Popular recipes: Patients with subclinical thyrotoxicosis, especially women, need to be monitored by an endocrinologist.

With timely diagnosis, monitoring of the condition and adequate treatment tactics, thyroid function is restored in most clinical cases. The risk of complications becomes minimal. However, failure to comply with medical instructions can have an unfavorable prognosis, leading to severe disability and even death.

Subclinical thyrotoxicosis is a rather rare disease, diagnosed in patients aged 18 to 55 years. Each age category has its own characteristics of the course of the disease and its manifestations. Doctors have proven the connection between the level of iodine in the body and the risk of thyrotoxicosis.

In elderly patients, the development of a serious illness can be provoked by an attempt to increase the iodine content by taking iodine-containing medications.

Features of the disease and causes of its occurrence

Subclinical thyrotoxicosis is one of the forms of the pathological process that causes significant changes in the body associated with increased production of thyroid-stimulating thyroid hormone. The main feature of the disease is that older women and representatives of the Negroid race are more susceptible to it.

The main reason for the development of subclinical thyrotoxicosis is an acute lack of iodine, which occurs in those who often deny themselves proper rest or are constantly in conditions difficult for normal existence. The correct diet, which should contain iodine, is also important. Their absence also negatively affects the health and quality of thyroid hormone production.

In order for the doctor to prescribe adequate and effective treatment, it is important for him to know the causes of the resulting dysfunction of the thyroid gland, changes in the levels of TSH, T3 and T4. Endocrinologists divide such causes into external and internal. External ones are:

taking oral contraceptives based on hormonal drugs;
surgical interventions;
taking medications that affect the functionality of the thyroid gland
treatment of diseases associated with insufficient iodine content.

Important! Subclinical means that it began to develop long before the first symptoms appeared. So, in the presence of Graves' disease, subclinical thyrotoxicosis does not manifest itself clearly.

Internal factors influencing the development of subclinical thyrotoxicosis are a violation of the general hormonal level in the postpartum period, the presence of such complex diseases as diffuse toxic goiter, consisting of many nodes. The existence of subclinical thyrotoxicosis in the patient’s body can be judged by changes in the functionality of some organs and systems:

failure of the heart and blood vessels;
nervous system disorders;
digestive tract dysfunction.

Symptoms of pathology

The disease manifests itself in the form of sleep disturbances and increased excitability, fatigue and inability to endure physical activity. The main manifestations of the disease can be considered:

irritability;
chronic fatigue;
sudden attacks of tachycardia with an increase in the number of heart contractions up to 100 beats per minute;
sweating;

dry mouth;
frequent rises in blood pressure;
frequent mood changes;
increased peristalsis;
constant feeling of hunger and lack of weight gain.

Another feature is that despite sleep disturbances, patients do not complain of being “overwhelmed” and cope well with their professional responsibilities.

Diagnostic methods

Subclinical thyrotoxicosis is one of the diseases that contribute to the occurrence of severe complications. Lack of timely and effective treatment can lead to the development of:

senile dementia;
coronary heart disease;
hypertension;
osteoporosis.

Timely contact with specialists and adequate treatment will help to avoid serious consequences and cope with the disease. Accurate diagnosis is carried out using a detailed examination, which includes:

blood test;
electrocardiography.

Important! A blood test allows you to establish the exact level of TG3 and TG4 in the patient’s body, as well as determine the content of thyroid-stimulating hormone if the levels of the first two hormones do not exceed the norm.

During an instrumental examination, the structure and parameters of the thyroid gland are studied using ultrasound radiation. An ECG can detect abnormalities in the heart.

Subclinical thyrotoxicosis occurs against the background of atrial fibrillation and causes the development of thrombosis or thromboembolism. Associated with this disease are:

atherosclerosis;
cardiac ischemia;
myocardial infarction;
angina pectoris.

It is important to pay attention to changes in the patient's weight. Violation of the levels of TSH, TG4 and TG3 leads to metabolic failure. This is especially true for fat metabolism. The patient is rapidly gaining weight.

During a visual examination, the doctor can detect not only a change in the appearance of the patient’s face, but with the development of Graves’ disease, visual acuity noticeably decreases and the appearance of the eyes changes. A characteristic sign of Graves' disease is.

Therapeutic measures are selected in accordance with the results of tests and instrumental examinations. In most cases, treatment is aimed at normalizing blood hemoglobin sugar levels, combating hormonal imbalances, eliminating the consequences of subclinical thyrotoxicosis in the form of heart and vascular diseases, and normalizing the functionality of the nervous system.

Therapy

In order to save a patient from subclinical thyrotoxicosis, doctors will need to do everything necessary to normalize the functioning of the thyroid gland. Drug treatment requires the prescription of drugs that affect the functionality of the thyroid gland. By acting directly on the gland itself, they reduce its activity. This helps reduce hormone production and restore previous function.

Often, endocrinologists prescribe glucocorticosteroids, but their dosage and regimen are developed individually in each individual case. The fact is that a huge role in the development of subclinical thyrotoxicosis is played by the patient’s age and the individual reaction of the body to the action of medications selected by the doctor.

One of the most effective methods of therapy is treatment with radioactive iodine. Once in the body, it accumulates in the structure of the thyroid gland, then its excess cells die and connective tissue appears in their place. Exceeding the dosage or an incorrectly chosen regimen for taking the drug leads to the fact that the level of iodine content increases noticeably, and the functionality of the gland decreases. Accordingly, the production of hormones decreases, which causes the development of hypothyroidism.

Often, doctors refuse emergency measures, being supporters of wait-and-see tactics. To maintain the required level of TSH, TG3 and TG4 in the patient’s body, he is prescribed lifelong hormonal therapy. If there are no special violations, then it is important to constantly monitor the condition and always be ready to provide maintenance therapy.

They are extremely popular among patients and doctors. Treatment with decoctions and infusions gives excellent results, but, in addition, endocrinologists strongly recommend that their patients spend some time several times a year in places where the environment and the quality of drinking water contribute to rapid recovery.

Many people suffering from subclinical thyrotoxicosis come for rest and treatment to sanatoriums and holiday homes located in the Amur region. Despite the lack of specialized medical centers here, Blagoveshchensk is recognized as one of the best cities where effective treatment of subclinical thyrotoxicosis is carried out.

If you are treating an ailment with the help of folk remedies prepared at home, you can use ancient recipes that have been known for a long time and do not require any rare and hard-to-find ingredients to prepare the compositions. However, only the attending physician can advise the exact prescription for each patient.

Subclinical thyrotoxicosis is a type of thyrotoxicosis, a condition caused by increased production of thyroid hormones, which have a pathological effect on health. The changes affect internal organs and also cause cosmetic defects: diffuse toxic goiter appears and the eyes become “bulging” - exophthalmos.

Thyrotoxicosis is divided into 3 degrees of severity; the subclinical form is considered separately. During this period, health deterioration is observed cyclically, so there is still debate among doctors: whether this condition requires special treatment or whether corrective methods and therapy for the underlying diseases that caused this pathology are sufficient.

Information about subclinical thyrotoxicosis

This condition is more common in women after menopause, and its occurrence is influenced by chronic diseases and external factors.

Doctors are alarmed by eye symptoms - with thyrotoxicosis, the appearance of the face changes, the eyes become bulging, and therefore visual acuity quickly decreases. This is how early Graves' disease makes itself felt.

Other internal reasons include the following factors:

thyroid adenoma;
postpartum hormonal changes;
multinodular diffuse toxic goiter.

In mild thyrotoxicosis, an excess of hormones can occur due to the use of medications prescribed for the treatment of thyroiditis - an inflammatory disease of the thyroid gland - iodine drugs, alpha-interferon, L-thyroxine.

In addition to eye symptoms and an enlarged thyroid gland, the following signs indicate subclinical thyrotoxicosis:

periodic attacks of tachycardia;
severe sweating, which is often mistaken for hot flashes;
mood swings, irritation;
insomnia;
periodic bouts of diarrhea;
increased urination;
temporary tremor of the limbs.

Unlike other types of thyrotoxicosis, weight loss does not occur; on the contrary, it may increase slightly.

If the correct diagnosis is not made in time, the body is depleted of useful substances necessary for normal life - mineral compounds are no longer absorbed - which provokes the development of osteoporosis, coronary artery disease, and senile dementia.

The risk of severe complication of coronary disease increases - the development of myocardial infarction, the occurrence of ischemic stroke.

Diagnosis of a dangerous condition

If hyperfunction of the thyroid gland is suspected, the following types of examination are recommended to the patient:

General blood tests and hormonal analysis to detect the content of the TSH hormone - thyrotropin - in a laboratory sample. If the syndrome is present, then the amount of the TSH hormone is reduced against the background of other indicators: T3, T4;
Conduct hardware examinations: ultrasound of the thyroid gland, ECG.

Based on the results of tests and studies, a treatment regimen for the condition is selected.

In most cases, the main treatment is aimed at normalizing blood sugar, increasing or decreasing hemoglobin, and normalizing the condition of the cardiovascular system.

Treatment of thyrotoxicosis

The main therapeutic measures for thyrotoxicosis are aimed at reducing the functional activity of the thyroid gland and normalizing it.

The standard treatment regimen is the prescription of drugs based on thiamazole and propylthiouracil - they directly affect the thyroid gland and block its functions. The treatment regimen is standard, but the doses and duration of the therapeutic course are selected for each patient individually - after the condition improves, they switch from a therapeutic dose to a maintenance dose.

In most cases, glucocorticosteroid hormones are prescribed, the doses of which are also adjusted depending on the patient’s age, stage of the disease and individual characteristics - the patient’s weight and metabolic level.

Treatment with radioactive iodine is considered one of the most modern methods of eliminating a condition in which the thyroid gland works at an increased rate. This method of adjustment helps to avoid surgery - removal of the thyroid gland.

With subclinical thyrotoxicosis, most endocrinologists are in a wait-and-see position. Until the condition causes persistent disturbances in the body - does not lead to a manifest form - it is not recommended to start hormonal therapy.

However, treatment of the disease that provoked hyperfunction of the thyroid gland begins immediately after its identification.

Treatment is not carried out in patients suffering from autoimmune and subacute thyroiditis and in pregnant women with physiological manifestations of thyrotoxicosis.

Since the syndrome develops in the second trimester of pregnancy and does not affect the condition of the fetus, slightly worsening the well-being of the expectant mother, the use of thyreostatics is unjustified - it can affect the physiological development of the baby.

However, after giving birth, the woman in labor will need mandatory diagnostic examinations and adjustments to her general condition if the thyroid gland does not stabilize. Women of childbearing age have an increased risk of developing thyrotoxicosis.

The older the patient is, the more pronounced the changes are. If, with subclinical thyrotoxicosis, endogenous subclinical hyperthyroidism is detected against the background of existing atrial fibrillation, then the use of thyreostatic therapy is considered a necessary measure.

In this case, they do not even take into account the degree of decrease in TSH production, since the risk of developing pathologies of the cardiovascular system increases - the development of atherosclerosis, the appearance of frequent arrhythmias.

Treatment with radioactive iodine may be considered to prolong life.

Traditional medicine cannot affect the functioning of the thyroid gland, so it is used only to relieve symptoms of concomitant diseases. Hawthorn tincture will help stabilize cardiac activity, a decoction of walnut partitions will relieve frequent visits to the toilet, rose hips will vitaminize the body. Increasing the amount of peaches and strawberries in the diet will not replace thyreostatics if they are prescribed.

However, a tactic has been developed that for TSH values from 0.10 to 0.45 mIU/l, dynamic monitoring is recommended: periodic testing - once every 6 months it is necessary to take a hormone test.

This condition is more common in women after menopause, and its occurrence is influenced by chronic diseases and external factors.

Other internal reasons include the following factors:

thyroid adenoma;
postpartum hormonal changes;
multinodular diffuse toxic goiter.

In addition to eye symptoms and an enlarged thyroid gland, the following signs indicate subclinical thyrotoxicosis:

periodic attacks of tachycardia;
severe sweating, which is often mistaken for hot flashes;
mood swings, irritation;
insomnia;
periodic bouts of diarrhea;
increased urination;
temporary tremor of the limbs.

Unlike other types of thyrotoxicosis, weight loss does not occur; on the contrary, it may increase slightly.

The risk of severe complication of coronary disease increases - the development of myocardial infarction, the occurrence of ischemic stroke.

Diagnosis of a dangerous condition

If hyperfunction of the thyroid gland is suspected, the following types of examination are recommended to the patient:

General blood tests and hormonal analysis to detect the content of the TSH hormone - thyrotropin - in a laboratory sample. If the syndrome is present, then the amount of the TSH hormone is reduced against the background of other indicators: T3, T4;
Conduct hardware examinations: ultrasound of the thyroid gland, ECG.

Based on the results of tests and studies, a treatment regimen for the condition is selected.

In most cases, the main treatment is aimed at normalizing blood sugar, increasing or decreasing hemoglobin, and normalizing the condition of the cardiovascular system.

Treatment of thyrotoxicosis

The main therapeutic measures for thyrotoxicosis are aimed at reducing the functional activity of the thyroid gland and normalizing it.

However, treatment of the disease that provoked hyperfunction of the thyroid gland begins immediately after its identification.

Treatment is not carried out in patients suffering from autoimmune and subacute thyroiditis and in pregnant women with physiological manifestations of thyrotoxicosis.

Treatment with radioactive iodine may be considered to prolong life.

However, a tactic has been developed that for TSH values from 0.10 to 0.45 mIU/l, dynamic monitoring is recommended: periodic testing - once every 6 months it is necessary to take a hormone test.

If TSH reproduction falls and its level drops below 0.10 mIU/l - this condition is called complete TSH suppression - treatment is recommended to begin if symptoms of concomitant diseases are detected:

osteoporosis;
progressive growth of goiter, causing disturbances in the swallowing process and difficulty breathing;
heart rhythm disturbance is a manifestation of tachycardia and arrhythmia.

Treatment of the digestive system is not required - correction of gastrointestinal disorders is carried out using an individually formulated diet.

A unified therapeutic strategy in modern medicine for the treatment of subclinical thyrotoxicosis has not been developed, since due to the periodicity of symptoms and a slight deterioration of the condition, it is rarely diagnosed.

In most cases, with subclinical hyperthyroidism, observation tactics are chosen.