What is hypothyroidism
Hypothyroidism is a deficiency of thyroid hormones. At the same time, a syndrome develops (a complex of certain pathological symptoms), which doctors define as a single term “hypothyroidism”.
Annually per 1000 people 4 new cases of hypothyroidism are detected,
Hypothyroidism is more common in women than in men.
Hypothyroidism is not a definitive diagnosis. This is a consequence, a result, which may have various causes (diseases, conditions).
Causes of Thyroid Hypothyroidism
- the absence or lack of active thyroid gland (autoimmune thyroiditis, effects of surgery or treatment with radioiodine, congenital thyroid abnormalities, consequences of non-autoimmune destructive thyroiditis, etc.);
- violation of the synthesis of thyroid hormones (severe iodine deficiency, medicinal damage to the thyroid gland, congenital defects of the synthesis of hormones);
- damage to the pituitary and / or hypothalamus, resulting in impaired synthesis of thyroliberin and TSH;
- tissue hypothyroidism (impaired cellular sensitivity to the effects of thyroid hormones, impaired thyroid hormone transport, impaired T4 to T3 transformation, etc.).
If the cause of hypothyroidism is a non-functioning thyroid gland, we are talking about primary hypothyroidism.
If the reason is a violation of the production of TSH, then we call hypothyroidism secondary.
In some cases, such as, for example, after thyroidectomy, with AIT and with congenital hypothyroidism, we are dealing with an irreversible situation,
Sometimes, for example, with postpartum, subacute and drug thyroiditis, the situation is reversible, that is, hypothyroidism is temporary.
Hypothyroidism can have many causes, but the most common of these is autoimmune thyroiditis (AIT). When AIT occurs, the destruction of thyrocytes (thyroid cells that produce hormones). In order for hypothyroidism to develop, most thyrocytes must die. Initially, while the smaller part of the cells died, the iron continues to work normally. The less healthy thyrocytes remain, the more noticeable the hormone production decreases. In response, on the principle of feedback, the pituitary gland increases the production of TSH, enhancing the stimulation of the thyroid gland.
For some time, due to hyperstimulation with high concentrations of TSH, the remaining thyroid cells continue to produce normal (low-normal) amounts of hormones. In the analyzes, one can see increased TSH and normal T4 free. This situation is called subclinical hypothyroidism. Bright clinical manifestations of hypothyroidism at this stage yet.
With the death of thyrocytes, less and less levothyroxine is produced; TSH is becoming higher. The manifest hypothyroidism develops. With manifest hypothyroidism, TSH is high, and T4 is free. reduced
If hypothyroidism takes a long time without treatment, then a severe clinical picture of myxedema develops: the disruption of all body systems due to a deficiency / absence of thyroid hormones. If time does not begin treatment, hypothyroid coma and death will develop.
Chronic lymphocytic thyroiditis
Women get 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 anti-thyroid antibodies in serum. In the hypertrophic (goiter) form of the disease, the thyroid gland is diffusely enlarged, dense, slightly bumpy, and in atrophic 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. At the same time, the thyroid gland is palpated as a solid mass. Riedel’s thyroiditis must be differentiated from thyroid cancer with an aspiration biopsy.
A twenty-year observation has shown that in women, the frequency of transition of 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’s disease — Birmer disease, premature ovarian failure, and vitilogyloma.
Secondary hypothyroidism is caused by impaired synthesis or release of TSH or thyroliberin. TSH deficiency occurs with the use of certain drugs, pituitary adenoma, Sheehan syndrome (postpartum pituitary infarction), radiation therapy, pituitary metastases, traumatic brain injury and surgery on the pituitary gland. The clinical picture is the same as in primary hypothyroidism, but may additionally include symptoms of hypopituitarism (adrenal insufficiency, hypogonadism, amenorrhea). With hormone-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 TSH level, the level and size of the pituitary gland also return to normal.
The diagnosis of secondary hypothyroidism is made if the level of free T4 is reduced against the background of a low or normal level of TSH. Secondary hypothyroidism should be suspected even if there is a shortage of other hormones, or if it is known that the patient suffers from a disease of the hypothalamus or pituitary gland.
Rare causes of hypothyroidism
The rare causes of hypothyroidism are thyroid blocking antibodies. These antibodies can cross the placenta and cause transient congenital hypothyroidism in the newborn. In about 5% of women with chronic lymphocytic thyroiditis, babies are born 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 during thyroid resection, 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 head and neck tumors. Occasionally hypothyroidism is observed in diseases such as hemochromatosis, scleroderma, sarcoidosis, and amyloidosis.
Hypothyroidism is caused by the use of certain medications. With a high intracellular concentration of iodide (which happens when taking iodine preparations in high doses), the Wolf – Chaikoff phenomenon is observed: iodine suppresses thyroglobulin iodization and the condensation of iodotyrosines. In healthy people, this phenomenon disappears in a few days, but iodine hypothyroidism can develop. The phenomenon of Wolf — Chaykov may cause iodine-containing amiodarone, radiopaque agents, a saturated solution of potassium iodide, kelp (in tablets). Povidone-iodine for local use (on the skin and mucous membranes) can have a systemic effect and also lead to transient iodine hypothyroidism. Lithium, perchlorate, propylthiouracil, tiamazol, interferon A, IL-2 can cause hypothyroidism due to the suppression of the synthesis or secretion of T4 and T3.
Symptoms, signs of hypothyroidism
Diagnosing hypothyroidism is both simple and difficult.
Just because the key to making a diagnosis is elevated TSH. (Recall the favorite saying of endocrinologists: “Investigate the TSH and sleep well.”) The study of TSH is available, cheap, informative.
If you suspect hypothyroidism, it is enough to take blood for TSH, and already after 2 hours the diagnosis of hypothyroidism will be confirmed or refuted.
It is difficult because, unfortunately, the symptoms that are far from always cause the doctors to suspect hypothyroidism. After all, people with hypothyroidism rarely turn to an endocrinologist. The symptoms that worry them are usually a reason to go to a cardiologist, a dermatologist, a gynecologist, a hematologist, a otolaryngologist, a neurologist. To anyone, but not to the endocrinologist.
Hypothyroidism – the great master of camouflage. He has many masks, and to consider a single cause under these masks – thyroid hormone deficiency – only the TSH study will help.
The fact is that in the hypothyroid syndrome all organs and systems are affected. None of the symptoms of hypothyroidism is specific for this disease. Exactly the same symptoms can occur in various diseases of the cardiovascular, respiratory, and digestive systems; can be observed in neurological, hematological, dermatological, rheumatological, psychiatric, gynecological practice.
With an amazing diversity in all the symptoms of hypothyroidism, one reason is a change in the metabolism in each cell of the body, associated with a deficiency / absence of T4 and T3: impaired protein synthesis, slower energy exchange, fluid retention.
Sometimes patients with hypothyroidism go from doctor to doctor for years, receiving useless appointments, suffering from increasing symptoms of the disease, not receiving the only necessary treatment – replacement therapy with thyroxine drugs.
Symptoms of hypothyroidism are diverse and can be expressed in varying degrees, from the complete absence of manifestations to severe multiorgan failure.
To understand how many masks in hypothyroidism, 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 voltage on the ECG, hydropericardium (fluid in the pericardium), atherosclerosis, high cholesterol, increased LDH.
Respiratory system: breath holding in sleep (sleep apnea syndrome), hoarseness, fluid in the pleural cavities, shortness of breath.
The 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, slow thought processes, neuropathy (pain in the extremities), decreased reflexes.
The urinogenital system: fluid retention, dense edema, any menstrual dysfunction, infertility, miscarriages, erectile dysfunction and ejaculation, decreased libido.
Skin: severe dryness, pallor, jaundice, peeling, thickening of the skin; hyperkeratosis of plantar areas; skin pigmentation on the elbows; brittle nails; dryness, thinning and hair loss.
Hematopoietic system: chronic anemia.
There is another “mask” associated with the diagnosis of “hypothyroidism”: this is the absence of hypothyroidism in the clinical picture typical of this disease. The patient has a complex of symptoms most characteristic of hypothyroidism (weakness, dry skin, constipation, edema, and
With hypothyroidism, metabolism slows down and heat production decreases. Basal metabolism can be halved, patients become very sensitive to cold (cold intolerance). O2 consumption, pulmonary gas exchange and erythropoiesis are reduced. Anemia develops. A decrease in lipolysis contributes to a moderate increase in body weight and hyperlipidemia (VLDL, LDL), and a reduction in the conversion of cholesterol to bile acids quickly leads to hypercholesterolemia and the development of atherosclerosis. Violation of glycogenolysis and gluconeogenesis causes hypoglycemia. Reducing the breakdown of glycosaminoglycans that bind water (mucopolysaccharides, mucin), contributes to their accumulation in various tissues. This gives the skin a pasty consistency, so the disease has received the name of myxedema (mucous edema). Sometimes carpal tunnel syndrome develops. Almost always marked swelling of the eyelids. Swelling of the vocal cords leads to hoarseness; swelling of the tongue affects articulation. In addition, fibronectin, collagen, plasma albumin is deposited in the skin. Reducing the conversion of carotene to vitamin A causes hyperkeratosis. Due to the accumulation of carotene skin acquires a yellowish tint. There is a hair loss. Due to the decrease in secretion of sweat and sebaceous glands, the skin becomes dry, and a decrease in heat production makes it cold to the touch.
Reducing heart stimulation with thyroid hormones reduces contractility, heart rate, PP, CB; sometimes systolic blood pressure decreases. With a marked deficiency of thyroid hormones, heart failure develops. Pleural and pericardial effusions are characteristic. Respiratory rate slows down, the reaction to hypercapnia and hypoxia is disturbed.
Diminished glomeruli and tubules in the kidneys. GFR, PP and channel capacity are reduced. Reduced renal excretion leads to water retention and NaCl. Due to the accumulation of fat, glycosaminoglycans, NaCl and water, the patient looks edematous.
In addition, protein synthesis in the liver is disturbed, and the rate of metabolism of steroid hormones and drugs decreases.
Reduced stimulation of the muscles of the intestine causes constipation. Impaired function of the muscles of the esophagus and the cardiac sphincter leads to gastroesophageal reflux and esophagitis.
Hypothyroidism decreases the activity and effectiveness of the autonomic nervous system. Neuromuscular excitability decreases, which causes a change in sensory functions, hyporeflection, loss of hearing, appetite, memory, depression and clouding of consciousness with the development of coma. These changes in adults are reversible.
The absence of thyroid hormones in the fetus and newborn causes irreversible damage to the brain. Thyroid hormones are required for the full development of dendrites and axons, the formation of synapses, myelination and glia formation, which is absolutely necessary for the development of the brain in the fetus and children during the first 2 years of life. A deficiency of thyroid hormones during fetal development significantly disrupts this development. If, after birth, the hormone deficiency is not replenished, irreversible brain damage occurs; brain function is not restored even with subsequent replacement therapy. Children with hypothyroidism are often deaf.
In addition, bone growth is delayed in these children. Growth retardation and impaired intelligence lead to typical signs of cretinism.
With a T3 / T4 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, inhibiting the release of gonadotropins and reducing fertility. TSH also promotes the growth of the thyroid gland, causing goiter. Finally, anomalies of gonadotropin secretion lead to impaired fertility.
Myxedema coma. Myxedema coma – life-threatening complication of hypothyroidism; it usually develops in patients with prolonged hypothyroidism and is characterized by a comatose state with severe hypothermia (body temperature 24-32.2 ° C), a lack of reflexes, convulsions, and respiratory depression with a delayed C02. Severe hypothermia can only be detected with a thermometer with an increased low temperature scale. The diagnosis must be made very quickly, because in the absence of immediate treatment the patient may die. The factors provoking myxedema coma include diseases, infections, injuries, medications, oppressive 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 measurement of serum TSH levels, 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, as a result of which paresthesia and tunnel syndromes can develop.
- The cardiovascular system. Most patients have bradycardia, which can be combined with mild hypertension. On the EEG, a flattening of the T wave and prolongation of the PQ interval are found. In the presence of a pericardial effusion, the amplitude of the R and R teeth decreases and the heart shadow on the radiograph increases. The QT interval can be lengthened, leading to ventricular premature beats. Possible reduction in myocardial contractility. Heart failure rarely occurs, since cardiac output is usually sufficient to provide 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 fragile; sometimes there is a loss of the outer half of the eyebrows. Patients often suffer from pain in the muscles and joints.
- Reproductive system. Typical violations of the menstrual cycle, 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.
- Gastrointestinal tract. Due to a decrease in GI motility, constipation occurs. There is a slight (no more than 5%) weight gain.
- Changes in laboratory parameters. "Blood tests show normocytic anemia, hyponatremia, increased CPK activity and serum LDL cholesterol levels.
The term “cretinism” was originally proposed to refer to the state of mentally retarded and undersized children from regions with severe iodine deficiency; such children differed puffiness of the face and swelling of the extremities. Deaf and mute signs and signs of pyramidal and extrapyramidal pathways were also frequently noted. In the US, white neonatal neonatal screening programs detect 1 case of sporadic hypothyroidism per 5,000, and among African American newborns only 1 in 32,000. (from the root of the tongue to the lower-front surface of the neck). The function of such an “ectopic gland” is reduced. The admission of thyroid-blocking antibodies from mothers with Hashimoto thyroiditis to the fetus may be the cause of the genesis of the thyroid gland and “atyreoid cretinism”, but in most of these cases the hypothyroidism in the newborn turns out to be transient. Other possible causes of neonatal hypothyroidism include exposure to the fetus iodide or antithyroid drugs taken by the mother, or treatment of thyrotoxicosis or thyroid cancer in the mother with radioactive iodine.
In almost all children with a birth weight of more than 2500 g, proximal tibial epiphyses and distal femoral epiphyses are already formed. Their absence causes to suspect hypothyroidism. The introduction of neonatal screening programs in the developed countries with the determination of the levels of TSH or T4 was a significant achievement of health care, since the early diagnosis of hypothyroidism prevents permanent mental retardation. A drop of blood, obtained by stabbing the heel of a child within 24-72 hours after birth, is applied to filter paper and sent to the central laboratory. Neonatal hypothyroidism is indicated by serum T4 levels below 6 µg% or TSH above 25 mU / L. The diagnosis is confirmed by repeated examination and radiographic signs of lagging of bone age. It should be remembered that in newborns, even with euthyroidism, if their mothers received insufficient treatment for hypothyroidism during pregnancy, some mental retardation is later discovered, which emphasizes the need to maintain euthyroidism in pregnant women.
Subclinical hypothyroidism of the thyroid gland
Subclinical (latent) hypothyroidism is diagnosed if the serum TSH level is elevated and the free T4 level is within the normal range. At the same time, antibodies to iodine peroxidase are often detected. In most cases, the disease is asymptomatic, although mild signs of hypothyroidism are possible. Patients with a family history of diabetes or other autoimmune diseases (especially type 1 diabetes), as well as patients with goiter, infertility, depression and hyperlipoproteidemia, are subject to examination. Treatment allows you to prevent the transition to a clinically expressed form, reduce LDL cholesterol, reduce some symptoms (if any), reduce goiter, restore ovulation, reduce the risk of cardiovascular diseases. The frequency of transition of subclinical hypothyroidism into a clinically expressed form is 5–10% per year, in the presence of antibodies to iodine peroxidase and high levels of TSH (more than 12 IU / l), this figure is higher.
Diagnosis of thyroid hypothyroidism
In the blood, the content of thyroxine, triiodothyronine is reduced and the concentration of thyrotropin is increased. An increase in cholesterol, creatine phosphokinase and aminotransferase levels is also characteristic. Blood tests determine anemia, leukopenia, lymphocytosis.
The most sensitive indicator is the serum TSH level; among certain groups of the population it is advisable to carry out its mass determination. In primary hypothyroidism, there is no suppression of the pituitary gland.
In many patients with primary hypothyroidism, the content of triiodothyronine (T3) in serum remains normal, which is probably due to enhanced stimulation of the defective thyroid gland with thyrotropic hormone, leading to preferential synthesis and secretion of the more active hormone – T3 Therefore, according to the level of T3 in the serum diagnose hypothyroidism.
Patients often develop anemia, usually normocytic normochromic of unknown etiology, but due to menorrhagia it can be hypochromic, and also (when combined with hypothyroidism with pernicious anemia or folate absorption) – macrocytic. Anemia is rarely severe (with hemoglobin levels
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 gland 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 are synthesized in pharmacological plants. For a long time, it was believed that a hypothyroidism medicine should contain both T4 (levothyroxine) and T3 (triiodothyronine). Until the end of the last century, preparations containing both hormones were produced, but it was later proved that it was not necessary to add T3 to drugs for hypothyroidism, since inside the T4 cells it turns into T3 as needed.
Patients often state that they do not want to take “chemistry.” Meanwhile, artificially obtained drugs are pure molecules of those substances that are needed to obtain specific therapeutic effects. There are no extra impurities in them, as, for example, in medicinal plants, and, accordingly, possible side effects are better studied and predictable.
Levothyroxine contained in the pill is the absolute analogue of natural levothyroxin, which produces a healthy thyroid gland. If we compare a thyroxin 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 correctly chosen replacement dose, treatment with levothyroxine is ABSOLUTELY SAFE and ABSOLUTELY EFFICIENT.
How is this very correct dose chosen? It is known that an adult requires normal thyroxin 1.6-1.7 μg / kg body weight for normal vital activity per day. Accordingly, with manifest hypothyroidism, the initial dose is easily calculated: we multiply the body weight (in kg) by 1.6.
For example, with a body weight of 65 kg, the total replacement dose calculated by this formula will be 104 μg per day (65 x 1.6 = 104). Since there are no tablets with a dosage of 104 µg, we give tablets containing the dose of levothyroxine closest to the calculated one. In this case, it will be a dosage of 100 micrograms.
Elderly patients and patients with cardiac problems who have lived for a long time in conditions of chronic hypothyroidism are treated with caution so that the metabolism can adapt to new conditions. First, a small dose is given, followed by a gradual increase until the calculated dose is reached.
Principles of levothyroxine dose titration
All patients receiving levothyroxine, to assess the effectiveness of treatment, only one analysis is given – TSH. The exceptions are pregnant women (T4 free) is additionally investigated and those who receive suppressive therapy after radical treatment of highly differentiated thyroid cancer (T4 free, in addition, thyroglobulin, AT to TG).
After the appointment of levothyroxine in a stable dose (
Assessing the TSH 2 months after the prescription of replacement therapy with levothyroxine in a constant dose, we are ready to say whether the dose is right.
if the TSH has entered the range of normal values (0.4-4.0), then the dose is adjusted correctly;
if ttg>4.0, then hypothyroidism is preserved, the dose of levothyroxine must be increased and the TSH re-evaluated after 2 months;
In some patients, the target TSH values differ from the standard corridor (0.4–4.0). These include pregnant women, small children, patients after the radical treatment of highly differentiated thyroid cancer.
Individuals with subclinical hypothyroidism usually do not need a full replacement dose of levothyroxine. In order to achieve stable euthyroidism, they need only small dosages of levothyroxine. The initial dose in these cases, as a rule, is 50 mg / day. (this is the minimum therapeutic dose for an adult).
It should be noted that the treatment of subclinical hypothyroidism is not always required and not all. 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 fertile age, as well as to those patients who have clinical symptoms of hypothyroidism: anemia, atherosclerosis, etc.
There are a lot of levothyroxine drugs (Eutirox, L-thyroxin and others) in the dosage market now in various dosages, which make it possible to conveniently select an individual dose for each patient.
In the pharmacy, you can get levothyroxine tablets from 25 μg to 150 μg in one tablet. Until recently, the “step” between doses was 25 μg,
Store levothyroxine tablets should be strictly in accordance with the instructions indicated on the box. In case of violation of the storage mode, the drug may lose its activity.
Do not forget that the tablet contains a very tiny dose of levothyroxine, calculated in micrograms: this is an almost invisible amount of active substance that can be placed on the tip of a pin. The tablet mainly consists of neutral fillers that stabilize the active substance. These fillers are slightly different for different companies, therefore, the activity of the drug may differ individually. Starting to take the drug of one company, try to continue to take the drug of the same company, so that you do not have to double-check 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 the simple but very important rules for taking levothyroxine:
- The prescribed dose should be taken daily, without interruption. No “drug holidays”, dose juggling, cancellation experiments and
Repeatedly observed an interesting phenomenon. Patients who, for some personal reasons, were afraid to start treatment with levothyroxine, often discontinued treatment on their own in the first days of treatment, explaining this by the “intolerance” of the drug, the appearance of unpleasant symptoms and
The main thing the patient should understand: Levothyroxine tablets are the hormone T4. There is no intolerance T4. This is a hormone without which our body cannot function normally.
It is possible that you are taking levothyroxine, and you are really worried about some unpleasant symptoms. Under normal TSH, it is pointless to look for a problem in levothyroxine. We must deal with the true cause of indisposition. You are no different from other people and you can also get sick, like those who have a thyroid gland working normally. To reduce all your diseases to the thyroid gland in this case is absurd 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. Price issue – 1 tablet every morning. It is not difficult. If a doctor prescribes lifelong treatment with levothyroxine, it means that drug withdrawal is unacceptable. There are no “treatment courses”.
Sometimes you have to see patients with hypothyroidism who stopped their treatment on their own, making sure that their TSH returned to normal. A common illusion arising from the successful treatment of chronic diseases is “I have been treated and recovered.” No, my dear, this is not a recovery, it is a high-quality medical control. While you are taking the chosen dose of medication, the results of your lab tests are normal, just like in healthy people. But after stopping a matched 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 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.
Many people live in the world with successfully compensated hypothyroidism. Every day, any of them, be it a great artist, ballet soloist, athletics champion or president of a great country, begins with a tablet of levothyroxine. And this does not prevent any of them from living brightly and happily. It does not hurt you!
Is hypothyroidism always incurable?
We already know that “hypothyroidism” is a syndrome that can occur 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, the outcome of which does not always form hypothyroidism. These include postpartum thyroiditis, subacute thyroiditis (de Kerven) and some others.
In any case, the prognosis will guide you to the prognosis of the disease.