Levothyroxine: instructions for use
Each tablet contains:
active ingredient - levothyroxine sodium 0.05 mg and 0.1 mg;
excipients - lactose monohydrate, sugar, calcium stearate (E-470), potato starch.
Tablets of color, white or white with a yellowish shade, with a biconvex surface.
Is a levorotatory isomer of thyroxin, after a partial metabolism in the liver and kidneys, it influences the development and growth of tissues and metabolism. In small doses, has an anabolic effect. In medium doses, it stimulates growth and development, increases the tissue's need for oxygen, stimulates the metabolism of proteins, fats and carbohydrates, and increases the functional activity of the cardiovascular and central nervous systems. In large doses, inhibits the production of thyrotropin-releasing hormone hypothalamus and thyroid-stimulating hormone of the pituitary gland. The therapeutic effect is observed after 7-12 days of taking the drug, during the same time the effect is preserved after discontinuation of the drug. The clinical effect of hypothyroidism appears after 3-5 days of taking the drug. Diffuse goiter decreases or disappears within 3-6 months, with late nodal stages, a significant reduction in the size of the thyroid gland is observed in 30% of cases, but almost all patients are prevented from further growth.
Indications for use
Hypothyroidism of various genesis (including during pregnancy), thyroid hormone deficiency, relapse of goiter (prevention after resection), euthyroid benign goiter, additional therapy for thyrotoxicosis with thyrostatic drugs after reaching the euthyroid state (not during pregnancy). Cancer of the thyroid gland (suppressive therapy, after the removal of the thyroid gland - replacement).
In the complex therapy: Graves disease, autoimmune thyroiditis, test for suppression of thyroid function.
Hypersensitivity, myocardial infarction in history; acute myocarditis, cardiopathy, chronic hyperthyroidism, in combination with thyreostatic drugs during pregnancy, sore throat, adrenal insufficiency; children's age up to 6 years (for this dosage form).
With caution used in: diseases of the cardiovascular system: coronary artery disease (atherosclerosis, angina, myocardial infarction in history); arterial hypertension, arrhythmias; diabetes; severe long-existing hypothyroidism; malabsorption syndrome (may require dose adjustment).
Pregnancy and lactation
Treatment with levothyroxine during pregnancy and lactation should be continued. Women with hypothyroidism who receive a maintenance dose of levotroksin, after the onset of pregnancy should be under the supervision of a physician, Levothyroxine passes through the hematoplacental barrier in the first trimester of pregnancy and does not go into the second and third trimesters. The drug is not recommended for use, at the same time, with thyrostatic agents that penetrate the placenta and v., As a result of this, may cause the development of thyroid hypofunction in the fetus. No information is available regarding the carcinogenic or teratogenic effects of levothyroxine.
Breastfeeding: The minimum amount of levothyroxine is excreted in breast milk and may cause hypothyroidism in a newborn baby. It is believed that in breast milk, the content of thyroid hormone is not enough to meet the needs of a newborn with a non-functioning thyroid gland.
Dosage and administration
Inside, in the morning, on an empty stomach, washed down with a small amount of liquid. Tablets should be taken regularly. If one pill is missed, the dose should not be increased during the subsequent pill.
If necessary, use of the drug in a lower dose than 100 .mkg, you should use drugs from other manufacturers, providing the possibility of the necessary dosage.
With hypothyroidism - the initial dose of 50-100 mcg per day, with a gradual increase (by 50 mcg every 2-3 weeks) to a maintenance one - 150-250 mcg per day, for children the initial dose - 12.5-50 mcg / day, a supporting dose - 100- 150 mcg per 1 'sq. M of body surface; In congenital hypothyroidism, children aged 6–12 years old — 4–5 mcg / kg / day, children 13–18 years old, for whom puberty is not finished — 2-3 mcg / kg / day, with completed puberty — 1.7 mcg / kg / day (for children under the age of 6 years, this dosage form is contraindicated).
After surgery for a malignant tumor of the thyroid gland - up to 300 micrograms per day. Children - the initial dose of 50 mg, supporting 100-150 mg per day.
With complex treatment of hyperthyroidism - 50-100 mcg per day.
For a suppression test - for 14 days, 200 mcg per day or 3 mg 1 time for 7 days before re-scintigram.
Euthyroid goiter and prevention of its recurrence after resection: for adults - 100–200 mcg per day, for children - 50–150 mcg per day.
When used in excessive doses - thyrotoxicosis (change in appetite, dysmenorrhea, chest pain, diarrhea, tachycardia, arrhythmia, fever, tremor, headache, irritability, lower extremity muscle cramps, nervousness, sweating, difficulty sleeping, vomiting, loss of body mass).
With frequent use, the phenomenon of hyperthyroidism.
In women of menopausal age, a decrease in bone density is possible.
Possible heart rhythm disturbance and ventricular hypertrophy.
When used in insufficiently effective doses, hypothyroidism (dysmenorrhea, constipation, dryness, puffiness of the skin, headache, lethargy, myalgia, drowsiness, weakness, apathy, increased body weight).
Pseudotumor of the brain in children (severe headaches).
Symptoms of severe overdose: thyrotoxic crisis with collapse and coma, sometimes delayed for several days after ingestion.
Other symptoms include chest pain, diarrhea, tachycardia, arrhythmia, fever, tremor, headache, irritability, muscle cramps of the lower extremities, nervousness, increased sweating, vomiting.
Treatment: the appointment of beta-blockers, intravenous glucocorticosteroids, plasmapheresis.
Interaction with other drugs
Reduces the effect of insulin and oral hypoglycemic drugs, cardiac glycosides (with low levels of thyroid hormones - the risk of toxicity of glycosides, with high (replacement therapy) - you can increase the dose of glycosides); enhances the effect of indirect anticoagulants (increased hypoprothrombinemic effect, it is necessary to change the dose according to the INR value), tricyclic antidepressants - a mutual increase in toxicity of both. Beta blockers cause a reduction in the conversion of T4 to TK.
Corticosteroids (gluco-and mineralocorticoid) - correction of their dose is necessary (the metabolism of corticoids is reduced with a low level of thyroid hormones and increased with a high). Ketamine, maprotiline - risk of hypertension, tachycardia, arrhythmia, dose adjustment is required. Growth hormone - acceleration of the closure of growth zones (treatment with levothyroxine is carried out before the use of growth hormone). Sympathomimetics - the risk of coronary complications in patients with coronary heart disease, an increase in the effects of both. Kolestiramine, Kolestipol, antacids, iron preparations, sucralfate reduce the "plasma concentration due to inhibition of intestinal absorption (the interval between administration is 4–5 hours). Phenytoin reduces the amount of levothyroxine associated with protein and the concentration of thyroxine (T4) by 15 and 25%, respectively Estrogens increase the concentration associated with thyroglobulin fraction (efficacy decreases) - increase the dose of levothyroxyTt. When used simultaneously with anabolic steroids * asparaginase, clofibrate, furosemide, salicylates, tamok Syphenom may be a pharmacokinetic interaction at the level of binding to the protein.The synthesis, secretion, distribution and metabolism of the drug are influenced by amiodarone, aminoglutetimid, para-aminosalicylic acid derivatives, ethionamide, antithyroid drugs, beta-adrenergic blockers, carbamazepine, chloro-hydrates, diazepam, and diazepam lovastatin, somatostatin.When used simultaneously with salicylates, furosemide (in high doses), clofibrate increases the concentration of the drug in the blood.
If necessary, the appointment of other drugs containing iodine, it is necessary to consult a doctor. It is recommended to periodically determine the concentration of thyroid-stimulating hormone in the blood, an increase in which indicates a dose deficiency. The adequacy of suppressive thyroid therapy is also evaluated by suppressing the capture of radioactive iodine. With a long-existing multinodular goiter, a stimulation test with thyrotropin-releasing hormone should be carried out before starting treatment. In most cases, hypothyroidism should restore metabolic status gradually, especially in elderly patients and patients with pathology of the cardiovascular system. Prior to treatment, the possibility of pituitary or hypothalamic hypothyroidism should be excluded. The drug contains lactose and should be administered with caution to patients with rare congenital galactose intolerance, Lapp lactase deficiency, or glucose-galactose malabsorption.
In patients with diseases of the cardiovascular system, the drug should be used in a low initial dose, increasing it slowly and at long intervals under constant ECG monitoring.
Elderly patients. In elderly patients and with long-term treatment of hypothyroidism, treatment should be carried out with caution, starting gradually with low doses. For elderly patients, an initial dose of 25 µg, which is then increased to a full maintenance dose within 6-12 weeks. At the stage of dose selection, it is necessary to use drugs from other manufacturers, providing for the possibility of dosing tablets of 25 μg.
Impact on the ability to drive vehicles and machinery: during the period of treatment, care must be taken when driving and engaging in other potentially hazardous activities that require increased concentration of attention and speed of psychomotor reactions.
10 tablets in a blister pack. On 5 planimetric packagings together with the instruction for medical use of medicine in a pack.
In the place protected from moisture and light at a temperature not higher than 25 ° C.
Keep out of the reach of children.
2 years. Do not use after the expiration date printed on the package.
Pharmacy sales terms
Levothyroxine analogs, synonyms and drugs of the group
L-thyroxine 150, L-Thyroxine 50 Berlin-Chemie, Eutirox
Calculate thyroid disease: symptoms of hypothyroidism
Thyroid disease today affects a huge number of people, especially women. But not all of them know ...
Most people, having slept through their morning jogging or falling asleep during their favorite series, say that they are simply tired. But, if they wanted to know the real reason for their fatigue, which chained them to the bed, they would have to talk to someone who has thyroid disease.
Forces are no more!
For me, feelings of fatigue and exhaustion were absolutely not characteristic. I have always been a very energetic person. Six hours of sleep at night was enough for me.
But since last fall I have become another person who I myself didn’t like very much. I barely got up in the morning to take the children to school, and then went back to bed, often falling asleep until 10 or even 11, while acutely suffering from the consciousness of my guilt.
But just at that moment, my younger sister was diagnosed with thyroid problems, and her doctor said that the disease could have a family history.
And when I read the list of possible symptoms of a thyroid disease: depression, constipation, hair loss, weight gain and others - everything fell into place. I have hypothyroidism. I am one of the millions of people suffering from this disease.
On the brakes!
The thyroid is a tiny, butterfly-shaped gland at the base of the neck that controls the energy flow in the body. Hypothyroidism, also called thyroid hypofunction, means that this gland does not produce enough hormones to do its job. The most common cause is Hashimoto thyroiditis, a condition that causes the body to produce antibodies that attack its own thyroid. A lack of thyroid hormones makes a person sluggish. Slow digestion causes constipation, reduced metabolism leads to weight gain and increased cholesterol, hair and skin, lacking many nutrients, become dry and coarse (and the hair may also fall out).
The brain also needs thyroid hormones to use oxygen and stimulate the production of serotonin and dopamine, which regulate emotions. That is why hypothyroidism can lead to depression and moodiness, not to mention fuzzy thinking, which almost every patient with this disease complains of. Other symptoms, such as weight gain, cramps and stomach discomfort, are not specific enough to make doctors think about problems with the thyroid gland, but they are no less unpleasant.
Some experts believe that today, women over 35 have a 35% risk of developing thyroid disease. But many experts think that these figures are even higher, because a significant proportion of patients are not aware of their diagnosis.
And here are the reasons for the unprecedented rise in popularity of the disease:
It is common nowadays everywhere. Many hypothyroid specialists recommend that patients try yoga, meditation, and other ways to relieve tension, which could help prevent immune system problems such as Hashimoto thyroiditis, the most common cause of hypothyroidism.
Some toxins destroy the human endocrine system, disrupting the synthesis of hormones. Currently, the American Association for the Study of Thyroid Diseases has addressed the topic of environmental impact on the function of this organ.
Too much or too little iodine, deficiency of selenium in the soil, fluoride in water and too much soy in today's food can also be responsible for the prevalence of hypothyroidism.
If you suspect you have hypothyroidism, check to see if you have the symptoms listed below:
- increased fatigue or total lack of strength
- severe sleepiness
- reduced tone
- unreasonable concern
- indifference to sex
- increased chilliness
- frequent convulsions
- unexplained weight gain despite dieting
- thinning or hair loss
- dry skin and hair
- high cholesterol
- high blood pressure
- painful or longer than normal menstruation
- low hoarse voice
If you find something from this list in your room, we recommend the following plan of action.
List your signs. Write them down. For example, you can not spend the day without a nap or you have recovered by 10 kg, despite walking 5 times a week and dieting.
Ask your relatives, including your brothers, sisters, parents, their brothers and sisters, cousins, grandparents, if they have any problems with the thyroid and have they ever received any additional thyroid hormones.
Tell the doctor about it and ask him to give you a TSH test. This is a blood test that checks the level of thyroid hormones. Find out your exact indicator, and not just whether it is in the "normal" range. Some expert endocrinologists now say that the norm is between 0.3 and 3.0. This means that TSH above 3 would indicate hypothyroidism. But many laboratories did not accept the new criteria for evaluating this indicator and still the result of 4 or even 5 is not regarded as high.
Recheck after 3 months. If you are prescribed a treatment, then you can understand if it helps.
Ask for a test for thyroid antibodies - Anti-TPO. If your TSH test is normal, but you feel unwell, this test can help determine if you have hypothyroidism.
Perform additional hormonal tests. Doctors need to check the levels of the hormones T3 and T4, which can give a more accurate picture of how your thyroid gland functions.
"One size" approach is impossible here - one size for all. You may need to take several trips to the doctors to get the right appointments, and subsequent treatment may also change. The meaning of treatment is in replacement therapy with synthetic analogues of thyroid hormones.
The doctor selects the dose individually, depending on the depth of the hypothyroidism, the patient's age, the condition of his cardiovascular system, and the presence of another pathology. With a properly selected dose of the drug, the level of thyroid stimulating hormone is within normal limits. The control is carried out 1 time in 6–12 months.
Diffuse nontoxic goiter: diagnosis, prevention, treatment
Diffuse non-toxic goiter (synonym - diffuse euthyroid goiter) is called a diffuse enlargement of the thyroid gland, which is not associated with dysfunction and is not a consequence of inflammatory and neoplastic processes in it.
As a rule, diffuse goiter is found in young people, and in women it occurs 3 times more often than in men. Especially often an enlargement of the thyroid gland is found in women during puberty, pregnancy, lactation and post menopausal period.
The main cause of endemic goiter is iodine deficiency. This etiological factor is valid throughout the Russian Federation. Criteria that indicate that the region is free from iodine deficiency are the frequency of goiter in adolescents less than 5%, the frequency of congenital hypothyroidism less than 3%, median ioduria more than 100 mg / l. For all regions of our country, there is a slight and moderate iodine deficiency. There are also a number of strumogenic substances, with an excessive supply of which into the body under conditions of iodine deficiency, the formation of goiter occurs. Some bacteria contain progotrin, which under the influence of certain enzymes is converted to goitrin, an active enzyme that inhibits the organization of iodine. Thiocyanates contained in certain types of vegetables inhibit the uptake of iodine by the thyroid gland, but this effect is leveled by an additional intake of iodine, while these effects of goutrin cannot be eliminated by this method. It should also be noted the negative impact of a lack of a number of vitamins and trace elements in conditions of iodine deficiency, such as retinol, cobalt, copper, zinc, molybdenum.
In addition to these, there are other causes of the development of diffuse euthyroid goiter. Defect enzyme systems that provide the synthesis of thyroid hormones, leads to the formation of sporadic goiter. With the development of some variants of the autoimmune pathology of the thyroid gland, its diffuse increase is characteristic while maintaining euthyroidism at the initial stages of development (for example, the hypertrophic form of autoimmune thyroiditis).
The impact of the above factors, combined with iodine deficiency and leads to the development of goiter.
Taking into account the fact that, nevertheless, the main cause of the development of diffuse non-toxic goiter is iodine deficiency, then we will consider in detail using what mechanisms the lack of iodine in the body leads to the formation of goiter. According to a number of researchers, and in particular, V.Fadeev , the pathogenesis of diffuse nontoxic goiter includes several main components: hyperplastic, associated with the effects of direct iodine deficiency and hypertrophic, the development of which is directly related to changes in thyroid stimulating hormone (TSH) levels.
Iodine deficiency in thyroid cells leads to a decrease in the content of iodinated lipids, the normal content of which ensures the inhibition of the activity of local tissue growth factors. With their lack of tissue growth factors (IGF-1, ERF, FGF) contribute to the division of thyrocytes, an increase in the number of thyroid cells (hyperplasia).
The main trophic stimulator of the thyroid gland is the thyroid stimulating hormone. With a regular decrease in the amount of thyroid hormones in conditions of iodine deficiency, TSH production somewhat increases, as well as the sensitivity of cells to it to a greater degree, with a decrease in the intrathyroid iodine content. Stimulation of TSH cells leads to an increase in the size of the thyroid cells (hypertrophy). In combination, both of these mechanisms cause a diffuse enlargement of the thyroid gland.
Subsequently, under conditions of iodine deficiency, adaptation mechanisms develop: an increase in iodine absorption by the thyroid gland, as well as preferential secretion of more active T3. An experienced clinician, who determined an enlargement of the thyroid gland during palpation, can assume the presence of goiter.
At present, the goiter classification proposed by WHO in 1962, revised in 2001, is used throughout the world, according to which the following degrees of thyroid enlargement are distinguished: 0 degree - there is no goiter (the volume of each lobe does not exceed the volume of the distal thumb of the patient’s thumb ); Grade I - goiter is palpable, but not visible in the normal position of the neck (there is no visible enlargement of the thyroid gland). This includes nodules that do not lead to an increase in the thyroid gland itself; Grade II - goiter is clearly visible in the normal position of the neck. For goiter, as a rule, asymptomatic. With its large size may have a cosmetic defect, compression of the trachea and esophagus.
To confirm this diagnosis will allow an ultrasound study to determine the volume of the thyroid gland. With its diffuse increase in women more than 18 ml, in men more than 25 ml, we can talk about the presence of goiter (an increase in the thyroid gland).
The next stage of the survey is to determine the functional state of the thyroid gland. Screening research method is to determine the level of thyroid stimulating hormone. When the TSH value is outside the normal range, the patient should determine the level of thyroid hormone free fractions in order to diagnose subclinical or manifest hypothyroidism or thyrotoxicosis. With a normal value of TSH, it is necessary to exclude the possible presence of chronic autoimmune thyroiditis, which will be indicated by an increase in the level of antibodies to TPO and a change in the echographic picture during ultrasound examination (hypoechogenicity and heterogeneity of the thyroid tissue). In the absence of large diagnostic signs characteristic of chronic autoimmune thyroiditis (according to the clinical guidelines of the Russian Association of Endocrinologists, 2002), a diffuse non-toxic goiter can be diagnosed to the patient.
In the presence of a retrosternal goiter, a thyroid gland scintigraphy is indicated. For large sizes of goiter with possible compression of the trachea and esophagus, it is advisable to conduct a chest X-ray with esophageal contrast barium.
There are several options for the conservative treatment of diffuse non-toxic goiter:
The first step is the use of monotherapy with iodine preparations in physiological doses. This therapy is etiotropic, aimed at restoring the intrathyroid iodine content. The reduction of goiter is somewhat delayed, however, this treatment option is quite effective for children and adolescents.
The use of thyroid hormone drugs allows for a rapid regression of the thyroid gland, however, after discontinuation of their use, withdrawal syndrome may occur. It develops due to the fact that when taking levothyroxine, the intrathyroid iodine content in the thyroid gland decreases, and after discontinuation of the drug, the thyroid gland enlarges due to hyperplastic processes (amid iodine deficiency) and hypertrophic (by eliminating the effect of suppressing TSH). Therapy with levothyroxine (Eutirox) (monotherapy or in combination with iodine preparations) should be carried out under the control of thyrothropin level. The target range is the TSH level close to the near limit of the norm (0.4–0.7 mU / l). After discontinuation of the drug, it is advisable to start taking potassium iodide.
The most pathogenetically justified treatment option for diffuse non-toxic goiter is the use of combination therapy: a combination of levothyroxine and potassium iodide. Therapy is carried out in 2 stages: at the first stage (on average, it can take from 6 months to 2 years), reduction of the goiter is achieved. Preparations of thyroid hormones provide a fairly rapid effect due to the suppression of the trophic effect of thyrotropin. The effect of iodine preparations is aimed at suppressing the hyperplastic effect of iodine deficiency. The second stage begins after reaching the normal size of the thyroid gland. Levothyroxine is canceled, continue to receive potassium iodide in prophylactic doses. In combination therapy, the need for levothyroxine is less than in monotherapy. A convenient option is a combined preparation containing 100 µg of levothyroxine sodium and 100 µg of potassium iodide - Iodtirox.
Surgical treatment of diffuse non-toxic goiter is indicated for large goiter sizes (accompanied by a cosmetic defect) and / or compression of surrounding organs.
There were also reports of the possible use of radioactive iodine therapy. Treatment with iodine 131 causes a reduction of up to 50% of the volume of the thyroid gland. As with the surgical method of treatment, the consequence is the development of hypothyroidism (up to 14% of all cases). Moreover, these cases are more often recorded in people with elevated levels of antibodies to TPO.
The remote consequences of the lack of treatment of diffuse non-toxic goiter is the formation of a nodular / multinodular goiter, with possible development in the subsequent functional autonomy of the thyroid gland, thyrotoxicosis with a corresponding effect on all human organs and systems (especially the cardiovascular system).
That is why the timely start of treatment of diffuse non-toxic goiter is especially important.
Measures to prevent the development of iodine deficiency disorders include mass and individual methods.
The measures of mass prevention is the use of iodized salt.
As an individual prevention of the development of iodine deficiency diseases, the American Thiological Association formulated recommended preventive daily dosages of potassium iodide for various groups: for newborns up to 6 months - 110 µg; 7-10 months - 130 mcg; 1-8 years - 90 mcg; 9-13 years old - 120 mcg; 14 and more - 150 mcg; pregnant women - 220 mcg; lactating women - 290 mcg.
One of the drugs used as a means of individual prevention and treatment of diffuse non-toxic goiter is Jodbalans®. This is a modern iodine preparation, produced in convenient dosages: one tablet contains 100 or 200 µg of potassium iodide. It should be taken in the morning after breakfast.