Hypothyroidism is a clinical syndrome caused by a persistent decrease in the level of thyroid hormones. According to a Colorado population-based study, the prevalence of hypothyroidism varies from 4 to 21% in women and from 3 to 16% in men, depending on age. In the age group 45-54 years, the incidence of hypothyroidism in women was 10%, in men 5% [Canaris G. et al., Arch Intern Med, 2000].
- Hypothyroidism, caused a decrease in the number of functioning thyroid tissue (thyroid)
• postoperative hypothyroidism
• postradiation hypothyroidism
• hypothyroidism, thyroid lesions resulting from autoimmune (autoimmune thyroiditis, Graves’ disease outcome in hypothyroidism)
• hypothyroidism, thyroid lesions resulting from viral
• at hypothyroidism background of thyroid neoplasms
- Hypothyroidism due to impaired embryonic development of the thyroid gland (congenital hypothyroidism)
- Hypothyroidism due to impaired synthesis of thyroid hormones
• endemic goiter with hypothyroidism
• sporadic goiter with hypothyroidism (defects in thyroid hormone biosynthesis at various biosynthetic levels)
• medical hypothyroidism (taking thyreostatics and a number of other drugs)
• goiter and hypothyroidism, developed as a result of eating food containing goitrogenic substances.
Hypothyroidism of central origin (secondary)
- hypothyroidism of pituitary genesis
- hypothyroidism of hypothalamic origin (or tertiary)
Hypothyroidism due to impaired transport, metabolism and action of thyroid hormones
- peripheral hypothyroidism
• generalized resistance to thyroid hormones
• partial peripheral resistance to
circulating thyroid hormones • T3 and T4 or TSH
All forms of hypothyroidism are based on a decrease in the level of thyroid hormones, which causes metabolic changes leading to disruption of the functioning of various organs and systems.
Clinical symptoms of hypothyroidism
There are no obvious differences in the clinical picture of primary and secondary hypothyroidism, except that secondary hypothyroidism is milder, because The thyroid gland has a residual secretion of thyroid hormones.
The clinical picture will largely depend on those thyroid diseases that led to the formation of hypothyroidism syndrome.
Diagnosis of hypothyroidism
To establish a diagnosis of hypothyroidism, it is usually sufficient to determine the concentration of TSH and free T4. Moreover, taking into account the fact that an increase in TSH levels is a very sensitive marker of primary hypothyroidism, measuring TSH is considered the best way to diagnose this condition.
Criteria for the diagnosis of
various forms of hypothyroidism
An elevated TSH level along with a decreased svT4 is an important diagnostic criterion for primary hypothyroidism. In hypothyroidism of central genesis, the TSH content in the blood is reduced or normal in combination with a reduced T4.
The most common causes of primary (thyroid disorders) hypothyroidism are:
• thyroid surgery;
• chronic autoimmune thyroiditis.
In 95% of patients, hypothyroidism is primary. The main diagnostic criteria for primary hypothyroidism:
• increased TSH, the level of thyroid hormones may be reduced;
• there is a thyroid disease.
In 5% of patients, hypothyroidism is secondary. The main diagnostic criteria for secondary (central nervous system disorders) hypothyroidism are:
• clinical signs of hypothyroidism are present,
• low basal TSH levels,
• total T4 – at the lower limit of normal or below normal,
• the patient has a disease of the central nervous system.
Severity of hypothyroidism:
• Subclinical hypothyroidism (or minimal thyroid insufficiency) – clinical symptoms of hypothyroidism may be absent, an increased level of TSH in the blood is determined with normal levels of thyroid hormones. Occurs in 10–20% of the population.
• Manifest hypothyroidism – accompanied by clinical manifestations, an increase in the level of TSH and a decrease in the level of thyroid hormones. It occurs in 1.5-2% of women and 0.2% of men, among people over 60 years of age – in 6% of women and 2.5% of men.
• Severe hypothyroidism (long-term) with an outcome in hypothyroid (myxedema) coma.
General principles of
“Gold standard” in the treatment of hypothyroidism of any etiology – replacement therapy with levothyroxine (L – T4) drugs, for example Eutirox.
Replacement therapy is necessary when it is necessary to achieve compensation for hypothyroidism, but there is no need to suppress TSH. For this, doses of Eutirox are used from 1.6 to 1.8 g per 1 kg of body weight per day. Against the background of thyroxine (T4) replacement therapy, the T3 concentration remains constant.
Monotherapy with levothyroxine (Eutirox) is optimal for the treatment of hypothyroidism. Existing in Russia levothyroxine preparations are available in dosages of 25 to 150 micrograms per 1 tablet that allows easy dosing of the drug, and the representation – lyayut a synthetic thyroxin (sodium salt thyroxine), which is identical to thyroxine produced by the thyroid gland. The drug is well absorbed in the gastrointestinal tract, and in hypothyroidism, its absorption is not impaired. When carrying out replacement therapy for primary hypothyroidism, the target TSH value is 0.5–1.5 mIU / L.
The goal of replacement therapy for central (secondary) hypothyroidism is to maintain thyroxine in the blood at a level corresponding to the upper third of the normal values for this indicator.
When carrying out replacement therapy, the estimated average dose of Eutirox is 75–150 mcg / day. To compensate for subclinical hypothyroidism, Eutirox is prescribed at the rate of 1 g per 1 kg of body weight per day, and the average estimated dose of the drug will be 50–75 g / day. Moreover, when deciding whether to start treatment for subclinical hypothyroidism, it should be borne in mind that:
• the appointment of replacement therapy with Eutirox is performed in case of persistent subclinical hypothyroidism or at least two-fold detection of the TSH level between 5 and 10 mMED / l;
• in case of a combination of pregnancy and subclinical hypothyroidism, a full replacement dose of Eutirox is prescribed immediately.
With uncompensated hypothyroidism (even subclinical!), Pregnancy is extremely unlikely. If pregnancy does occur, then treatment of hypothyroidism should be started immediately, and during pregnancy, the need for thyroxine increases on average by 45% of the estimated initial dose. If pregnancy occurs in a woman with compensated hypothyroidism, then the dose of Eutirox should be increased in accordance with the increased need for it. A pregnant woman with uncompensated hypothyroidism has an increased risk of obstetric complications:
• intrauterine fetal death;
• placental abruption;
• perinatal complications.
Thyroid hormone therapy (Eutirox) significantly improves both the course and the outcome of pregnancy.
Thus, during pregnancy, the estimated dose of Eutirox is 2.0-2.2 g per 1 kg of body weight per day. The severity and duration of hypothyroidism are the main criteria that determine the doctor’s tactics at the time of initiation of treatment. At the initial stage of treatment of hypothyroidism, the patient’s age and the presence of concomitant pathology, primarily diseases of the cardiovascular system, should be taken into account.
For patients without cardiac pathology under 55 years of age, Eutirox is prescribed at the rate of 1.6–1.8 g per 1 kg of body weight per day. At the same time, the approximate initial dose: women – 75-100 mcg / day, men – 100-150 mcg / day.
For patients with cardiac pathology or over 55 years of age, Eutirox is prescribed at the rate of 0.9 g per 1 kg of weight. The initial dose of the drug is 12.5-25 mcg / day, and it should be increased by 12.5-25 mcg with an interval of 2 months until the TSH level in the blood normalizes. When cardiac symptoms appear or worsen, it is necessary to correct cardiac therapy.
Eutirox is taken in the morning, on an empty stomach, 30 minutes before meals, preferably with plain water.
The following points are important.
• Subjective improvement of the patient’s condition with proper treatment of hypothyroidism will occur gradually, over several weeks.
• The full therapeutic effect (euthyroidism) is achieved no earlier than 2-3 months after the start of therapy.
• Total T4 usually returns to normal after 5–6 days. after starting treatment.
• Total T3 returns to normal 2–4 weeks after starting treatment.
• The TSH level decreases to normal not earlier than after 3–6 months. after starting treatment.
Thus, the main task of treatment is to restore the normal physiological functions of all organs and systems disturbed due to hypothyroidism. In both primary and secondary (tertiary) hypothyroidism, the basis of treatment is adequate replacement therapy with thyroid hormone drugs. Cri – teriem adequacy of treatment is the disappearance of clinical and laboratory manifestations of hypothyroidism.
The more severe the hypothyroidism and the longer it has been uncompensated, the higher the general susceptibility of the body to thyroid hormones will be, and this is especially true for cardiomyocytes. Therefore, the process of adaptation to the drug should be gradual and smooth, regardless of the patient’s age.
Treatment for all forms of hypothyroidism is substitutional and lifelong. The only exception is hypothyroidism caused by the administration of any medications or substances that block the production of thyroid hormones.
Monitoring. Patients receiving an adjusted dose of Eutirox are advised to test their TSH levels annually. The TSH level is not affected by the time of blood sampling and the interval after taking Eutirox.