- Causes of acquired hypothyroidism
- What happens in the body?
- risk groups
- The main symptoms of acquired hypothyroidism
- Diagnosis of acquired hypothyroidism
- Treatment of acquired hypothyroidism
- The main causes of congenital hypothyroidism
- What happens in the body with congenital hypothyroidism?
- Symptoms of congenital hypothyroidism
- Diagnosis and treatment of congenital hypothyroidism
Hypothyroidism is a condition of the body characterized by a deficiency of thyroid hormones. Hormonal insufficiency may be primary due to thyroid disease or secondary, when there are no pathological changes in the gland itself, and the lack of hormones due to the action of other factors. It is believed that primary hypothyroidism occurs in almost 99% of cases.
There are hypothyroidism:
Congenital hypothyroidism is caused by hypoplasia or the absence of the thyroid gland, when thyroid hormones are either completely absent or their production is insignificant. In some situations, there is a genetic defect in enzymes involved in the formation of these hormones, as a result of which iodine uptake by the thyroid cells is impaired, another type of genetic change is a violation of the structure of the protein portion of thyroglobulin. In these cases, the thyroid gland synthesizes defective molecules of active thyroid hormones that are not perceived by the cells of the body.
Acquired hypothyroidism develops as a result of thyroid diseases that have arisen in the course of a person’s life. For example:
- after removal of a portion of the thyroid gland by surgery;
- when its tissue is destroyed by ionizing radiation (treatment with radioactive iodine preparations, irradiation of the neck organs, etc.);
- after taking certain medications: lithium preparations, beta-blockers, adrenal cortex hormones, vitamin A in large doses;
- with iodine deficiency in food and the development of some forms of endemic goiter.
According to the mechanism of development distinguish hypothyroidism:
- primary (thyrogenic),
- secondary (pituitary),
- tertiary (hypothalamic),
Primary hypothyroidism is when pathological changes initially develop in the thyroid gland itself, for example, its congenital hypoplasia or hypothyroidism resulting from the removal of goiter.
Secondary hypothyroidism is when everything is fine with the thyroid gland itself, however, thyrotropin deficiency occurs, which is produced in the pituitary gland and normally should trigger the synthesis of thyroid hormones in the thyroid gland itself. The causes of the development of secondary hypothyroidism can be hemorrhage in the pituitary gland, tumors or inflammatory processes in a given area of the brain, oxygen starvation of cells due to blood loss. Also, the production of thyrotropin in the pituitary gland can be inhibited by certain drugs, for example: apomorphine, reserpine, anti-Parkinsonian drugs.
Tertiary hypothyroidism - in this case there is a deficiency of thyroliberin, which is produced in the hypothalamus and triggers the production of thyrotropin in the pituitary gland, which directly controls the activity of the thyroid gland.
Peripheral hypothyroidism is characterized by a decrease in the sensitivity of body tissues and cell receptors to the action of thyroid hormones. The reasons for the development of this state are not well understood.
Acquired hypothyroidism in varying degrees, is most common among diseases of the thyroid gland. Most often it develops as a result of chronic autoimmune thyroiditis or results from the removal of a large amount of thyroid tissue during surgery.
Causes of Acquired Hypothyroidism
In most cases, persistent hypothyroidism develops due to chronic autoimmune thyroiditis, removal of a part of the thyroid gland or treatment with radioactive iodine.
Transient (temporary, transient) hypothyroidism is observed when taking thyreostatic drugs or large doses of iodine. Acquired hypothyroidism can be observed in newborns and pregnant women due to severe iodine deficiency, when this element practically does not come with food (these conditions are usually called transient neonatal hyperthyrotropinemia and gestational hypiroxinemia).
Acquired secondary hypothyroidism is a consequence of the destructive processes observed in the pituitary microadenomas or suprasellar structures, as well as after surgical interventions in this area.
What happens in the body?
A deficiency of thyroid hormones affects the functioning of almost all organs and body systems:
- oxygen consumption by cells decreases (cellular respiration actually suffers),
- reduced energy production
- There is a shortage of a number of enzymes, the production of which depends on the energy resource of the cell,
- Myxedema appears - mucinous edema (hyaluronic acid accumulates in the connective tissue, which “pulls” the liquid on itself),
- violated almost all types of metabolism.
The following categories of the population are at risk of developing hypothyroidism:
- in the presence of thyroid disease, including thyroiditis;
- suffering from pernicious anemia, diabetes;
- use some drugs (lithium salts, amiodarone, preparations of radioactive iodine, etc.);
- If there are changes in the biochemical blood tests: a high atherogenic index, hyponatremia, increased CPK (creatine phosphokinase) and LDH (lactate dehydrogenase), as well as an increase in prolactin.
The main symptoms of acquired hypothyroidism
Diagnosis of acquired hypothyroidism in some cases may be difficult, since some symptoms of hypothyroidism can be observed in 15% of adults suffering from mental or somatic diseases, but with a normally functioning thyroid gland.
Classic Primary Hypothyroidism
Classical hypothyroidism is characterized by the following symptoms and syndromes:
1. Exchange hypothermic syndrome : yellowness of the skin, obesity, early development of atherosclerosis, high blood cholesterol, chilliness, decrease in body temperature.
2. Connective tissue - myxedematous edema:
- swelling of the face, including in the periorbital area,
- the mucous membranes of the auditory tube and nose (hearing loss, difficulty breathing through the nose),
- tongue (visible teeth),
- vocal cords (hoarseness),
- meninges, pleura, pericardium (polyserositis).
3. Nervous system:
- memory loss
- development of secondary pituitary adenoma,
- muscle tension and slow relaxation,
4. Cardiovascular system:
- myxedema heart (slow pulse, increase in heart size),
- development of heart failure.
5. Digestive organs:
- enlarged liver
- propensity to develop gallstones,
- development of biliary dyskinesia.
6. Circulatory system:
- Anemia of various types (megaloblastic, iron deficient, hypo-or normochromic).
7. Reproductive system:
- violation of menstrual function until its complete disappearance,
- galactorrhea (milk secretion from the mammary glands).
8. Leather and its derivatives:
- fragility and dullness of hair,
- their increased loss and slow growth,
- dry skin
- thin, exfoliated and scribbled nails.
If hypothyroidism remains without appropriate treatment for a long time, then myxedema (hypothyroid) coma may develop. Its main manifestations are:
- hypothermia (up to 30 0 С),
- reduced respiration and heart rate,
- intestinal obstruction due to a sharp decrease in peristalsis,
- change of consciousness (stupor, coma).
Without timely treatment, mortality is up to 80%.
Features of the course of secondary acquired hypothyroidism
Diagnosis of Acquired Hypothyroidism
In the diagnosis of hypothyroidism can distinguish several main points:
1. Primary and re-examination of a doctor who identifies complaints and symptoms characteristic of hypothyroidism, and also analyzes the results of the examination and carries out the differential diagnosis of various diseases that have a similar manifestation.
2. Laboratory and instrumental examination:
- complete blood count (decrease in hemoglobin, nature of anemia),
- biochemical blood tests (high cholesterol, hypoproteinemia, etc.),
- study of the level of thyroid hormones (thyroxine, triiodothyronine), as well as pituitary thyrotropin under normal conditions and with the help of a thyroliberine test, when 500 μg of thyroliberin is administered intravenously,
- Thyroid ultrasound,
- determination of bone age (for children).
Treatment of Acquired Hypothyroidism
Hypothyroidism is treated by an endocrinologist who, if necessary, can attract other specialists. Self-medication of hypothyroidism is unacceptable due to possible deterioration of health.
If possible, it is necessary to eliminate the cause of the development of hypothyroidism, for example:
- repeal drugs that cause a decrease in thyroid hormone activity,
- treat thyroiditis,
- normalize iodine intake in food.
The very deficiency of thyroid hormones is filled by means of replacement therapy with levothyroxine and similar drugs. Life-long thyroid hormones are prescribed in the event of the development of hypothyroidism due to its removal, irradiation, or if it is impossible to restore its function for other reasons. Symptomatic treatment is also conducted depending on the prevalence of certain disorders (for example, prescription of drugs that reduce cholesterol).
Treatment of hypothyroid coma is often carried out in conditions of resuscitation and includes intensive measures aimed at correcting and ensuring vital functions and eliminating the deficiency of thyroid hormones.
The prognosis for the daily intake of thyroid hormones is favorable: patients lead a normal life. In cases where there is no treatment for hypothyroidism, the clinical manifestations may worsen until the onset of mexedematous coma.
The main causes of congenital hypothyroidism
The main causes of congenital hypothyroidism are:
- Absence or hypoplasia of the thyroid tissue (its agenesis, hypoplasia, dystopia).
- The effect on the child's thyroid gland of maternal antibodies that circulate in the blood of women suffering from autoimmune thyroiditis.
- Hereditary defects in T4 synthesis (defects in thyroid peroxidase, thyroglobulin, etc.).
- Hypothalamic-pituitary congenital hypothyroidism.
What happens in the body with congenital hypothyroidism?
While the fetus is in the maternal organism, the absence of its own thyroid hormones is compensated by the action of the maternal ones, however, immediately after birth, their level in the baby’s body begins to decrease sharply.
If during the neonatal period the deficiency of these hormones is not compensated, then irreversible changes occur in the brain and other parts of the nervous system, leading to dementia of varying degrees. If treatment with thyroid hormones is initiated during the first week of a child’s life, then neuropsychological development practically does not suffer.
Symptoms of congenital hypothyroidism
Symptoms of congenital hypothyroidism do not contribute to the early diagnosis of the disease and are fully manifested from the 3rd month of life. However, an experienced specialist can detect the following signs of hypothyroidism at an early stage:
- late terms of birth (from 40 weeks and more),
- prolonged jaundice (more than 7 days),
- high weight (at birth),
- an increase in the tongue (half-open mouth with a "spread" tongue) and thyroid gland,
- late discharge of meconium,
- deep voice when crying crying
- puffiness in the form of pillows-seals on the back surfaces of the feet, hands, as well as in the subclavian fossae,
- swelling of the face, lips, eyelids,
- enlarged rear fontanelle,
- umbilical hernia.
At 3-4 months without adequate treatment appear:
- poor weight gain,
- hypothermia (hands and feet cold to the touch),
- loss of appetite
- dry skin
- increased fragility and dryness of hair,
- difficulty swallowing
- muscle hypotonia.
After 5–6 months of life:
- signs of disproportionate growth (late closing of fontanelles, wide and sunken nose),
- delayed physical and psychomotor development.
Diagnosis and treatment of congenital hypothyroidism
Since the clinical picture can be erased at first, a neonatal screening is performed to diagnose congenital hypothyroidism. To do this, the level of TSH is determined in dried blood stains on filter paper taken from the baby’s heel on the 4–5th day of his life (preterm screening is performed from day 7 to day 14). An earlier diagnosis (on the 2nd, 3rd day) leads to false positive results.
Substitution therapy is prescribed depending on the results of the TSH level:
- up to 20 mCU / ml - the norm, no therapeutic measures are carried out;
- 20-50 uU / ml is a doubtful result that requires re-conducting a study, which includes the determination of TSH and T4: L-thyroxin is prescribed at T4 less than 120 nmol / l, and TSH more than 20 μE / ml .;
- 50–100 µU / ml - suspicion of hypothyroidism, treatment is prescribed immediately and can be canceled with a positive result upon re-examination;
- more than 100 mCU / ml - high probability of hypothyroidism, replacement therapy is prescribed even in the absence of clinical manifestations of the disease.
After 2 weeks and 1–1.5 months from the start of therapy, a control study of TSH and T4 is conducted, and at the age of 1 year, the diagnosis is clarified by canceling L-thyroxine for 2 weeks and then measuring the TSH and T4 levels. If, as a result, normal results are obtained, treatment is stopped.
With timely initiated treatment (in the first or second week of life), the prognosis is favorable, but without appropriate replacement therapy, signs of a delay in neuropsychic development up to severe forms of dementia progress.