Autoimmune thyroiditis. Autoimmune pathology in integrative medicine Treatment of autoimmune thyroiditis

This article was written for doctors of various specialties.

Official medicine considers autoimmune diseases incurable. The theory of the occurrence of autoimmune aggression is complex and confusing, so treatment tactics provide only symptomatic procedures that do not affect the underlying causes of the disease. Cause-and-effect relationships cannot be put into a coherent concept.

The general theory of autoimmunity is a dysregulation of the immune system and the appearance of “errors” in it, leading to auto-aggression.

An interesting fact that we often identify using the ATM diagnostic complex (K. Schimmel’s method) is the presence of general immunodeficiency in autoimmune diseases (psoriasis, UC, lupus erythematosus, rheumatoid arthritis, autoimmune thyroiditis). It is difficult to imagine that in the absence of an immune response to invasive pathogens (viruses, fungi, bacteria, worms) in immunodeficiency states, immune aggression against one’s own antigens develops. If the number of autoantigens in the body is too large and constantly reproduced, the immune system spends its biological potential on their destruction, which leads to general immunodeficiency. The immune system works on this problem, ignoring genetically alien life forms that have entered the body.

When exposed to a pathological factor leading to cell death, the body sends a command to increase proliferation, which inevitably leads to the appearance of a large number of young cells designed to compensate for the loss from dead cells. Pathology occurs at a time when cells do not have time to differentiate into functionally active ones for various reasons (lack of vitamins, microelements, impaired breathing and nutrition due to insufficient capillary circulation, etc. .) This leads to embryonication of organs, which induces a system of organ-specific autosystems.

In other words, the body, with the help of autoantibodies, gets rid of undifferentiated cells that pose a threat to the entire body.

The appearance of autoantigens and autoantibodies is associated with the process of progressive tissue embryonication under conditions of increased pathological proliferation. These conditions are otherwise called precancerous with varying degrees of severity of pathology.

It is clear that this process is secondary, since the primary cause is the influence of a pathological factor leading to cell death.

For example, with psoriasis, one of the causes should be considered stress, leading to spasm of the arteries in the skin. This leads to cell death as a result of cessation of blood circulation, increased proliferation (200 times higher than normal), embryonication and the subsequent production of specific antibodies designed to eliminate this pathology.

In autoimmune thyroiditis, the root cause is a “weak liver”, in which the antitoxic and metabolic function is significantly reduced. Such a liver is not able to neutralize spent thyroid hormones (thyroxine, triiodothyronine), and their amount accumulates in the blood. Autoimmune aggression in this case is aimed at the hormones themselves, their precursors (thyropobulin), and thyroid cells in order to reduce the concentration of thyroid hormones in the body. Another option for autoimmune thyroiditis may be irradiation, leading to changes in the DNA of cells, viral or bacterial infection, accumulation of “waste and toxins” in the thyroid cells, etc.

In connection with the above, it becomes clear that the accumulation of embryonic young cells in tissues enhances their “foreignness”, while simultaneously provoking autoimmune aggression. This “foreignness” is characterized by the appearance in the tissue of another antigenic structure, perceived by the immune system as a target for an autoimmune attack.

1. The causes of autoimmune processes can be bacteria, worms, viruses, injuries, tissue metabolism disorders, radiation, and the administration of certain medications and vaccines. That is, any reasons the impact of which leads to the formation of a foreign antigenic structure (in other words, a foreign protein)

G. Reckeweg defined autoimmune diseases in the IV cellular phase of “slagging of the body.” In these phases, when toxins and wastes penetrate into cells, cellular structures are disrupted and an antigenic structure is formed (see methods - homotoxicology). Since the “biological barrier” (after which complete tissue restoration is impossible) passes between stages III and IV of disease states, the treatment of autoimmune diseases seems to be a rather long and complex process.

Unfortunately, there are catastrophically few doctors capable of assessing the condition of the body on the basis of objective standard tests. A system for training doctors in the principles of integrative medicine is needed. Only such specialists are able to determine the correct tactics for treating autoimmune diseases, taking into account the entire chain of pathological processes. Being within the strict framework of “standard protocols”, official medicine limits the ability of specialists to carry out non-standard treatment of autoimmune diseases that require knowledge from a variety of fields: immunology, pathophysiology, virology, hematology, pharmacology, therapy, endocrinology.

Step-by-step treatment plan for autoimmune diseases (author’s method)

Cleansing the intestines, liver, blood, blood vessels (see section “Methods”).

Oxidant therapy (ozone therapy, iodine therapy, “dead” water, etc.).

Antioxidant therapy (freshly squeezed juices, glutathione, vitamin E, C, A, D).

The use of unsaturated fatty acids Omega 3-6-9 to restore cell membranes.

The use of B vitamins.

Application of microelements.

External and internal use of kaolin clay (silicon).

Detoxification (rheosorbilate, reamberin, heptral, thiotriazoline, sodium thiosulfate).

Metabolic restoration of the liver (Berlition, Essentiale, Karsil, Liv 52).

Restoring blood pH (sodium bicarbonate).

Ion detox + oxygen enrichment (hardware treatment, ultraviolet irradiation, skin massage with vitamins A, D, E and clay).

Points 1-12 are carried out within 14 days simultaneously

Restoration of blood circulation (actovegin, mexidol, l-lysine, hardware treatment of STSEK, catholyte).

Program for restoring psycho-emotional balance and anti-stress therapy.

Points 13-14 are carried out simultaneously for 7 days.

Reduced level of immune reactions (solu-medrol, medrol, methotrexate, thymodepressin).

Use of the adrenergic blocker doxazosin (Cardura).

Continuation of antifungal therapy (intraconazole).

Points 15-16-17 are carried out simultaneously for 14-28 days (until all signs of the disease disappear).

Restoration of immunity (thymalin, immunofan, cycloferon, polyoxidonium, lykopid, liasthene).

Restoring adrenal function (synacthen-depot, pantethine, pantothenic acid, cranberry, vitamin C, licorice, viburnum, raw eggs, etc.).

Autohemotherapy according to Filatov’s method.

Introduction of foreign protein (Kapustin method, pyrogenal).

Taking transfer factor.

Taking doxazosin.

Points 18-23 are carried out simultaneously for 30-40 days.

Carrying out such treatment guarantees a complete cure for autoimmune diseases.

The “mistake” of the immune system and the breaking of the “vicious” autoimmune circle can only be accomplished in such a complex way, implying:

body cleansing

restoration of blood circulation

restoration of metabolic liver function

restoration of metabolism

saturation of the body with silicon

anti-stress treatment (hypnosis)

immunocorrection: decrease in the level of immunity, increase in the level of immunity, introduction of a foreign protein, autohemotherapy according to Filatov, administration of a transfactor

restoration of adrenal function

Failure to complete any step of this scheme again forms a “vicious circle”, which can lead to relapse of the disease.

The effectiveness of treatment of autoimmune diseases increases significantly if patients follow a rich vegetarian diet (nuts, legumes, fruits, vegetables) with plenty of freshly squeezed juices (2 liters per day) during the entire course of treatment. After the course of treatment, you can switch to separate meals.

During and after the course of treatment, drink at least 2 liters of water. per day.

Immunomodulator

Active ingredient

Glucosaminylmuramyl dipeptide (GMDP)

Release form, composition and packaging

Pills white, round, flat-cylindrical, with a chamfer and a notch.

Excipients: lactose monohydrate - 184.7 mg, sugar (sucrose) - 12.5 mg, potato starch - 40 mg, methylcellulose - 0.3 mg, calcium stearate - 2.5 mg.

10 pcs. - contour cellular packaging (1) - cardboard packs.

Pharmacological action

Pharmacodynamics

The active ingredient of Lykopid tablets is glucosaminylmuramyl dipeptide (GMDP) - a synthetic analogue of the structural fragment of the membrane (peptidoglycan) of bacterial cells. GMDP is an activator of innate and acquired immunity, strengthens the body’s defense against viral, bacterial and fungal infections; has an adjuvant effect in the development of immunological reactions.

The biological activity of the drug is realized through the binding of GMDP to the intracellular receptor protein NOD2, localized in the cytoplasm of phagocytes (neutrophils, macrophages, dendritic cells). The drug stimulates the functional (bactericidal, cytotoxic) activity of phagocytes, enhances their presentation of antigens, the proliferation of T- and B-lymphocytes, increases the synthesis of specific antibodies, and helps normalize the balance of Th1/Th2 lymphocytes towards the predominance of Th1. The pharmacological action is carried out by enhancing the production of key interleukins (interleukin-1, interleukin-6, interleukin-12), TNF alpha, interferon gamma, colony-stimulating factors. The drug increases the activity of natural killer cells.

Lykopid has low toxicity (LD 50 exceeds the therapeutic dose by 49,000 times or more). In the experiment, when administered orally in doses 100 times higher than the therapeutic dose, the drug does not have a toxic effect on the central nervous system and cardiovascular system, and does not cause pathological changes in internal organs.

Lykopid does not have embryotoxic or teratogenic effects and does not cause chromosomal or gene mutations.

Experimental studies conducted on animals provided data on the antitumor activity of the drug Lykopid (GMDP).

Pharmacokinetics

The bioavailability of the drug when taken orally is 7-13%. The degree of binding to blood is weak. The time to reach Cmax is 1.5 hours after administration. T 1/2 - 4.29 hours. Does not form active metabolites, is excreted mainly through the kidneys unchanged.

Indications

The drug is used in adults in the complex treatment of diseases accompanied by secondary immunodeficiency states:

• acute and chronic purulent-inflammatory and soft tissues, including purulent-septic postoperative complications;
• sexually transmitted infections (human papillomavirus infection, chronic trichomoniasis);
• herpetic infection (including ophthalmoherpes);
• psoriasis (including);
• pulmonary tuberculosis.

Contraindications

• hypersensitivity to glucosaminylmuramyl dipeptide and other components of the drug;
• pregnancy;
• lactation period (breastfeeding);
• children under 18 years of age;
• autoimmune in the acute phase;
• conditions accompanied by febrile temperature (>38°C) at the time of taking the drug;
• rare congenital metabolic disorders (alactasia, galactosemia, lactase deficiency, sucrase/isomaltase deficiency, fructose intolerance, glucose-galactose malabsorption);
• use in autoimmune diseases is not recommended due to the lack of clinical data.

Lykopid 10 mg with caution used in elderly people, strictly under the supervision of a physician.

Dosage

Likopid is taken orally on an empty stomach, 30 minutes before meals.

If you miss a dose, if passed no more than 12 hours from the scheduled time, the patient may take the missed dose; in case it has passed more than 12 hours from the scheduled time of administration, you must take only the next dose according to the schedule and not take the missed one.

Purulent-inflammatory diseases of the skin and soft tissues, acute and chronic, severe, including purulent-septic postoperative complications:

Herpetic infection (recurrent course, severe forms): 10 mg 1 time/day for 6 days.

For ophthalmoherpes: 10 mg 2 times/day for 3 days. After a break of 3 days, the course of treatment is repeated.

Sexually transmitted infections (human papillomavirus infection, chronic trichomoniasis): 10 mg 1 time/day for 10 days.

Psoriasis: 10–20 mg 1 time/day for 10 days and then five doses every other day, 10–20 mg 1 time/day.

For severe psoriasis and extensive damage (including psoriatic arthritis): 10 mg 2 times/day for 20 days.

Pulmonary tuberculosis: 10 mg 1 time/day for 10 days.

Side effects

Often (1–10%)- arthralgia (joint pain), myalgia (); at the beginning of treatment, there may be a short-term increase in body temperature to subfebrile values ​​(up to 37.9°C), which is not an indication for discontinuation of the drug. Most often, the side effects described above are observed when taking Lykopid tablets in high doses (20 mg).

Rarely (0.01-0.1%)- short-term increase in body temperature to febrile values ​​(>38.0°C). If body temperature rises >38.0°C, antipyretics can be taken, which does not reduce the pharmacological effects of Lykopid tablets.

Very rarely (<0.01%) - diarrhea.

If any of the side effects indicated in the instructions worsen or the patient notices any other side effects, the doctor should be informed.

Overdose

Cases of drug overdose are unknown.

Symptoms: Based on the pharmacological properties of the drug, in case of overdose, a rise in body temperature to subfebrile (up to 37.9 ° C) values ​​may be observed.

Treatment: If necessary, symptomatic therapy (antipyretic drugs) is carried out and sorbents are prescribed. A specific antidote is unknown.

Drug interactions

The drug increases the effectiveness of drugs, there is synergy with antiviral and antifungal drugs.

Antacids and sorbents significantly reduce the bioavailability of the drug.

GCS reduce the biological effect of the drug Lykopid.

Special instructions

At the beginning of taking the drug Likopid 10 mg, an exacerbation of the symptoms of chronic and latent diseases is possible, associated with the main pharmacological effects of the drug.

In elderly people, Likopid 10 mg is used with caution, strictly under the supervision of a physician. Elderly patients are recommended to start treatment with half doses (1/2 of the therapeutic dose), in the absence of side effects, increasing the dose of the drug to the required therapeutic dose.

The decision to prescribe Licopid tablets 10 mg to patients with a combination of diagnoses of psoriasis and gout should be made by a doctor when assessing the risk/benefit ratio, due to the potential risk of exacerbation of gouty arthritis and joint swelling. If the doctor decides to prescribe the drug Licopid tablets 10 mg in a situation where the patient has a combination of diagnoses of psoriasis and gout, treatment should begin with low doses, in the absence of side effects, increasing the dose to a therapeutic one.

Each Likopid 10 mg tablet contains sucrose in the amount of 0.001 XE (bread units), which should be taken into account in patients with diabetes.

Each Likopid 10 mg tablet contains 0.184 grams of lactose, which should be taken into account by patients suffering from hypolactasia (lactose intolerance, in which the body experiences a decrease in the level of lactase, the enzyme necessary to digest lactose).

Impact on the ability to drive vehicles and operate machinery

Does not affect the ability to drive vehicles and complex machinery.

Pregnancy and lactation

Taking Likopid 10 mg is contraindicated for women during pregnancy and breastfeeding.

Conditions for dispensing from pharmacies

The drug is available with a prescription.

Storage conditions and periods

The drug should be stored in a dry place, protected from light, out of reach of children, at a temperature not exceeding 25°C. Shelf life - 5 years. Do not use after expiration date.

Licopid

ATX:

L03A Immunostimulants

Pharmacological group

Other immunomodulators

Nosological classification (ICD-10)

- A15-A19 Tuberculosis
- A41 Other septicemia
- A60 Anogenital herpetic viral infection
- B00 Infections caused by herpes simplex virus
- B00.5 Herpetic eye disease
- B19 Viral hepatitis, unspecified
- B34.4 Papovavirus infection, unspecified
- D84.9 Immunodeficiency, unspecified
- J18 Pneumonia without specifying the pathogen
- J31 Chronic rhinitis, nasopharyngitis and pharyngitis
- J37 Chronic laryngitis and laryngotracheitis
- J40 Bronchitis, not specified as acute or chronic
- J42 Chronic bronchitis, unspecified
- K73 Chronic hepatitis, not elsewhere classified
- L08.9 Local infection of skin and subcutaneous tissue, unspecified
- L40 Psoriasis
- Z100* CLASS XXII Surgical practice

Composition and release form

Tablets 1 tablet.
Glucosaminylmuramyl dipeptide (GMDP):
- 1 mg
- 10 mg
excipients: lactose; sucrose; potato starch; methylcellulose; calcium stearate
in a blister pack 10 pcs.; in a cardboard pack 1 or 2 packages.

Description of the dosage form

Round flat-cylindrical tablets of white color with a chamfer. Tablets with a dosage of 10 mg have a risk.

Pharmacological action

Pharmacological action - immunomodulatory.

Pharmacokinetics

The bioavailability of the drug when taken orally is 7-13%. The degree of binding to blood albumin is weak. Does not form active metabolites. Tmax - 1.5 hours, T1/2 - 4.29 hours. Excreted from the body unchanged, mainly through the kidneys.

Pharmacodynamics

The biological activity of the drug is due to the presence of specific receptors (NOD-2) for glucosaminylmuramyl dipeptide (GMDP), localized in the endoplasm of phagocytes and T-lymphocytes. The drug stimulates the functional (bactericidal, cytotoxic) activity of phagocytes (neutrophils, macrophages), enhances the proliferation of T- and B-lymphocytes, and increases the synthesis of specific antibodies. The pharmacological action is carried out by enhancing the production of interleukins (IL-1, IL-6, IL-12), tumor necrosis factor-alpha, interferon gamma, and colony-stimulating factors. The drug increases the activity of natural killer cells.

Indications for the drug Likopid

Complex therapy of conditions accompanied by secondary immunodeficiencies in adults and children.

Adults (1 and 10 mg tablets):
chronic lung infections;
acute and chronic purulent-inflammatory diseases of the skin and soft tissues, including purulent-septic postoperative complications;
herpetic infection (including ophthalmoherpes);
papillomavirus infection;
chronic viral hepatitis B and C;
psoriasis (including arthropathic form);
pulmonary tuberculosis.

Children (1 mg tablets only):
acute and chronic purulent-inflammatory diseases of the skin and soft tissues;
chronic infection of the upper and lower respiratory tract, both in the acute stage and in remission;
herpetic infections of any localization;
chronic viral hepatitis B and C.

Contraindications

individual hypersensitivity to the drug;
pregnancy;
lactation;
autoimmune thyroiditis in the acute phase;
conditions in diseases accompanied by high fever or hyperthermia (>38 °C).

Use during pregnancy and breastfeeding

Contraindicated during pregnancy. Breastfeeding should be stopped during treatment.

Side effects of the drug Likopid

At the beginning of treatment, a short-term increase in body temperature (not higher than 37.9 °C) may be observed, which is not an indication for discontinuation of the drug. No other side effects were identified during treatment with Likopid.

Interaction

The drug increases the effectiveness of semisynthetic penicillins, fluoroquinolones, cephalosporins, and polyene derivatives. There is synergy with antiviral and antifungal drugs. Antacids and sorbents significantly reduce the bioavailability of the drug. GCS reduce the biological effect of Lykopid. It is not advisable to combine Licopid with sulfonamide drugs and tetracyclines.

Overdose

Cases of overdose are unknown.

Directions for use and doses

Adults: table. 1 mg sublingually and tab. 10 mg orally, on an empty stomach, 30 minutes before meals.
To prevent postoperative complications, Likopid is prescribed 1 mg sublingually once a day for 10 days.
For the treatment of purulent-septic lesions of the skin and soft tissues of moderate severity, incl. and postoperative - 2 mg sublingually 2-3 times a day for 10 days.
In the treatment of severe purulent-septic processes - 10 mg orally once a day for 10 days.
For chronic lung infections - 1-2 mg sublingually once a day for 10 days.
For pulmonary tuberculosis - 10 mg 1 time per day under the tongue for 10 days.
For mild herpes infection - 2 mg 1-2 times a day sublingually for 6 days; for severe forms - 10 mg 1-2 times a day sublingually for 6 days.
For ophthalmic herpes - 10 mg orally 2 times a day for 3 days. After a 3-day break, the course of treatment is repeated.
For lesions of the cervix of the uterus by the human papillomavirus - 10 mg orally 1 time per day for 10 days.
For psoriasis - 10-20 mg orally 1-2 times a day for 10 days and then 10-20 mg every other day for the next 10 days. For severe forms and extensive damage (including arthropathic form) - 10 mg 2 times a day for 20 days.

For children aged 1-16 years, Likopid is available only in the form of 1 mg tablets.
For newborns with a protracted course of infectious diseases (pneumonia, bronchitis, enterocolitis, sepsis, postoperative complications, etc.) - 0.5 mg orally 2 times a day for 7-10 days.
In the treatment of chronic respiratory tract infections and purulent skin infections - 1 mg orally 1 time per day for 10 days.
When treating herpes infection (regardless of location) - 1 mg 3 times a day orally for 10 days.
In the treatment of chronic viral hepatitis B and C - 1 mg orally 3 times a day for 20 days.

Special instructions

Does not affect the ability to drive a car or operate complex machinery.

Shelf life of the drug Likopid

5 years.

Storage conditions for the drug Likopid

List B: In a dry place, protected from light, at a temperature not exceeding 25 °C.

angela 2018-11-13 22:15:08

Good afternoon I am being treated by an infectious disease specialist for herpes type 6. After taking acyclovir 0.2 mg 5t per day for 7 days and licopid 10 mg. A herpes rash broke out on my body once a day for 10 days. Is this a normal situation?

Good afternoon. Did the doctor confirm your diagnosis? Is the rash really of herpetic etiology? Contact a dermatologist to clarify the diagnosis. This situation is casuistic.

Alena 2018-08-18 03:25:12

After I took the course of Lykopid 10, the muscles of my legs (calves) began to ache, just when I went to bed the feeling was unbearable, when will it go away

Menshchikova Galina Vladimirovna Dermatovenerologist, dermato-oncologist. Candidate of Medical Sciences. Doctor of the first category. More than 15 years of experience answers:

Good afternoon. The instructions do not contain the side effect you mentioned.

Sergey 2018-07-25 23:20:46

Can it be used for psoriasis and HIV infection?

For these pathologies, only after agreement with the attending physician, as they can affect the course of the underlying somatic disease.

Natalia 2018-02-07 17:39:04

My daughter has frequent colds, sore throats and tonsillitis. The doctor prescribed Lycopid 10 mg, and she is 16 years old, and the instructions say that this dose is from 18 years old. Tell me, is it dangerous for her to drink 10 mg?

Bagaeva Madina Dermatovenerologist, member of the Moscow Society of Dermatovenerologists and Cosmetologists named after. A.I. Pospelova answers:

The use of this drug at an earlier age is widely used.

Elena 2017-12-06 17:38:29

Is it possible to take Likopid and Anaferon for children at the same time?

Bagaeva Madina Dermatovenerologist, member of the Moscow Society of Dermatovenerologists and Cosmetologists named after. A.I. Pospelova answers:

Hello! Can.

Lyudmila 2017-11-19 09:21:55

Hello. My daughter (14 years old) had a temperature of 36.8 to 37.4 for two weeks, and was prescribed Lycopid 10 mg. Could there be a side effect in the form of knee pain?

Primarily, an autoimmune disease develops when the immune system, which protects the body from disease, decides to attack healthy cells because it mistakes them as foreign. Autoimmunity is most easily understood as a "hyperimmune" condition. Depending on the type of autoimmune disease, it can affect one or many different types of body tissue. Simply suppressing the immune system is also not enough to reverse all the inflammation, degeneration, and loss of tissue structure and function that occurs during the autoimmune process.

“Healthy eating,” with an emphasis on alternating a cleansing and detoxifying diet with a reparative diet, is a natural way to curb immune system overreaction. A variety of metabolic, functional laboratory tests are recommended to identify "immune stimulants" and then determine diet, supplementation and lifestyle program to manage the problem. Initially, most patients choose a natural and medical approach. However, over time, as your body recovers, you may become less rigid in your adherence to these strategies in treating and managing your disease.

Causes of autoimmune diseases

Currently, scientists have not paid enough attention to identifying the causes or risk factors that contribute to the development of autoimmune conditions such as multiple sclerosis, lupus, rheumatoid arthritis, scleroderma, and even some forms of diabetes. Constant stress, toxins, trauma and poor nutrition, plus genetic predisposition, contribute to the emergence of aggression of the immune system against the tissues of its own body (sensitive tissues of the body are destroyed).

Autoimmune disease and thyroid function

Along with the obesity epidemic, hypothyroidism often occurs due to low thyroid function, causing a person to gain weight, and the two conditions are often related. When the thyroid gland or its hormones become the target of an immune attack, the result can be decreased thyroid function, a condition that can be difficult to diagnose in the early stages. This is why it is extremely important for nutritionists and healthcare professionals to learn to recognize symptoms and manifestations in the early stages. Hypothyroidism, if left untreated, can contribute to unwanted weight gain and a variety of debilitating symptoms that can lead to serious health problems.

What is the thyroid gland and how does it work?

The thyroid gland is a small butterfly-shaped gland located at the base of the throat, under the Adam's apple, responsible for producing several hormones that affect the energy production of almost every cell, tissue and organ in the body. It controls metabolism, regulates body temperature, and affects body weight, muscle strength, energy levels and fertility.

The primary hormones produced by the thyroid gland (T4 and T3) are formed from the amino acid tyrosine and iodine. Hormone production depends on the hypothalamus, which monitors the body's need for more thyroid hormones and signals the pituitary gland to release these hormones. Thyroid-stimulating hormone, released from the pituitary gland, controls and influences the production of the above hormones. Thyroid-stimulating hormone levels rise and fall in response to fluctuations in these hormones in the blood.

Hypothyroidism can occur when dysfunction occurs in any of these glands, resulting in a lack of thyroid hormone production. It can also be the result of other problems, such as: ineffective conversion of the T4 prehormone to T3 hormone or insensitivity of hormone receptors in cells. An underactive thyroid gland contributes to a myriad of physiological effects throughout the body.

Autoimmune thyroiditis

Autoimmune thyroiditis is the most commonly diagnosed form of hypothyroidism in developed countries, with symptoms affecting approximately 2% of the population. What makes this disease more insidious is that a significant number of patients diagnosed with autoimmune thyroiditis do not have any symptoms. Another small percentage of men and women suffer from a subclinical form of this disease, i.e. their symptoms are practically invisible, and the disease is extremely difficult to detect using clinical tests.

Who is at risk for developing autoimmune thyroiditis?

Autoimmune thyroiditis can appear at any age, even in young children, and can occur in both sexes. However, this disease is most common among women, usually between the ages of 30 and 50. At age 60, scientists estimate that 20% of women have hypothyroidism. According to various estimates, women get sick 10 to 50 times more often than men. This is believed to be because in women, the system that regulates immunity also regulates the reproductive cycle.

What causes autoimmune thyroiditis?

Research shows that the combination of genetic predisposition and environmental pollution can become a significant risk factor for the development of autoimmune thyroiditis. Both autoimmune thyroiditis and Basedow's disease, being in families with a history of autoimmune diseases increases the risk of developing them. In addition, there are many environmental factors that can trigger this disease. Experts believe that it is likely that many factors, rather than just one, contribute to the development of hypothyroidism.

Toxins are of particular concern, especially those created from petrochemicals such as plastics (found in the water bottles we drink), pesticides, fertilizers, dioxin, body care products, and contaminants found in the air and water supplies. water - contain substances that mimic the body's estrogens. These xenoestrogens are potent endocrine disruptors and affect hormone balance. In particular, both dental fillings and fluorides in toothpastes and water are also endocrine disruptors. Mercury amalgams are especially dangerous (since they are very close to the throat) and can pose a serious threat to the thyroid gland.

Possible risk factors:

• Viral, bacterial infections or candidiasis.
• Chronic stress, enough to cause adrenal insufficiency, prevents the conversion of T4 to T3 and weakens the body's immune defenses.
• Pregnancy – causes changes in the hormonal and immune systems in sensitive women during pregnancy or after childbirth. (see Autoimmune thyroiditis and pregnancy)
• Trauma – surgery or accident.
• Nutrient deficiencies – particularly iodine and/or selenium deficiency.
• Bacteria in food – primarily Yersinia enterocolitica.

Symptoms

As stated above, autoimmune thyroiditis may be asymptomatic, but when symptoms appear, they usually begin with a gradual enlargement of the thyroid gland (goiter) and/or the gradual development of hypothyroidism, with the following symptoms:

• anemia (both iron deficiency and malignant)
• mental fog (forgetfulness, slow thinking, constant loss of energy)
• chest pain
• cold intolerance
• very cold hands and feet
• cold weather worsens symptoms
• dry, rough skin
• early graying of hair
• exhaustion after exercise
• frequent colds and flu (severe recovery from these diseases)
• headaches, including migraines
• high cholesterol, especially LDL
• infertility and miscarriages
• low basal temperature
• low libido
• muscle cramps and/or sensitivity
• hair loss
• restless legs syndrome
• severe premenstrual syndrome
• sleep disorders
• slow speech
• fatigue and muscle aches
• weak, brittle nails
• weight gain (obesity)

Other less common symptoms include high blood pressure and excess earwax. Low thyroid function can also have profound health consequences, including short stature, decreased concentration, and decreased IQ in children born to mothers with hypothyroidism and, quite possibly, an increased risk of developing cardiovascular disease.

What to eat if you have autoimmune thyroiditis

Once you are diagnosed with autoimmune thyroiditis, you need to balance your diet so that you help the body stop inflammation, balance hormonal levels, and help the thyroid gland produce hormones and convert them properly. When antibodies to thyroid cells are detected in the body, doctors prescribe taking the synthetic hormone T4 (levothyroxine), and in addition to drug therapy, nutritionists recommend starting to follow a certain therapeutic diet (see Diet for autoimmune thyroiditis of the thyroid gland).

Nutritional support for the thyroid gland is the shortest path to recovery. Eating a diet rich in high-quality proteins and fats, rich in fresh organic vegetables, fruits, nuts, seeds, certain types of whole grains and other nutritious foods is key. It is highly recommended to consume increased amounts of protein, as low thyroid function reduces the body's ability to utilize the proteins consumed. However, people whose metabolism is driven primarily by their adrenal glands, thyroid glands, or gonads require minor dietary changes despite a diagnosis of AIT. Also, in addition to three main meals, try to also have two to three snacks a day to maintain your energy levels throughout the day.

Squirrels

It is recommended to consume 40 grams of protein at each meal, especially animal proteins. Additionally, at least 20 grams of protein should be consumed with each snack, and eating cold-water fish is an exceptional choice because it contains omega-3 fatty acids. Whey protein is also a good source, but if you are vegan or vegetarian, good plant-based protein sources for you include:

• pace
• almond
• flax or hemp seeds

Healthy fats

Consume 4-6 tablespoons of “healthy fats” daily from avocados, nuts and seeds (especially pumpkin, chia and flax seeds), organic butter and ghee, olive oil and coconut milk, meats and vegetable oils. Coconut oil is very beneficial for the thyroid gland due to the lauric acid it contains, which calms the endocrine system. The medium chain fatty acids in coconut products are quickly absorbed and are an excellent source of energy for the body and are also beneficial for weight loss!

Antioxidant Rich Foods

People with autoimmune thyroiditis should also focus on eating plenty of foods rich in antioxidants, as these are essential to fight the damage caused by free radicals caused by inflammation. Emphasis should be placed on eating foods that contain large amounts of vitamin A, as they are especially beneficial due to the fact that people with autoimmune diseases often develop vitamin A deficiency. The reason for this is that their bodies often cannot efficiently convert beta -carotene to vitamin A. Other nutrients with antioxidant properties that people with autoimmune thyroiditis may be deficient in include vitamins C and E, iodine, zinc and selenium.

• Foods rich in vitamin A and beta-carotene: carrots, veal liver, fish oil, eggs, Greek yogurt, lightly cooked spinach, kale, collard greens, chard, zucchini, red peppers, apricots, cantaloupe and sweet potatoes.
• Vitamin C Rich Foods: red bell pepper, parsley, broccoli, citrus fruits, romaine lettuce.
• Vitamin E Rich Foods: Lightly sautéed mustard greens and Swiss chard, sunflower seeds, almonds, avocado.
• Foods rich in iodine: seaweed (especially very high quality dulse and kelp), seafood (mercury free and wild caught, not fish farmed).
• Zinc-rich foods: oysters, crab, beef (from natural-fed cows), sesame and pumpkin seeds.
• Selenium-rich foods: Brazil nuts, crimini mushrooms, cod, shrimp, halibut, snapper, oats, sunflower seeds, brown rice (read more about selenium here - Selenium: benefits and harm to the body).

Vegetables

Consume at least 900 grams of colorful vegetables, lightly cooked or raw, daily. Avoid eating vegetables from the cabbage family (collard, broccoli, cauliflower, turnips, etc.) raw, as these vegetables suppress thyroid function. However, you should not be too zealous - everything should be in moderation.

Carbohydrates

Fruits, grains and starchy vegetables should be consumed in moderation. Eat 500 grams of fruit per day, plus 100 to 200 grams once or twice daily of whole grains or starchy vegetables. Whole grains should be consumed in soaked or sprouted form - this will make them more digestible. This is very important for people with weakened digestion, as this condition is often seen in people with hypothyroidism.

Water

Drink at least 8 glasses of clean, filtered water daily. Avoid drinking water with chlorine and fluoride, as these elements are halogens and compete with iodine, which can lead to thyroid dysfunction. Also, remember: it is not wise to buy water in plastic bottles!

Functional foods and nutritional supplements

For people with a lot of health problems, taking nutritional supplements in the form of dietary powder is a great idea. You can take undenatured whey protein concentrate (or other protein powder for those who are dairy intolerant or vegan/vegetarian), kelp blends, cereal grasses, sea vegetables, fiber blends including flaxseed meal and apple pectin.

It is recommended to take anti-inflammatory extracts of organic fruits and vegetables, as well as other therapeutic ingredients such as aloe vera, detoxifying herbs, ionic minerals, probiotic bacteria (fermented milk, probiotics, sauerkraut, etc.) and digestive enzymes. This combination provides the body with easily digestible protein rich in sulfur-containing amino acids that help cleanse the body of toxins; healing chlorophyll and anti-inflammatory nutrients that help cool down an overheated immune system and cleanse the blood, thyroid and thyroid hormones of impurities.

You can use these foods as meal replacements by taking them as a smoothie or simply adding them to warm or cool liquids (water or tea). By mixing them with coconut water, you can further improve your health.

Best Herbal Dietary Supplements

Herbal dietary supplements are sold in many forms, mostly in the form of capsules and tablets, which are usually taken several times a day. This supplementation schedule is not something everyone can strictly follow. Powders can be taken once a day and are much more convenient. Since different products have different ingredients, it makes sense to use more than one and alternate them. Some of the best such products are It Works Greens™, Athletic Greens® and Garden of Life Perfect Food Green. They can be mixed with water or added to purees. Again, a supplement cannot replace a healthy diet, but a good herbal supplement can certainly make a significant difference to your diet.

What not to eat if you have autoimmune thyroiditis

Gluten is contraindicated in AIT

Unsaturated oils(including canola oil): These oils promote hypothyroidism because they are high in inflammation-promoting omega-6 fatty acids, and they tend to become rancid before they are bottled (or rancid in clear bottles).

GMO soybeans: Endocrine disruptor and considered somewhat toxic. Soy is considered a good source of protein, but GMO soy is not recommended for patients with autoimmune thyroiditis, even in small quantities, as such soy damages the hormonal system. The exception to this rule is fermented soy products (from natural soybeans) such as tempeh, natto and miso.

Spirulina and other algae: Although iodine deficiency may help cause hypothyroidism, American Thyroid Association warns that attempting to treat the disorder by consuming large doses of iodine, including the iodine found in sea vegetables such as spirulina, may worsen the symptoms of the condition. This is especially true if hypothyroidism is caused by autoimmune thyroiditis (Hashimoto's disease), an autoimmune disease in which the thyroid tissue is attacked by the body's own immune cells. Excessive amounts of iodine can stimulate these cells to become more active, worsening the autoimmune process.

What else is possible with autoimmune thyroiditis?

Since autoimmune thyroiditis can impair digestion, it is a good idea to support digestion with enzymes and probiotics, and supplement your diet with additional nutrients that the body is most often deficient in with this disease.

• Natural Multivitamins Directions: Take as directed on package.
• Antioxidant Supplements: Take as directed daily.
• Essential fatty acids: from fish or flax; 1000-2000 mg per day in two doses.
• B Vitamin Supplements: Take in capsule or tablet form, but preferably use nutritional yeast.
• Calcium: 250-300 mg (1-2 at bedtime). Calcium and iron should be taken two hours before or after you take thyroid medications so they don't interfere with their absorption. Read more about which form of calcium to choose and how they differ here - Which calcium is better - an overview of forms of calcium.
• Magnesium: 200 mg 2 times a day.
• Selenium: Supplementing the diet with selenium supplements (200 mcg) for 3 months has been found to significantly reduce thyroid peroxidase autoantibodies and significantly improve well-being and/or mood. Note: Selenomethionine is recommended. If you are pregnant, do not exceed 400 mcg per day!
• Iodine: If supplements do not contain 150-200 mcg of iodine, use kelp supplements at 2-3 grams per day. This has been shown to help lower antibody levels.
• Vitamin D3: In autoimmune diseases, the human body is deficient in vitamin D3, so supplementation with this vitamin is recommended to ensure optimal immune function and thyroid hormone production. Take 1,000 to 5,000 IU of vitamin D3 daily to get your body's levels of this vitamin up to the desired level. After this, you must adhere to maintenance dosages (as recommended by your doctor).
• L-tyrosine: Hormones are synthesized from tyrosine in the thyroid gland. Taking it makes it possible to improve the functions of the thyroid gland, adrenal glands and pituitary gland. L-tyrosine is recommended to be taken daily at 500 mg twice a day, but low levels of this amino acid rarely occur, so not all people with autoimmune thyroiditis and hypothyroidism need its supplements.
• Chromium: 200 mcg per day.
• Iron: If your blood test shows iron deficiency, take calcium and iron two hours before or after you take your thyroid medications, as the medication will otherwise interfere with their absorption.
• Zinc: If tests show zinc deficiency, take a zinc supplement of 50 mg per day.

Additional nutritional supplements:

• Take a variety of free-form amino acids (two 500 mg capsules) daily.
• Taurine (two capsules of 500 mg per day).
• Proteolytic enzymes on an empty stomach to eliminate inflammation.

Vegans may need to supplement with nutrients not normally found in sufficient amounts in their non-animal diet. They are recommended to take additional vitamin B12, vitamin D, L-carnitine, zinc and selenium.

• Reduce your calorie intake by about 30% and stop eating before you feel full, trying to eat nutrient-dense foods. (Indicated to improve both immune and thyroid function).
• “Eat breakfast like a king, lunch like a prince, and dinner like a pauper” to prevent your body from overloading with food at night, since eating too much in the evening can contribute to weight gain.

Autoimmune thyroiditis (AIT) is a chronic pathological disorder of the thyroid gland, which is caused by autoimmune reactions. The disease is characterized by damage to the follicular structures responsible for the formation of thyroid hormones as a result of an attack by T-lymphocytes due to an error in identifying the cells of one’s own body.

This disease is not rare, as it accounts for about a third of all thyroid disorders. Women are more prone to the disease; in men, such a disorder is diagnosed twenty times less often. The pathology develops mainly from 40 to 55 years, but in recent decades there has been a tendency towards the disease in younger people and children.

Autoimmune thyroiditis consists of several pathological conditions of similar genesis.

There are the following types of illness:

1. Chronic AIT, the older name for this disease is. The chronic form may also be called lymphomatous or lymphocytic thyroiditis. The essence of the pathology is the abnormal penetration of T-lymphocytes into the underlying glandular tissue. This pathological process causes an abnormally high concentration of antibodies in relation to parenchymal cells, which causes disruption of the organ and even its structure. In this case, the concentration of iodine-containing thyroid hormones in the blood decreases, and hypothyroidism forms. This type of disease is chronic, inherited through generations and can be one of many autoimmune processes in the body.
2. – the most studied form of the disease, since this pathology occurs much more often than other variants of AIT. The reason is the excessive reactivation of protective mechanisms after childbirth (during pregnancy, a woman’s immunity is suppressed, which has important biological significance for the fetus). If a woman in labor has a predisposition, then the likelihood of developing pathology is quite high.
3. Painless or silent AIT- this is similar to postpartum thyroiditis, but the pathology has no connection with bearing a child and the exact causes of its occurrence are currently unknown. It is characterized by the absence of pain syndrome.
4. Cytokine-induced thyroiditis– a pathology that occurs as a side effect of long-term use of interferon in people with blood diseases or hepatitis C.

Note. All of the above types of pathology, except for chronic thyroiditis, are distinguished by their similarity in the same sequence of pathological processes in the organ. The first stages are characterized by the development of destructive thyrotoxicosis, which is subsequently replaced by transient hypothyroidism.

Clinical forms of the disease

Autoimmune thyroiditis differs in symptomatic and morphological features, so it is usually divided into forms, listed in the table.

Table. Clinical forms of autoimmune thyroiditis:

Form of the disease	Description
	There is no clinical picture, but there are immunological symptoms. The thyroid gland is unchanged or slightly enlarged, but not more than grade 2. The parenchyma is homogeneous, without compactions, minor signs of thyroid or The secretion of hormones is not impaired.
	Goiter (enlargement of the thyroid gland) is observed. The symptoms are caused by mild manifestations of low or high secretion of thyroid hormones. Ultrasound shows diffuse enlargement of the entire organ or the presence of nodular formations, as well as both signs at the same time, which happens somewhat less frequently. This form is often characterized by normal synthetic activity or moderate hypersecretion, but as the disease progresses, synthesis decreases and abundant hormone production is replaced by hypothyroidism.
	The clinical picture corresponds to hypothyroidism, and the size of the organ remains normal or slightly decreases. This form of the disease is typical for older people, and in young patients this is possible only after exposure to significant doses of radiation.

Please note. In the most severe cases of the atrophic form of autoimmune thyroiditis, significant destruction of synthetic cells is observed, due to which a significant part of the thyroid gland is destroyed, while its functional activity drops to the lowest levels.

Stages of Hashimoto's disease:

	Stage 1 - hyperthyroidism	Stage 2 - euthyroidism	Stage 3 – irreversible hypothyroidism
Description	Characterized by a sharp increase in antibodies to thyrocytes, their massive destruction and the release of large amounts of thyroid hormones into the blood	Gradually, the concentration of hormones decreases to normal levels, and a period of imaginary well-being begins. Antibodies continue to destroy thyroid tissue	Due to the continuous destruction of thyroid cells, its activity gradually decreases, and the patient develops irreversible hypothyroidism. The extreme degree of development of the disease is the complete replacement of glandular cells of the thyroid gland with connective tissue.
Duration	The first 6 months from the onset of the disease	6-9 (up to 12) months from the onset of the disease	After 9-12 months from the onset of the disease and beyond
Characteristic symptoms	Irritability, insomnia Tachycardia, palpitations (“heart pounding”) Feeling of a lump in the throat Sore throat, coughing Various menstrual cycle disorders	At this stage of the disease, clinical symptoms are usually absent. The patient feels well, laboratory tests for thyroid hormones are within normal limits. Pathological changes in the organ can only be noticed with the help of ultrasound: its structure becomes heterogeneous, cysts appear in it, and then dense connective tissue nodes	Drowsiness, weakness, fatigue Lethargy, decreased mental and motor activity Disturbance of all types of metabolism: fat (increased cholesterol levels in the blood), protein (acceleration of tissue breakdown), carbohydrate (increased risk of developing diabetes) and water-salt Dense swelling, puffiness of the face, hands and feet Brittle nails, hair loss Poor tolerance to low temperatures, chilliness Bradycardia (decreased heart rate), arrhythmia Menstrual dysfunction, infertility, early menopause in women Thyroid enlargement

Rare forms of the disease

In addition to the forms listed above, immune thyroiditis has several rather rare forms:

1. Juvenile.
2. With the formation of nodes.

Now about each of them in more detail.

Juvenile form

Develops in childhood and, most often, adolescence.

Manifestations:

1. Specific changes detected during ultrasound.
2. AT-TPO is detected in the blood.

Juvenile autoimmune thyroiditis, which has a fairly favorable prognosis, most often heals spontaneously when the patient reaches the age of 18–20 years. But, in rare cases, it is still possible for the pathology to become chronic.

Why the disease develops is not completely clear to modern science. It is believed that it can be triggered by hormonal changes in the child’s body during its transition to puberty.

Thyroiditis with nodular formation

This form manifests itself by an increase in the titer of AT-TPO, as well as changes in the picture that ultrasound gives - here there is a continuous change in the configuration and size of the nodes, sometimes merging, sometimes dividing, sometimes increasing, sometimes decreasing. Confirmation of the diagnosis is made using a fine-needle aspiration biopsy, which will provide accurate information about the tissue of which the nodes are composed.

This type of AIT can not be treated, except in extreme cases when the size of the thyroid gland has grown so much that the gland has displaced or compressed other organs - the esophagus or trachea. This situation is an indication for surgical intervention.

Reasons

Hereditary condition alone will not be enough for the formation of the disease.

In order to provoke the development of autoimmune thyroiditis, exposure to the adverse factors listed below will be required:

• history of viral respiratory diseases;
• the presence of constant sources of infection and infectious foci, for example, diseased tonsils, caries, chronic rhinitis of a bacterial nature and other diseases;
• unfavorable environmental circumstances: increased background radiation, iodine deficiency, the presence of toxins, especially chlorine and fluorine compounds, which provoke excessive aggressiveness of T-lymphocytes;
• self-medication with hormonal and iodine preparations, or their long-term use;
• excessive passion for tanning, especially during hours of active infrared radiation;
• severe stressful situations.

Scientists have identified a connection between a person’s immune status and his emotional sphere.

It manifests itself as follows:

• Stressful situations and depression provoke the production of certain hormones;
• These biologically active substances lead the body to attack itself;
• The antibodies involved in this attack use the thyroid gland as a target.

As a result, autoimmune thyroiditis develops, the psychosomatics of which are initially expressed in frequent depressive states. That is why so often people suffering from this pathology are indifferent to what is happening in the world around them, often have a bad mood and low physical activity.

Interesting: Quite often it is a poor psychological, rather than physical, condition that prompts patients to seek medical help for this pathology.

Symptoms

As mentioned above, the initial stages (euthyroid and subclinical phases) do not have a clearly defined clinical picture. Very rarely during these periods, an increase in the organ in the form of a goiter is possible.

In this case, a person feels discomfort in the neck (pressure or lump), he quickly gets tired, the body weakens and mild joint pain may be observed. Most often, symptoms appear in the first few years, when the disease is just beginning to develop.

The signs are caused by ongoing processes that correspond to the indicated phases. As the tissue structure is destroyed, the disease lingers in the euthyroid phase, after which it progresses to persistent hypothyroidism.

Postpartum AIT manifests itself as mild thyrotoxicosis 4 months after birth. A woman usually becomes more tired and loses weight.

It is not often that the symptoms are more pronounced (sweating, tachycardia, feeling of fever, muscle tremors and other obvious signs). The hypothyroid phase begins at the end of the fifth month after the birth of the child; not often this can be associated with the development of a depressive postpartum state.

Please note. Painless thyroiditis manifests itself as barely noticeable, almost asymptomatic thyrotoxicosis.

Diagnostics

Diagnosing AIT before decreased hormone concentrations begin to appear is not so easy. To make a diagnosis, the endocrinologist takes into account the symptoms and test results obtained during the diagnosis. If relatives have this disease, then this fact confirms that the person has autoimmune thyroiditis.

Test results indicating the disease:

• leukocytosis in the blood;
• an immunogram shows the presence of antibodies to thyroid hormones;
• a biochemical blood test shows changes in the content of thyroid hormones and TSH;
• Ultrasound helps determine the echogenicity of the parenchyma, the size of the gland, the presence of nodules or compactions;
• a fine-needle biopsy will allow you to select thyroid tissue for histological analysis; with autoimmune thyroiditis, a pathologically large accumulation of lymphocytes is detected in the tissues of the organ.

An important feature of making a reliable diagnosis is the simultaneous presence of the following indicators:

• increased level of antibodies to the thyroid parenchyma (AT-TPO);
• hypoechogenicity of the tissue structure;
• the presence of signs characteristic of low hypothyroidism.

If any of the above three signs is absent, then we can only talk about the probable presence of the disease, since the first two signs cannot reliably indicate the presence of AIT.

As a rule, therapy is prescribed when the disease enters the hypothyroid phase. This determines the fact that before the onset of this phase there is no urgent need to determine the diagnosis and prescribe appropriate therapy.

Changes detected by ultrasound examination

In addition to objective and laboratory data, there are also echo signs of thyroiditis, which consist of a decrease in the echogenicity of the thyroid gland and the development of pronounced changes that are diffuse in nature.

The photo shows that the thyroid gland affected by autoimmune thyroiditis has a darker color than a healthy one, and its structure is very heterogeneous - its tissue is sometimes darker and sometimes lighter in different places.

Quite often, ultrasound diagnostic specialists, along with the heterogeneity of the organ structure, detect darker lesions. However, they are not always real nodes.

This is what foci of pronounced inflammation look like on ultrasound. Their name is “pseudo-nodes”. In order to clarify the nature of these compactions that appear in the thyroid tissue during autoimmune thyroiditis, if their size is 10 millimeters or more, a biopsy is performed.

Histological examination of the sample taken will help answer the question of its origin. Such structures can turn out to be “pseudonodules” against the background of AIT, and benign colloid nodules, and malignant neoplasms.

Histological features

When examining a sample of thyroid tissue, the following histological signs of thyroiditis can be detected:

1. Infiltration of immune elements into organ tissue(lymphocytes penetrate them, saturating their structure). The predominant elements in this process are plasma cells. Infiltration can be of varying degrees of saturation, and is also divided into diffuse (a widespread process) and focal (lymphomaplasmocytic elements are localized in certain places).
2. Growth of lymphoid follicles, in which there are breeding centers.
3. The appearance of large cells of oxyphilic light epithelial tissue, called Hurthle or Ashkinazi cells. They are formed due to the intensification of most processes occurring in the thyroid gland. Ashkinazi cells exhibit powerful metabolic activity. However, their origin and development are not associated with the processes of destruction, dystrophy or oncogenesis in the affected thyroid gland. They are designed to enhance the natural processes for which the thyroid tissue is responsible and which suffer under the influence of the pathological process.
4. Regenerative processes. In contrast to the lymphocytic infiltration that develops during autoimmune thyroiditis, the thyroid gland tries to recover and forms areas of healthy functional epithelial cells, which in some cases have a papillary appearance. These growths are benign. In general, autoimmune processes are characterized by manifestations of reparative regeneration, which has a clear tendency to increase the volume of interfollicular epithelial tissue.
5. Fibrosis of thyroid tissue, in which there is a thickening of the network of argyrophilic fibers prone to collagenization. The result of such processes may be the division of organ tissue into distinct lobular segments. Tissue fibrosis is more typical for diffuse autoimmune thyroiditis than for focal one.

Treatment

There is no specific treatment for autoimmune thyroiditis in medical practice today, so there is no way to stop the disease before the body begins to feel a lack of thyroid hormones. During the hour of the thyrotoxic phase, doctors do not recommend using drugs that stabilize excessive production of hormones (thiamazole, propylthiouracil or others), because in this case there is no hypersecretion, and the hormonal level temporarily increases due to the breakdown of follicles and the release of thyroid-stimulating hormones. If cardiac activity is impaired, the patient is prescribed beta-blockers

If the thyroid gland is underactive, a person will be forced to take hormonal medications (hormone replacement therapy). Glucocorticoids are indicated if a combination of AIT with subacute thyroiditis is diagnosed.

This condition often occurs during cold seasons. The use of non-hormonal anti-inflammatory drugs, for example, diclofenac and others, is also indicated. Medications that correct the activity of the immune system must be prescribed. In case of organ atrophy, surgical intervention will be required.

Depending on the course, type and severity of Hashimoto’s disease, treatment can be carried out in three directions:

1. Drug therapy with drugs of synthetic analogues of thyroid hormones (Eutirox, L-thyroxine). Replacement treatment helps fight progressive hypothyroidism, but the dose of the drug must be constantly increased.
2. Surgical removal of thyroid tissue is usually prescribed when the organ is almost completely destroyed. After surgical treatment, lifelong hormonal replacement therapy is also required.
3. Computer reflexology is one of the promising methods for treating Hashimoto’s disease. It is based on the effect of low-frequency direct current on biologically active points, which leads to stimulation of nervous, immune and endocrine processes in the tissues of the thyroid gland and restoration of the organ’s functioning. It is too early to say that an effective remedy has been found for the treatment of autoimmune thyroiditis, but the method gives positive results and is being successfully introduced into medical practice.

What are the restrictions?

Patients who suffer from AIT must adhere to certain restrictions so as not to provoke the development of another relapse.

Autoimmune thyroiditis - contraindications:

1. Many people mistakenly believe that if the thyroid gland is dysfunctional, iodine-containing medications are necessary. In fact, these medications can both help and harm, so in this case it is important not to self-medicate, even if we are talking about “healthy” vitamins or mineral complexes. For example, iodine in autoimmune thyroiditis increases the number of antibodies that destroy thyroid cells. Only a doctor, based on the results of T3 and T4 tests, has the right to prescribe iodine-containing drugs for the main treatment.
2. In cases of selenium deficiency, the conversion of T3 and T4 is disrupted, which leads to the development of hypothyroidism. In other words, this trace element synthesizes a hormone that creates energy in cells. When a disorder occurs, the thyroid gland improves its functioning by increasing its surface area (it grows, nodes or cysts appear on it). But the microelement is still missing! Thus, selenium plays an important role in autoimmune thyroiditis. However, it is not prescribed in all cases: if the patient has thyrotoxicosis, then this microelement is contraindicated.
3. Many patients are interested in whether it is possible to get vaccinated (for example, against influenza) if the thyroid gland is dysfunctional? Endocrinologists note that autoimmune thyroiditis and vaccinations are not compatible concepts. The fact is that AIT is a serious immune disorder, so vaccination can only aggravate the hormonal imbalance.

Forecast

In general, if adequate treatment is prescribed, the prognosis is relatively positive. If therapy is started during the first destructive transformations in the organ, then the negative processes slow down and the disease enters a period of prolonged remission.

Often, a satisfactory condition persists for 12-15 years or more, although exacerbations are not excluded during these periods. The presence of signs of AIT and corresponding antibodies in the blood are symptoms indicating the formation of hypothyroidism in the future.

If the disease occurs after childbirth, then the probability of developing AIT during a second pregnancy is 70%. Of all women in labor suffering from postpartum syndrome, one third develop a stable form of hypothyroidism.

Prevention

There is currently no specific prevention that would completely eliminate the development of the disease. It is extremely important to detect signs of a developing disease as early as possible and promptly begin the correct therapy to compensate for the insufficient production of thyroid hormones.

At risk are women with an increased immune response to thyroid cells (TPO AT test) who are planning to become pregnant. In such patients, strict monitoring of the functioning of the organ is necessary during pregnancy and after childbirth.

Questions

Hello doctor! I passed laboratory tests, the results of which showed that TSH for AIT was 8.48 µIU/ml (normal 0.27 – 4.2). The endocrinologist prescribed a decoction of walnut septa, outlined the course of treatment and scheduled the next consultation in 3 weeks. Is this qualified treatment for the disease? Or do I need to take medications? Maybe hormonal drugs?

Hello! Have you had an ultrasound examination? What changes have occurred in the thyroid gland since the last examination? Or was it primary?

It is difficult to give recommendations with such an insignificant description of symptoms. If your endocrinologist has on hand not only the results of laboratory tests, but also instrumental ones, then the treatment recommended to you is quite competent and must be followed.

Good evening! Tell me, when diagnosing AIT of the thyroid gland, how long do they live with it? My treating specialist did not give me an answer to this question. By the time I got home to contact you, I was exhausted. Thank you in advance for your answer.

Hello! Patients with autoimmune thyroiditis live quite a long time. The disease may not progress at all. If hypothyroidism develops, drug treatment is prescribed.

If the effectiveness of medication is low, a specialist may prescribe surgery, after which you will be prescribed hormone replacement therapy. Try not to focus too much on the disease, but at the same time follow all the recommendations of the specialist treating you. I wish you good luck with your treatment.