What is hypothyroidism?

is a process that occurs due to a lack of thyroid hormones in the thyroid gland. This disease occurs in about one in a thousand men and nineteen out of a thousand women. Often there are cases when the disease is difficult to detect, and for a long time. The reason for the diagnostic difficulties is that the disease occurs and develops slowly, and it is characterized by signs that make it difficult to recognize hypothyroidism. Usually the symptoms are mistaken for simple overwork, in women - for pregnancy or something else.

Due to the occurrence and spread of this disease, the main metabolic processes in the body are inhibited, since thyroid hormones are responsible for energy metabolism.

It rarely becomes a separate disease associated with the pathology of the thyroid gland alone;

Not an independent disease and should not be the only diagnosis (except in rare cases);

It becomes a complication or a natural consequence of any pathology of the thyroid gland with the exception of hyperthyroidism;

It is based on functional disorders in the form of insufficient production of thyroid hormones (triiodothyronine, tetraiodothyronine (thyroxine),), their inferiority or premature inactivation in tissues;

It causes a violation of the general hormonal background and metabolic processes in the body.

Each of these points requires a little clarification. After all, the prevalence of this pathology is very wide, which causes a high interest among the population regarding the expansion of knowledge about it. Another name for extreme hypothyroidism is myxedema.

Hypothyroidism is rarely a single disease or the only diagnosis.

If we consider this statement from a pathogenetic point of view, then it is 100% true. The only exceptions are those cases when it is impossible to establish the primary cause of hypothyroidism, or clinical signs of hypothyroidism are recorded against the background of a normal amount of thyroid hormones. Then this disease may be the only diagnosis that sounds like "idiopathic hypothyroidism."

In all other cases, there must necessarily be a primary disease that caused a violation of the functional abilities of the thyroid gland in relation to the synthesis of thyroid hormones. Prolonged course of hypothyroidism will certainly cause severe disorders in the body, which will be displayed as a layering of other diseases, in which it will become an unfavorable background for their further progression.

Hypothyroidism is a functional pathology of the thyroid gland with damage to the whole body.

Hypothyroidism is based not on organic changes in the tissues of the thyroid gland and their structural restructuring, but on a violation of the ability to synthesize the corresponding hormones (thyroxine, triiodothyronine, calcitonin).

The consequences that arise in this case cause other functional and even organo-anatomical disorders in almost all organs and tissues. After all, thyroid hormones are involved in important biochemical reactions that regulate the metabolic processes of protein and mineral metabolism and the synthesis of steroid and sex hormones, the growth and development of the musculoskeletal system, the functional abilities of the heart and brain. Hypothyroidism causes not only difficulty in the functioning of these organs, but also a violation of their anatomical structure.

Despite the fact that hypothyroidism is a functional disorder manifested by thyroid dysfunction, its consequences and complications are of an organic nature. The disease causes a violation of the normal structure of target organs that are dependent on thyroid hormones. At the same time, the thyroid gland itself, as a rule, also changes its structure, but the changes are not due to hypothyroidism, but to the disease that caused it!

Hypothyroidism - a syndrome of general hormonal imbalance

The endocrine system of the human body functions as a closed circuit. The loss of one of its links will necessarily slow down the work of the others. This is exactly what happens with hypothyroidism.

After all, the hormones thyroxine, triiodothyronine and calcitonin interact with:

Pituitary hormones that regulate the functioning of the thyroid gland - their lack stimulates the production of thyroid-stimulating hormone, which provokes the growth of the thyroid gland in diffuse volume, in the form of nodes or cancerous;

Other tropic hormones of the hypothalamic-pituitary system - against the background of a decrease in thyroid and increased activity of thyroid-stimulating hormone, an increase in the amount of prolactin is possible. Such changes lead to permanent galactorrhea and changes in the mammary glands, and also further disrupt the synthesis of sex hormones by the ovaries;

Steroid hormones of the sex glands and adrenal glands - the activity of their synthesis is significantly reduced, since thyroid hormones cannot provide adequate activity of protein metabolism in the liver. As a result, there is a lack of building material for steroids, which for the most part consist of protein, and hormonal insufficiency of the testicles, ovaries and adrenal glands;

Parathyroid glands - a lack of calcitonin causes a violation of calcium metabolism, which is the result of the leaching of calcium ions from the bone tissue from excessive parathyroid hormone activity.

In what case can hypothyroidism be an independent disease?

Those clinical variants of hypothyroidism, when the thyroid gland synthesizes a sufficient amount of hormones and their concentration in the blood is normal, are referred to as paradoxical types of the disease. This is truly incredible and seemingly impossible. After all, if thyroid hormones are produced normally, then where can the symptoms of hypothyroidism come from? It turns out that this also happens.

The main mechanism of this kind of conditions is the abnormal structure of thyroid hormones or their rapid destruction in the blood. Various autoimmune conditions are capable of triggering such pathological processes against the background of systemic diseases or after suffering a severe pathology (infections, injuries, pancreatic necrosis,). Despite a sufficient amount of the hormone circulating in the plasma, it is not able to fully fulfill its purpose, as it is inactivated by the person's own immune cells. In the same way, clinical hypothyroidism also occurs when thyroxine receptors in its target organs are destroyed.

The clinical picture of hypothyroidism can be represented by symptoms of the underlying disease of the thyroid gland, which caused its dysfunction, and direct signs of hypothyroidism.

In short, the main symptoms of hypothyroidism are:

menstrual irregularities in women;

a sharp weight gain, albeit insignificant. It is caused by a drop in metabolic rate, but appetite is reduced, which prevents a significant increase in body weight;

Musculoskeletal system

Severe general weakness and impotence;

Decreased muscle tone and strength;

Nervous system

Lethargy and apathy;

Numbness of the limbs;

Decreased reflexes;

Depressive and hallucinatory syndromes;

Decrease in memory and mental and intellectual abilities, up to cretinism;

Decreased hearing and visual acuity.

endocrine disorders

Dysfunction of the adrenal glands, manifested by an increase in the main symptoms of hypothyroidism;

menstrual disorders;

Galactorrhea (excretion of milk from the mammary glands in the absence of breastfeeding);

Damage to the blood system

Decreased hemoglobin and iron deficiency anemia;

Megaloblastic anemia;

Violation of digestion and the presence of undigested food particles in the feces;

Decreased amount of daily urine.

The main and one of the first symptoms of hypothyroidism are: skin lesions with severe dense swelling of soft tissues, combined with general weakness, bradycardia, mental and sexual disorders!

Causes of hypothyroidism

Hypothyroidism, as an endocrine disease, can occur due to direct damage to the thyroid gland and due to other pathologies associated with a violation of the functions and structure of the organs that regulate its work.

The main causes of hypothyroidism and etiological classification are given in the form of a table.

Etiological type of hypothyroidism	Immediate causes and diseases
Primary (it is based on damage to the thyroid gland, which leads to its functional inferiority)	Congenital factors: Underdevelopment of the thyroid gland (hypo- and aplasia); Hereditary fermentopathy with damage to thyroid enzymes involved in the synthesis of thyroid hormones; Acquired parentage factors: Condition after removal of the thyroid gland (strumectomy); Ionizing radiation during radiation therapy of tumor diseases, or natural origin in areas of man-made disasters associated with nuclear emissions; Treatment with radioactive iodine preparations; Thyroiditis (inflammatory processes of the thyroid gland) of microbial and autoimmune origin; Iodine deficiency states and endemic against their background; Overdose of drugs that inhibit the synthesis of thyroid hormones and amiodarone; Tumor lesion of the thyroid gland.
Secondary (caused by a decrease in the activity of the pituitary gland in relation to the ability to synthesize thyroid-stimulating hormone)	Ischemic damage to the pituitary gland with cerebral vessels or acute severe anemia against the background of bleeding; Inflammation of intracranial structures in the pituitary region of the brain; Tumor transformation of cells of the adenohypophyseal region; Damage to the pituitary gland against the background of autoimmune diseases; The toxic effect of drugs on glandular pituitary cells (levodopa, parlodel).
Tertiary (represented by damage to the hypothalamic nuclei)	Meningoencephalitis involving the hypothalamic zone; Severe traumatic brain injury; Intracerebral tumors; Therapy with serotonin drugs.
Peripheral (violation of the action of existing thyroid hormones)	Autoimmune processes during which antibodies to thyroid hormones are formed; Congenital or hereditary disorders of the structure of receptors in tissues through which thyroid hormones carry out their action; Enzymopathies of the kidneys and liver, leading to a violation of the conversion of thyroxine to triiodothyronine; Defects in transport proteins that transport hormones into organ cells.

This disease can be very well camouflaged. The lack of thyroid hormones, especially in females, causes depression, a constant bad mood, and a feeling of incomprehensible sadness. In a sick person, intelligence can be hidden or openly reduced, attention and memory become poor, and cognitive function decreases. It becomes difficult for a person to fall asleep, insomnia begins, or, conversely, regularly sleeps.

The longer an undetected and untreated disease has spread since its onset, the greater the likelihood of an intracranial hypertension syndrome. A person complains of regular pain in the head. The patient can live in peace, thinking that the cervical (or some other) is to blame. Suspicions are also caused by muscle pain in the arms, a feeling of weakness in them, tingling and goosebumps. Hypothyroidism is also mistaken for heart disease, as the blood pressure and blood levels of the patient increase.

In the case of female hypothyroidism, mastopathy may develop, and menstruation fails.

Another sign of the disease is swelling of certain parts of the body. Eyelids swell more often, other places less often, but edema is still the main indicator of the presence of hypothyroidism. A repeated decrease in immunity in humans can have an impact on the appearance of the disease. And it can occur even with the smallest violation of the functioning of the thyroid gland. Another sign is this, which occurs because the thyroid gland is responsible for hematopoiesis.

Hypothyroidism in more than 95% of cases is primary and due to. Therefore, when clinical manifestations of hypothyroidism are detected, it is this organ that is examined first of all!

Almost all cases of hypothyroidism are associated with a direct violation of the structure and functioning of the organ responsible for the synthesis of thyroid hormones. This organ is the thyroid gland. It is quite logical that the criteria for the degree of the pathological process in any organ are the severity of changes in its structure and the ability to perform the function that it is supposed to perform. With regard to primary hypothyroidism, the causal relationship is built in such a way that the thyroid gland, due to a violation of its structure, is not able to synthesize the hormones T4 and T3. This causes the clinical manifestations of hypothyroidism, which are superimposed on the symptoms of the underlying disease.

The main diseases of the thyroid gland that can cause primary hypothyroidism include congenital diseases in the form of underdevelopment or complete absence of the organ, inflammatory changes (thyroiditis), cancerous tumors and common endemic goiter with insufficient intake of iodine. Complete or partial removal of the thyroid gland also causes hypothyroidism of varying severity.

To conduct a differential diagnosis between all types of hypothyroidism and confirm the primary type will help:

Clinical findings - the presence of signs of damage to the thyroid gland (its enlargement, the presence of nodes, difficulty swallowing and sore throat) along with symptoms of hypothyroidism;

Data from ultrasound, MRI or radioisotope diagnostics, indicating the presence of structural changes in the thyroid gland and a decrease in its functional abilities;

Blood test to determine plasma concentration of thyroid hormones: T4, T3, TSH. In primary hypothyroidism, T3 and T4 levels are always low. TSH compensatory increases in order to enhance the stimulation of the thyroid gland to produce hormones, or remains within the normal range.

Secondary hypothyroidism is a type of decrease in the functional abilities of the thyroid gland, which occurs not as a result of damage to its tissues, but due to a violation of the regulation of functional activity in relation to hormone production. The thyroid gland, like any organ of the endocrine system, depends on the regulatory glands. These are the pituitary and hypothalamus. Speaking of secondary hypothyroidism, they mean a violation of the activity of hypothalamic thyroid-stimulating hormone. It is either not produced by the pituitary gland, or acquires an abnormal structure. In any case, a situation arises in which an anatomically healthy and unchanged thyroid gland is not able to synthesize thyroxine.

Various intracerebral pathological processes in the form of traumatic injuries, tumors, circulatory disorders in the cerebral arteries, and autoimmune destruction can cause damage to the glandular cells of the pituitary gland. With regard to clinical manifestations, secondary hypothyroidism differs from primary in that symptoms of damage to other endocrine glands, ovaries and adrenal glands, join the typical clinical picture. This causes more severe than with primary hypothyroidism, disorders of the muscular system and the heart, severe intellectual impairment, sexual disorders in the form of persistent amenorrhea and, atrophy of the genital organs and mammary glands, excessive hair growth, sexual infantilism and electrolyte disorders.

Confirming secondary hypothyroidism can help:

Absence of clinical and instrumental signs of damage to the thyroid gland with a clear clinical picture of hypothyroidism;

Data of X-ray examination of the skull in two projections with the study of the area of ​​the Turkish saddle, where the pituitary gland is located;

Computed tomography and MRI of the head, which will help determine the presence or absence of objective causes that caused secondary hypothyroidism;

Blood test to determine plasma concentrations of specific thyroid and pituitary hormones. Diagnostic criteria for secondary hypothyroidism are a decrease in the level of T3, T4 and TSH.

In some cases, we have to talk about tertiary hypothyroidism. It is also not associated with diseases of the thyroid gland, but is due to a violation of the regulation of its activity. In this case, the pathogenetic chain will be even more complicated, since the work of not one, but two links of regulatory processes is disrupted. The nuclei of the hypothalamic part of the brain are affected, which are responsible for the synthesis of hormones that regulate the activity of hormone production by the pituitary gland. In the case of tertiary hypothyroidism, everything looks like this: the hypothalamus does not produce thyreoliberin - the pituitary gland does not produce TSH - the thyroid gland does not produce thyroid hormones.

Hypothyroidism can be conditionally divided into clinical forms of moderate and severe. It all depends on the amount of thyroid hormones produced by the thyroid gland. If they are not present at all, the consequences will be simply catastrophic, and such hypothyroidism will become extremely severe. This form of hypothyroidism is called myxedema. With a partially preserved ability of the thyroid gland to produce hormones, the functioning of the body is disrupted, but such consequences are quite reversible and compatible with everyday life.

Patients with hypothyroidism should be aware that the following consequences may occur without appropriate hormone replacement therapy.

In children:

Lagging behind the child in mental and physical development, up to cretinism;

Delay in the appearance of secondary sexual characteristics, up to complete infantilism;

A sharp decrease in the defenses of the immune system, which is manifested by frequent colds, severe exacerbations of chronic infections;

Severe weakness and inability of the child to carry physical activity.

In adults:

Decreased mental abilities, memory and intelligence;

Persistent heart problems;

Persistent lowering of blood pressure;

Prolonged course of chronic diseases and infectious processes;

Disorders of menstrual function;

Atrophy of the ovaries, external genital organs and mammary glands;

Sexual impotence, impotence and infertility;

Hypothyroid coma (a critical decrease in hormone levels, leading to severe metabolic disorders up to a critical drop in cardiac activity and the brain, accompanied by a persistent loss of consciousness).

All the severe consequences of hypothyroidism can be avoided by careful attention to the existing problem in the early stages of its development. The sooner the diagnosis is detailed and the appropriate hormone replacement therapy is started, the fewer disorders will occur in the body!

The treatment process for hypothyroidism involves the impact on the main links of this disease and includes the following methods:

Etiotropic therapy

It involves treating the underlying disease or condition that caused hypothyroidism. Unfortunately, this kind of help is not always possible. Even when it is possible to act on the true cause of hypothyroidism, the effect is rare.

In the complex of etiotropic therapy, according to indications, the following can be used:

Iodine preparations (iodomarin, potassium iodide). Indicated for endemic goiter due to iodine deficiency in food and its insufficient intake into the body;

Adequate treatment of inflammatory and other diseases of the thyroid gland that caused hypothyroidism;

X-ray therapy or other treatments for diseases of the hypothalamic-pituitary system;

Pathogenetic and symptomatic therapy

It suggests a slowdown in the progression of pathological changes in organs and tissues that occur against the background of the absence of thyroid hormones. This type of treatment can never be used as an independent, and always complements the basic treatment with hormonal drugs.

Patients with hypothyroidism are prescribed:

Cardioprotectors (riboxin, trimetazidine, preductal, mildronate, ATP);

Cardiac glycosides (digoxin, strophanthin, corglicon) in the presence of signs of heart failure;

Vitamin preparations (ascorbic acid, neurobex, milgama, aevit, tocopherol, multivitamin complexes);

Preparations of sex hormones in women to normalize menstrual function and ovulation;

Preparations for improving metabolic processes in the brain (nootropics, neuroprotectors).

Replacement therapy with hormonal drugs

This type of treatment is the only correct solution for hypothyroidism. Hormones should become basic. All other activities are supportive. The principle of hormone replacement therapy is simple: the artificial introduction of thyroid hormones into the body.

Of the drugs containing thyroid hormones, thyroxine and triiodothyronine can be used. If earlier the second drug was used much more often, then modern endocrinologists have come to the conclusion that its use is inappropriate. T3 has a negative effect on the myocardium, aggravating heart damage against the background of hypothyroidism. The only situation where it can be more effective than thyroxine is a hypothyroid coma, in which intravenous administration of triiodothyronine has a fairly rapid therapeutic effect.

As for T4 hormone replacement therapy, it involves the use of drugs containing levothyroxine (L-thyroxine). In the pharmacy network, they can be purchased under the following names:

Euthyrox;

Bagothyrox;

L-thyroxine;

When prescribing thyroxin preparations, it is important to adhere to the following principles:

Lifetime admission is expected. The exception is cases of temporary primary hypothyroidism that occurs against the background of the pathology of the thyroid gland and in the early postoperative period after the removal of its part;

Gradual selection of the dose, taking into account the severity of hormonal deficiency, the age of the patient, the duration of the disease. The following pattern can be traced: the longer and more pronounced untreated hypothyroidism, the higher the body's sensitivity to the action of hormonal drugs;

Mandatory monitoring of the effectiveness of treatment based on signs of clinical improvement and according to the hormonal spectrum of the blood (increase in the concentration of T4, T3 and a decrease in TSH);

Use of small dosages in patients with concomitant heart disease. The dose in such patients should be increased very slowly under ECG control;

The expediency of a subsequent dose increase is evaluated after the maximum possible manifestation of the effectiveness of the previous one (at least 4-6 weeks).

The most effective treatment for hypothyroidism is L-thyroxine replacement therapy. Its dosage, frequency and mode of administration should be determined only by an endocrinologist under the control of the hormonal blood spectrum and clinical data!

Education: Diploma of the Russian State Medical University N. I. Pirogov, specialty "Medicine" (2004). Residency at the Moscow State University of Medicine and Dentistry, diploma in Endocrinology (2006).

Catad_tema Anesthesiology-reanimatology - articles

Catad_tema Diseases of the thyroid gland - articles

Life-threatening complications of hypothyroidism

E.A.Troshina, M.Yu.Yukina
Federal State Institution Endocrinological Research Center of Rosmedtekhnologii, Moscow

Hypothyroidism is a symptom complex of changes in various organs and systems, caused by a decrease in the level of thyroid hormones.

The quality of life of patients with hypothyroidism who constantly receive replacement therapy with levothyroxine differs slightly from that of patients without hypothyroidism. Hypothyroidism itself becomes a way of life for the patient, not a disease.

However, in the absence of timely adequate treatment of hypothyroidism, the risk of complications increases. Hypothyroid coma (HC) is a rare, life-threatening complication of hypothyroidism. First of all, it develops in elderly patients for a long time un- or poorly treated. Patients with GC die predominantly from respiratory and heart failure, in some cases from cardiac tamponade. Even with promptly initiated vigorous therapy, 40% of patients die.

Clinical symptoms of hypothyroidism develop in a patient with a gradual increase. Most often, hypothyroidism is characteristic of patients operated on the thyroid gland (primary postoperative hypothyroidism).

The doctor should suspect the presence of hypothyroidism syndrome in an elderly patient and determine the level of thyroid-stimulating hormone (TSH) in the blood serum if the patient had any history of thyroid disease or received medications that can provoke the development of hypothyroidism. In addition, the presence of constipation resistant to conventional treatment, cardiomyopathy, anemia of unknown origin, dementia, should be a reason to rule out hypothyroidism in an elderly patient.

Laboratory diagnostics

Laboratory parameters for the diagnosis of hypothyroidism are the determination of basal (not stimulated) TSH and free T 4 and T 3 values. A normal basal TSH level rules out hypothyroidism. With elevated basal TSH, the diagnosis is confirmed by the detection of low concentrations of free T 4 and T 3 .

Mistakes in diagnosing hypothyroidism

The diagnosis of hypothyroidism is often untimely, since in its initial stage the detected symptoms are extremely non-specific. In addition, hypothyroidism syndrome can imitate various non-thyroid diseases, which is associated with multiple organ lesions found in conditions of thyroid hormone deficiency. Very often, manifestations of hypothyroidism in the elderly are considered by the doctor and patient as signs of normal aging. Indeed, symptoms such as dry skin, alopecia, loss of appetite, weakness, dementia, etc., are similar to the manifestations of the aging process. Typical symptoms of hypothyroidism are detected only in 25-50% of older people, while the rest have either extremely mild symptoms, or hypothyroidism is clinically manifested as some kind of monosymptom.

Clinical diagnostics

Clinical symptoms of hypothyroidism

General symptoms Fatigue, fatigue, weakness Weight gain, chilliness Cardiovascular symptoms Sinus bradycardia Heart failure cardiomegaly Pericarditis Arterial hypotension or paradoxical hypertension Respiratory system respiratory failure, hypercapnia Leather and its derivatives Dry skin, hair loss Thickening of nails Loss of the lateral parts of the eyebrows Skin coloration is pale with a yellowish tinge Nervous system Apathy, drowsiness, disturbance concentration Memory impairment Depressive psychoses Stupor and coma Hyporeflexia

Musculoskeletal system muscle weakness Muscular atrophy Violation of skeletal formation in children Gastrointestinal tract Lack of appetite Constipation, megacolon, ileus Sex organs In women: cycle disorder like amenorrhea or menorrhagia Infertility In men: lack of libido, decreased potency, gynecomastia Metabolism Decreased basal metabolism Weight gain, obesity High cholesterol, hypoglycemia Fluid retention with volume expansion tongue, swelling of the face, especially the eyelids Laboratory data Hyponatremia Anemia Increasing creatine kinase levels Thyroid Goiter or its absence

hypothyroid coma

Resolving factors are severe comorbidities, surgery, trauma, sedatives and drugs, and hypothermia.

The basis of the pathogenesis of GC is alveolar hypoventilation followed by hypoxia of vital organs, resulting in a decrease in body temperature, bradycardia and hypoglycemia. With untimely assistance, a fatal outcome is possible. Mortality in HC ranges from 60 to 90%.

All symptoms of hypothyroidism increase in the patient. Drowsiness, disorientation, coma are expressed. Body temperature is reduced to 34-35 ° C, bradycardia occurs. The skin is cold, pasty.

The main symptom of GC is a decrease in body temperature. Coma is accompanied by progressive changes in the central nervous system, inhibition of all types of reflexes. Changes in the central nervous system lead to an increase in bradycardia, a decrease in blood pressure and hypoglycemia.

Cardiovascular disorders that develop in a patient with GC are often the cause of death. Peripheral hemodynamic parameters are among the first to respond to changes in the concentration of thyroid hormones. Hypothyroidism is accompanied by a decrease in heart rate (HR). The bradycardia that occurs with hypothyroidism is reversible when euthyroidism is achieved.

Another effect in hypothyroidism is a change in total peripheral vascular resistance (OPVR). Hypothyroidism causes an increase in peripheral vascular resistance, with which, to a certain extent, the development of diastolic arterial hypertension (AH) is associated. Diastolic hypertension in hypothyroidism is common. In patients with hypothyroidism and the presence of hypertension, the content of aldosterone and renin in the blood plasma is reduced, i.e. diastolic hypertension in hypothyroidism is hyporeninic in nature.

The proposed causes of impaired vasodilating function in hypothyroidism are: decreased generation of vasodilating substances and/or resistance to them of vascular smooth muscle cells; decrease in the concentration of atrial Na-uretic peptide.

The state of hypothyroidism is characterized by a decrease in the number of β-adrenergic receptors, which is associated with a lower likelihood of developing arrhythmias. However, it has been established that norepinephrine secretion and its content in blood plasma are increased in persons with hypothyroidism. Norepinephrine, being mainly an adrenergic stimulant, can contribute to spasm of the coronary arteries.

Hypothyroidism is characterized by a decrease in myocardial contractility, a decrease in ejection fraction, and the development of heart failure. The state of hypothyroidism is also accompanied by prolongation of diastole, an increase in the time of isovolumetric relaxation of the left ventricle.

Treatment of hypothyroidism

Since GC is the result of either the lack of treatment of hypothyroidism or inadequate therapy for this syndrome and is an extremely serious condition with high mortality, a doctor of any specialty should be aware of the algorithms for treating hypothyroidism and the drugs used for this.

It is very important to recognize hypothyroidism in time, which can be diagnosed by only one indicator of hormonal analysis - TSH, and prescribe replacement therapy with Euthyrox. Its difference from other thyroid hormone preparations is the ability to easily select the desired dosage - 25,50,75,100, 125 or 150 mcg, which greatly facilitates the replacement therapy of hypothyroidism.

Dosing regimen of the drug
EUTHIROX (levothyroxine sodium)
Set individually depending on the indications, the effect of treatment and laboratory data. The entire daily dose is taken 1 time / day in the morning, at least 30 minutes before breakfast and washed down with liquid.
With hypothyroidism at the beginning of treatment, a dose of 50 mcg / day is prescribed. The dose is increased by 25-50 mcg every 2-4 weeks until signs of a euthyroid state are achieved.
In patients with long-term hypothyroidism, myxedema and, especially, in cases where there are diseases of the cardiovascular system, the initial dose of the drug should not exceed 25 mcg / day. In most patients, the effective dose does not exceed 200 mcg / day. The lack of an adequate effect when prescribing 300 mcg / day indicates malabsorption or that the patient does not take the prescribed dose of Euthyrox. Adequate therapy usually leads to normalization of the level of thyroid-stimulating hormone and thyroxine (T 4) in plasma after 2-3 weeks of treatment.

A summary of the manufacturer's information on dosage of drugs in adults is provided. Before prescribing the drug, carefully read the instructions.

Treatment of GC
The main task of the treatment of GC is the restoration of normal physiological functions of all organs and systems that are impaired due to hypothyroidism. The criterion for the adequacy of treatment is the disappearance of clinical and laboratory manifestations of hypothyroidism.

The severity and duration of hypothyroidism are the main criteria that determine the doctor's tactics at the time of initiation of treatment.

The more severe hypothyroidism and the longer it has not been compensated, the higher will be the general susceptibility of the body to thyroid hormones, especially for cardiomyocytes.

The main therapeutic measures for GC:

1. Replacement therapy with thyroid hormone preparations (levothyroxine).
2. The use of glucocorticoids.
3. The fight against hypoventilation and hypercapnia, oxygen therapy.
4. Elimination of hypoglycemia.
5. Normalization of the activity of the cardiovascular system.
6. Elimination of severe anemia.
7. Elimination of hypothermia.
8. Treatment of concomitant infectious and inflammatory diseases and elimination of other causes that led to the development of coma.

GC treatment is carried out in a specialized intensive care unit and is aimed at increasing the level of thyroid hormones, combating hypothermia, and eliminating cardiovascular and neurovegetative disorders.

The treatment of GC is based on the principle of maximum administration of thyroid hormones, primarily levothyroxine, through a tube, either drip or intramuscular injections.

The goal of the treatment of hypothyroidism is stable normalization of the TSH level within the normal range (0.4-4.0 mcU/l). In adults, euthyroidism is usually achieved with levothyroxine at a dose of 1.6-1.8 µg/kg body weight per day. The initial dose of the drug and the time to reach the full replacement dose is determined individually, depending on age, body weight and the presence of concomitant heart disease. It is possible to gradually achieve a full replacement dose of levothyroxine - an increase of 25 mcg every 8-10 weeks. The need for levothyroxine decreases with age. Some older people may receive less than 1 mcg/kg of the drug per day.

The need for levothyroxine increases during pregnancy. Evaluation of thyroid function in pregnant women, which involves the study of the level of TSH and free T 4 , is appropriate in each trimester of pregnancy. The dose of the drug should ensure the maintenance of a low-normal TSH level.

In postmenopausal hypothyroid women on estrogen replacement therapy, an increase in the dose of levothyroxine may be necessary to maintain normal TSH levels.

The level of TSH, after changing the dose of levothyroxine, is examined no earlier than after 8-10 weeks. Patients receiving a selected dose of a hormonal drug are recommended to have their TSH levels checked annually. The TSH level is not affected by the time of blood sampling and the interval after taking levothyroxine. If, in addition to this, the determination of the level of free T 4 is used to assess the adequacy of therapy, the drug should not be taken in the morning before blood sampling, since for about 9 hours after taking levothyroxine, the level of free T 4 in the blood is increased by 15-20%. Ideally, the drug should be taken on an empty stomach at the same time of day and at least 4 hours apart before or after taking other drugs or vitamins. Taking drugs and compounds such as cholestyramine, ferrous sulfate, soy proteins, sucralfate and antacids containing aluminum hydroxide reduces the absorption of levothyroxine, which may require an increase in its dose. You may need to increase the dose of this drug if you are taking rifampin and anticonvulsants that change hormone metabolism.

Thyroid disease is the most common endocrine pathology. Hypothyroidism deserves special attention, the symptoms of which are often perceived as whims and banal laziness - it is diagnosed in 2-4% of the population (among women 45-50 years old - 6-8%) and leads to disruption of the whole organism. That is why every woman should know the symptoms of hypothyroidism and methods of its effective treatment.

Hypothyroidism - what is it?

Hypothyroidism is a painful condition associated with a persistent deficiency (low production or rapid destruction) of the thyroid hormones thyroxine (T4) and triiodothyronine (T3) against the background of an increase in the pituitary hormone TSH.

These hormones perform the following functions:

• Responsible for the normal growth and development of the body;
• Control the work of the heart, nervous and digestive systems, affect the reproductive function and the musculoskeletal system;
• Regulate metabolism at all levels - lipid, carbohydrate, protein, water-salt;
• Participate in the formation of immunity and anti-stress resistance.

Symptoms of hypothyroidism are caused by a violation of the above functions, and the severity of the clinical picture directly depends on the degree of hormonal deficiency.

Lead to hypothyroidism:

• Small size of the thyroid gland and its aplasia, hereditary insufficiency of hormone production (congenital hypothyroidism);
• Organic pathology of the thyroid gland (primary hypothyroidism) - thyroiditis, nodular goiter, tumors, abscess, tuberculosis;
• Medical manipulations - resection or complete removal of the thyroid gland, radioactive iodine therapy and taking drugs with thyrostatic action (corticosteroids, Mercazolil, Dopamine, medicines for the treatment of hepatitis, etc.);
• Lack of iodine from food (long-term endemic goiter);
• Dysfunction of the pituitary and hypothalamus (secondary hypothyroidism) - brain injury, pituitary tumors, hemorrhages;
• Autoimmune disorders (rapid inactivation of hormones) and their deiodination in the blood.

Hypothyroid insufficiency is not an independent disease and always occurs against the background of another disease. However, the cause of the disease is not always possible to identify.

Hypothyroidism in its development goes through the following stages:

1. Subclinical - the thyroid gland, reflexively making up for the lack of hormones, grows in size. At the same time, the level of T3 and T4 remains normal, and the TSH indicator is somewhat overestimated.
2. Manifest - a continuing increase in the level of TSH and a decrease in T4 provokes external manifestations of the disease.
3. Compensated - hormonal deficiency is replenished with drug therapy.
4. Decompensated - an irreplaceable level of hormones leads to serious consequences up to cretinism, heart failure and myxedematous coma.

Symptoms of hypothyroidism and the first signs

The clinical picture of hypothyroid insufficiency is associated with a slowdown in metabolic processes and is manifested by symptoms from almost all organs and systems. So, for the symptoms of hypothyroidism in women, violations are characteristic:

• Skin

The first signs of hypothyroidism of the thyroid gland are manifested by brittle nails with the formation of grooves on the nail plates, dull color and massive hair loss. Pallor of the skin with scaly foci and areas of hyperkeratosis on the elbows and feet is noted. Slight jaundice is possible due to an enlarged liver, a decrease in body temperature to 35ºС.

For patients with hypothyroidism, a puffy appearance of the face is characteristic: bags under the eyes, swelling of the lips and tongue (traces of teeth along the edges of the tongue), swelling of the legs / arms. Swelling of the nasal mucosa leads to difficulty in breathing and a violation of the sense of smell.

At the same time, diuretics, with a decrease in the daily amount of urine due to inhibition of kidney function, do not reduce swelling, only exacerbating the failure of the water-salt balance.

There is also some weight gain. Restraint of body weight growth is due to lack of appetite and impaired digestion. However, it is almost impossible to lose those extra pounds.

• Heart

The heart responds to a lack of hormones (less than 55 beats / min), low blood pressure, arrhythmia and frequent attacks of the type of angina pectoris. The doctor can fix the deafness of heart tones, expanded borders of the heart.

However, in advanced cases, an atypical reaction of the cardiovascular system is often recorded - persistent tachycardia, hypertension.

• Musculoskeletal system

Weakness, sometimes reaching complete impotence, is due to a decrease in muscle tone, and physical endurance decreases. And the slow process of muscle relaxation leads to stiffness in movements and periodic convulsive twitches of individual muscles.

With congenital hypothyroidism, symptoms of disproportionate development are fixed: shortened limbs with a long torso.

• Nervous system

The state of causeless apathy gradually develops into depression. Memory suffers noticeably, and a violation of mental abilities in congenital hypothyroidism leads to the development of cretinism. In this plane, the symptoms of hypothyroidism in women are manifested by numbness of the limbs, problems with vision and hearing.

• Blood

The hematopoietic system reacts to hypothyroid insufficiency with anemia, which increases the manifestations of general weakness. Reduced immunity is manifested by frequent colds. Less often, leukopenia is recorded in the blood test.

• Digestion

Hypothyroidism often causes gastrointestinal symptoms. Intestinal atony leads to constipation, and gastritis occurs with constant pain and excruciating nausea. The process of digestion of food is also disturbed - undigested elements are found in the feces.

• Endocrine abnormalities

Hypothyroidism causes a chain of hormonal disorders. Inadequate adrenal function exacerbates the manifestations of the disease. Reproductive function suffers: impotence in men, frigidity and menstrual irregularities in women.

Hypothyroidism is an excellent masker. Often, thyroid hormone deficiency, especially at the subclinical stage, is confused with heart disease, fatigue syndrome, depression and other diseases.

However, the treatment of hypothyroidism will be effective only with the appointment of adequate therapy with drugs that compensate for hormonal deficiency.

Symptoms of hypothyroidism in women - features

Often, the symptoms of hypothyroidism in women are ignored: the severity of the condition is in no way linked to the complaints made. A puffy face, an “extinct” look (with the normal functioning of the thyroid gland, a woman’s eyes shine!), Problems with hair and nails raise doubts about her own attractiveness.

Often from women with hypothyroid insufficiency, you can hear:

• Sufficient sleep does not bring rest to the body. The morning starts with a feeling of weakness.
• I do not want anything, although there is no apparent reason for apathy.
• Constant chilliness, regardless of the weather and clothing.
• Pathological forgetfulness, very poor memory (signs are often associated with atherosclerosis due to high cholesterol in hypothyroidism).
• Fainting due to hypotonia and slowing down of speech.
• Lack of sexual desire, excess hair all over the body.
• The occurrence of cystic formations in the chest and uterus.
• Violation of the menstrual cycle (irregularity of menstruation), earlier.

Hypothyroidism of the thyroid gland in women can occur during pregnancy due to a lack of iodine intake. But if hypothyroidism is limited to the subclinical stage, the woman's condition returns to normal after childbirth.

Sometimes hypothyroidism continues in the postpartum period, this is due to the inhibition of the pituitary gland.

Diagnosis of hypothyroidism

The diagnosis is based on the analysis of indicators. Hypothyroidism is diagnosed when the level of thyroxine is less than 140-50 nmol/l and triiodothyronine is less than 3.85-1.50 mmol/l.

At the same time, the increase in TSH occurs in a logarithmic progression: even with a slight lack of T4, a significant increase in TSH is recorded. The degree of deficiency of the hormones T3 and T4 determines the severity of the disease.

To identify the causative disease, an ultrasound examination of the thyroid gland (identification of nodes), an x-ray or CT scan of the head is prescribed to exclude a pituitary tumor.

The main treatment for hypothyroidism in women is the elimination of hormonal deficiency with the help of drug-induced synthetic hormones. Depending on the blood counts, the doctor individually selects the drug, starting treatment with a minimum dose.

Widely used therapeutic agents are L-thyroxine, Thyreoidin, Thyroxine, Thyreocomb. The effectiveness of the prescribed dose is checked by a repeated study of the level of hormones.

Also in the treatment of hypothyroidism, dietary supplements such as Endonorm are used. The herbal composition regulates the production of the TSH hormone, has a symptomatic effect (normalizes the functioning of the reproductive system, adrenal glands, improves immunity) and does not have serious side effects, unlike synthetic hormones.

However, dietary supplements are not an alternative replacement for hormone therapy, treatment with Endorm and others is used only with the approval of the treating endocrinologist.

With timely treatment of hypothyroidism and regular use of hormonal agents, the patient remains able to work. At the same time, twice a year, it is necessary to control the level of hormones and adjust the dosage of drugs.

After surgical resection of the thyroid gland, replacement therapy is carried out for life. The most serious side effect of synthetic hormones is the gradual extinction of thyroid function and its atrophy, which leads to an increase in the dosage of drugs.

Hypothyroidism is especially severe in children. Children's brains are especially sensitive to a lack of iodine and thyroid hormones. The delay in physical development is accompanied by low intelligence and poor learning.

Complications

The developing disease is fraught with myocardial infarction, frequent pneumonia and mexedematous coma. Hypothyroid coma most often occurs in older people who forget to take medications prescribed by a doctor to treat hypothyroidism, and threatens the patient's life.

Against the background of a decrease in temperature to 30ºС, depression of consciousness and respiration occurs, symptoms of heart failure increase, fluid accumulates in the body and diuresis decreases.

• Fatal outcome in myxedematous coma - up to 40% of patients.

Hypothyroidism- a clinical syndrome that develops as a result of reduced thyroid function.

The thyroid gland is one of the most important parts of the endocrine system. The hormones produced by this gland affect the intrauterine formation of the central nervous system of the fetus, growth and psychophysical development in childhood, as well as the intensity of metabolism, heat production, reproductive function, protein synthesis, calcium metabolism and many other processes throughout life.

The production of thyroid hormones is regulated by the hypothalamic-pituitary system. The main thyroid hormones are thyroxine (T4) and triiodothyronine (T3). Thyroxine, the molecule of which contains 4 iodine atoms, is much less active than triiodothyronine, which is formed after the separation of 1 iodine atom from thyroxine.

Causes of hypothyroidism

Hypothyroidism can have various origins:

• The most common option (it is also called primary hypothyroidism) develops as a result of pathology in the thyroid gland itself. This may be its congenital underdevelopment, the synthesis of abnormal hormones, damage to the gland by an autoimmune process, ionizing radiation, deficiency or impaired absorption of iodine, hypothyroidism as a result of taking medications, removal of the gland or radioiodine therapy.
• Reduced thyroid function may also be associated with pathology of the hypothalamic-pituitary system - reduced production of thyroid-stimulating hormone (TSH) by the pituitary gland and thyroliberin - by the hypothalamus.
• In rare cases, symptoms of hypothyroidism are observed even with normal production of thyroid-stimulating hormones - this is due to the reduced sensitivity of tissue receptors to these hormones.

congenital hypothyroidism

Women are subject to the development of this syndrome almost 20 times more often than men. Hypothyroidism is a fairly common problem, but it is rarely recognized in a timely manner. The exception is congenital hypothyroidism, since recently all newborns undergo mandatory screening for this type of pathology. This is dictated by the fact that unrecognized and, as a result, untreated congenital hypothyroidism is fraught with gross and irreversible disorders in the growth and development of the child - dwarfism, severe mental retardation, cretinism, mental disorders, deafness, underdevelopment of the organs of the reproductive system, etc. Timely treatment allows avoid these consequences.

Autoimmune hypothyroidism

Of the acquired forms, timely correction is usually obtained in cases of hypothyroidism, which naturally develop as a result of resection of the gland or radioiodine therapy. But the vast majority of cases involve autoimmune thyroiditis- symptoms develop gradually, they are nonspecific, not always pronounced, and for many years not only the patients themselves, but also the doctors can regard them as the result of fatigue or stress.

Symptoms of hypothyroidism

The main symptoms of hypothyroidism:

• low body temperature, constant feeling of chilliness, poor cold tolerance;
• weight gain, obesity;
• general puffiness, puffiness (hence another name for hypothyroidism - "myxedema", which means "mucous edema");
• swelling of the mucous membranes of the nose, larynx, Eustachian tube, leading to difficulty breathing, coarsening of the voice, hearing impairment;
• slowness, drowsiness, memory impairment, slowing down of thought processes, reduced emotional background, depressive states, decreased performance;
• pain in muscles and joints;
• slow heart rate, lowering systolic blood pressure;
• constipation, biliary dyskinesia, decreased secretory function of the stomach;
• pale and dry skin, brittleness and increased hair loss, stratification of nails;
• disorders in the work of the reproductive system - menstrual irregularities up to the absence of menstruation and infertility;
• it is also possible the development of anemia, decreased immunity, etc.

The ultimate manifestation of hypothyroidism is hypothyroid or myxedematous coma- it develops with long-term hypothyroidism without appropriate treatment. It is expressed in the increase of the listed symptoms with the transition to a coma with a threat to life. It can be provoked by an infectious disease transferred against the background of existing hypothyroidism, stress, hypothermia, increased stress. It most often occurs in the elderly, usually in women.

Diagnostics

As in the case of hyperthyroidism, the determination of the level of T3, T4 and TSH in the blood is of paramount diagnostic importance. In primary hypothyroidism, TSH will be significantly elevated, while T3 and T4 will be lowered.

To clarify the cause of hypothyroidism, antithyroid antibodies are determined, ultrasound, MRI of the brain (to assess the state of the hypothalamic-pituitary system in case of suspected central hypothyroidism). In childhood, an X-ray examination of the skeleton is performed with the determination of bone age. Because due to the long course of the pathological process, other organs and systems also suffer, observation may be required, for example, by a cardiologist, gastroenterologist, with all the necessary research methods.

Treatment of hypothyroidism

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Hypothyroidism is treated by an endocrinologist. Treatment usually consists of lifelong thyroid hormone replacement. The dosage is selected individually.

The use of nutritional supplements or preparations containing iodine in areas where this element is lacking is of preventive importance. This is especially important during pregnancy and lactation, as well as in childhood.

Hypothyroidism is a deficiency of thyroid hormones. At the same time, a syndrome develops (a complex of certain pathological symptoms), which doctors define with the single term “hypothyroidism”.

Annually for 1000 people. 4 new cases of hypothyroidism are detected, i.e. we can say that the syndrome of hypothyroidism is a common occurrence in the human population.

Hypothyroidism is more common in women than in men.

Hypothyroidism is not yet a definitive diagnosis. This is a consequence, an outcome, which can have various causes (diseases, conditions).

Causes of hypothyroidism of the thyroid gland

• absence or deficiency of active thyroid tissue (autoimmune thyroiditis, consequences of surgery or radioiodine treatment, congenital anomalies of the thyroid gland, consequences of non-autoimmune destructive thyroiditis, etc.);
• violation of the synthesis of thyroid hormones (severe iodine deficiency, drug damage to the thyroid gland, congenital defects in the synthesis of hormones);
• damage to the pituitary gland and / or hypothalamus, leading to a violation of the synthesis of thyroliberin and TSH;
• tissue hypothyroidism (impaired cellular sensitivity to the effects of thyroid hormones, impaired transport of thyroid hormones, impaired conversion of T 4 to T 3, etc.).

If the cause of hypothyroidism is an inactive thyroid gland, we speak of primary hypothyroidism.

If the cause is a violation of TSH production, then we call hypothyroidism secondary.

In some cases, as, for example, after thyroidectomy, with AIT and with congenital hypothyroidism, we are dealing with an irreversible situation, i.e. hypothyroidism will persist for the rest of your life, and replacement treatment must be for LIFETIME.

Sometimes, for example, with postpartum, subacute and drug-induced thyroiditis, the situation is reversible, that is, hypothyroidism is temporary.

Hypothyroidism can have many causes, but the most common is autoimmune thyroiditis (AIT). With AIT, the destruction of thyrocytes (thyroid cells that produce hormones) occurs. For hypothyroidism to develop, most thyrocytes must die. At first, while a smaller part of the cells died, the gland continues to work normally. The less healthy thyrocytes remain, the more markedly the production of hormones decreases. In response, in a feedback loop, the pituitary gland increases TSH production, increasing thyroid stimulation.

For some time, due to hyperstimulation by high concentrations of TSH, the remaining thyroid cells continue to produce normal (low-normal) amounts of hormones. In the analyzes, you can see an increased TSH and a normal T 4 free. This situation is called subclinical hypothyroidism. There are no clear clinical manifestations of hypothyroidism at this stage.

As thyrocytes die, less and less levothyroxine is produced; TTG becomes more and more high. Manifest hypothyroidism develops. With overt hypothyroidism, TSH is high, and T 4 is free. reduced.

If hypothyroidism proceeds for a long time without treatment, then a severe clinical picture develops - myxedema: a malfunction of all body systems due to a deficiency / absence of thyroid hormones. If treatment is not started in time, hypothyroid coma and death will develop.

Diagnosis	Causes	Thyroid	TSH level	Antibodies
Chronic lymphocytic thyroiditis (Hashimoto's thyroiditis)	autoimmune disease	First dense, symmetrically enlarged, then atrophy develops	Promoted	Antibodies to iodide peroxidase
Complications after radical treatment	Radioactive iodine treatment or surgery (thyroidectomy, thyroidectomy)	atrophied or absent	Promoted	Perhaps a persistent increase in the titer of antithyroid antibodies characteristic of diffuse toxic goiter (to thyroglobulin and iodide peroxidase)
Secondary hypothyroidism	Damage to the pituitary or hypothalamus, drugs	Normal size or reduced	Normal or increased against the background of a decrease in the level of T 4; often reduced biological activity of TSH	Missing
Subacute thyroiditis	Viral infection, autoimmune disorders	Slightly enlarged	Transient increase in the hypothyroid stage	Transient increase in antibody titer to iodide peroxidase

Chronic lymphocytic thyroiditis

Women suffer from it 5-7 times more often than men. The prevalence of hypothyroidism increases with age; according to one study, 33% of women over 70 have serum anti-thyroid antibodies. In the hypertrophic (goiter) form of the disease, the thyroid gland is diffusely enlarged, dense, slightly bumpy, and in the atrophic form it has normal dimensions. Aspiration biopsy reveals lymphocytic infiltration. A rare form of chronic thyroiditis - chronic fibrous thyroiditis (Riedel's thyroiditis) - is characterized by fibrosis of the thyroid gland and adjacent tissues. In this case, the thyroid gland is palpated as a solid volumetric formation. Riedel's thyroiditis must be differentiated from thyroid cancer by aspiration biopsy.

Twenty-year follow-up showed that in women the frequency of transition from subclinical hypothyroidism to clinically pronounced is 4.3% per year. The higher the antibody titer, the faster this transition occurs. It is important to remember that chronic lymphocytic thyroiditis is often combined with other endocrine autoimmune diseases: type 1 diabetes mellitus (antibodies to iodide peroxidase are detected in 30% of women with this disease), primary adrenal insufficiency, Addison-Birmer disease, premature ovarian failure and vitiligo.

Secondary hypothyroidism

Secondary hypothyroidism is caused by a violation of the synthesis or release of TSH or thyroliberin. TSH deficiency occurs with certain drugs, pituitary adenoma, Sheehan's syndrome (postpartum pituitary infarction), radiation therapy, pituitary metastases, traumatic brain injury, and pituitary surgery. The clinical picture is the same as in primary hypothyroidism, but may additionally include symptoms of hypopituitarism (adrenal insufficiency, hypogonadism, amenorrhea). With hormonally active adenoma, there may be signs of hypersecretion of hormones - prolactin, growth hormone, cortisol. In primary hypothyroidism, there is a significant increase in prolactin levels and even an increase in the pituitary gland. After normalization of the TSH level, the level and size of the pituitary gland also return to normal.

The diagnosis of secondary hypothyroidism is made when the free T4 level is reduced against the background of a low or normal TSH level. Secondary hypothyroidism should also be suspected if there is a deficiency of other hormones or if the patient is known to have a disease of the hypothalamus or pituitary gland.

Rare causes of hypothyroidism

Rare causes of hypothyroidism include thyroid-blocking antibodies. These antibodies can cross the placenta and cause transient congenital hypothyroidism in newborns. Approximately 5% of women with chronic lymphocytic thyroiditis give birth to children with transient congenital hypothyroidism, probably due to thyroid-blocking antibodies.

Other causes are thyroidectomy and radiation therapy. After thyroidectomy, hypothyroidism develops within a few weeks, and with resection of the thyroid gland, the frequency and rate of development of hypothyroidism depend on the volume of the remaining tissue. Hypothyroidism often occurs as a result of radiation therapy for lymphogranulomatosis and malignant tumors of the head and neck. Occasionally, hypothyroidism is observed in diseases such as hemochromatosis, scleroderma, sarcoidosis, and amyloidosis.

Drug-induced hypothyroidism

Hypothyroidism is caused by the use of certain drugs. With a high intracellular concentration of iodide (which happens when taking iodine preparations in high doses), the Wolf-Chaikov phenomenon is observed: iodine inhibits the iodization of thyroglobulin and the condensation of iodotyrosines. In healthy people, this phenomenon disappears after a few days, but iodine hypothyroidism may develop. The Wolff-Chaikov phenomenon can be caused by amiodarone containing a large amount of iodine, radiopaque agents, a saturated solution of potassium iodide, kelp (in tablets). Povidone-iodine for topical application (on the skin and mucous membranes) is able to have a systemic effect and also lead to transient iodine hypothyroidism. Lithium, perchlorate, propylthiouracil, thiamazole, interferon a, IL-2 can cause hypothyroidism due to suppression of the synthesis or secretion of T 4 and T 3 .

Symptoms, signs of hypothyroidism of the thyroid gland

Diagnosing hypothyroidism is both simple and difficult.

Simply because the "key" to the diagnosis is an elevated TSH. (Recall a favorite saying of endocrinologists: "Research TSH and sleep well.") TSH research is available, cheap, informative.

If hypothyroidism is suspected, it is enough to take blood for TSH, and after 2 hours the diagnosis of hypothyroidism will be confirmed or refuted.

It is difficult because, unfortunately, the symptoms that are not always present cause doctors to suspect hypothyroidism. After all, people with hypothyroidism rarely turn to an endocrinologist. The symptoms that bother them are usually a reason to go to a cardiologist, dermatologist, gynecologist, hematologist, otolaryngologist, neurologist ... To anyone, but not to an endocrinologist.

Hypothyroidism is a great master of camouflage. He has many masks, and only a study of TSH will help to consider under these masks a single cause - a deficiency of thyroid hormones.

The fact is that with the syndrome of hypothyroidism, all organs and systems suffer. None of the symptoms of hypothyroidism is specific to this disease. Exactly the same symptoms can occur in various diseases of the cardiovascular, respiratory, digestive systems; can be observed in neurological, hematological, dermatological, rheumatological, psychiatric, gynecological practice.

With a surprising variety, all the symptoms of hypothyroidism have one reason - a change in metabolism in every cell of the body associated with a deficiency / absence of T 4 and T 3: impaired protein synthesis, slowing down energy metabolism, fluid retention.

Sometimes patients with hypothyroidism go from doctor to doctor for years, receiving useless appointments, suffering from increasing symptoms of the disease, without receiving the only necessary treatment - thyroxine replacement therapy.

Symptoms of hypothyroidism are diverse and can be expressed in varying degrees, from the complete absence of manifestations to severe multiple organ failure.

To understand how many masks hypothyroidism has, consider its manifestations in the work of organs and systems.

Cardiovascular system: increased diastolic (lower) blood pressure, bradycardia (rare pulse), sometimes tachycardia (increased heart rate), low ECG voltage, hydropericardium (fluid in the pericardium), atherosclerosis, high cholesterol, increased LDH.

Respiratory system: holding your breath during sleep (sleep apnea syndrome), hoarseness, fluid in the pleural cavities, shortness of breath.

Digestive system: chronic constipation, loss of appetite, biliary dyskinesia, gallstones, increased transaminases (ACT and ALT).

Nervous system: weakness, drowsiness, fatigue, depression, memory impairment, dementia, hearing loss, slowing of thought processes, neuropathy (pain in the limbs), decreased reflexes.

Genitourinary system: fluid retention, dense edema, any menstrual dysfunction, infertility, miscarriages, erectile dysfunction and ejaculation, decreased libido.

Skin: severe dryness, pallor, yellowness, peeling, thickening of the skin; hyperkeratosis of the plantar areas; skin pigmentation on the elbows; fragility of nails; dryness, thinning and hair loss.

Hematopoietic system: chronic anemia.

There is another "mask" associated with the diagnosis of "hypothyroidism": it is the absence of hypothyroidism with a clinical picture typical of this disease. The patient has a complex of symptoms most characteristic of hypothyroidism (weakness, dry skin, constipation, edema, etc.) with a normal level of TSH and T 4 free. This phenomenon is sometimes referred to as "hypothyroidism without hypothyroidism". Those. in fact, the patient does not have hypothyroidism, it is necessary to look for another cause of the symptoms and treat it, but the picture is so vivid that it is difficult to believe in the absence of hypothyroidism, and the doctor (and sometimes the patient himself) repeatedly rechecks TSH and T4, suspecting a laboratory error.

Hypothyroidism slows metabolism and reduces heat production. BMR may be halved and patients become very sensitive to cold (cold intolerance). O 2 consumption, gas exchange in the lungs and erythropoiesis are reduced. Anemia develops. A decrease in lipolysis contributes to a moderate increase in body weight and hyperlipidemia (VLDL, LDL), and a decrease in the conversion of cholesterol into bile acids quickly leads to hypercholesterolemia and the development of atherosclerosis. Violation of glycogenolysis and gluconeogenesis causes hypoglycemia. Reducing the breakdown of water-binding glycosaminoglycans (mucopolysaccharides, mucin) contributes to their accumulation in various tissues. This gives the skin a doughy consistency, so the disease is called myxedema (mucous edema). Sometimes carpal tunnel syndrome develops. Swelling of the eyelids is almost always noted. Swelling of the vocal cords leads to hoarseness; swelling of the tongue affects articulation. In addition, fibronectin, collagen, and plasma albumin are deposited in the skin. Reduced conversion of carotene to vitamin A causes hyperkeratosis. Due to the accumulation of carotene, the skin acquires a yellowish tint. Hair loss is noted. Due to the decrease in the secretion of sweat and sebaceous glands, the skin becomes dry, and the decrease in heat production makes it cold to the touch.

Reduced stimulation of the heart with thyroid hormones reduces contractility, heart rate, VR, CO; sometimes systolic blood pressure decreases. With a pronounced deficiency of thyroid hormones, heart failure develops. Pleural and pericardial effusions are characteristic. The respiratory rate slows down, the response to hypercapnia and hypoxia is disturbed.

The glomeruli and tubules in the kidneys are reduced. GFR, PP and tubular throughput are reduced. Decreased renal excretion leads to water and NaCl retention. Due to the accumulation of fat, glycosaminoglycans, NaCl and water, the patient appears edematous.

In addition, protein synthesis in the liver is disrupted, and the rate of metabolism of steroid hormones and drugs decreases.

Decreased stimulation of the intestinal musculature causes constipation. Dysfunction of the muscles of the esophagus and cardiac sphincter leads to gastroesophageal reflux and esophagitis.

Hypothyroidism reduces the activity and efficiency of the autonomic nervous system. Neuromuscular excitability decreases, which causes a change in sensory functions, hyporeflexia, loss of hearing, appetite, memory, depression and clouding of consciousness with the development of coma. These changes in adults are reversible.

The lack of thyroid hormones in the fetus and newborn causes irreversible brain damage. Thyroid hormones are required for the full development of dendrites and axons, synapse formation, myelination and glial formation, which are absolutely essential for brain development in the fetus and children during the first 2 years of life. Deficiency of thyroid hormones during fetal development significantly impairs this development. If the hormone deficiency is not replenished after birth, irreversible brain damage occurs; brain function is not restored even with subsequent replacement therapy. Children with hypothyroidism often suffer from deafness.

In addition, these children have delayed bone growth. Stunting and impaired intelligence lead to typical signs of cretinism.

With T 3 /T 4 deficiency, the secretion of TRH and TSH is not inhibited. TRH stimulates the formation of not only TSH, but also prolactin, and therefore causes hyperprolactinemia, which further leads to galactorrhea, inhibition of the release of gonadotropins and reduced fertility. TSH also promotes the growth of the thyroid gland, causing a goiter. Finally, anomalies in the secretion of gonadotropins lead to impaired reproductive function.

Myxedema coma. Myxedema coma is a life-threatening complication of hypothyroidism; it usually develops in patients with prolonged hypothyroidism and is characterized by a coma with severe hypothermia (body temperature 24-32.2 ° C), absence of reflexes, convulsions and respiratory depression with CO2 retention. Severe hypothermia can only be detected with a thermometer with an enlarged low temperature scale. The diagnosis must be established very quickly, because in the absence of immediate treatment, the patient may die. Factors that provoke myxedema coma include diseases, infections, injuries, drugs that depress the central nervous system, and cold.

The clinical picture of hypothyroidism is diverse and depends on the duration and severity of thyroid hormone deficiency. The variety of manifestations is due to the possibility of damage to any organs and systems. However, due to the widespread use of serum TSH measurements, hypothyroidism is usually diagnosed before the onset of classic symptoms.

• CNS. Patients complain of memory impairment and depression. The accumulation of hydrophilic glycosaminoglycans in the skin leads to compression of the nerve trunks, resulting in paresthesia and tunnel syndromes.
• The cardiovascular system. Most patients have bradycardia, which may be associated with mild arterial hypertension. The EEG shows flattening of the T wave and prolongation of the PQ interval. In the presence of pericardial effusion, the amplitude of the R and P waves decreases and the shadow of the heart on the radiograph increases. The QT interval may be prolonged, leading to ventricular premature beats. Possible decrease in myocardial contractility. Heart failure is rare because cardiac output is usually sufficient to meet the reduced tissue oxygen demand.
• Musculoskeletal system and connective tissue. In hypothyroidism, glycosaminoglycans can be deposited in the subcutaneous tissue, causing puffiness of the face and swelling of the legs. The skin is usually dry, the hair is coarse and brittle; sometimes there is a loss of the outer half of the eyebrows. Patients often experience pain in the muscles and joints.
• reproductive system. Characterized by menstrual irregularities, as well as menorrhagia on the background of anovulatory cycles. In severe hypothyroidism, as a result of stimulation of the lactotropic cells of the adenohypophysis with thyroliberin, the level of prolactin increases and galactorrhea develops.
• GIT. Due to a decrease in gastrointestinal motility, constipation occurs. There is a slight (no more than 5%) weight gain.
• Changes in laboratory parameters. “Blood tests reveal normocytic anemia, hyponatremia, increased CPK activity and serum LDL cholesterol levels.

Newborns (cretinism)

The term "cretinism" was originally proposed to refer to the condition of mentally retarded and short children from regions with severe iodine deficiency; such children were distinguished by puffiness of the face and swelling of the extremities. Deaf-muteness and signs of disorders of the pyramidal and extrapyramidal pathways were also often noted. In the United States, neonatal screening programs detect 1 in 5,000 "sporadic" hypothyroidism among white newborns, and only 1 in 32,000 among African American newborns. (from the root of the tongue to the lower anterior surface of the neck). The function of such an "ectopic gland" is reduced. The transfer of thyroid-blocking antibodies from a mother with Hashimoto's thyroiditis to the fetus may be the cause of thyroid agenesis and "athyroid cretinism", but in most of these cases, hypothyroidism in newborns is transient. Other possible causes of neonatal hypothyroidism include exposure of the fetus to iodide or antithyroid drugs taken by the mother, or treatment of thyrotoxicosis or thyroid cancer in the mother with radioactive iodine.

Almost all children with a birth weight of more than 2500 g have already formed proximal tibial epiphyses and distal femoral epiphyses. Their absence makes one suspect hypothyroidism. The introduction in developed countries of newborn screening programs with the determination of TSH or T 4 levels has been a significant public health achievement, since early diagnosis of hypothyroidism can prevent permanent mental retardation. A drop of blood obtained by pricking the baby's heel 24-72 hours after birth is applied to filter paper and sent to the central laboratory. Neonatal hypothyroidism is indicated by a serum T4 level below 6 µg% or TSH above 25 mU/L. The diagnosis is confirmed by repeated examination and radiological signs of bone age lag. It should be remembered that in newborns, even with euthyroidism, if their mothers were not adequately treated for hypothyroidism during pregnancy, they later show some mental retardation, which emphasizes the need to maintain euthyroidism in pregnant women.

Subclinical hypothyroidism of the thyroid gland

Subclinical (latent) hypothyroidism is diagnosed when serum TSH is elevated and free T4 is within normal limits. In this case, antibodies to iodide peroxidase are often detected. In most cases, the disease is asymptomatic, although mild signs of hypothyroidism are possible. Patients with a family history aggravated by thyroid disease or other autoimmune diseases (especially type 1 diabetes mellitus), as well as patients with goiter, infertility, depression and hyperlipoproteinemia, are subject to examination. Treatment can prevent the transition to a clinically pronounced form, lower LDL cholesterol, reduce some symptoms (if any), reduce goiter, restore ovulation, reduce the risk of cardiovascular disease. The frequency of transition of subclinical hypothyroidism to a clinically pronounced form is 5-10% per year, in the presence of antibodies to iodide peroxidase and high levels of TSH (more than 12 IU / l), this figure is higher.

Diagnosis of hypothyroidism of the thyroid gland

In the blood, the content of thyroxine, triiodothyronine is reduced and the concentration of thyrotropin is increased. An increase in the content of cholesterol, creatine phosphokinase and aminotransferases is also characteristic. In blood tests, anemia, leukopenia, lymphocytosis are determined.

The most sensitive indicator is the level of TSH in serum; among certain groups of the population, it is advisable to carry out its mass determination. In primary hypothyroidism, there is no inhibition of the pituitary gland.

In many patients with primary hypothyroidism, the content of triiodothyronine (T 3) in serum remains normal, which is probably due to increased stimulation of the defective thyroid gland by thyroid-stimulating hormone, leading to the predominant synthesis and secretion of the more active hormone - T 3 Therefore, according to the level of T 3 in serum It is not always possible to diagnose hypothyroidism.

Patients often develop anemia, usually normocytic normochromic of unknown etiology, but due to menorrhagia, it can be hypochromic, and also (when hypothyroidism is combined with pernicious anemia or folate malabsorption) - macrocytic. Anemia is rarely severe (with hemoglobin levels<9 г%) и по мере коррекции гипометаболизма исчезает. Иногда это требует 6-9 мес.

In primary hypothyroidism, serum cholesterol is usually elevated; in secondary hypothyroidism, its increase is less pronounced.

Complications of hypothyroidism of the thyroid gland

Myxedema coma

Myxedematous (hypothyroid) coma is an extremely rare condition, which is the final stage of untreated hypothyroidism. It is characterized by progressive weakness, stupor, hypothermia, hypoglycemia, and hyponatremia, and eventually death. Myxedema coma usually develops in winter in older people with underlying lung and vascular disease.

History usually includes thyroid disease, radioiodine therapy, thyroidectomy, or neck radiation. Characterized by a gradual increase in drowsiness, turning into a stupor. Examination reveals bradycardia and severe hyponatremia; body temperature can drop to 24°C. Myxedematous coma is usually recorded in obese older women; the skin has a yellowish tint, the voice is hoarse, the tongue is enlarged, the hair is thinned, the eyes are swollen. In typical cases, dynamic intestinal obstruction and slow reflexes occur. There may be signs of pneumonia, myocardial infarction, cerebral artery thrombosis, or gastrointestinal bleeding. Sometimes there are convulsions, hemorrhages, hypo- or hypercalcemia. The diagnosis of myxedematous coma is confirmed by the milky appearance of the serum, high concentrations of carotene and cholesterol in it, as well as an increased level of protein in the cerebrospinal fluid. The content of SHT 4 in serum is reduced, and TSH is sharply increased. Antithyroid autoantibodies are usually found in high titers, suggesting Hashimoto's thyroiditis as the cause of severe hypothyroidism. The ECG shows sinus bradycardia with low waveform voltage. If rapid laboratory testing is not possible (which happens quite often), the diagnosis is made on the basis of clinical signs.

The manifestations of myxedema coma are based on three main factors:

1. CO 2 retention and hypoxia;
2. violation of water and electrolyte metabolism;
3. hypothermia.

The first of these is mainly due to a sharp inhibition of the response to hypoxia and hypercapnia, although obesity, heart failure, intestinal obstruction, immobility, pneumonia, pleural or peritoneal effusion, CNS depression and weakness of the respiratory muscles also play a role. Respiratory disorders often reach an extremely severe degree, and it is almost always necessary to resort to artificial ventilation of the lungs. Thyroid hormones eliminate hypothermia and improve the ventilatory response to hypoxia. The main violation of water-electrolyte metabolism is water intoxication, caused by a decrease in kidney perfusion and free water retention. This leads to hyponatremia, which is most easily corrected by restricting free water intake. Hypothermia often goes unrecognized because mercury does not fall below 34°C in a conventional thermometer. Therefore, it is necessary to use thermometers with a wider scale. Rapid warming of patients with myxedema coma is contraindicated. Therapy T 4 is usually accompanied by an increase in body temperature.

Factors provoking the development of myxedema coma in patients with severe hypothyroidism include heart failure, pneumonia, and the use of sedatives or narcotic drugs. Before obtaining laboratory data on the normal function of the adrenal glands, it is recommended to administer to patients not only thyroid hormones, but also glucocorticoids. Myxedema coma due to primary thyroid insufficiency must be distinguished from coma due to central hypothyroidism. In the latter case, glucocorticoid replacement therapy is of particular importance.

Hypothyroidism and heart disease

Previously, the treatment of patients with severe hypothyroidism and cardiovascular disease faced great difficulties, since replacement therapy with levothyroxine sometimes led to exacerbation of angina pectoris, heart failure, or the development of myocardial infarction. Currently, β-blockers, coronary angioplasty or coronary artery bypass grafting can initially eliminate coronary heart disease, which ensures better tolerability of subsequent thyroxine replacement therapy.

Hypothyroidism and neuropsychiatric diseases

Hypothyroidism is often accompanied by depression, which can reach a significant degree. Less often, in severe hypothyroidism, confusion, paranoid delusions, and even a manic state (“myxedematous psychosis”) are observed. Determination of the levels of fT 4 and TSH in the serum of mentally ill people is a reliable way to identify such cases. These patients require T 4 therapy, not just psychopharmacological agents. Some authors recommend the use of thyroid hormones for depression, even in the absence of hypothyroidism, but the effectiveness of such treatment remains unproven.

Treatment of hypothyroidism of the thyroid gland

Once the diagnosis of hypothyroidism has been made, treatment is not particularly difficult.

The goal of treatment for hypothyroidism is to compensate for the deficiency of thyroid hormones.

Many years ago, drugs for the treatment of hypothyroidism were made from the thyroid glands of animals. As you know, the thyroid gland contains not only T4, but also a small amount of T3. In recent decades, all drugs for the treatment of hypothyroidism have been synthesized in pharmaceutical factories. For a long time, it was believed that a cure for hypothyroidism should contain both T4 (levothyroxine) and T3 (triiodothyronine). Until the end of the last century, preparations containing both hormones were produced, but later it was proved that it was not necessary to add T 3 to hypothyroidism drugs, since inside the cells T4 turns into T 3 as needed.

Patients often state that they do not want to take "chemo". Meanwhile, drugs obtained artificially are pure molecules of those substances that are needed to obtain specific therapeutic effects. They do not contain unnecessary impurities, as, for example, in medicinal plants, and, accordingly, possible side effects are better studied and predictable.

Levothyroxine contained in the tablet is an absolute analogue of natural levothyroxine, which is produced by a healthy thyroid gland. If we compare a thyroxine molecule obtained from a living organism with a thyroxine molecule made in a laboratory, there will be no difference between them.

This means that with a properly selected replacement dose, treatment with levothyroxine is ABSOLUTELY SAFE and ABSOLUTELY EFFECTIVE.

How is this most correct dose selected? It is known that an adult needs 1.6 - 1.7 µg/kg of body weight of thyroxine per day for normal life. Accordingly, with overt hypothyroidism, the initial dose is easily calculated: multiply body weight (in kg) by 1.6.

For example, with a body weight of 65 kg, the total replacement dose calculated using this formula will be 104 micrograms per day (65 x 1.6 = 104). Since there are no tablets with a dosage of 104 mcg, we give tablets containing a dose of levothyroxine closest to the calculated one. In this case, it will be a dosage of 100 mcg.

Elderly patients and patients with cardiac problems who have lived for a long time in conditions of chronic hypothyroidism, treatment is prescribed with caution so that the metabolism has time to adapt to new conditions. First, a small dose is given, followed by a gradual increase until the calculated dose is reached.

Principles of dose titration of levothyroxine

All patients receiving levothyroxine, to evaluate the effectiveness of treatment, take only one test - TSH. The exceptions are pregnant women (T 4 free is additionally studied) and persons receiving suppressive therapy after radical treatment of highly differentiated thyroid cancer (additionally T 4 free, thyroglobulin, AT to TG).

After the appointment of levothyroxine at a stable dose (i.e. the same dosage every day, without gaps and violations of the drug), TSH can be assessed as a criterion for the effectiveness of treatment after 7-8 weeks. Doing this earlier is pointless and uninformative. TSH is a very accurate indicator of the level of thyroid hormones and is inversely logarithmic to their average concentrations. Even with a slight deficiency of thyroid hormones, TSH increases many times over. It takes about two months for TSH levels to “settle down” with regular treatment for hypothyroidism.

Having assessed TSH 2 months after the appointment of replacement therapy with levothyroxine at a constant dose, we are ready to say whether the dose is correctly selected.

if TSH entered the corridor of normal values ​​​​(0.4-4.0), then the dose was chosen correctly;

if TSH>4.0, then hypothyroidism persists, the dose of levothyroxine should be increased and TSH re-evaluated after 2 months;

if TSH<4,0, значит, доза левотироксина избыточна, имеется лекарственный тиреотоксикоз; дозу надо уменьшить и проконтролировать ТТГ через 2 месяца.

It usually takes from 2 months to a year to select the correct replacement dose. On average 4-6 months.

In some patients, the target TSH values ​​differ from the standard corridor (0.4 - 4.0). This includes pregnant women, young children, patients after radical treatment of well-differentiated thyroid cancer.

Individuals with subclinical hypothyroidism usually do not require a full replacement dose of levothyroxine. To achieve stable euthyroidism, small doses of levothyroxine are sufficient for them. The initial dose in these cases, as a rule, is 50 mcg / day. (this is the minimum therapeutic dose for an adult).

It should be noted that treatment of subclinical hypothyroidism is not always required and not for everyone. Sometimes observational tactics are sufficient, since in some cases subclinical hypothyroidism proceeds without harm to the patient's condition. But there are clinical groups in which the treatment of subclinical hypothyroidism must be prescribed.

In subclinical hypothyroidism, levothyroxine is always prescribed to pregnant women and women of childbearing age, as well as to those patients who have pronounced clinical symptoms of hypothyroidism: anemia, atherosclerosis, etc.

There are many levothyroxine preparations (Eutirox, L-thyroxine, and others) in various dosages on the drug market now, which make it convenient to select an individual dose for each patient.

In a pharmacy, you can get levothyroxine tablets from 25 micrograms to 150 micrograms in one tablet. Until recently, the “step” between doses was 25 mcg, i.e. levothyroxine tablets were available at 25.50, 75, 100, 125, 150 mcg. For the convenience of titration, many companies now produce tablets with intermediate dosages: 37, 62, 87, 112, 137 mcg. Sometimes, in order to accurately select the dose, it is necessary to divide the tablets into halves and quarters, but this is not very convenient and may lead to improper storage of the “fragments” of tablets prepared for taking.

Store levothyroxine tablets strictly in accordance with the instructions on the box. If the storage regimen is violated, the drug may lose its activity.

Remember that a tablet contains a very tiny dose of levothyroxine, calculated in micrograms: this is an almost invisible amount of the active substance that can be placed on the tip of a pin. The tablet mainly consists of neutral excipients that stabilize the active substance. For different companies, these fillers are slightly different, so the activity of the drug may vary individually. Starting to take the drug of one company, try to continue taking the drug of the same company in the future, so that you do not have to double-check the TSH and titrate the dose of the drug every time.

How to take levothyroxine?

In order for the treatment to be effective and the patient to feel no worse than healthy peers, it is necessary to follow simple, but very important rules for taking levothyroxine:

• The prescribed dose of the drug should be taken daily, without interruption. No drug holidays, dose juggling, withdrawal experiments, etc. are not allowed.
• The drug should be taken strictly on an empty stomach with a small amount of water. (You can not drink levothyroxine with juice, fizzy drinks, coffee, tea, milk, etc. - the active substance from this may be partially or completely destroyed.)
• After taking the drug, you must wait at least 30 minutes before taking food or other medicines.
• If you accidentally forget to take the drug, then do not increase the dose the next day; take your usual dose of medication, and if a TSH test is due in the coming weeks, then notify your doctor about skipping it, because. the result of the analysis may be uninformative.
• If you develop tachycardia, irregular heartbeat, sweating, increased blood pressure, weight loss, tell your doctor immediately. You may be taking an overdose of levothyroxine and have symptoms of thyrotoxicosis following the overdose. It is necessary to urgently investigate TSH: if it is less than 0.4 μIU / ml, then the doctor will adjust the dose of the drug. (The exception is pregnant women and people after radical treatment of well-differentiated thyroid cancer; they have other target TSH values.) If TSH is not reduced, then there is no drug-induced thyrotoxicosis, dose adjustment is not required. The causes of the symptoms that appear will be determined by the doctor, but they are not associated with taking levothyroxine.

Repeatedly observed an interesting phenomenon. Patients who, for some personal reasons, were afraid to start treatment with levothyroxine, often canceled treatment on their own in the first days of taking it, explaining this by “intolerance” to the drug, the appearance of unpleasant symptoms, etc. I had to tell them the “terrible secret of endocrinologists”: any clinical effects of levothyroxine preparations appear only after one and a half to two weeks, so much time is required for T4, taken in the form of a tablet, to turn into an active form of the hormone and begin to affect metabolism.

The main thing that the patient must understand is that levothyroxine tablets are a T4 hormone. There is no T4 intolerance. This is a hormone without which our body cannot function normally.

It is possible that you are taking levothyroxine, and some unpleasant symptoms are really bothering you. With normal TSH, it is pointless to look for a problem in levothyroxine. We must deal with the true cause of the malaise. You are no different from other people and can also get sick, like those whose thyroid gland is working normally. To reduce all your diseases to the thyroid gland in this case is ridiculous and illogical.

Regular intake of levothyroxine in the right dose will provide you with a quality of life indistinguishable from the quality of life of people with a healthy thyroid gland. The price of the issue is 1 tablet every morning. That's not difficult.
If the doctor prescribes lifelong treatment with levothyroxine, then the withdrawal of the drug is unacceptable. We are not talking about any "courses of treatment".

Sometimes you see patients with hypothyroidism who stop treatment on their own after making sure that their TSH has returned to normal. A common illusion that comes with successful chronic disease management is "I'm cured and I'm cured." No, my dears, this is not a recovery, this is a quality medical control. As long as you are taking the correct dose of medication, your lab results are normal, the same as in healthy people. But after the cessation of the selected treatment, the disease will get out of control and will again destroy your life.

If you are going on vacation or on a business trip, do not forget to stock up on the road with levothyroxine. Of course, this is not a shortage and you will find your drug in any pharmacy in the world, but we have already agreed that it is better not to change the manufacturer without special need.

There are many people in the world with successfully compensated hypothyroidism. Every day of any of them, whether it be a great artist, a ballet soloist, an athletics champion or the president of a great country, begins with a levothyroxine pill. And this does not prevent any of them from living brightly and happily. It won't hurt you either!

Is hypothyroidism always incurable?

We already know that "hypothyroidism" is a syndrome that can be observed in various diseases and conditions of the thyroid gland. In addition to autoimmune thyroiditis (AIT), in which there is an irreversible loss of thyroid cells and, accordingly, thyroid function, there are other thyroiditis, which do not always result in hypothyroidism. This includes postpartum thyroiditis, subacute thyroiditis (de Quervain) and some others.

In any case, the attending physician will acquaint you with the prognosis of the disease.

Summing up

1. Hypothyroidism is a syndrome caused by a deficiency/absence of thyroid hormones.
2. The symptoms of hypothyroidism are varied and non-specific.
3. The only way to confirm/rule out hypothyroidism is to test for TSH
4. Depending on the causes, hypothyroidism can be irreversible or reversible.
5. Hypothyroidism can be subclinical (hidden) and overt (obvious). In subclinical hypothyroidism, TSH is elevated, T 4 free. fine; with overt hypothyroidism, TSH is elevated, T 4 free. lowered.
6. Treatment of hypothyroidism - replacement therapy with levothyroxine (T 4).
7. With a properly selected dose of levothyroxine, the quality of life of a patient with hypothyroidism does not differ from that of people with a healthy thyroid gland.