What is Diffuse (Endemic) Goiter?
Endemic goiter is an enlargement of the thyroid gland that develops as a result of iodine deficiency in people living in certain geographical areas with iodine deficiency in the environment (that is, in an area endemic for goiter).
The normal growth and development of a person depends on the proper functioning of the endocrine system, in particular on the activity of the thyroid gland. Chronic iodine deficiency leads to proliferation of gland tissue and a change in its functional capabilities.
Causes of Diffuse (Endemic) Goiter
The main reason for the development of endemic goiter is the insufficient intake of iodine in the body.
Iodine is a trace element necessary for the biosynthesis of thyroid hormones – thyroxine and triiodothyronine. Iodine enters the human body with food, water, air. 90% of the daily need for iodine is provided by food, 4-5% – water, about 4-5% – comes with air. Iodine is found in fish, meat, seaweed, shrimp and other products of the sea, milk and dairy products, water, including mineral, iodized table salt, buckwheat and oatmeal, beans, lettuce, beets, grapes, milk chocolate, eggs, potatoes.
When iodine is ingested in smaller quantities than the required daily requirement, a compensatory increase in the thyroid gland develops, i.e., goiter.
Distinguish between absolute iodine deficiency (i.e., deficiency of iodine intake with food and water) and relative iodine deficiency, caused not by iodine deficiency in the environment and food, but by diseases of the gastrointestinal tract and impaired iodine absorption in the intestine, some iodine blockade of the thyroid gland drugs (cordarone, potassium perchlorate, nitrates, lithium carbonate, sulfonamides, some antibiotics), a congenital defect in the thyroid hormone biosynthesis eze.
Factors predisposing to the development of endemic goiter:
- heredity burdened by goiter;
- genetic defects in the biosynthesis of thyroid hormones;
- water pollution by urochrome, nitrates, a high content of calcium, humic substances in it, which makes it difficult to absorb iodine;
- deficiency of microelements of zinc, manganese, selenium, molybdenum, cobalt, copper and excess calcium in the environment and food products. Copper deficiency reduces the activity of iodinase involved in the addition of iodine to the tyrosyl radical, and also reduces the activity of cytochrome oxidase, ceruloplasmin. Cobalt deficiency reduces thyroid iodine oxidase activity. An imbalance of trace elements contributes to the disruption of the biosynthesis of thyroid hormones;
- the use of drugs that block the transport of iodide into the cells of the thyroid gland (periodate, potassium perchlorate);
- the use of drugs that disrupt the organization of iodine in the thyroid gland (derivatives of thiourea, thiouracil, some sulfonamides, para-aminobenzoic acid, aminosalicylic acid);
- the presence of strumogenic factors in the products. Natural strumogens can be divided into two groups. One group includes thiocyanates and isocyanates, which are mainly found in plants of the Crucifera family (white cabbage, cauliflower, broccoli, Brussels sprouts, turnip, turnip, horseradish, lettuce, and rape). Thiocyanates and isocyanates block the capture of iodides by the thyroid gland and accelerate its release from the gland. Another group of strumogens is cyanogenic glycosides contained in cassava, corn, sweet potatoes, lima beans;
- the impact of infectious and inflammatory processes, especially chronic, helminthic infestations, poor sanitary and hygienic and social conditions. In these situations, the compensatory ability of the thyroid gland to maintain an optimal level of thyroid hormones in the blood decreases sharply.
Pathogenesis during Diffuse (Endemic) Goiter
1. Compensatory thyroid hyperplasia as a response to a low intake of iodine in the body and, therefore, a low intrathyroid concentration of iodine, insufficient for normal secretion of thyroid hormones. Often, an increase in the thyroid gland in volume does not provide an optimal level of thyroid hormones and hypothyroidism develops. In response to a decrease in the level of thyroid hormones in the blood, an increase in the secretion of thyrotropin is observed, which leads first to diffuse hyperplasia of the gland, and then to the development of nodular forms of goiter. By increasing the mass of tissue, the thyroid gland is trying to increase the synthesis of hormones in conditions of insufficient intake of iodine in the body. However, the concentration of iodine in the thyroid gland is reduced (normally the thyroid gland contains 500 μg of iodine per 1 g of tissue).
A reflection of adaptive mechanisms developing in conditions of goiter endemic is also an increase in the formation of T3 from T4.
With prolonged iodine deficiency, not only hyperplasia and hypertrophy of thyroid cells develop, but also their focal dystrophy, necrobiosis, and sclerosis. Hormonally inactive compounds (thyroalbumin, etc.) appear in the blood of patients, which helps to reduce the synthesis of thyroxin, increase the level of thyrotropin and further growth of the thyroid gland and the formation of nodes in it.
2. Of great importance in the development of goiter is also the insufficient synthesis of thyroglobulin in endemic areas, which leads to insufficient formation of thyroxine.
3. Autoimmune factors, according to modern concepts, play a large role in the development of endemic goiter. Patients with endemic goiter have violations of cellular and humoral immunity. Enzymatic defects in hormone synthesis are accompanied by the release of abnormal iodized proteins into the bloodstream, which contributes to the development of autoimmune processes, autoimmune aggression and degenerative processes in the thyroid gland. In response to the damaging effects of autoimmune processes, hyperplasia of the thyroid gland develops, which supports the state of euthyroidism. However, a long-existing autoimmune process in the thyroid gland leads to a gradual decrease in the functional activity of the gland – hypothyroidism.
It has been established that already in the initial stages of endemic goiter, there is latent or subclinical (“chemical”) hypothyroidism, which contributes to the further growth of goiter and the formation of nodular forms.
Symptoms of Diffuse (Endemic) Goiter
- The degree of enlargement of the thyroid gland.
0 – No goiter.
l – Lobes larger than the distal phalanx of the thumb. The goiter is palpable, but not visible.
II – Goiter is palpable and visible to the eye.
- The form of endemic goiter (morphological).
2.3. Mixed (diffuse-nodal).
- The functional state of the thyroid gland.
3.1. Euthyroid goiter.
- Localization of goiter:
4.1. Usually located.
4.2. Partially sternal.
4.4. Distilled goiter from embryonic bookmarks (goiter of the tongue root, additional lobe of the thyroid gland).
Symptoms of an endemic goiter are determined by the shape, size of the goiter, and the functional state of the thyroid gland. Even with an euthyroid state, patients can complain of general weakness, fatigue, headache, discomfort in the heart. Typically, these complaints appear with large degrees of enlargement of the gland and reflect functional disorders of the nervous and cardiovascular systems.
With an increase in goiter and compression of the adjacent organs, complaints appear about a feeling of pressure in the neck, more pronounced in the supine position, shortness of breath, sometimes swallowing, with compression of the trachea there may be asthma attacks, dry cough. The enlarged thyroid gland is moderately dense.
Distinguish diffuse, nodular and mixed forms of goiter.
Diffuse goiter is characterized by a uniform increase in the thyroid gland in the absence of local seals in it. Nodular goiter is characterized by a tumor-like growth of thyroid tissue in the form of a node, the remaining parts of the gland are usually not enlarged and are not felt. With mixed goiter, there is a combination of diffuse hyperplasia and a node.
In addition to the usual location of the goiter on the anterior surface of the neck, its atypical localization is found: sternal, annular (around the trachea), sublingual, lingual, tracheal, from the additional elements of the thyroid gland.
Depending on the functional state of the thyroid gland, euthyroid and hypothyroid goiter are distinguished. 70-80% of patients have an euthyroid state.
One of the most severe manifestations of hypothyroidism in endemic goiter is cretinism, the clinical symptoms of which begin in childhood. Characteristic signs of cretinism are pronounced hypothyroidism, marked lag in physical, mental, mental, intellectual development, short stature, tongue-tied, sometimes deaf-mute, delayed bone maturation.
Complications of an endemic goiter, as a rule, develop with large degrees of enlargement of the thyroid gland:
- compression of the esophagus, trachea, adjacent nerves and blood vessels;
- the development of “goiter heart” – that is, hyperfunction and expansion of the right heart due to mechanical obstruction of blood circulation due to compression of the adjacent vessels;
- hemorrhage into the thyroid parenchyma followed by calcification;
- strumitis (inflammation of the goiter of the thyroid gland, clinically similar to subacute thyroiditis);
- malignant degeneration of goiter altered thyroid gland (usually nodular forms).
Diagnosis of Diffuse (Endemic) Goiter
Laboratory and instrumental data
- General analysis of blood and urine without significant changes.
- The absorption of 131 I by the thyroid gland was increased after 24 hours (more than 50%), this is a consequence of iodine deficiency in the thyroid gland.
- Excretion of iodine with urine: indicators are reduced, as a rule, less than 50 mcg / day.
Normally, the median (geometric mean) urinary iodine content in adults and schoolchildren exceeds 100 mcg / L. It is advisable to use this indicator for assessing iodine deficiency in a population, and not in an individual patient being examined, since its indicators are very variable, vary from day to day, are influenced by many factors, in particular, a high-calorie diet increases urinary iodine excretion, and low-calorie – reduces.
- Determination of the content in the blood of T3, T4, thyrotropin. In clinically euthyroid patients, the content in the blood of T3 and T4 is within normal limits or there may be a slight increase in T3 with a tendency to decrease T4 level at a normal level of thyrotropin. This is a compensatory reaction of the thyroid gland – to maintain the euthyroid state, the conversion of less active T4 to more active T3 increases. In subhypothyroid patients, the T4 level in the blood decreases or is located at the lower limit of the norm, and the T3 level is at the upper limit of the norm, the thyrotropin content is either increased or close to the upper limit of the norm. With the development of hypothyroidism, the content in the blood of T3, T4 is reduced, and the level of thyrotropin is increased.
- Determination of thyroglobulin in the blood. The concentration of thyroglobulin in the blood in all age groups varies inversely with the intake of iodine, especially in newborns. The less iodine enters the body, that is, the greater the iodine deficiency, the higher the content of thyroglobulin in the blood.
- Ultrasound of the thyroid gland. With a diffuse form, a diffuse enlargement of the thyroid gland of various degrees is detected, it is possible to detect areas of fibrosis.Thyroid tissue is often heterogeneous, often its echogenicity is reduced. Nodal forms of endemic goiter have the following features:
– in most cases, the nodes are multiple, much less often – single;
– nodes are visualized as formations of a round, oval or irregular shape;
– the contours of the nodes can be either clear, with a well-defined capsule in the form of a thin rim of increased echogenicity, and fuzzy;
– echogenicity of nodes is more often than average intensity, however, it is both increased and decreased;
– often in the nodes are determined echo-negative zones (accumulation of colloid or hemorrhage in the node);
– possible detection in nodes of hyperechoic inclusions with an acoustic shadow – calcifications;
– multinodular goiter can be combined with adenomas (the frequency of adenomas in multinodular goiters is about 24%) and carcinomas (according to published data, from 1-6 to 17%). Adenomas are oval or rounded, the contours are clear, echogenicity is lowered, medium or high. Adenomas of medium and increased echogenicity have a hypoechoic rim (“halo sign”). In the adenoma, lesions with fluid and calcifications can be determined.
Malignant nodes have the following characteristics:
– fuzzy contours;
– solid structure;
– increased echogenicity;
– the presence of microcalcifications (in 37-40% of thyroid carcinomas);
– an increase in regional lymph nodes.
The upper limits of the normal thyroid volume in adults:
– men – 25 ml (cm3);
– women – 18 ml (cm3).
- Radioisotope scanning of the thyroid gland reveals a uniform distribution of the isotope and a diffuse increase in the size of the gland of various degrees (with diffuse shape) or the presence of “cold” or “warm” nodes in the nodular form. With the development of hypothyroidism, the accumulation of the isotope by the gland is sharply reduced.
- Puncture biopsy of the thyroid gland under the control of ultrasound reveals the following characteristic changes in punctate:
– with colloid goiter – a large number of homogeneous masses of the colloid, thyroid epithelial cells are few;
– with parenchymal goiter – lack of colloid, a lot of thyroid epithelial cells (cubic, flattened), a significant admixture of blood due to abundant vascularization of the gland;
– with nodular goiter (it is most often colloidal) – the presence of a colloid, the hemorrhagic nature of punctate with an admixture of fresh or altered red blood cells, macrophages, dystrophic changes in thyroid cells, lymphoid elements is possible.
Screening program for endemic goiter:
– General analysis of blood and urine.
– Ultrasound of the thyroid gland.
– Determination of the content in the blood of T3, T4, thyroglobulin, thyrotropin.
– Determination of daily urinary excretion of iodine.
– X-ray of the esophagus with large sizes of goiter (detection of compression of the esophagus).
– Immunogram: the content of B- and T-lymphocytes, subpopulations of T-lymphocytes, immunoglobulins, antibodies to thyroglobulin and the microsomal fraction of the follicular epithelium.
– Thyroid biopsy under ultrasound guidance.
Treatment of Diffuse (Endemic) Goiter
The tactics of treatment of endemic goiter largely depends on the degree of enlargement of the thyroid gland and the state of gland function. With a small increase in the size of the gland (goiter of the first degree), they are usually limited to the appointment of potassium iodide, a necessarily intermittent course, of products rich in iodine.
If there is a decrease in thyroid function, synthetic analogues of thyroid hormones or combination drugs (thyrotome, levothyroxine) are prescribed, under the control of the content of thyroid hormones in the blood. If the form of the goiter is nodular, the nodes are large or rapidly growing, leading to compression of the surrounding organs, surgical treatment of the goiter is performed. After the operation, thyroid hormones are prescribed to prevent the re-development of goiter.
Prevention of Diffuse (Endemic) Goiter
Prevention of endemic goiter is massive and individual.
Mass prophylaxis of goiter is the addition of potassium iodate to sodium chloride – iodization. 20-40 g of potassium iodate are added per ton of sodium chloride. Such table salt should not be stored for more than the period indicated on the package, since iodine salts are destroyed, the same happens when the salt is stored in a humid atmosphere. It is necessary to salt food after cooking. When heated, iodine evaporates.
Individual prophylaxis is prescribed to patients who underwent thyroid surgery, temporarily living in the region endemic for goiter, working with strumogenic substances. At the same time, iodine rich foods are recommended: seaweed, sea fish and seafood, walnuts, persimmons.